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  • 1
    Electronic Resource
    Electronic Resource
    Shadow price principles applied to regulated pricing of natural gas (1984)
    Springer
    Annals of operations research 2 (1984), S. 285-316 
    Details
    ISSN: 1572-9338
    Keywords: Regulation ; shadow price ; economics ; markets ; natural gas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics , Economics
    Notes: Abstract Inclusion of the shadow prices for natural gas in a dynamic fuels model for the United States shows that the primary reason for the relatively large, fly-up in new marginal gas prices in the early 1980's was the release of the pent-up price effects of the U.S. government's price regulations. In accordance with principles, the shadow price of natural gas fell siginificantly following de-regulation of the highcost gas (section 107) in 1980, which represented the precursor for downward adjustments in marginal wellhead prices of new high-cost gas and drilling activity. The modeling results show that no significant fly-up in new marginal gas prices for lower-cost gas (section 102) is likely to occur in 1985, when its phased de-regulation ends and it is finally de-regulated, because no shadow price precursor currently exists for this gas. Shadow price principles clear up the primary misconceptions with regard to natural gas pricing. This application indicates the significance of shadow price principles for regulated pricing in general.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01874745
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  • 2
    Electronic Resource
    Electronic Resource
    Food and water consumption during the reproductive cycle of female German cockroaches (1983)
    Springer
    Entomologia experimentalis et applicata 34 (1983), S. 51-57 
    Details
    ISSN: 1570-7458
    Keywords: Blattella ; German cockroach ; Females ; Reproductive cycle ; Food intake ; Water intake ; Regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Description / Table of Contents: Résumé L'examen de la consommation d'eau et d'aliments par les femelles adultes de Blattella germanica a été lié au cycle reproductif. La consommation individuelle quotidienne des insectes a été reliée à certains évènements marquants dans chacun de quatre cycles de production d'oothèque. Les pics d'alimentation et d'absorption se produisaient pendant la période de maturation des oeufs, mais disparaissaient brutalement à l'apparition de chaque oothèque. Pendant la période où les femelles portent les oothèques, elles s'alimentent et s'abreuvent parcimonieusement. Le rôle éventuel joué par l'alimentation et particulièrement l'absorption dans la régulation de la reproduction de cet important insecte nuisible est examiné.
    Notes: Summary Food and water consumption by adult female German cockroaches has been examined in relation to the reproductive cycle. Daily consumption was recorded for individual insects and was related to certain landmark events in each of four egg-case production cycles. It was shown that peaks of feeding and drinking occur during the egg maturation period, but are abruptly terminated at the appearance of each egg case. During the period when females carry the egg case, they feed and drink sparingly. The possible role played by feeding and especially drinking in the regulation of reproduction in this important pest species is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00300899
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of penitrem A on rat's performances in passive avoidance and Morris water maze tests (1997)
    Springer
    Mycopathologia 138 (1997), S. 99-104 
    Details
    ISSN: 1573-0832
    Keywords: Learning ; Memory ; Morris water maze ; Passive avoidance ; Penitrem A ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Intraperitoneal administration of the mycotoxin penitrem A 30 min before a training session in passive avoidance task, impaired performance of rats subjected to a test-session 24 h after. This effect was not antagonised by pretraining administration of physostigmine or bicuculline. Administration of penitrem A 20 min before a training session or 30 min before a test-session did not impair performance. In the Morris water maze, doses of penitrem A that induces slight to moderate tremors, but not a lower dose, disrupted place learning. These results suggest that penitrem A disrupts the processes that take place at the time of acquisition, but not those just after acquisition, and does not alter the restitution of information. This effect would not be related to a decrease of cholinergic neurotransmission nor to a stimulation of GABA A receptors. Nevertheless, it could not be totally excluded that the performance impairments induced by penitrem A would be secondary to a motor disruption.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006853600205
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  • 4
    Electronic Resource
    Electronic Resource
    Intercalary regeneration and level interactions in the fresh-water planarianDugesia lugubris (1984)
    Springer
    Development genes and evolution 193 (1984), S. 149-157 
    Details
    ISSN: 1432-041X
    Keywords: Intercalary regeneration ; Regulation ; Morphallaxis ; Planarians
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary In the planarianDugesia lugubris, when two originally widely separated body levels are joined together, intercalary regeneration is induced. The whole sequence of levels normally intervening between the two levels joined are reformed by one of the two associated pieces. Generally regeneration is accomplished by morphallactic remodelling. This process starts at the margin of the suture, which was originally nearer to the head, and progressively extends through the piece, which is entirely remodelled if it is too short. Thus, a head cut at the level of the eyes and joined to a tail is totally reshaped, forming a new head with a new pair of eyes and a new prepharyngeal zone in which the original eyes persist. When the head piece is too short, the pharynx is not produced by the regenerate, but secondarily through remodelling of the tail piece. Remodelling of the head piece is also observed when it is joined to a prepharyngeal piece. When a head piece is joined in reverse orientation to a tail piece, the remodelling, which is directed by the tail, leads to the reversal of polarity in the head tissues. When the head piece is entirely remodelled it forms an anterior extremity, a new head with new eyes and a prepharyngeal zone containing the original eyes. After joining the preocular level to a prepharyngeal level the intercalary regenerate is entirely built up by dedifferentiated cells (epimorphosis), which are produced by the prepharyngeal tissues (the margin which represents the more posterior level). The results do not support Child's concept of dominance and are interpreted in the light of the concept of cell sociology.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00848890
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  • 5
    Electronic Resource
    Electronic Resource
    Regulation and the modification of axial properties in partial embryos of the nemertean, Cerebratulus lacteus (1997)
    Springer
    Development genes and evolution 207 (1997), S. 42-50 
    Details
    ISSN: 1432-041X
    Keywords: Key words Cell lineage ; Dorsoventral axis ; Nemertea ; Regulation ; Spiralians
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  Embryos acquire axial properties (e.g., the animal-vegetal, dorsoventral and bilateral axes) at various times over the course of their normal developmental programs. In the spiral-cleaving nemertean, Cerebratulus lacteus, lineage tracing studies have shown that the dorsoventral axis is set up prior to the first cleavage division; however, blastomeres isolated at the two-cell stage will regulate to form apparently perfect, miniature pilidium larvae. We have examined the nature of axial specification in this organism by determining whether partial embryos retain the original embryonic/larval axial properties of the intact embryo, or whether new axial relationships are generated as a consequence of the regulatory process. Single blastomeres in two-cell stage embryos were injected with lineage tracer, and were then bisected along the second cleavage plane at the four-cell stage. Thus, the relationship between the plane of the first cleavage division and various developmental axes could be followed throughout development in the ”half-embryos”. While some embryo fragments appear to retain their original animal-vegetal and dorsoventral axes, many fragments generate novel axial properties. These results indicate that axial properties set up and used during normal development in C. lacteus can be completely reorganized during the course of regulation. While certain embryonic axes, such as the animal-vegetal and dorsoventral axes, appear to be set up prior to first cleavage, these axes and associated cell fates are not irreversibly fixed until later stages of development in normal intact embryos. In C. lacteus, the process whereby these properties are ultimately determined is apparently controlled by complex sets of cell-cell interactions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004270050090
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  • 6
    Electronic Resource
    Electronic Resource
    Ferricyanide reductase of rose plasma membranes is regulated by nitrogen supply (1996)
    Springer
    Plant cell reports 15 (1996), S. 833-835 
    Details
    ISSN: 1432-203X
    Keywords: Ferricyanide reduction ; Nitrogen ; Regulation ; Rosa damascena ; Suspension culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The ability of suspension-cultured rose (Rosa damascena Mill. cv Gloire de Guilan) cells to reduce ferricyanide is decreased by 50% during an overnight incubation in a low-nutrient (1 mM CaCl2, 0.1 mM KCl) solution. This loss is not observed when nitrate and/or glutamate is added to the low-nutrient medium, but it occurs in medium containing all the components needed for normal growth except nitrate plus glutamate. Thus, the cells possess both constitutive and inducible enzymes for the reduction of ferricyanide, and nitrate or glutamate is both necessary and sufficient to stimulate the production of the inducible enzyme.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233150
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  • 7
    Electronic Resource
    Electronic Resource
    Sink-cell-specific activity of a potato ADP-glucose pyrophosphorylase B-subunit promoter in transgenic potato and tomato plants (1997)
    Springer
    Planta 203 (1997), S. 133-139 
    Details
    ISSN: 1432-2048
    Keywords: Key words: ADP-glucose pyrophosphorylase B (small) subunit ; Transcription ; Regulation ; Solanum ; Lycopersicon ; Sucrose induction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract. The 5′-flanking region of a B (small) subunit gene of ADP-glucose pyrophosphorylase (EC 2.2.7.27) – called the agpB1 promoter – was cloned from the potato cultivar Désirée and its activity studied in transgenic potato (Solanumtuberosum L.) and tomato (Lycopersiconesculentum Mill.) plants using the gusA reporter gene. In potato, high β-glucuronidase (GUS) activity was found in the storage tissues of developing tubers, but gusA expression was also detected in phloem-associated parenchymas in stolons, stems and petioles, as well as in the starch sheath adjacent to the vascular tissues in leaf veins, stems and petioles. In leaves, promoter activity was limited to stomatal guard cells and to the starch sheath of the major veins, with no detectable activity in the mesophyll. No expression was observed in roots. β-Glucuronidase activity was finally detected in pollen grains and in ovary placental tissues. The potato promoter::gusA construct was introduced in transgenic tomatoes and was shown to be highly regulated during fruit development, with a tight parallelism between GUS activity, the extractable ADP-glucose pyrophosphorylase activity and fruit starch content. In conclusion, the agpB1 promoter appears to be specific to sink tissues, contrasting with the sAGP gene recently described by P.A. Nakata and T.W. Okita (1996 Mol Gen Genet 250: 581–592) which is transcribed in both sink and source tissues. Furthermore, and in contrast to sAGP, agpB1 transcription is stimulated by sucrose.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004250050174
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  • 8
    Electronic Resource
    Electronic Resource
    Regulation of two alcohol dehydrogenases in Aspergillus nidulans (1984)
    Springer
    Current genetics 8 (1984), S. 253-259 
    Details
    ISSN: 1432-0983
    Keywords: Regulation ; Alcohol dehydrogenases ; Aspergillus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary In Aspergillus nidulans there are two alcohol dehydrogenases. In the presence of ethanol, alcohol dehydrogenase I (AHH I) is induced and alcohol dehydrogenase II (ADH II) is repressed. ADH I and ADH II have molecular weights of 39,000 and 36,000 respectively. At least ADH I is under the control of alcR, a transacting regulatory gene that is adjacent to alcA (the structural gene for ADH I, Pateman et al. 1983). Mutations in the alcR regulatory gene result in non inducibility of ADH I specific mRNA. Extreme alcA and alcR mutations result in derepressed levels of ADH II, and it is not clear whether alcR controls ADH II directly or through its control of ADH I synthesis. Both enzymes are subject to carbon catabolite repression. Induction of ADH I and ADH II operates at the level of synthesis or processing of mRNA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00419721
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  • 9
    Electronic Resource
    Electronic Resource
    Cloning and characterization of a Neurospora crassa ribosomal protein gene, crps-7 (1997)
    Springer
    Current genetics 31 (1997), S. 139-143 
    Details
    ISSN: 1432-0983
    Keywords: Key words Ribosomal protein ; Fungus ; Neurospora crassa ; Regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract A Neurospora crassa ribosomal protein gene, crps-7, was isolated from a genomic DNA library closely linked to the morphological gene ro-2. Sequence analysis and a computerized database search revealed a high degree of homology to the Xenopus laevis rps8 and rat rps7 gene, as well as to uncharacterized ORFs from two yeast species. Comparison with a nearly full-length cDNA clone revealed two introns, one of which is in a conserved position shared with the Xenopus gene. Although a number of sequence motifs common to other N. crassa ribosomal protein genes are present upstream of the crps-7 gene, mRNA abundance is not tightly regulated by carbon availability. Relative transcript levels during nitrogen limitation and thermal stress were also examined.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050188
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  • 10
    Electronic Resource
    Electronic Resource
    Expression of the arylsulphatase reporter gene under the control of the nit1 promoter in Chlamydomonas reinhardtii (1997)
    Springer
    Current genetics 31 (1997), S. 264-271 
    Details
    ISSN: 1432-0983
    Keywords: Key words Nitrate reductase ; Regulation ; Arylsulphatase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In Chlamydomonas reinhardtii, the expression of the nit1 gene encoding nitrate reductase is dependent on the nature of the nitrogen source and on other environmental factors. We have fused the nit1 promoter region to the arylsulphatase (ars) reporter gene lacking its own promoter and introduced this chimeric construction (nit1/ars) into a wall-less strain of C. reinhardtii. A new and sensitive method, based on the use of α-naphthylsulphate as a substrate and a diazonium salt as a chromogenic post-coupling agent, was developed to detect the activity of arylsulphatase (an enzyme which is almost completely secreted in the culture medium) both in vitro and in agar plates. The transformants carrying nit1/ars did not express arylsulphatase when grown in ammonium-sufficient medium but readily accumulated the enzyme in ammonium-free medium either supplemented, or not supplemented, with nitrate or nitrite. The nit1/ars construct, however, was not expressed in the nit2 mutant lacking a specific transcription regulator controlling the expression of nit1. These results, together with the observation that the transcription of nit1/ars is initiated at the same sites as the nit1 endogenous gene, confirms the hypothesis that the regulation of nit1 expression takes place mainly at the transcriptional level. The expression of the ars gene from the nit1 promoter was high enough to allow direct measurements of arylsulphatase activities in pools of transformants without prior isolation of nit1/ars clones. This original procedure has permitted the analysis of the effects of nested deletions in the nit1 promoter region on the expression of the reporter gene. The results indicate that the –282 to –198 sequence is required for transcription to occur and that the –751 to –282 region contains several elements mediating nit1 expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050204
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  • 11
    Electronic Resource
    Electronic Resource
    Trans-nuclear action of the nit-2 regulatory gene product and study of two additional nitrogen control genes in Neurospora crassa (1983)
    Springer
    Current genetics 7 (1983), S. 51-56 
    Details
    ISSN: 1432-0983
    Keywords: Neurospora crassa ; Nitrogen metabolism ; Regulation ; Heterokaryons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The nit-2 gene of Neurospora crassa is a major regulatory gene for control of nitrogen metabolism. Synthesis of the enzyme L-amino acid oxidase requires a functional nit-2 gene product and is also controlled by amino acid induction and nitrogen catabolite repression. Electrophoretic variants of L-amino acid oxidase have been employed to demonstrate that in heterokaryons, a nit-2 + gene product can turn on the expression of this enzyme in its own nucleus and also in nuclei that possess a nit-2 mutant. This trans-nuclear effect is only partial since the variant coded for in the nucleus containing the nit-2 mutant allele is always present in lower amounts than the alternative form. Two additional putative nitrogen control genes, MS5 and en(am)1, have been found to have clear effects upon the expression of L-amino acid oxidase. The en(am)1 mutant appears to result in an unusual case of reversal of the control present in wild-type: the enzyme is expressed in a constitutive fashion and inducers, required for enzyme synthesis in wild-type, actually reduce the level of L-amino acid oxidase in en(am)1. The MS5 mutant shows a substantial release from the usual nitrogen catabolite repression exerted by glutamine in wild-type.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00365680
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  • 12
    Electronic Resource
    Electronic Resource
    ALG/alg: a single gene controlling the utilization of lactate in the presence of antimycin in the yeast Saccharomyces cerevisiae (1984)
    Springer
    Current genetics 8 (1984), S. 407-411 
    Details
    ISSN: 1432-0983
    Keywords: Regulation ; Lactate utilization ; Mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary A strain dependent growth on lactate in the presence of antimycin A (AA) has been observed — the strain D261 can grow on lactate and AA, whereas in the strain K8/6C antimycin A prevents the utilization of lactate and the induction of LDH. Genetic analysis demonstrates that growth on lactate in the presence of AA segregates from D261 as a single nuclear factor which we indicate by ALG1 and alg1 in its dominant and recessive states. alg1 complements the gene(s) which give(s) rise to the same phenotype in K8/6C. The analysis of the regulation by lactate of LDH in the absence and presence of AA and in rho − cells shows that growth on lactate and antimycin A is not corretated with the induction by lactate of LDH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00433906
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  • 13
    Electronic Resource
    Electronic Resource
    Ammonia and light effect on nitrogenase activity in nitrogen-limited continuous cultures of Rhodopseudomonas capsulata. Role of glutamine synthetase (1984)
    Springer
    Archives of microbiology 139 (1984), S. 326-331 
    Details
    ISSN: 1432-072X
    Keywords: Rhodopseudomonas capsulata ; Continuous cultures ; Nitrogenase ; Glutamine synthetase ; H2 production ; Regulation ; Light ; Ammonia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Nitrogen-limited continuous cultures of Rhodopseudomonas capsulata were used to investigate some aspects of the regulation of nitrogenase activity. The role of glutamine synthetase (GS) in this regulation was examined by measuring changes of its adenylylation state when the light intensity and the nitrogen source were varied. Maximal nitrogenase activity was observed at a dilution rate corresponding to about one third of the maximum specific growth rate (μmax), both in ammonia- and in glutamate-limited cultures. At higher dilution rates, both GS and nitrogenase were inactivated by ammonia. Determination of the kinetics of inhibition of both enzymes indicated that the degree of inactivation of nitrogenase and the adenylylation state of GS were not closely related. Increase of light intensity stimulated nitrogenase activity dramatically. Conversely, a shift-down in light intensity to a limiting value resulted in a decrease of nitrogenase activity suggesting that synthesis was inhibited. On the other hand, the adenylylation state of glutamine synthetase appeared to be unaffected by changes in light intensity, indicating that GS is probably not involved in the regulation of nitrogenase expression by light.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00408374
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  • 14
    Electronic Resource
    Electronic Resource
    Contrasting modes of photosynthetic enzyme regulation in oxygenic and anoxygenic prokaryotes (1984)
    Springer
    Archives of microbiology 139 (1984), S. 124-129 
    Details
    ISSN: 1432-072X
    Keywords: Photosynthesis ; Regulation ; Thioredoxin ; Cyanobacterium ; Chromatium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Enzymes that are regulated by the ferredoxin/thioredoxin system in chloroplasts — fructose-1,6-bisphosphatase (FBPase), sedoheptulose-1,7-bisphosphatase purified from two different types of photosynthetic prokaryotes (cyanobacteria, purple sulfur bacteria) and tested for a response to thioredoxins. Each of the enzymes from the cyanobacterium Nostoc muscorum, an oxygenic organism known to contain the ferredoxin/thioredoxin system, was activated by thioredoxins that had been reduced either chemically by dithiothreitol or photochemically by reduced ferredoxin and ferredoxin-thioredoxin reductase. Like their chloroplast counterparts, N. muscorum FBPase and SBPase were activated preferentially by reduced thioredoxin f. SBPase was also partially activated by thioredoxin m. PRK, which was present in two regulatory forms in N. muscorum, was activated similarly by thioredoxins f and m. Despite sharing the capacity for regulation by thioredoxins, the cyanobacterial FBPase and SBPase target enzymes differed antigenically from their chloroplast counterparts. The corresponding enzymes from Chromatium vinosum, an anoxygenic photosynthetic purple bacterium found recently to contain the NADP/thioredoxin sytem, differed from both those of cyanobacteria and chloroplasts in showing no response to reduced thioredoxin. Instead, C. vinosum FBPase, SBPase, and PRK activities were regulated by a metabolite effector, 5′-AMP. The evidence is in accord with the conclusion that thioredoxins function in regulating the reductive pentose phosphate cycle in oxygenic prokaryotes (cyanobacteria) that contain the ferredoxin/thioredoxin system, but not in anoxygenic prokaryotes (photosynthetic purple bacteria) that contain the NADP/thioredoxin system. In organisms of the latter type, enzyme effectors seem to play a dominant role in regulating photosynthetic carbon dioxide assimilation.
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    URL: http://dx.doi.org/10.1007/BF00401986
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  • 15
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    Regulatory O2 tensions for the synthesis of fermentation products in Escherichia coli and relation to aerobic respiration (1997)
    Springer
    Archives of microbiology 168 (1997), S. 290-296 
    Details
    ISSN: 1432-072X
    Keywords: Key wordsEscherichia coli ; (Mixed acid) fermentation ; Facultative anaerobic metabolism ; O2 ; Aerobic ; respiration ; Regulation ; FNR ; ArcA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In an oxystat, the synthesis of the fermentation products formate, acetate, ethanol, lactate, and succinate of Escherichia coli was studied as a function of the O2 tension (pO2) in the medium. The pO2 values that gave rise to half-maximal synthesis of the products (pO0.5) were 0.2–0.4 mbar for ethanol, acetate, and succinate, and 1 mbar for formate. The pO0.5 for the expression of the adhE gene encoding alcohol dehydrogenase was approximately 0.8 mbar. Thus, the pO2 for the onset of fermentation was distinctly lower than that for anaerobic respiration (pO0.5≤ 5 mbar), which was determined earlier. An essential role for quinol oxidase bd in microaerobic growth was demonstrated. A mutant deficient for quinol oxidase bd produced lactate as a fermentation product during growth at microoxic conditions (approximately 10 mbar O2), in contrast to the wild-type or a quinol-oxidase-bo-deficient strain. In the presence of nitrate, the amount of lactate was largely decreased. Therefore, under microoxic conditions, the pO2 appears to be too high for (mixed acid) fermentation to function and too low for aerobic respiration by quinol oxidase bo.
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    URL: http://dx.doi.org/10.1007/s002030050501
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  • 16
    Electronic Resource
    Electronic Resource
    The molecular regulation of the reductive pentose phosphate pathway in Proteobacteria and Cyanobacteria (1996)
    Springer
    Archives of microbiology 166 (1996), S. 141-150 
    Details
    ISSN: 1432-072X
    Keywords: Key words CBB pathway ; CO2 fixation ; Transcription ; Regulation ; Proteobacteria ; Cyanobacteria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In phototrophic and chemoautotrophic proteobacteria, genes encoding enzymes of the Calvin-Benson-Bassham pathway of CO2 fixation are often found in clusters that are transcribed from a single promoter under control of the LysR-type transcriptional activator, CbbR. Mutations affecting CbbR prevent induction of cbb genes. Gel-retardation assays have demonstrated CbbR binding to putative regulatory regions of cbb operons, and in two cases, footprinting experiments have delimited the nucleotide sequence protected by CbbR. Fusion of cbb control sequences to reporter genes has allowed the regions required for promoter activity to be defined, and recent experiments indicate that the cbb regulon in Rhodobacter is controlled by a global two-component signal transduction system that also regulates other metabolic processes in this organism. Different ways of regulating CBB cycle enzymes that also have roles in heterotrophic metabolism have recently been discovered. In cyanobacteria, the genes of the CBB pathway are organized and regulated differently, and these oxygen-evolving phototrophic bacteria have evolved different strategies to control the assimilation of CO2.
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    URL: http://dx.doi.org/10.1007/s002030050369
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  • 17
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    Electronic Resource
    Regulation of phosphate uptake kinetics inOscillatoria agardhii (1984)
    Springer
    Archives of microbiology 139 (1984), S. 28-32 
    Details
    ISSN: 1432-072X
    Keywords: Cyanobacterium ; Phosphate ; Uptake ; Kinetics ; Regulation ; Pulse ; Steady state
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In order to study phosphate uptake kinetics the cyanobacteriumOscillatoria agardhii was grown in continuous culture under a phosphorus limitation. The affinity of the uptake system reflected in the initial slope of the uptake rate versus external substrate concentration curve (dV/ds) was found to be unaffected by the growth wate. The maximum phosphate uptake rate (V m ) decreased as the growth rate was increased. Attempts were made to relate the decrease ofV m to the increase in phosphorus content of the cells that occurred a higher growth rates. Accumulation of phosphate during pulse experiments indeed resulted in a decrease ofV m . However feedback regulation ofV m by accumulated phosphorus was found to occur only to a small extent in steady state growing cells. The main part of the regulation of the activity of the phosphate uptake system seemingly is determined by a long term process that is, at least longer than 2 h. The presence of short term feedback inhibition by accumulated phosphorus on the activity of the uptake system provides an explanation of the phenomenon thatOscillatoria agardhii is not able to grow at nearμ max growth rates under a phosphorus limitation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00692707
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  • 18
    Electronic Resource
    Electronic Resource
    Cyclophosphamide-induced changes in rodent odontogenesis (1983)
    Springer
    Cell & tissue research 234 (1983), S. 679-689 
    Details
    ISSN: 1432-0878
    Keywords: Odontogenesis ; Rats ; Cyclophosphamide ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Cyclophosphamide-induced changes in rodent odontogenesis were investigated by light and electron microscopy in four-day-old Sprague Dawley rats given one injection of 40 mg/kg of body weight of cyclophosphamide and killed at intervals of one hour, one day, one week and two weeks. Incisor and molar teeth were dissected from the animals, fixed in 2.0% glutaraldehyde in 0.1 M sodium cacodylate with 3.4% sucrose, and subsequently some were incubated for alkaline phosphatase reaction, and embedded in Spurr's medium for sectioning at light- and electron-microscopic levels. From three days a cell-sparse zone was created in the pulp in the growing end of the tooth and progressive cellular changes were observed which became more severe in the one-week and two-week specimens. Subodontoblast and adjacent pulpal cells were the most affected showing nuclear changes, damage to, or loss of, organelles, and inclusion bodies. Odontogenic epithelium was less affected and odontoblasts appeared to be unaffected by the drug. A new irregular matrix was laid down in the defect area and seemed to be the product of depolarized odontoblasts. This new matrix showed alkaline phosphatase activity, as did the cells embedded in it, and later it became mineralized. It is speculated that the polarity of odontoblasts might be maintained by an intact subodontoblastic layer; when this is lost the odontoblasts become depolarized and capable of secreting matrix from both ends.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00218659
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  • 19
    Electronic Resource
    Electronic Resource
    Localization and diurnal expression of mRNA encoding the β1-adrenoceptor in the rat pineal gland: an in situ hybridization study (1997)
    Springer
    Cell & tissue research 288 (1997), S. 279-284 
    Details
    ISSN: 1432-0878
    Keywords: Key words: Adrenoceptors ; Diurnal rhythms ; Regulation ; In situ hybridization ; Pineal gland ; Rat (Wistar)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. The rat pinealocyte is stimulated by norepinephrine, which is released from sympathetic nerve fibers innervating the gland. Norepinephrine binds to β1-adrenoceptors situated on the pinealocyte cell membrane. Ligand binding to these receptors exhibits a diurnal rhythm, with the largest number occurring in the late part of the light phase when the release of norepinephrine is minimal. By using in situ hybridization with a cDNA antisense oligonucleotide probe recognizing mRNA encoding the rat β1-adrenoceptor, we have demonstrated a stronger hybridization signal in the rat pineal gland than in other brain regions. Cells containing β1-mRNA are located in the superficial pineal gland, the deep pineal gland, and the pineal stalk. However, the number of receptors varies considerably between the individual pinealocytes. The β1-mRNA in situ hybridization signal for mRNA encoding the β1-adrenoceptor of the rat pineal has been quantified over a 24-h period; the strongest signal is found at mid-dark and the weakest signal at mid-light, indicating that the transcriptional regulation of β1-mRNA synthesis in the rat pineal is diurnal. In addition, maximal receptor protein expression occurs late in the light phase in the rat pineal and is thus considerably delayed compared with its peak mRNA synthesis. This lag time indicates that the β1-receptor is regulated at the translational or post-translational level. Removal of the sympathetic input to the pineal gland by superior cervical ganglionectomy decreases the β1-mRNA signal in the gland.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004410050813
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  • 20
    Electronic Resource
    Electronic Resource
    Differential expression of genes in thevir regulon ofStreptococcus pyogenes is controlled by transcription termination (1996)
    Springer
    Molecular genetics and genomics 250 (1996), S. 207-213 
    Details
    ISSN: 1617-4623
    Keywords: Regulation ; C5a peptidase ; M protein ; Transcription termination ; Streptococcus pyogenes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Streptococcal C5a peptidase (SCP), encoded byscpA inStreptococcus pyogenes, is a surface molecule which is able to cleave and inactivate the chemotactic factor C5a. ThescpA gene is part of thevir regulon and subject to positive regulation by the Mga protein. It is down-regulated compared to another Mga-activated gene,emm. A chloramphenicol acetyltransferase (CAT) reporter gene was used to measurescpA promoter activity. Previous work had shown that when a large portion of thescpA promoter region was deleted, expression of CAT increased relative to the wild-type. This deleted region was found to contain an inverted repeat. In this study we show that the inverted repeat in the leader mRNA is the site of transcription termination, which down-regulates expression ofscpA. This is a novel mechanism for regulation of gene expression inS. pyogenes. A specific deletion of the inverted repeat in thescpA promoter-CAT reporter construct was made using inverse PCR. Expression was measured from single-copy chromosomal integrants. When the inverted repeat was deleted, expression increased. Furthermore, Northern hybridization confirmed the existence of a truncated transcript, consistent with a transcription termination mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02174180
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  • 21
    Electronic Resource
    Electronic Resource
    Identification of cis-acting DNA sequences involved in the transcription of the virulence regulatory gene spvR  in Salmonella typhimurium (1996)
    Springer
    Molecular genetics and genomics 251 (1996), S. 225-235 
    Details
    ISSN: 1617-4623
    Keywords: Key words Salmonella typhimurium ; rpoS ; spv ; Virulence plasmid ; Regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  The SpvR protein is a DNA-binding protein of the LysR family, required for the transcription of the spvABCD virulence operon of Salmonella typhimurium. An alternative sigma factor, σS (RpoS), in conjunction with SpvR, controls the transcription of the spvR gene. In this study, we used a combination of primer extension experiments and deletion/fusion analyses of the spvR gene to identify sequences involved in spvR transcription in S. typhimurium. When induced in the stationary phase of growth in rich medium or during carbon starvation, transcription of spvR in S. typhimurium is driven by a single promoter (spvRp1) and initiates 17 nucleotides upstream of the spvR start codon. The level of spvR transcription originating at spvRp1 was 20-fold higher in the wild-type strain than in the rpoS mutant. In both strains, however, transcription at spvRp1 requires the SpvR protein. 5′ Deletions up to position −86, relative to the spvR start codon, did not inhibit inducibility by σS and/or SpvR. In contrast, 5′ deletion up to −75 abolished the activation of spvRp1 by SpvR in both the wild-type strain and rpoS mutant. Within the 11-bp sequence lying between position −86 and position −75, a 10-bp consensus motif TNTNTGCANA, present in both the spvR and spvA promoter regions, was identified and may contain the DNA recognition site for SpvR. In addition, we detected initiation of transcription within the spvR coding region. This finding may have implications for comparative studies of regulation with spvR gene fusions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02172922
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  • 22
    Electronic Resource
    Electronic Resource
    Identification of cis-acting DNA sequences involved in the transcription of the virulence regulatory genespvR inSalmonella typhimurium (1996)
    Springer
    Molecular genetics and genomics 251 (1996), S. 225-235 
    Details
    ISSN: 1617-4623
    Keywords: Salmonella typhimurium ; rpoS ; spv ; Virulence plasmid ; Regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The SpvR protein is a DNA-binding protein of the LysR family, required for the transcription of thespvABCD virulence operon ofSalmonella typhimurium. An alternative sigma factor, σS (RpoS), in conjunction with SpvR, controls the transcription of thespvR gene. In this study, we used a combination of primer extension experiments and deletion/fusion analyses of thespvR gene to identify sequences involved inspvR transcription inS. typhimurium. When induced in the stationary phase of growth in rich medium or during carbon starvation, transcription ofspvR inS. typhimurium is driven by a single promoter (spvRp1) and initiates 17 nucleotides upstream of thespvR start codon. The level ofspvR transcription originating atspvRp1 was 20-fold higher in the wild-type strain than in therpoS mutant. In both strains, however, transcription atspvRp1 requires the SpvR protein. 5′ Deletions up to position −86, relative to thespvR start codon, did not inhibit inducibility by σS and/or SpvR. In contrast, 5′ deletion up to −75 abolished the activation ofspvRp1 by SpvR in both the wild-type strain andrpoS mutant. Within the 11-bp sequence lying between position −86 and position −75, a 10-bp consensus motif TNTNTGCANA, present in both thespvR andspvA promoter regions, was identified and may contain the DNA recognition site for SpvR. In addition, we detected initiation of transcription within thespvR coding region. This finding may have implications for comparative studies of regulation withspvR gene fusions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02172922
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  • 23
    Electronic Resource
    Electronic Resource
    Regulation of SNM1, an inducible Saccharomyces cerevisiae gene required for repair of DNA cross-links (1996)
    Springer
    Molecular genetics and genomics 250 (1996), S. 162-168 
    Details
    ISSN: 1617-4623
    Keywords: Key words DNA repair ; Regulation ; Gene fusion ; DRE element ; Saccharomyces cerevisiae
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  The interstrand cross-link repair gene SNM1 of Saccharomyces cerevisiae was examined for regulation in response to DNA-damaging agents. Induction of SNM1-lacZ fusions was detected in response to nitrogen mustard, cis-platinum (II) diamine dichloride, UV light, and 8-methoxypsoralen +UVA, but not after heat-shock treatment or incubation with 2-dimethylaminoethylchloride, methylmethane sulfonate or 4-nitroquinoline-N-oxide. The promoter of SNM1 contains a 15 bp motif, which shows homology to the DRE2 box of the RAD2 promoter. Similar motifs have been found in promoter regions of other damage-inducible DNA repair genes. Deletion of this motif results in loss of inducibility of SNM1. Also, a putative negative upstream regulation sequence was found to be responsible for repression of constitutive transcription of SNM1. Surprisingly, no inducibility of SNM1 was found after treatment with DNA-damaging agents in strains without an intact DUN1 gene, while regulation seems unchanged in sad1 mutants.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02174175
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  • 24
    Electronic Resource
    Electronic Resource
    Regulation ofSNM1, an inducibleSaccharomyces cerevisiae gene required for repair of DNA cross-links (1996)
    Springer
    Molecular genetics and genomics 250 (1996), S. 162-168 
    Details
    ISSN: 1617-4623
    Keywords: DNA repair ; Regulation ; Gene fusion ; DRE element ; Saccharomyces cerevisiae
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The interstrand cross-link repair geneSNM1 ofSaccharomyces cerevisiae was examined for regulation in response to DNA-damaging agents. Induction ofSNM1-lacZ fusions was detected in response to nitrogen mustard, cis-platinum (II) diamine dichloride, UV light, and 8-methoxypsoralen + UVA, but not after heat-shock treatment or incubation with 2-dimethyl-aminoethylchloride, methylmethane sulfonate or 4-nitroquinoline-N-oxide. The promoter ofSNM1 contains a 15 bp motif, which shows homology to the DRE2 box of theRAD2 promoter. Similar motifs have been found in promoter regions of other damage-inducible DNA repair genes. Deletion of this motif results in loss of inducibility ofSNM1. Also, a putative negative up-stream regulation sequence was found to be responsible for repression of constitutive transcription ofSNM1. Surprisingly, no inducibility ofSNM1 was found after treatment with DNA-damaging agents in strains without an intactDUN1 gene, while regulation seems unchanged insad1 mutants.
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    URL: http://dx.doi.org/10.1007/BF02174175
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  • 25
    Electronic Resource
    Electronic Resource
    Novel, developmentally specific control of Ds transposition in maize (1997)
    Springer
    Molecular genetics and genomics 256 (1997), S. 158-168 
    Details
    ISSN: 1617-4623
    Keywords: Key words Transposon ; Ac ; Regulation ; Zea mays ; Excision
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Plants form their gametes late in somatic development and, as a result, often pass somatic mutations on to their progeny. Classic examples of this process are the germinal revertants of unstable, Ac/Ds transposon-induced kernel mutations in maize: frequent and early reversion events during somatic development are generally correlated with a high frequency of revertant gametes. We have characterized a Ds allele of the maize waxy(wx) gene, wx-m5:CS7, for which the correlation between somatic and germinal reversion frequencies no longer holds. The ability of wx-m5:CS7 (CS7) to produce revertant gametes is suppressed ∼100-fold in comparison with a second Ds allele, wx-m5:CS8 (CS8), which has an identical insertion at Wx and the same frequent and early somatic reversion pattern in endosperm. The excision of Ds from wx is not reduced 100-fold in the somatic tissues of CS7 plants as compared with CS8 plants. Suppressed formation of CS7 revertant gametes is independent of the Ac transposase source and is heritably passed to the embryos of progeny kernels; however, frequent and early somatic reversion is observed again in endosperms of these progeny kernels. This suppression appears to be caused by a dominant mutation in a trans-acting product that can suppress the germinal reversion of other Ds-induced alleles as well; the mutation is tightly linked to Wx but is not in the CS7 Ds itself. Taken together, the data suggest a novel mode of developmental control of Ac/Ds elements by the host plant, suppressing element excision in the shoot meristem.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004380050557
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  • 26
    Electronic Resource
    Electronic Resource
    The effects of regulations on state liquor prices (1996)
    Springer
    Empirica 23 (1996), S. 303-316 
    Details
    ISSN: 1573-6911
    Keywords: Regulation ; liquor ; fair trade ; L3 ; L5
    Source: Springer Online Journal Archives 1860-2000
    Topics: Economics
    Notes: Abstract Several estimation methods agree that state regulations such as resale price maintenance and retail price posting affected the prices of liquor brands up to the mid-1970s in the US states in which the distribution system is privately owned; before-versus-after analysis using the quasiexperimental method provides the strongest evidence. The effects of particular regulations are not so clearcut, however. In the 1970s, the regulations supporting these practices began to be removed. The regulations that continued in effect seem to have lost their potency about that time. The effects of regulation no longer are seen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00924975
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  • 27
    Electronic Resource
    Electronic Resource
    A note on price cap regulation and competition (1996)
    Springer
    Review of industrial organization 11 (1996), S. 459-471 
    Details
    ISSN: 1573-7160
    Keywords: Regulation ; incentives ; price caps ; competition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Economics
    Notes: Abstract This paper examines the properties of a price-cap regulatory regime similar in design to a plan recently proposed by AGT Ltd. in hearings on Alternative Forms of Regulation before the Canadian Radio-television and Telecommunications Commission. The price-cap plan incorporates a number of novel features which include (i) quantity weights that evolve through time rather than remaining fixed; (ii) adjustments for productivity that incorporate yardstick competition; and (iii) allowing the weights to reflect the firm's market power or absence thereof in the presence of competition. Hence, should competitive circumstances permit, the regulatory regime allows for its own sunset.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00157773
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  • 28
    Electronic Resource
    Electronic Resource
    Critique of proportional hypotheses and methods for back-calculation of fish growth (1996)
    Springer
    Environmental biology of fishes 46 (1996), S. 309-320 
    Details
    ISSN: 1573-5133
    Keywords: Individual growth ; Growth compensation ; Regulation ; Ontogenetic allometry ; Cyprinus carpio ; Leuciscus cephalus ; Rutilus rutilus ; Abramis brama
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Synopsis Hypotheses which assume a contant proportional deviation of the individual size of fish scales (S) or body (L) from mean size throughout life are biologically insignificant. Growth is considered and illustrated as a complex self-regulating process which continuously changes throughout ontogeny. Speed and form of changes of the growth of individual fish depend mainly on the initial size of the specimen and on the habitat. Consider five main types of changes of the L-S regression lines for individual fish with different initial sizes. They are basically different from the current proportional model of individual growth. The regression lines for individual fish cannot and should not be used for back-calculating L from S either by proportional or by regression methods, as individual L(S)/theoretical L(S) ratio, determined at the time of capture, are usually considerably different, compared to the previous years. For back-calculation of the average L values from average S values the use of separate equations for each age-group or for the whole subpopulation are recommended.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00005008
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  • 29
    Electronic Resource
    Electronic Resource
    Effects of saturated fatty acids on amylase release from exocrine pancreatic segments of sheep, rats, hamsters, field voles and mice (1996)
    Springer
    Journal of comparative physiology 166 (1996), S. 305-309 
    Details
    ISSN: 1432-136X
    Keywords: Key words Exocrine pancreas ; Fatty acids ; Amylase release ; Sheep ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  Stimulatory effects of saturated fatty acids consisting of 4 (butyrate), 8 (octanoate), 12 (laurate) and 16 (palmitate) carbon atoms, as well as acetylcholine on pancreatic amylase release were assessed in tissue segments isolated from sheep, rats, hamsters, field voles and mice. The amount of amylase release induced by the fatty acids (1 μmol ⋅ l-1 to 10 mml ⋅ l-1) and by acetylcholine (10 nmol ⋅ l-1 to 100 μmol ⋅ l-1) increased in a concentration-dependent manner, and the maximum response in response to the fatty acids was obtained at the maximal dose used. The maximum increase in amylase release in response to butyrate or octanoate was highly and significantly (r=0.974, P〈0.001) dependent on the log value of the mean body mass in the following order: sheep〉rats〉hamsters〉field voles〉mice. On the other hand, the response to laurate and palmitate was variable among animal species. Addition of atropine (1.4 μmol ⋅ l-1) to the medium did not reduce the responses to octanoate stimulation, but significantly reduced acetylcholineinduced responses, implying that the effects of the fatty acids were not mediated through activation of muscarinic acetylcholine receptors. Reduction of calcium ion concentration in the medium significantly inhibited the responses induced by the fatty acids and acetylcholine, suggesting that amylase release depends on extracellular calcium ions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003600050012
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  • 30
    Electronic Resource
    Electronic Resource
    Evidence for the short-term regulation of glycolytic flux in the isolated perfused ventricle of the land snail Helix lucorum (L.) after treatment with serotonin (5-hydroxytryptamine) (1997)
    Springer
    Journal of comparative physiology 167 (1997), S. 508-516 
    Details
    ISSN: 1432-136X
    Keywords: Key words Gastropod ; Glycolysis ; Heart ; Mollusc ; Perfusion ; Regulation ; Serotonin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The glycolytic flux and the regulation of phosphofructokinase (PFK) activity by fructose 2,6-bisphosphate and covalent modification was investigated in isolated ventricles of land snail Helix lucorum perfused with or without serotonin. Serotonin evoked a significant increase in the level of glycolytic intermediates and a threefold increase of glycolytic flux. Studies of saturation curves of PFK for the substrate fructose 6-phosphate at pH similar to intracellular pH of heart muscle showed that serotonin increases enzyme sensitivity to activation by fructose 6-phosphate. Moreover, PFK preparations from ventricles perfused with serotonin exhibited lower K a values for the activators AMP and fructose 2,6-bisphosphate, compared with the enzyme preparations from serotonin-untreated ventricles. The results suggest that PFK was converted to a more active form when exposed to serotonin. In vitro experiments of PFK phosphorylation showed that the conversion of the enzyme to a more active form was possibly due to its phosphorylation by an endogenous cyclic-AMP-dependent protein kinase. The concentration of fructose 2,6-bisphosphate increased in serotonin-treated ventricles and it exerted a synergistic effect with AMP on the activation of PFK. The bound fraction of glycolytic enzymes increased in the serotonin-treated ventricles only after the 4th min of perfusion. The results suggest that the stimulation of glycolytic flux in the ventricles of H. lucorum in the first minutes of perfusion with serotonin was partly due to the activation of PFK via enzyme molecule covalent modification and to increase of fructose 2,6-bisphosphate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003600050103
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  • 31
    Electronic Resource
    Electronic Resource
    Effects of saturated fatty acids on amylase release from exocrine pancreatic segments of sheep, rats, hamsters, field voles and mice (1996)
    Springer
    Journal of comparative physiology 166 (1996), S. 305-309 
    Details
    ISSN: 1432-136X
    Keywords: Exocrine pancreas ; Fatty acids ; Amylase release ; Sheep ; Rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Stimulatory effects of saturated fatty acids consisting of 4 (butyrate), 8 (octanoate), 12 (laurate) and 16 (palmitate) carbon atoms, as well as acetylcholine on pancreatic amylase release were assessed in tissue segments isolated from sheep, rats, hamsters, field voles and mice. The amount of amylase release induced by the fatty acids (1 μmol·l−1 to 10 mml·l−1) and by acetylcholine (10 nmol·l−1 to 100 μmol·l−1) increased in a concentration-dependent manner, and the maximum response in response to the fatty acids was obtained at the maximal dose used. The maximum increase in amylase release in response to butyrate or octanoate was highly and significantly (r=0.974,P〈0.001) dependent on the log value of the mean body mass in the following order: sheep 〉 rats 〉 hamsters 〉 field voles 〉 mice. On the other hand, the response to laurate and palmitate was variable among animal species. Addition of atropine (1.4 μmol·l−1) to the medium did not reduce the responses to octanoate stimulation, but significantly reduced acetylcholine-induced responses implying that the effects of the fatty acids were not mediated through activation of muscarinic acetylcholine receptors. Reduction of calcium ion concentration in the medium significantly inhibited the responses induced by the fatty acids and acetylcholine, suggesting that amylase release depends on extracellular calcium ions.
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  • 32
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    Electronic Resource
    Electronic rotameter for quantitative evaluation of rotational behaviour in rats after unilateral lesions of the nigrostriatal dopamine system (1984)
    Springer
    Medical & biological engineering & computing 22 (1984), S. 361-366 
    Details
    ISSN: 1741-0444
    Keywords: Drugs ; Psychology ; Rats ; Rotameter
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02442107
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  • 33
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    Identification of procaryotic developmental stages by statistical analyses of two-dimensional gel patterns (1997)
    Weinheim : Wiley-Blackwell
    Electrophoresis 18 (1997), S. 1418-1428 
    Details
    ISSN: 0173-0835
    Keywords: Two-dimentional polyacrylamide gel electrophoresis ; Streptomyces ; Development ; Multivariate ; Regulation ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Multivariate statistical comparisons of two-dimensional protein (2-D) gel patterns were used for the first time to define stages of a biological developmental system. The differentiating procaryote, Streptomyces coelicolor, was radiolabeled in liquid cultures at 16 intervals during development, and radioactive proteins were separated and quantified on 2-D gels. Cluster, principal component, and correlation analyses classified these gel patterns into four distinct groups, each reflecting a pattern of gene expression specific for a stage of development. These studies focused our attention on a phase of arrested growth as a key regulatory transition leading to secondary metabolism and a phase of renewed growth. Proteins whose synthesis was switched on or off during the “transitional” phase (some 21 and 18, respectively) were identified and will be the focus of future studies designed to identify their physiological or regulatory function.
    Additional Material: 9 Ill.
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    URL: http://dx.doi.org/10.1002/elps.1150180817
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    A comparison of selected mRNA and protein abundances in human liver (1997)
    Weinheim : Wiley-Blackwell
    Electrophoresis 18 (1997), S. 533-537 
    Details
    ISSN: 0173-0835
    Keywords: Messenger RNA ; Two-dimensional polyacrylamide gel electrophoresis ; Transcript image ; Liver ; Regulation ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: In order to obtain an estimate of the overall level of correlation between mRNA and protein abundances for a well-characterized pharmaceutically relevant biological system, we have analyzed human liver by quantitative two-dimensional electrophoresis (for protein abundances) and by Transcript Image methodology (for mRNA abundances). Incyte's LifeSeq™ database was searched for expressed sequence tag (EST) sequences corresponding to a series of 23 proteins identified on 2-D maps in the Large Scale Biology (LSB) Molecular Anatomy™ database, resulting in estimated abundances for 19 messages (4 were undetected) among 7926 liver clones sequenced. A correlation coefficient of 0.48 was obtained between the mRNA and protein abundances determined by the two approaches, suggesting that post-transcriptional regulation of gene expression is a frequent phenomenon in higher organisms. A comparison with published data (Kawamoto, S., et al., Gene 1996, 174, 151-158) on the abundances of liver mRNAs for plasma proteins (secreted by the liver) suggests that higher abundance messages are strongly enriched in secreted sequences. Our data confirms this: of the 50 most abundant liver mRNAs, 29 coded for secreted proteins, while none of the 50 most abundant proteins appeared to be secreted products (although four plasma and red blood cell proteins were presents in this group as contaminants from tissue blood).
    Additional Material: 3 Ill.
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    URL: http://dx.doi.org/10.1002/elps.1150180333
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  • 35
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    Unknown
    Reply to Comment on Taxes, Subsidies, and Advertising Efficacy in Changing Eating Behavior: An Experimental Study (2014)
    Oxford University Press
    Details
    Publication Date: 2014-12-03
    Keywords: C91 - Laboratory, Individual Behavior, I18 - Government Policy ; Regulation ; Public Health
    Print ISSN: 2040-5790
    Electronic ISSN: 2040-5804
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Economics
    Published by Oxford University Press
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    PAPER CURRENT
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    Do Neighborhood Parks and Playgrounds Reduce Childhood Obesity? (2014)
    Oxford University Press
    Details
    Publication Date: 2014-01-22
    Description: Using the 2007 National Survey of Children's Health data, we find a statistically and economically significant effect of neighborhood parks and playgrounds on childhood obesity based on covariate matching estimators. The park/playground effect depends on gender, age, race, household income, neighborhood safety, and other neighborhood amenities. The results suggest that adding a neighborhood park/playground may reduce the obesity rate and make children more fit, but relevant interventions must consider socioeconomic status of the targeted children as well as other neighborhood amenities.
    Keywords: I18 - Government Policy ; Regulation ; Public Health, I38 - Government Policy ; Provision and Effects of Welfare Programs, R53 - Public Facility Location Analysis ; Public Investment and Capital Stock
    Print ISSN: 0002-9092
    Electronic ISSN: 1467-8276
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Economics
    Published by Oxford University Press
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    The Economics of Information, Deep Capture, and the Obesity Debate (2014)
    Oxford University Press
    Details
    Publication Date: 2014-03-21
    Description: The economic theory of regulatory capture predicts that industry groups will attempt to influence their regulators (for example, by lobbying for rules that exclude competition). It has been suggested that the same logic applies to any powerful institution with the ability to affect industry profits. When the aim of industry is to alter the public’s perception of its product (for example, by disseminating favorable messages to the news media or via an advertising campaign, or by funding industry-friendly scientific research), the end result has been dubbed deep capture. We develop a formal model of deep capture, in which consumers have imperfect information about product quality, and a dominant producer is able to increase his profits by altering the parameters of the consumer’s search problem. We demonstrate the empirical relevance of the phenomenon with a discussion of the food industry response to the obesity epidemic.
    Keywords: D18 - Consumer Protection, D83 - Search ; Learning ; Information and Knowledge ; Communication ; Belief, I18 - Government Policy ; Regulation ; Public Health, L15 - Information and Product Quality ; Standardization and Compatibility, L51 - Economics of Regulation
    Print ISSN: 0002-9092
    Electronic ISSN: 1467-8276
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Economics
    Published by Oxford University Press
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    Sub-therapeutic Antibiotics and the Efficiency of U.S. Hog Farms (2014)
    Oxford University Press
    Details
    Publication Date: 2014-04-05
    Description: A substantial share of U.S. hog producers incorporate antimicrobial drugs into their livestock's feed or water at sub-therapeutic levels to promote feed efficiency and weight gain. Recently, in response to concerns that the overuse of antibiotics in livestock could promote the development of antimicrobial drug-resistant bacteria, the U.S. Food and Drug Administration adopted a strategy to phase out the use of antibiotics for production purposes. This study uses a stochastic frontier model and data from the 2009 USDA Agricultural Resource Management Survey of feeder-to-finish hog producers to estimate the potential effects on hog output and output variability resulting from a ban on antibiotics used for growth promotion. We use propensity score nearest neighbor matching to create a balanced sample of sub-therapeutic antibiotic (STA) users and nonusers. We estimate the frontier model for the pooled sample and separately for users and non-users—which allows for a flexible interaction between STA use and the production technology. Point estimates for the matched sample indicate that STA use has a small positive effect on productivity and production risk, increasing output by 1.0–1.3% and reducing the standard deviation of unexplained output by 1.4%. The results indicate that improvements in productivity resulted exclusively from technological improvement rather than from an increase in technical efficiency.
    Keywords: D24 - Production ; Cost ; Capital and Total Factor Productivity ; Capacity, I18 - Government Policy ; Regulation ; Public Health, Q12 - Micro Analysis of Farm Firms, Farm Households, and Farm Input Markets, Q18 - Agricultural Policy ; Food Policy
    Print ISSN: 0002-9092
    Electronic ISSN: 1467-8276
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Economics
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  • 39
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    Are you smart enough to know what to eat? A critique of behavioural economics as justification for regulation (2014)
    Oxford University Press
    Details
    Publication Date: 2014-07-03
    Description: With the rise of behavioural economics has come the belief that decision-making biases justify paternalistic policies. Such views challenge the notion of consumer sovereignty and the validity of traditional approaches of economic welfare analysis. While behavioural economics might improve the effectiveness of policies that are already justified on some other market-failure grounds, this article argues that the existence of cognitive failures, alone, do not justify government regulation. If one abandons the idea that consumers know what is in their best interest, judging the merits of policies becomes arbitrary and reflects only what a paternalist wants for others. The typical behavioural economic experiment occurs with college students devoid of real-world context. The biases found in such setting may not extrapolate well to conditions where people have more experience and knowledge, and where they can learn from past mistakes. Even when behavioural biases persist in the ‘real world’, consumers face incentives to engage in activities that protect them from the adverse consequences of the biases, and public policies that shield people from such consequences reduce incentives to self-regulate. The article concludes with some ideas for future research and a discussion of the merits of freedom of choice.
    Keywords: D03 - Behavioral Economics ; Underlying Principles, I18 - Government Policy ; Regulation ; Public Health, Q18 - Agricultural Policy ; Food Policy
    Print ISSN: 0165-1587
    Electronic ISSN: 1464-3618
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Economics
    Published by Oxford University Press
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  • 40
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    The Short-Run Impact of the Healthy Incentives Pilot Program on Fruit and Vegetable Intake (2014)
    Oxford University Press
    Details
    Publication Date: 2014-09-02
    Description: In response to low consumption levels of fruits and vegetables by Supplemental Nutrition Assistance Program (SNAP) participants, the USDA Food and Nutrition Service created the Healthy Incentives Pilot (HIP) to test the efficacy of providing a 30% incentive for purchases of targeted fruits and vegetables (TFVs). Four to six months after implementation, mean daily TFV intake for adult HIP participants was 0.22 cup-equivalents higher (24% higher) than for control-group SNAP participants. These impact estimates with a random-assignment research design generally agree with previously published nonexperimental elasticity estimates, which imply that a pure price reduction of 30% would increase fruit and vegetable consumption by about 20%.
    Keywords: I18 - Government Policy ; Regulation ; Public Health, I38 - Government Policy ; Provision and Effects of Welfare Programs
    Print ISSN: 0002-9092
    Electronic ISSN: 1467-8276
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Economics
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  • 41
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    IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Peraldi, P -- Budavari, A -- Ellis, R -- White, M F -- Spiegelman, B M -- DK 42539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571133" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*metabolism ; Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance/*physiology ; Male ; Mice ; Muscle, Skeletal/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism/*physiology ; Phosphorylation ; Rats ; Rats, Zucker ; Receptor, Insulin/*antagonists & inhibitors/metabolism ; Serine/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 42
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    Angiopoietin-2, a natural antagonist for Tie2 that disrupts in vivo angiogenesis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: Angiogenesis is thought to depend on a precise balance of positive and negative regulation. Angiopoietin-1 (Ang1) is an angiogenic factor that signals through the endothelial cell-specific Tie2 receptor tyrosine kinase. Like vascular endothelial growth factor, Ang1 is essential for normal vascular development in the mouse. An Ang1 relative, termed angiopoietin-2 (Ang2), was identified by homology screening and shown to be a naturally occurring antagonist for Ang1 and Tie2. Transgenic overexpression of Ang2 disrupts blood vessel formation in the mouse embryo. In adult mice and humans, Ang2 is expressed only at sites of vascular remodeling. Natural antagonists for vertebrate receptor tyrosine kinases are atypical; thus, the discovery of a negative regulator acting on Tie2 emphasizes the need for exquisite regulation of this angiogenic receptor system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maisonpierre, P C -- Suri, C -- Jones, P F -- Bartunkova, S -- Wiegand, S J -- Radziejewski, C -- Compton, D -- McClain, J -- Aldrich, T H -- Papadopoulos, N -- Daly, T J -- Davis, S -- Sato, T N -- Yancopoulos, G D -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):55-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals Inc., 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204896" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Blood Vessels/embryology/*metabolism ; Cells, Cultured ; Cloning, Molecular ; Embryo, Mammalian/metabolism ; Endothelial Growth Factors/genetics/metabolism ; Endothelium, Vascular/*cytology/metabolism ; Female ; Humans ; Ligands ; Lymphokines/genetics/metabolism ; Membrane Glycoproteins/antagonists & inhibitors/metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/chemistry/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Receptor, TIE-2 ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 43
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    Amidation of bioactive peptides: the structure of peptidylglycine alpha-hydroxylating monooxygenase (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-21
    Description: Many neuropeptides and peptide hormones require amidation at the carboxyl terminus for activity. Peptidylglycine alpha-amidating monooxygenase (PAM) catalyzes the amidation of these diverse physiological regulators. The amino-terminal domain of the bifunctional PAM protein is a peptidylglycine alpha-hydroxylating monooxygenase (PHM) with two coppers that cycle through cupric and cuprous oxidation states. The anomalous signal of the endogenous coppers was used to determine the structure of the catalytic core of oxidized rat PHM with and without bound peptide substrate. These structures strongly suggest that the PHM reaction proceeds via activation of substrate by a copper-bound oxygen species. The mechanistic and structural insight gained from the PHM structures can be directly extended to dopamine beta-monooxygenase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prigge, S T -- Kolhekar, A S -- Eipper, B A -- Mains, R E -- Amzel, L M -- DK32949/DK/NIDDK NIH HHS/ -- GM44692/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1300-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biophysical Chemistry, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9360928" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Catalysis ; Copper/chemistry/metabolism ; Crystallography, X-Ray ; Dipeptides/metabolism ; Dopamine beta-Hydroxylase/chemistry/metabolism ; Electrons ; Hydroxylation ; Ligands ; Mixed Function Oxygenases/*chemistry/metabolism ; Models, Molecular ; *Multienzyme Complexes ; Oxidation-Reduction ; Oxygen/metabolism ; Peptides/metabolism ; *Protein Conformation ; Protein Structure, Secondary ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 44
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    Gene discovery offers tentative clues to Parkinson's (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):1973.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Genetic Markers ; Humans ; Lewy Bodies/chemistry ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/analysis/chemistry/*genetics ; Oxidative Stress ; Parkinson Disease/etiology/*genetics ; Point Mutation ; Protein Conformation ; Protein Folding ; Rats ; Synucleins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 45
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    NGF signals ride a trolley to nucleus (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9289850" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Axonal Transport ; Axons/*metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; Gene Expression Regulation ; Nerve Growth Factors/*metabolism ; Neurons/*metabolism ; Proto-Oncogene Proteins/metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, trkA ; Receptors, Nerve Growth Factor/metabolism ; *Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 46
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    Neurogenesis in postnatal rat spinal cord: a study in primary culture (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: Spinal cord injuries result in paralysis, because when damaged neurons die they are not replaced. Neurogenesis of electrophysiologically functional neurons occurred in spinal cord cultured from postnatal rats. In these cultures, the numbers of immunocytochemically identified neurons increased over time. Additionally, neurons identified immunocytochemically or electrophysiologically incorporated bromodeoxyuridine, confirming they had differentiated from mitotic cells in vitro. These findings suggest that postnatal spinal cord retains the capacity to generate functional neurons. The presence of neuronal precursor cells in postnatal spinal cord may offer new therapeutic approaches for restoration of function to individuals with spinal cord injuries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kehl, L J -- Fairbanks, C A -- Laughlin, T M -- Wilcox, G L -- DA07097/DA/NIDA NIH HHS/ -- DA07234/DA/NIDA NIH HHS/ -- DE00225/DE/NIDCR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):586-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA. 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110976" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Bromodeoxyuridine/metabolism ; Cell Differentiation ; Cells, Cultured ; Culture Media ; Glial Fibrillary Acidic Protein/analysis ; Immunohistochemistry ; Mitosis ; Neurons/chemistry/*cytology/metabolism ; Phosphopyruvate Hydratase/analysis ; Rats ; Spinal Cord/chemistry/*cytology ; Tubulin/analysis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 47
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    Rat model for Gulf War syndrome? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1404.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411763" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Disease Models, Animal ; Hippocampus/*drug effects/metabolism ; Humans ; Isoflurophate/*toxicity ; Maze Learning/drug effects ; Military Personnel ; Nicotinic Antagonists/toxicity ; Persian Gulf Syndrome/*chemically induced/metabolism ; Rats ; Receptors, Nicotinic/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 48
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    Marijuana: harder than thought? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):1967-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221496" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/drug effects/metabolism ; Animals ; Brain/*drug effects/metabolism ; *Cannabis ; Corticotropin-Releasing Hormone/*metabolism ; Dopamine/*metabolism ; Dronabinol/adverse effects/*pharmacology ; Humans ; Naloxone/pharmacology ; Nucleus Accumbens/drug effects/metabolism ; Rats ; Substance Withdrawal Syndrome/*metabolism ; Substance-Related Disorders/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 49
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    Regulatory phosphorylation of AMPA-type glutamate receptors by CaM-KII during long-term potentiation (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: Long-term potentiation (LTP), a cellular model of learning and memory, requires calcium-dependent protein kinases. Induction of LTP increased the phosphorus-32 labeling of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors (AMPA-Rs), which mediate rapid excitatory synaptic transmission. This AMPA-R phosphorylation appeared to be catalyzed by Ca2+- and calmodulin-dependent protein kinase II (CaM-KII): (i) it correlated with the activation and autophosphorylation of CaM-KII, (ii) it was blocked by the CaM-KII inhibitor KN-62, and (iii) its phosphorus-32 peptide map was the same as that of GluR1 coexpressed with activated CaM-KII in HEK-293 cells. This covalent modulation of AMPA-Rs in LTP provides a postsynaptic molecular mechanism for synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barria, A -- Muller, D -- Derkach, V -- Griffith, L C -- Soderling, T R -- NS27037/NS/NINDS NIH HHS/ -- R01 GM054408/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2042-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland, OR 97201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197267" target="_blank"〉PubMed〈/a〉
    Keywords: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/analogs & derivatives/pharmacology ; 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Line ; Enzyme Inhibitors/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Hippocampus/*metabolism ; Humans ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Male ; Peptide Mapping ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/*metabolism ; Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 50
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    Large porous particles for pulmonary drug delivery (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-20
    Description: A new type of inhalation aerosol, characterized by particles of small mass density and large size, permitted the highly efficient delivery of inhaled therapeutics into the systemic circulation. Particles with mass densities less than 0.4 gram per cubic centimeter and mean diameters exceeding 5 micrometers were inspired deep into the lungs and escaped the lungs' natural clearance mechanisms until the inhaled particles delivered their therapeutic payload. Inhalation of large porous insulin particles resulted in elevated systemic levels of insulin and suppressed systemic glucose levels for 96 hours, whereas small nonporous insulin particles had this effect for only 4 hours. High systemic bioavailability of testosterone was also achieved by inhalation delivery of porous particles with a mean diameter (20 micrometers) approximately 10 times that of conventional inhaled therapeutic particles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edwards, D A -- Hanes, J -- Caponetti, G -- Hrkach, J -- Ben-Jebria, A -- Eskew, M L -- Mintzes, J -- Deaver, D -- Lotan, N -- Langer, R -- GM26698/GM/NIGMS NIH HHS/ -- HD29125/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1868-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Engineering, Pennsylvania State University, 204 Fenske Laboratory, University Park, PA 16802, USA. dxe11@psuv.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9188534" target="_blank"〉PubMed〈/a〉
    Keywords: *Administration, Inhalation ; Aerosols ; Animals ; Biological Availability ; Blood Glucose/analysis ; Bronchoalveolar Lavage ; *Drug Carriers ; Drug Compounding ; Insulin/administration & dosage/blood/pharmacokinetics ; *Lactic Acid ; *Lung ; Male ; Particle Size ; *Polyglycolic Acid ; *Polylysine ; *Polymers ; Rats ; Rats, Sprague-Dawley ; Testosterone/administration & dosage/blood/pharmacokinetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 51
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    Experiments in a Parkinson's rat model (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pallini, R -- Consales, A -- Lauretti, L -- Fernandez, E -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):389-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9518368" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dopamine/physiology ; Fluorescent Dyes/*metabolism ; *Genetic Therapy ; Genetic Vectors ; Glial Cell Line-Derived Neurotrophic Factor ; Nerve Degeneration ; Nerve Growth Factors/genetics ; Nerve Tissue Proteins/*genetics ; Neurons/metabolism/pathology ; *Neuroprotective Agents ; Oxidopamine/pharmacology ; Parkinson Disease/pathology/*therapy ; Rats ; *Stilbamidines ; Substantia Nigra/metabolism/*pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 52
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    A neural substrate of prediction and reward (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-14
    Description: The capacity to predict future events permits a creature to detect, model, and manipulate the causal structure of its interactions with its environment. Behavioral experiments suggest that learning is driven by changes in the expectations about future salient events such as rewards and punishments. Physiological work has recently complemented these studies by identifying dopaminergic neurons in the primate whose fluctuating output apparently signals changes or errors in the predictions of future salient and rewarding events. Taken together, these findings can be understood through quantitative theories of adaptive optimizing control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schultz, W -- Dayan, P -- Montague, P R -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1593-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology, University of Fribourg, CH-1700 Fribourg, Switzerland. Wolfram.Schultz@unifr.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054347" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Computer Simulation ; Conditioning (Psychology) ; Cues ; Dopamine/*physiology ; *Learning ; Mesencephalon/*physiology ; *Models, Neurological ; Neurons/*physiology ; Rats ; *Reward
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Alternative cleavage of Alzheimer-associated presenilins during apoptosis by a caspase-3 family protease (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-18
    Description: Most cases of early-onset familial Alzheimer's disease (FAD) are caused by mutations in the genes encoding the presenilin 1 (PS1) and PS2 proteins, both of which undergo regulated endoproteolytic processing. During apoptosis, PS1 and PS2 were shown to be cleaved at sites distal to their normal cleavage sites by a caspase-3 family protease. In cells expressing PS2 containing the asparagine-141 FAD mutant, the ratio of alternative to normal PS2 cleavage fragments was increased relative to wild-type PS2-expressing cells, suggesting a potential role for apoptosis-associated cleavage of presenilins in the pathogenesis of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, T W -- Pettingell, W H -- Jung, Y K -- Kovacs, D M -- Tanzi, R E -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):373-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics and Aging Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9219695" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics/metabolism/pathology ; Amino Acid Chloromethyl Ketones/pharmacology ; Amino Acid Substitution ; Animals ; *Apoptosis ; Caspase 3 ; *Caspases ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Enzyme Activation ; Etoposide/pharmacology ; Membrane Proteins/chemistry/genetics/*metabolism ; Mutation ; Oligopeptides/pharmacology ; Phosphorylation ; Presenilin-1 ; Presenilin-2 ; Rats ; Staurosporine/pharmacology ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    NMDA channel regulation by channel-associated protein tyrosine kinase Src (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: The N-methyl-D-aspartate (NMDA) receptor mediates synaptic transmission and plasticity in the central nervous system (CNS) and is regulated by tyrosine phosphorylation. In membrane patches excised from mammalian central neurons, the endogenous tyrosine kinase Src was shown to regulate the activity of NMDA channels. The action of Src required a sequence [Src(40-58)] within the noncatalytic, unique domain of Src. In addition, Src coprecipitated with NMDA receptor proteins. Finally, endogenous Src regulated the function of NMDA receptors at synapses. Thus, NMDA receptor regulation by Src may be important in development, plasticity, and pathology in the CNS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, X M -- Askalan, R -- Keil, G J 2nd -- Salter, M W -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):674-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Hospital for Sick Children, Department of Physiology, University of Toronto, Toronto, Ontario, M5G 1X8 Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005855" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Ion Channel Gating ; Ion Channels/*metabolism ; Molecular Sequence Data ; N-Methylaspartate/metabolism ; Neurons/*metabolism ; Oligopeptides/pharmacology ; Patch-Clamp Techniques ; Phosphorylation ; Phosphotyrosine/metabolism ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Spinal Cord/cytology ; Synapses/*metabolism ; Synaptic Transmission ; src-Family Kinases/chemistry/*metabolism
    Print ISSN: 0036-8075
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    Fear of hope (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, W -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):1907.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9333941" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cell Transplantation ; Genetic Therapy ; Humans ; Immunotherapy ; *Nerve Regeneration ; Neuroglia/*transplantation ; Olfactory Bulb/cytology/transplantation ; Rats ; Spinal Cord Injuries/surgery/*therapy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    The product of the proto-oncogene c-cbl: a negative regulator of the Syk tyrosine kinase (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-18
    Description: Engagement of antigen and immunoglobulin receptors on hematopoietic cells is directly coupled to activation of nonreceptor protein tyrosine kinases (PTKs) that then phosphorylate critical intracellular substrates. In mast cells stimulated through the FcvarepsilonRI receptor, activation of several PTKs including Syk leads to degranulation and release of such mediators of the allergic response as histamine and serotonin. Regulation of Syk function occurred through interaction with the Cbl protein, itself a PTK substrate in this system. Overexpression of Cbl led to inhibition of Syk and suppression of serotonin release from mast cells, demonstrating its ability to inhibit a nonreceptor tyrosine kinase. Complex adaptor proteins such as Cbl can directly regulate the functions of the proteins they bind.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ota, Y -- Samelson, L E -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):418-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-5430, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9103201" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Degranulation ; Enzyme Precursors/antagonists & inhibitors/*metabolism ; Genetic Vectors ; Intracellular Signaling Peptides and Proteins ; Mast Cells/*metabolism ; Mutation ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-cbl ; Rats ; Receptors, IgE/metabolism ; Receptors, IgG/metabolism ; Recombinant Proteins/metabolism ; Serotonin/metabolism ; Signal Transduction ; Tumor Cells, Cultured ; *Ubiquitin-Protein Ligases ; Vaccinia virus
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Enzyme-inhibitor-like tuning of Ca(2+) channel connectivity with calmodulin (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-02-09
    Description: Ca(2+) channels and calmodulin (CaM) are two prominent signalling hubs that synergistically affect functions as diverse as cardiac excitability, synaptic plasticity and gene transcription. It is therefore fitting that these hubs are in some sense coordinated, as the opening of Ca(V)1-2 Ca(2+) channels are regulated by a single CaM constitutively complexed with channels. The Ca(2+)-free form of CaM (apoCaM) is already pre-associated with the isoleucine-glutamine (IQ) domain on the channel carboxy terminus, and subsequent Ca(2+) binding to this 'resident' CaM drives conformational changes that then trigger regulation of channel opening. Another potential avenue for channel-CaM coordination could arise from the absence of Ca(2+) regulation in channels lacking a pre-associated CaM. Natural fluctuations in CaM concentrations might then influence the fraction of regulable channels and, thereby, the overall strength of Ca(2+) feedback. However, the prevailing view has been that the ultrastrong affinity of channels for apoCaM ensures their saturation with CaM, yielding a significant form of concentration independence between Ca(2+) channels and CaM. Here we show that significant exceptions to this autonomy exist, by combining electrophysiology (to characterize channel regulation) with optical fluorescence resonance energy transfer (FRET) sensor determination of free-apoCaM concentration in live cells. This approach translates quantitative CaM biochemistry from the traditional test-tube context into the realm of functioning holochannels within intact cells. From this perspective, we find that long splice forms of Ca(V)1.3 and Ca(V)1.4 channels include a distal carboxy tail that resembles an enzyme competitive inhibitor that retunes channel affinity for apoCaM such that natural CaM variations affect the strength of Ca(2+) feedback modulation. Given the ubiquity of these channels, the connection between ambient CaM levels and Ca(2+) entry through channels is broadly significant for Ca(2+) homeostasis. Strategies such as ours promise key advances for the in situ analysis of signalling molecules resistant to in vitro reconstitution, such as Ca(2+) channels.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553577/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553577/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, Xiaodong -- Yang, Philemon S -- Yang, Wanjun -- Yue, David T -- P30 DC005211/DC/NIDCD NIH HHS/ -- R01 DC000276/DC/NIDCD NIH HHS/ -- England -- Nature. 2010 Feb 18;463(7283):968-72. doi: 10.1038/nature08766. Epub 2010 Feb 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Calcium Signals Laboratory, Department of Biomedical Engineering, The Johns Hopkins University School of Medicine, Ross Building, Room 713, 720 Rutland Avenue, Baltimore, Maryland 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20139964" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Apoproteins/analysis/metabolism ; Binding, Competitive/drug effects ; Calcium/analysis/metabolism/pharmacology ; Calcium Channel Blockers/*chemistry/*metabolism ; Calcium Channels/*chemistry/genetics/*metabolism ; Calmodulin/analysis/*metabolism ; Cell Line ; Cell Survival ; Electrophysiology ; *Feedback, Physiological ; Fluorescence Resonance Energy Transfer ; Humans ; Protein Structure, Tertiary ; Rats ; Recombinant Fusion Proteins/chemistry/genetics/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Still prime time for primates (2010)
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    Publication Date: 2010-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2010 May 20;465(7296):267. doi: 10.1038/465267a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20485389" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Rights/trends ; Animals ; Animals, Laboratory/anatomy & histology/physiology ; Cognition/*physiology ; Empathy/physiology ; Humans ; Mice ; *Models, Animal ; Neurosciences/*methods/trends ; Prefrontal Cortex/anatomy & histology/physiology ; Primates/*anatomy & histology/*physiology ; Rats
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Neuroscience: Editing out fear (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-01-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Quirk, Gregory J -- Milad, Mohammed R -- England -- Nature. 2010 Jan 7;463(7277):36-7. doi: 10.1038/463036a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20054384" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning, Classical/*physiology ; Cues ; Electroshock ; Extinction, Psychological/*physiology ; Fear/*physiology/*psychology ; Humans ; Memory/*physiology ; Models, Neurological ; Models, Psychological ; Neuronal Plasticity/*physiology ; Photic Stimulation ; Rats ; Stress Disorders, Post-Traumatic/therapy ; Time Factors
    Print ISSN: 0028-0836
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    Affinity gradients drive copper to cellular destinations (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-05-14
    Description: Copper is an essential trace element for eukaryotes and most prokaryotes. However, intracellular free copper must be strictly limited because of its toxic side effects. Complex systems for copper trafficking evolved to satisfy cellular requirements while minimizing toxicity. The factors driving the copper transfer between protein partners along cellular copper routes are, however, not fully rationalized. Until now, inconsistent, scattered and incomparable data on the copper-binding affinities of copper proteins have been reported. Here we determine, through a unified electrospray ionization mass spectrometry (ESI-MS)-based strategy, in an environment that mimics the cellular redox milieu, the apparent Cu(I)-binding affinities for a representative set of intracellular copper proteins involved in enzymatic redox catalysis, in copper trafficking to and within various cellular compartments, and in copper storage. The resulting thermodynamic data show that copper is drawn to the enzymes that require it by passing from one copper protein site to another, exploiting gradients of increasing copper-binding affinity. This result complements the finding that fast copper-transfer pathways require metal-mediated protein-protein interactions and therefore protein-protein specific recognition. Together with Cu,Zn-SOD1, metallothioneins have the highest affinity for copper(I), and may play special roles in the regulation of cellular copper distribution; however, for kinetic reasons they cannot demetallate copper enzymes. Our study provides the thermodynamic basis for the kinetic processes that lead to the distribution of cellular copper.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Banci, Lucia -- Bertini, Ivano -- Ciofi-Baffoni, Simone -- Kozyreva, Tatiana -- Zovo, Kairit -- Palumaa, Peep -- England -- Nature. 2010 Jun 3;465(7298):645-8. doi: 10.1038/nature09018. Epub 2010 May 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Magnetic Resonance Center CERM and Department of Chemistry, University of Florence, Via Luigi Sacconi 6, 50019, Sesto Fiorentino, Florence, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20463663" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biocatalysis ; Carrier Proteins/*metabolism ; Cations, Monovalent/metabolism ; Copper/isolation & purification/*metabolism ; Cyclooxygenase 2/chemistry/metabolism ; Dithiothreitol/metabolism ; Glutathione/metabolism ; Humans ; Intracellular Space/*metabolism ; Ion Transport ; Kinetics ; Ligands ; Metallothionein/metabolism ; Mitochondria, Liver ; Oxidation-Reduction ; Protein Binding ; Rats ; Spectrometry, Mass, Electrospray Ionization ; Thermodynamics
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    Change of purpose (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-05-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉England -- Nature. 2010 May 20;465(7296):267-8. doi: 10.1038/465267b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20485388" target="_blank"〉PubMed〈/a〉
    Keywords: Acidosis, Lactic/drug therapy ; Animals ; Antineoplastic Agents/pharmacology/therapeutic use ; Clinical Trials as Topic/economics ; Dichloroacetic Acid/pharmacology/therapeutic use ; Drug Industry/*economics/methods/trends ; Humans ; Off-Label Use/*economics ; Patents as Topic/*legislation & jurisprudence ; Rats ; United States
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    Toxicology: The big test for bisphenol A (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-04-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borrell, Brendan -- England -- Nature. 2010 Apr 22;464(7292):1122-4. doi: 10.1038/4641122a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20414285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzhydryl Compounds ; Chemical Industry/methods/standards ; Endocrine Disruptors/adverse effects/toxicity ; Estrogens, Non-Steroidal/adverse effects/toxicity ; Female ; Guidelines as Topic ; Humans ; Infant ; Male ; Mice ; National Institute of Environmental Health Sciences (U.S.) ; Neoplasms/chemically induced/etiology ; Phenols/adverse effects/*toxicity ; Rats ; Toxicity Tests/methods/standards ; Toxicology/economics/*methods/*standards ; United States ; United States Environmental Protection Agency ; Validation Studies as Topic
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    Sensitivity to perturbations in vivo implies high noise and suggests rate coding in cortex (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-07-03
    Description: It is well known that neural activity exhibits variability, in the sense that identical sensory stimuli produce different responses, but it has been difficult to determine what this variability means. Is it noise, or does it carry important information-about, for example, the internal state of the organism? Here we address this issue from the bottom up, by asking whether small perturbations to activity in cortical networks are amplified. Based on in vivo whole-cell patch-clamp recordings in rat barrel cortex, we find that a perturbation consisting of a single extra spike in one neuron produces approximately 28 additional spikes in its postsynaptic targets. We also show, using simultaneous intra- and extracellular recordings, that a single spike in a neuron produces a detectable increase in firing rate in the local network. Theoretical analysis indicates that this amplification leads to intrinsic, stimulus-independent variations in membrane potential of the order of +/-2.2-4.5 mV-variations that are pure noise, and so carry no information at all. Therefore, for the brain to perform reliable computations, it must either use a rate code, or generate very large, fast depolarizing events, such as those proposed by the theory of synfire chains. However, in our in vivo recordings, we found that such events were very rare. Our findings are thus consistent with the idea that cortex is likely to use primarily a rate code.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898896/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898896/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉London, Michael -- Roth, Arnd -- Beeren, Lisa -- Hausser, Michael -- Latham, Peter E -- G0500244/Medical Research Council/United Kingdom -- R01 MH062447-08/MH/NIMH NIH HHS/ -- R01 MH62447/MH/NIMH NIH HHS/ -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Jul 1;466(7302):123-7. doi: 10.1038/nature09086.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wolfson Institute for Biomedical Research and Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20596024" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Animals ; Artifacts ; Cerebral Cortex/cytology/*physiology ; *Models, Neurological ; Neurons/metabolism ; Patch-Clamp Techniques ; Probability ; Rats ; Rats, Sprague-Dawley ; Stochastic Processes
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    Metabolic disorders: Fathers' nutritional legacy (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skinner, Michael K -- England -- Nature. 2010 Oct 21;467(7318):922-3. doi: 10.1038/467922a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962833" target="_blank"〉PubMed〈/a〉
    Keywords: Adiposity/drug effects ; Animals ; Body Weight/drug effects ; DNA Methylation ; Diabetes Mellitus, Type 2/etiology/genetics/pathology/physiopathology ; Diet/*adverse effects ; Dietary Fats/*administration & dosage/*adverse effects ; Epigenesis, Genetic/drug effects ; *Fathers ; Female ; Gene Expression Profiling ; Glucose Intolerance/etiology/pathology/physiopathology ; Insulin/secretion ; Insulin-Secreting Cells/metabolism/*pathology/secretion ; Male ; Obesity/etiology/genetics/pathology/physiopathology ; Paternal Exposure/*adverse effects ; Rats ; Spermatozoa/drug effects/metabolism
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    L1 retrotransposition in neurons is modulated by MeCP2 (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-11-19
    Description: Long interspersed nuclear elements-1 (LINE-1 or L1s) are abundant retrotransposons that comprise approximately 20% of mammalian genomes. Active L1 retrotransposons can impact the genome in a variety of ways, creating insertions, deletions, new splice sites or gene expression fine-tuning. We have shown previously that L1 retrotransposons are capable of mobilization in neuronal progenitor cells from rodents and humans and evidence of massive L1 insertions was observed in adult brain tissues but not in other somatic tissues. In addition, L1 mobility in the adult hippocampus can be influenced by the environment. The neuronal specificity of somatic L1 retrotransposition in neural progenitors is partially due to the transition of a Sox2/HDAC1 repressor complex to a Wnt-mediated T-cell factor/lymphoid enhancer factor (TCF/LEF) transcriptional activator. The transcriptional switch accompanies chromatin remodelling during neuronal differentiation, allowing a transient stimulation of L1 transcription. The activity of L1 retrotransposons during brain development can have an impact on gene expression and neuronal function, thereby increasing brain-specific genetic mosaicism. Further understanding of the molecular mechanisms that regulate L1 expression should provide new insights into the role of L1 retrotransposition during brain development. Here we show that L1 neuronal transcription and retrotransposition in rodents are increased in the absence of methyl-CpG-binding protein 2 (MeCP2), a protein involved in global DNA methylation and human neurodevelopmental diseases. Using neuronal progenitor cells derived from human induced pluripotent stem cells and human tissues, we revealed that patients with Rett syndrome (RTT), carrying MeCP2 mutations, have increased susceptibility for L1 retrotransposition. Our data demonstrate that L1 retrotransposition can be controlled in a tissue-specific manner and that disease-related genetic mutations can influence the frequency of neuronal L1 retrotransposition. Our findings add a new level of complexity to the molecular events that can lead to neurological disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059197/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059197/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muotri, Alysson R -- Marchetto, Maria C N -- Coufal, Nicole G -- Oefner, Ruth -- Yeo, Gene -- Nakashima, Kinichi -- Gage, Fred H -- 1-DP2-OD006495-01/OD/NIH HHS/ -- DP2 OD006495/OD/NIH HHS/ -- DP2 OD006495-01/OD/NIH HHS/ -- R01 MH088485/MH/NIMH NIH HHS/ -- R01 MH088485-03/MH/NIMH NIH HHS/ -- R01MH088485/MH/NIMH NIH HHS/ -- England -- Nature. 2010 Nov 18;468(7322):443-6. doi: 10.1038/nature09544.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California San Diego, School of Medicine, Department of Pediatrics/Rady Children's Hospital San Diego, La Jolla, California 92093-0695, USA. muotri@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21085180" target="_blank"〉PubMed〈/a〉
    Keywords: 5' Untranslated Regions/genetics ; Animals ; Brain/cytology/metabolism ; DNA Methylation ; Gene Silencing ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Long Interspersed Nucleotide Elements/*genetics ; Male ; Methyl-CpG-Binding Protein 2/deficiency/genetics/*metabolism ; Methylation ; Mice ; Neuroepithelial Cells/metabolism ; Neurons/*metabolism ; Organ Specificity ; Promoter Regions, Genetic/genetics ; Rats ; Recombination, Genetic/*genetics ; Rett Syndrome/genetics/pathology ; Transcription, Genetic/genetics
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    Fine-tuning of pre-balanced excitation and inhibition during auditory cortical development (2010)
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    Publication Date: 2010-06-19
    Description: Functional receptive fields of neurons in sensory cortices undergo progressive refinement during development. Such refinement may be attributed to the pruning of non-optimal excitatory inputs, reshaping of the excitatory tuning profile through modifying the strengths of individual inputs, or strengthening of cortical inhibition. These models have not been directly tested because of the technical difficulties in assaying the spatiotemporal patterns of functional synaptic inputs during development. Here we apply in vivo whole-cell voltage-clamp recordings to the recipient layer 4 neurons in the rat primary auditory cortex (A1) to determine the developmental changes in the frequency-intensity tonal receptive fields (TRFs) of their excitatory and inhibitory inputs. Surprisingly, we observe co-tuned excitation and inhibition immediately after the onset of hearing, suggesting that a tripartite thalamocortical circuit with relatively strong feedforward inhibition is formed independently of auditory experience. The frequency ranges of tone-driven excitatory and inhibitory inputs first expand within a few days of the onset of hearing and then persist into adulthood. The latter phase is accompanied by a sharpening of the excitatory but not inhibitory frequency tuning profile, which results in relatively broader inhibitory tuning in adult A1 neurons. Thus the development of cortical synaptic TRFs after the onset of hearing is marked by a slight breakdown of previously formed excitation-inhibition balance. Our results suggest that functional refinement of cortical TRFs does not require a selective pruning of inputs, but may depend more on a fine adjustment of excitatory input strengths.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909826/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909826/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Yujiao J -- Wu, Guangying K -- Liu, Bao-Hua -- Li, Pingyang -- Zhou, Mu -- Xiao, Zhongju -- Tao, Huizhong W -- Zhang, Li I -- EY018718/EY/NEI NIH HHS/ -- EY019049/EY/NEI NIH HHS/ -- R01 DC008983/DC/NIDCD NIH HHS/ -- R01 DC008983-01/DC/NIDCD NIH HHS/ -- R01 DC008983-02/DC/NIDCD NIH HHS/ -- R01 DC008983-03/DC/NIDCD NIH HHS/ -- R01 DC008983-04/DC/NIDCD NIH HHS/ -- R01 EY019049/EY/NEI NIH HHS/ -- R01 EY019049-02/EY/NEI NIH HHS/ -- R01DC008983/DC/NIDCD NIH HHS/ -- R03 DC006814/DC/NIDCD NIH HHS/ -- R03 DC006814-01A1/DC/NIDCD NIH HHS/ -- R03 DC006814-02/DC/NIDCD NIH HHS/ -- R03 DC006814-03/DC/NIDCD NIH HHS/ -- R21 DC008588/DC/NIDCD NIH HHS/ -- R21 DC008588-01/DC/NIDCD NIH HHS/ -- R21 DC008588-02/DC/NIDCD NIH HHS/ -- R21DC008588/DC/NIDCD NIH HHS/ -- UL1 RR025755/RR/NCRR NIH HHS/ -- England -- Nature. 2010 Jun 17;465(7300):927-31. doi: 10.1038/nature09079.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California 90089, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20559386" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Animals ; Auditory Cortex/growth & development/*physiology ; Auditory Pathways/physiology ; Electrical Synapses/physiology ; Excitatory Postsynaptic Potentials/*physiology ; Hearing/physiology ; Neural Inhibition/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Sensory Receptor Cells/*physiology ; Time Factors
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    LRRC26 auxiliary protein allows BK channel activation at resting voltage without calcium (2010)
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    Publication Date: 2010-07-09
    Description: Large-conductance, voltage- and calcium-activated potassium (BK, or K(Ca)1.1) channels are ubiquitously expressed in electrically excitable and non-excitable cells, either as alpha-subunit (BKalpha) tetramers or together with tissue specific auxiliary beta-subunits (beta1-beta4). Activation of BK channels typically requires coincident membrane depolarization and elevation in free cytosolic Ca(2+) concentration ([Ca(2+)](i)), which are not physiological conditions for most non-excitable cells. Here we present evidence that in non-excitable LNCaP prostate cancer cells, BK channels can be activated at negative voltages without rises in [Ca(2+)](i) through their complex with an auxiliary protein, leucine-rich repeat (LRR)-containing protein 26 (LRRC26). LRRC26 modulates the gating of a BK channel by enhancing the allosteric coupling between voltage-sensor activation and the channel's closed-open transition. This finding reveals a novel auxiliary protein of a voltage-gated ion channel that gives an unprecedentedly large negative shift ( approximately -140 mV) in voltage dependence and provides a molecular basis for activation of BK channels at physiological voltages and calcium levels in non-excitable cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, Jiusheng -- Aldrich, Richard W -- England -- Nature. 2010 Jul 22;466(7305):513-6. doi: 10.1038/nature09162. Epub 2010 Jul 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, Center for Learning and Memory, University of Texas, Austin, Texas 78712, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20613726" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Amino Acid Sequence ; Animals ; *Calcium/analysis ; Cell Line, Tumor ; Humans ; Ion Channel Gating/*physiology ; Large-Conductance Calcium-Activated Potassium Channels/genetics/*metabolism ; Male ; Membrane Potentials ; Mice ; Molecular Sequence Data ; Neoplasm Proteins/chemistry/genetics/*metabolism ; Prostatic Neoplasms/metabolism ; Rats
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    Chronic DLL4 blockade induces vascular neoplasms (2010)
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    Publication Date: 2010-02-12
    Description: Delta-like 4 (DLL4)-mediated Notch signalling has emerged as an attractive target for cancer therapy. However, the potential side effects of blocking this pathway remain uncertain. Here we show that chronic DLL4 blockade causes pathological activation of endothelial cells, disrupts normal organ homeostasis and induces vascular tumours, raising important safety concerns.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, Minhong -- Callahan, Christopher A -- Beyer, Joseph C -- Allamneni, Krishna P -- Zhang, Gu -- Ridgway, John Brady -- Niessen, Kyle -- Plowman, Greg D -- England -- Nature. 2010 Feb 11;463(7282):E6-7. doi: 10.1038/nature08751.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Tumor Biology and Angiogenesis, Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA. minhong@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20147986" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*adverse effects/pharmacology ; Drug-Induced Liver Injury/pathology/physiopathology ; Endothelial Cells/drug effects/pathology ; Humans ; Intracellular Signaling Peptides and Proteins/*antagonists & ; inhibitors/metabolism ; Macaca fascicularis ; Membrane Proteins/*antagonists & inhibitors/metabolism ; Mice ; Rats ; Receptors, Notch/metabolism ; Signal Transduction ; Vascular Neoplasms/*chemically induced
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    A trans-acting locus regulates an anti-viral expression network and type 1 diabetes risk (2010)
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    Publication Date: 2010-09-10
    Description: Combined analyses of gene networks and DNA sequence variation can provide new insights into the aetiology of common diseases that may not be apparent from genome-wide association studies alone. Recent advances in rat genomics are facilitating systems-genetics approaches. Here we report the use of integrated genome-wide approaches across seven rat tissues to identify gene networks and the loci underlying their regulation. We defined an interferon regulatory factor 7 (IRF7)-driven inflammatory network (IDIN) enriched for viral response genes, which represents a molecular biomarker for macrophages and which was regulated in multiple tissues by a locus on rat chromosome 15q25. We show that Epstein-Barr virus induced gene 2 (Ebi2, also known as Gpr183), which lies at this locus and controls B lymphocyte migration, is expressed in macrophages and regulates the IDIN. The human orthologous locus on chromosome 13q32 controlled the human equivalent of the IDIN, which was conserved in monocytes. IDIN genes were more likely to associate with susceptibility to type 1 diabetes (T1D)-a macrophage-associated autoimmune disease-than randomly selected immune response genes (P = 8.85 x 10(-6)). The human locus controlling the IDIN was associated with the risk of T1D at single nucleotide polymorphism rs9585056 (P = 7.0 x 10(-10); odds ratio, 1.15), which was one of five single nucleotide polymorphisms in this region associated with EBI2 (GPR183) expression. These data implicate IRF7 network genes and their regulatory locus in the pathogenesis of T1D.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3657719/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3657719/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heinig, Matthias -- Petretto, Enrico -- Wallace, Chris -- Bottolo, Leonardo -- Rotival, Maxime -- Lu, Han -- Li, Yoyo -- Sarwar, Rizwan -- Langley, Sarah R -- Bauerfeind, Anja -- Hummel, Oliver -- Lee, Young-Ae -- Paskas, Svetlana -- Rintisch, Carola -- Saar, Kathrin -- Cooper, Jason -- Buchan, Rachel -- Gray, Elizabeth E -- Cyster, Jason G -- Cardiogenics Consortium -- Erdmann, Jeanette -- Hengstenberg, Christian -- Maouche, Seraya -- Ouwehand, Willem H -- Rice, Catherine M -- Samani, Nilesh J -- Schunkert, Heribert -- Goodall, Alison H -- Schulz, Herbert -- Roider, Helge G -- Vingron, Martin -- Blankenberg, Stefan -- Munzel, Thomas -- Zeller, Tanja -- Szymczak, Silke -- Ziegler, Andreas -- Tiret, Laurence -- Smyth, Deborah J -- Pravenec, Michal -- Aitman, Timothy J -- Cambien, Francois -- Clayton, David -- Todd, John A -- Hubner, Norbert -- Cook, Stuart A -- 061858/Wellcome Trust/United Kingdom -- 076113/Wellcome Trust/United Kingdom -- 089989/Wellcome Trust/United Kingdom -- MC_U120061454/Medical Research Council/United Kingdom -- MC_U120085815/Medical Research Council/United Kingdom -- MC_U120097112/Medical Research Council/United Kingdom -- P301/10/0290/British Heart Foundation/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Sep 23;467(7314):460-4. doi: 10.1038/nature09386. Epub 2010 Sep 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Delbruck-Center for Molecular Medicine (MDC), Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20827270" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosomes, Human, Pair 13/genetics ; Chromosomes, Mammalian/genetics ; Diabetes Mellitus, Type 1/*genetics/immunology ; Gene Regulatory Networks/genetics ; Genetic Loci/*genetics ; Genetic Predisposition to Disease/*genetics ; Genome-Wide Association Study ; Humans ; Immunity, Innate/*genetics ; Inflammation/genetics/immunology ; Interferon Regulatory Factor-7/immunology ; Macrophages/immunology/metabolism ; Organ Specificity ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/genetics ; Rats ; Receptors, G-Protein-Coupled/genetics/metabolism ; Viruses/*immunology
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    Long-term potentiation depends on release of D-serine from astrocytes (2010)
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    Publication Date: 2010-01-16
    Description: Long-term potentiation (LTP) of synaptic transmission provides an experimental model for studying mechanisms of memory. The classical form of LTP relies on N-methyl-D-aspartate receptors (NMDARs), and it has been shown that astroglia can regulate their activation through Ca(2+)-dependent release of the NMDAR co-agonist D-serine. Release of D-serine from glia enables LTP in cultures and explains a correlation between glial coverage of synapses and LTP in the supraoptic nucleus. However, increases in Ca(2+) concentration in astroglia can also release other signalling molecules, most prominently glutamate, ATP and tumour necrosis factor-alpha, whereas neurons themselves can synthesize and supply D-serine. Furthermore, loading an astrocyte with exogenous Ca(2+) buffers does not suppress LTP in hippocampal area CA1 (refs 14-16), and the physiological relevance of experiments in cultures or strong exogenous stimuli applied to astrocytes has been questioned. The involvement of glia in LTP induction therefore remains controversial. Here we show that clamping internal Ca(2+) in individual CA1 astrocytes blocks LTP induction at nearby excitatory synapses by decreasing the occupancy of the NMDAR co-agonist sites. This LTP blockade can be reversed by exogenous D-serine or glycine, whereas depletion of D-serine or disruption of exocytosis in an individual astrocyte blocks local LTP. We therefore demonstrate that Ca(2+)-dependent release of D-serine from an astrocyte controls NMDAR-dependent plasticity in many thousands of excitatory synapses nearby.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807667/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807667/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henneberger, Christian -- Papouin, Thomas -- Oliet, Stephane H R -- Rusakov, Dmitri A -- 084311/Wellcome Trust/United Kingdom -- G0600368/Medical Research Council/United Kingdom -- G0600368(77987)/Medical Research Council/United Kingdom -- G0802216/Medical Research Council/United Kingdom -- G0802216(89644)/Medical Research Council/United Kingdom -- G0900613/Medical Research Council/United Kingdom -- G0900613(91064)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2010 Jan 14;463(7278):232-6. doi: 10.1038/nature08673.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UCL Institute of Neurology, University College London, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology/drug effects/metabolism/*secretion ; Calcium/antagonists & inhibitors/metabolism ; Exocytosis/drug effects ; Glycine/pharmacology ; Hippocampus/cytology/drug effects/physiology ; Long-Term Potentiation/drug effects/*physiology ; Male ; Memory/drug effects/physiology ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/agonists/metabolism ; Serine/biosynthesis/metabolism/pharmacology/*secretion ; Synapses/drug effects/metabolism
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    Termination of autophagy and reformation of lysosomes regulated by mTOR (2010)
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    Publication Date: 2010-06-08
    Description: Autophagy is an evolutionarily conserved process by which cytoplasmic proteins and organelles are catabolized. During starvation, the protein TOR (target of rapamycin), a nutrient-responsive kinase, is inhibited, and this induces autophagy. In autophagy, double-membrane autophagosomes envelop and sequester intracellular components and then fuse with lysosomes to form autolysosomes, which degrade their contents to regenerate nutrients. Current models of autophagy terminate with the degradation of the autophagosome cargo in autolysosomes, but the regulation of autophagy in response to nutrients and the subsequent fate of the autolysosome are poorly understood. Here we show that mTOR signalling in rat kidney cells is inhibited during initiation of autophagy, but reactivated by prolonged starvation. Reactivation of mTOR is autophagy-dependent and requires the degradation of autolysosomal products. Increased mTOR activity attenuates autophagy and generates proto-lysosomal tubules and vesicles that extrude from autolysosomes and ultimately mature into functional lysosomes, thereby restoring the full complement of lysosomes in the cell-a process we identify in multiple animal species. Thus, an evolutionarily conserved cycle in autophagy governs nutrient sensing and lysosome homeostasis during starvation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920749/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920749/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Li -- McPhee, Christina K -- Zheng, Lixin -- Mardones, Gonzalo A -- Rong, Yueguang -- Peng, Junya -- Mi, Na -- Zhao, Ying -- Liu, Zhihua -- Wan, Fengyi -- Hailey, Dale W -- Oorschot, Viola -- Klumperman, Judith -- Baehrecke, Eric H -- Lenardo, Michael J -- 2010CB833704/CB/NCI NIH HHS/ -- GM079431/GM/NIGMS NIH HHS/ -- R01 GM079431/GM/NIGMS NIH HHS/ -- Z01 AI000718-13/Intramural NIH HHS/ -- Z01 AI000718-14/Intramural NIH HHS/ -- ZIA AI000718-15/Intramural NIH HHS/ -- England -- Nature. 2010 Jun 17;465(7300):942-6. doi: 10.1038/nature09076. Epub 2010 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20526321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/*physiology ; Cell Line ; Cercopithecus aethiops ; HeLa Cells ; Homeostasis/physiology ; Humans ; Intracellular Signaling Peptides and Proteins/*metabolism ; Lysosomes/*metabolism/ultrastructure ; *Nutritional Physiological Phenomena ; Protein-Serine-Threonine Kinases/*metabolism ; Rats ; Signal Transduction ; TOR Serine-Threonine Kinases ; Vero Cells
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    Chronic high-fat diet in fathers programs beta-cell dysfunction in female rat offspring (2010)
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    Publication Date: 2010-10-22
    Description: The global prevalence of obesity is increasing across most ages in both sexes. This is contributing to the early emergence of type 2 diabetes and its related epidemic. Having either parent obese is an independent risk factor for childhood obesity. Although the detrimental impacts of diet-induced maternal obesity on adiposity and metabolism in offspring are well established, the extent of any contribution of obese fathers is unclear, particularly the role of non-genetic factors in the causal pathway. Here we show that paternal high-fat-diet (HFD) exposure programs beta-cell 'dysfunction' in rat F(1) female offspring. Chronic HFD consumption in Sprague-Dawley fathers induced increased body weight, adiposity, impaired glucose tolerance and insulin sensitivity. Relative to controls, their female offspring had an early onset of impaired insulin secretion and glucose tolerance that worsened with time, and normal adiposity. Paternal HFD altered the expression of 642 pancreatic islet genes in adult female offspring (P 〈 0.01); genes belonged to 13 functional clusters, including cation and ATP binding, cytoskeleton and intracellular transport. Broader pathway analysis of 2,492 genes differentially expressed (P 〈 0.05) demonstrated involvement of calcium-, MAPK- and Wnt-signalling pathways, apoptosis and the cell cycle. Hypomethylation of the Il13ra2 gene, which showed the highest fold difference in expression (1.76-fold increase), was demonstrated. This is the first report in mammals of non-genetic, intergenerational transmission of metabolic sequelae of a HFD from father to offspring.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ng, Sheau-Fang -- Lin, Ruby C Y -- Laybutt, D Ross -- Barres, Romain -- Owens, Julie A -- Morris, Margaret J -- England -- Nature. 2010 Oct 21;467(7318):963-6. doi: 10.1038/nature09491.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, School of Medical Sciences, University of New South Wales, New South Wales, Sydney 2052, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962845" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Adiposity/drug effects ; Aging/genetics ; Animals ; Apoptosis/genetics ; Body Weight/drug effects ; Cations/metabolism ; Cell Cycle/genetics ; Cytoskeleton/metabolism ; DNA Methylation/drug effects ; Diabetes Mellitus, Type 2/etiology/pathology/physiopathology ; Diet/*adverse effects ; Dietary Fats/*administration & dosage/*adverse effects ; Epigenesis, Genetic/drug effects ; *Fathers ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Glucose/pharmacology ; Glucose Intolerance/etiology/pathology/physiopathology ; Glucose Tolerance Test ; Homeostasis/drug effects ; Insulin/secretion ; Insulin-Secreting Cells/metabolism/*pathology/secretion ; Litter Size ; Male ; Obesity/etiology/pathology/physiopathology ; Paternal Exposure/*adverse effects ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/genetics
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    Striatal microRNA controls cocaine intake through CREB signalling (2010)
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    Publication Date: 2010-07-09
    Description: Cocaine addiction is characterized by a gradual loss of control over drug use, but the molecular mechanisms regulating vulnerability to this process remain unclear. Here we report that microRNA-212 (miR-212) is upregulated in the dorsal striatum of rats with a history of extended access to cocaine. Striatal miR-212 decreases responsiveness to the motivational properties of cocaine by markedly amplifying the stimulatory effects of the drug on cAMP response element binding protein (CREB) signalling. This action occurs through miR-212-enhanced Raf1 activity, resulting in adenylyl cyclase sensitization and increased expression of the essential CREB co-activator TORC (transducer of regulated CREB; also known as CRTC). Our findings indicate that striatal miR-212 signalling has a key role in determining vulnerability to cocaine addiction, reveal new molecular regulators that control the complex actions of cocaine in brain reward circuitries and provide an entirely new direction for the development of anti-addiction therapeutics based on the modulation of noncoding RNAs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2916751/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2916751/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hollander, Jonathan A -- Im, Heh-In -- Amelio, Antonio L -- Kocerha, Jannet -- Bali, Purva -- Lu, Qun -- Willoughby, David -- Wahlestedt, Claes -- Conkright, Michael D -- Kenny, Paul J -- F32 CA134121/CA/NCI NIH HHS/ -- F32 DA024932/DA/NIDA NIH HHS/ -- R01 DA025983/DA/NIDA NIH HHS/ -- R01 DA025983-03/DA/NIDA NIH HHS/ -- England -- Nature. 2010 Jul 8;466(7303):197-202. doi: 10.1038/nature09202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Behavioral and Molecular Neuroscience, Department of Molecular Therapeutics, The Scripps Research Institute, Scripps Florida, Jupiter, Florida 33458, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20613834" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Cocaine/*metabolism/pharmacology ; Cocaine-Related Disorders/drug therapy/enzymology/*genetics/*metabolism ; Cyclic AMP Response Element-Binding Protein/*metabolism ; MAP Kinase Kinase Kinases/metabolism ; Male ; MicroRNAs/biosynthesis/genetics/*metabolism ; Neostriatum/drug effects/*metabolism ; Rats ; Rats, Wistar ; Reward ; *Signal Transduction/drug effects ; Transcription Factors/metabolism ; Up-Regulation/drug effects
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    Global and local fMRI signals driven by neurons defined optogenetically by type and wiring (2010)
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    Publication Date: 2010-05-18
    Description: Despite a rapidly-growing scientific and clinical brain imaging literature based on functional magnetic resonance imaging (fMRI) using blood oxygenation level-dependent (BOLD) signals, it remains controversial whether BOLD signals in a particular region can be caused by activation of local excitatory neurons. This difficult question is central to the interpretation and utility of BOLD, with major significance for fMRI studies in basic research and clinical applications. Using a novel integrated technology unifying optogenetic control of inputs with high-field fMRI signal readouts, we show here that specific stimulation of local CaMKIIalpha-expressing excitatory neurons, either in the neocortex or thalamus, elicits positive BOLD signals at the stimulus location with classical kinetics. We also show that optogenetic fMRI (of MRI) allows visualization of the causal effects of specific cell types defined not only by genetic identity and cell body location, but also by axonal projection target. Finally, we show that of MRI within the living and intact mammalian brain reveals BOLD signals in downstream targets distant from the stimulus, indicating that this approach can be used to map the global effects of controlling a local cell population. In this respect, unlike both conventional fMRI studies based on correlations and fMRI with electrical stimulation that will also directly drive afferent and nearby axons, this of MRI approach provides causal information about the global circuits recruited by defined local neuronal activity patterns. Together these findings provide an empirical foundation for the widely-used fMRI BOLD signal, and the features of of MRI define a potent tool that may be suitable for functional circuit analysis as well as global phenotyping of dysfunctional circuitry.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3177305/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3177305/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Jin Hyung -- Durand, Remy -- Gradinaru, Viviana -- Zhang, Feng -- Goshen, Inbal -- Kim, Dae-Shik -- Fenno, Lief E -- Ramakrishnan, Charu -- Deisseroth, Karl -- 1K99EB008738/EB/NIBIB NIH HHS/ -- R00 EB008738/EB/NIBIB NIH HHS/ -- R00 EB008738-03/EB/NIBIB NIH HHS/ -- England -- Nature. 2010 Jun 10;465(7299):788-92. doi: 10.1038/nature09108.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Electrical Engineering, Psychiatry and Biobehavioral Sciences, Bioengineering, and Radiology, University of California, Los Angeles, California 90095, USA. ljinhy@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20473285" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/radiation effects ; Anesthesia ; Animals ; Brain/anatomy & histology/blood supply/*cytology/*radiation effects ; Cerebrovascular Circulation/radiation effects ; Chlorophyta ; Luminescent Measurements ; Luminescent Proteins/genetics/metabolism ; *Magnetic Resonance Imaging ; Motor Cortex/blood supply/cytology/metabolism/radiation effects ; Neural Pathways/*radiation effects ; Neurons/classification/cytology/*metabolism/*radiation effects ; Oxygen/blood/metabolism ; Photic Stimulation ; Rats ; Rhodopsin/genetics/metabolism/radiation effects ; Thalamus/blood supply/cytology/metabolism/radiation effects
    Print ISSN: 0028-0836
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    Did the bunny sell or sully the story on toxicity testing? (2010)
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    Publication Date: 2010-02-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Backmann, Jan -- England -- Nature. 2010 Feb 11;463(7282):729. doi: 10.1038/463729d.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20148010" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Testing Alternatives/methods ; Animals ; Animals, Laboratory ; Chemical Industry/*methods ; Europe ; *Models, Animal ; Periodicals as Topic/standards ; *Rabbits ; Rats ; Reproduction/drug effects ; Toxicity Tests/*methods
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    Neuroscience: Astrocytes as aide-memoires (2010)
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    Publication Date: 2010-01-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santello, Mirko -- Volterra, Andrea -- England -- Nature. 2010 Jan 14;463(7278):169-70. doi: 10.1038/463169a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075911" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/cytology/*metabolism/secretion ; Calcium/antagonists & inhibitors/*metabolism ; Hippocampus/cytology/physiology ; Long-Term Potentiation/*physiology ; Memory/*physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/agonists/metabolism ; Serine/metabolism/secretion ; Synapses/*metabolism
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    Conversion of adult pancreatic alpha-cells to beta-cells after extreme beta-cell loss (2010)
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    Publication Date: 2010-04-07
    Description: Pancreatic insulin-producing beta-cells have a long lifespan, such that in healthy conditions they replicate little during a lifetime. Nevertheless, they show increased self-duplication after increased metabolic demand or after injury (that is, beta-cell loss). It is not known whether adult mammals can differentiate (regenerate) new beta-cells after extreme, total beta-cell loss, as in diabetes. This would indicate differentiation from precursors or another heterologous (non-beta-cell) source. Here we show beta-cell regeneration in a transgenic model of diphtheria-toxin-induced acute selective near-total beta-cell ablation. If given insulin, the mice survived and showed beta-cell mass augmentation with time. Lineage-tracing to label the glucagon-producing alpha-cells before beta-cell ablation tracked large fractions of regenerated beta-cells as deriving from alpha-cells, revealing a previously disregarded degree of pancreatic cell plasticity. Such inter-endocrine spontaneous adult cell conversion could be harnessed towards methods of producing beta-cells for diabetes therapies, either in differentiation settings in vitro or in induced regeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877635/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877635/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thorel, Fabrizio -- Nepote, Virginie -- Avril, Isabelle -- Kohno, Kenji -- Desgraz, Renaud -- Chera, Simona -- Herrera, Pedro L -- U01 DK072522/DK/NIDDK NIH HHS/ -- U01 DK072522-01/DK/NIDDK NIH HHS/ -- U01 DK072522-02/DK/NIDDK NIH HHS/ -- U01 DK072522-03/DK/NIDDK NIH HHS/ -- U01 DK072522-04/DK/NIDDK NIH HHS/ -- U01 DK072522-05/DK/NIDDK NIH HHS/ -- England -- Nature. 2010 Apr 22;464(7292):1149-54. doi: 10.1038/nature08894. Epub 2010 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Physiology & Metabolism, University of Geneva Faculty of Medicine, 1 rue Michel-Servet, CH-1211 Geneva 4, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20364121" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/metabolism ; Cell Count ; Cell Death/drug effects ; Cell Differentiation/*physiology ; Cell Lineage ; Cell Proliferation ; Cell Transdifferentiation/*physiology ; Cellular Reprogramming ; Diphtheria Toxin/pharmacology/toxicity ; Female ; Glucagon/biosynthesis/genetics/secretion ; Glucagon-Secreting Cells/*cytology/metabolism/secretion ; Humans ; Insulin/biosynthesis/pharmacology/secretion ; Insulin-Secreting Cells/*cytology/drug effects/metabolism/secretion ; Male ; Mice ; Mice, Transgenic ; Rats ; Regeneration/physiology
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    Circulating mitochondrial DAMPs cause inflammatory responses to injury (2010)
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    Publication Date: 2010-03-06
    Description: Injury causes a systemic inflammatory response syndrome (SIRS) that is clinically much like sepsis. Microbial pathogen-associated molecular patterns (PAMPs) activate innate immunocytes through pattern recognition receptors. Similarly, cellular injury can release endogenous 'damage'-associated molecular patterns (DAMPs) that activate innate immunity. Mitochondria are evolutionary endosymbionts that were derived from bacteria and so might bear bacterial molecular motifs. Here we show that injury releases mitochondrial DAMPs (MTDs) into the circulation with functionally important immune consequences. MTDs include formyl peptides and mitochondrial DNA. These activate human polymorphonuclear neutrophils (PMNs) through formyl peptide receptor-1 and Toll-like receptor (TLR) 9, respectively. MTDs promote PMN Ca(2+) flux and phosphorylation of mitogen-activated protein (MAP) kinases, thus leading to PMN migration and degranulation in vitro and in vivo. Circulating MTDs can elicit neutrophil-mediated organ injury. Cellular disruption by trauma releases mitochondrial DAMPs with evolutionarily conserved similarities to bacterial PAMPs into the circulation. These signal through innate immune pathways identical to those activated in sepsis to create a sepsis-like state. The release of such mitochondrial 'enemies within' by cellular injury is a key link between trauma, inflammation and SIRS.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2843437/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2843437/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Qin -- Raoof, Mustafa -- Chen, Yu -- Sumi, Yuka -- Sursal, Tolga -- Junger, Wolfgang -- Brohi, Karim -- Itagaki, Kiyoshi -- Hauser, Carl J -- R01 GM059179/GM/NIGMS NIH HHS/ -- R01 GM059179-08/GM/NIGMS NIH HHS/ -- R01 GM059179-09/GM/NIGMS NIH HHS/ -- England -- Nature. 2010 Mar 4;464(7285):104-7. doi: 10.1038/nature08780.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, Division of Trauma, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20203610" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Lung Injury/immunology/pathology ; Animals ; Calcium Signaling ; Cells, Cultured ; CpG Islands/immunology ; DNA, Mitochondrial/blood/immunology ; Femur/injuries ; Fractures, Bone/immunology/pathology ; Humans ; Immunity, Innate/immunology ; Liver/immunology/injuries/pathology ; Male ; Mitochondria/*immunology/*secretion ; Mitogen-Activated Protein Kinases/metabolism ; Muscle, Skeletal/immunology/pathology ; N-Formylmethionine Leucyl-Phenylalanine/immunology/metabolism ; Neutrophils/enzymology/immunology/metabolism ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Receptors, Formyl Peptide/metabolism ; Sepsis/immunology/metabolism/microbiology ; Systemic Inflammatory Response ; Syndrome/blood/*complications/*immunology/pathology ; Toll-Like Receptor 9/metabolism ; Wounds and Injuries/blood/*complications/*immunology/pathology
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    Neuroscience: fMRI under the spotlight (2010)
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    Publication Date: 2010-06-11
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2996390/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2996390/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leopold, David A -- ZIA MH002838-06/Intramural NIH HHS/ -- ZIC MH002899-04/Intramural NIH HHS/ -- England -- Nature. 2010 Jun 10;465(7299):700-1. doi: 10.1038/465700a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20535195" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/radiation effects ; Anesthesia ; Animals ; Brain/*cytology/*radiation effects ; Cerebrovascular Circulation/radiation effects ; Humans ; *Magnetic Resonance Imaging ; Mice ; Motor Cortex/cytology/metabolism/radiation effects ; Neural Pathways/*radiation effects ; Neurons/*metabolism/*radiation effects ; Photic Stimulation ; Rats ; Rhodopsin/metabolism/radiation effects ; Thalamus/cytology/metabolism/radiation effects
    Print ISSN: 0028-0836
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    An intrinsic vasopressin system in the olfactory bulb is involved in social recognition (2010)
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    Publication Date: 2010-02-26
    Description: Many peptides, when released as chemical messengers within the brain, have powerful influences on complex behaviours. Most strikingly, vasopressin and oxytocin, once thought of as circulating hormones whose actions were confined to peripheral organs, are now known to be released in the brain, where they have fundamentally important roles in social behaviours. In humans, disruptions of these peptide systems have been linked to several neurobehavioural disorders, including Prader-Willi syndrome, affective disorders and obsessive-compulsive disorder, and polymorphisms of V1a vasopressin receptor have been linked to autism. Here we report that the rat olfactory bulb contains a large population of interneurons which express vasopressin, that blocking the actions of vasopressin in the olfactory bulb impairs the social recognition abilities of rats and that vasopressin agonists and antagonists can modulate the processing of information by olfactory bulb neurons. The findings indicate that social information is processed in part by a vasopressin system intrinsic to the olfactory system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842245/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2842245/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tobin, Vicky A -- Hashimoto, Hirofumi -- Wacker, Douglas W -- Takayanagi, Yuki -- Langnaese, Kristina -- Caquineau, Celine -- Noack, Julia -- Landgraf, Rainer -- Onaka, Tatsushi -- Leng, Gareth -- Meddle, Simone L -- Engelmann, Mario -- Ludwig, Mike -- BB/F019009/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0700176/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2010 Mar 18;464(7287):413-7. doi: 10.1038/nature08826. Epub 2010 Feb 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Integrative Physiology, University of Edinburgh, Edinburgh EH8 9XD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20182426" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antidiuretic Hormone Receptor Antagonists ; Interneurons/drug effects/metabolism ; Olfactory Bulb/cytology/*metabolism ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Receptors, Vasopressin/metabolism ; Recognition (Psychology)/drug effects/*physiology ; *Social Behavior ; Vasopressins/antagonists & inhibitors/*metabolism
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    S-glutathionylation uncouples eNOS and regulates its cellular and vascular function (2010)
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    Publication Date: 2010-12-24
    Description: Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)(*-)), which are key mediators of cellular signalling. In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg. In the absence of BH(4), NO synthesis is abrogated and instead O(2)(*-) is generated. While NOS dysfunction occurs in diseases with redox stress, BH(4) repletion only partly restores NOS activity and NOS-dependent vasodilation. This suggests that there is an as yet unidentified redox-regulated mechanism controlling NOS function. Protein thiols can undergo S-glutathionylation, a reversible protein modification involved in cellular signalling and adaptation. Under oxidative stress, S-glutathionylation occurs through thiol-disulphide exchange with oxidized glutathione or reaction of oxidant-induced protein thiyl radicals with reduced glutathione. Cysteine residues are critical for the maintenance of eNOS function; we therefore speculated that oxidative stress could alter eNOS activity through S-glutathionylation. Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)(*-) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function. We show that eNOS S-glutathionylation in endothelial cells, with loss of NO and gain of O(2)(*-) generation, is associated with impaired endothelium-dependent vasodilation. In hypertensive vessels, eNOS S-glutathionylation is increased with impaired endothelium-dependent vasodilation that is restored by thiol-specific reducing agents, which reverse this S-glutathionylation. Thus, S-glutathionylation of eNOS is a pivotal switch providing redox regulation of cellular signalling, endothelial function and vascular tone.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370391/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Chun-An -- Wang, Tse-Yao -- Varadharaj, Saradhadevi -- Reyes, Levy A -- Hemann, Craig -- Talukder, M A Hassan -- Chen, Yeong-Renn -- Druhan, Lawrence J -- Zweier, Jay L -- K99 HL103846/HL/NHLBI NIH HHS/ -- K99 HL103846-02/HL/NHLBI NIH HHS/ -- R01 HL038324/HL/NHLBI NIH HHS/ -- R01 HL038324-20/HL/NHLBI NIH HHS/ -- R01 HL063744/HL/NHLBI NIH HHS/ -- R01 HL063744-09/HL/NHLBI NIH HHS/ -- R01HL103846/HL/NHLBI NIH HHS/ -- R01HL38324/HL/NHLBI NIH HHS/ -- R01HL63744/HL/NHLBI NIH HHS/ -- R01HL65608/HL/NHLBI NIH HHS/ -- R01HL83237/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1115-8. doi: 10.1038/nature09599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, Department of Internal Medicine, College of Medicine, Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Dithiothreitol/pharmacology ; Endothelial Cells/metabolism ; Endothelium, Vascular/*metabolism ; Glutathione/*metabolism ; Humans ; Male ; Mercaptoethanol/pharmacology ; Mutation ; Nitric Oxide Synthase Type III/genetics/*metabolism ; Oxidation-Reduction ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Rats, Sprague-Dawley ; Reducing Agents/pharmacology ; Signal Transduction ; Vasodilation/physiology
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    N-myristoyltransferase inhibitors as new leads to treat sleeping sickness (2010)
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    Publication Date: 2010-04-03
    Description: African sleeping sickness or human African trypanosomiasis, caused by Trypanosoma brucei spp., is responsible for approximately 30,000 deaths each year. Available treatments for this disease are poor, with unacceptable efficacy and safety profiles, particularly in the late stage of the disease when the parasite has infected the central nervous system. Here we report the validation of a molecular target and the discovery of associated lead compounds with the potential to address this lack of suitable treatments. Inhibition of this target-T. brucei N-myristoyltransferase-leads to rapid killing of trypanosomes both in vitro and in vivo and cures trypanosomiasis in mice. These high-affinity inhibitors bind into the peptide substrate pocket of the enzyme and inhibit protein N-myristoylation in trypanosomes. The compounds identified have promising pharmaceutical properties and represent an opportunity to develop oral drugs to treat this devastating disease. Our studies validate T. brucei N-myristoyltransferase as a promising therapeutic target for human African trypanosomiasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917743/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917743/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frearson, Julie A -- Brand, Stephen -- McElroy, Stuart P -- Cleghorn, Laura A T -- Smid, Ondrej -- Stojanovski, Laste -- Price, Helen P -- Guther, M Lucia S -- Torrie, Leah S -- Robinson, David A -- Hallyburton, Irene -- Mpamhanga, Chidochangu P -- Brannigan, James A -- Wilkinson, Anthony J -- Hodgkinson, Michael -- Hui, Raymond -- Qiu, Wei -- Raimi, Olawale G -- van Aalten, Daan M F -- Brenk, Ruth -- Gilbert, Ian H -- Read, Kevin D -- Fairlamb, Alan H -- Ferguson, Michael A J -- Smith, Deborah F -- Wyatt, Paul G -- 077503/Wellcome Trust/United Kingdom -- 077705/Wellcome Trust/United Kingdom -- 085622/Wellcome Trust/United Kingdom -- 087590/Wellcome Trust/United Kingdom -- 1097737/Canadian Institutes of Health Research/Canada -- G0900138/Medical Research Council/United Kingdom -- G0900138(90614)/Medical Research Council/United Kingdom -- WT077503/Wellcome Trust/United Kingdom -- WT077705/Wellcome Trust/United Kingdom -- WT083481,/Wellcome Trust/United Kingdom -- WT085622/Wellcome Trust/United Kingdom -- England -- Nature. 2010 Apr 1;464(7289):728-32. doi: 10.1038/nature08893.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Drug Discovery Unit, Division of Biological Chemistry and Drug Discovery, University of Dundee, Dundee DD1 5EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20360736" target="_blank"〉PubMed〈/a〉
    Keywords: Acyltransferases/*antagonists & inhibitors/metabolism ; Aminopyridines/chemistry/metabolism/pharmacology/therapeutic use ; Animals ; Antiparasitic Agents/chemistry/metabolism/*pharmacology/*therapeutic use ; Enzyme Assays ; Enzyme Inhibitors/chemistry/metabolism/pharmacology/therapeutic use ; Female ; Humans ; Mice ; Molecular Structure ; Pyrazoles/chemistry/metabolism/pharmacology/therapeutic use ; Rats ; Sulfonamides/chemistry/metabolism/pharmacology/therapeutic use ; Time Factors ; Trypanosoma brucei brucei/*drug effects/*enzymology/growth & development ; Trypanosomiasis, African/*drug therapy/*parasitology
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    The histone variant macroH2A suppresses melanoma progression through regulation of CDK8 (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-12-24
    Description: Cancer is a disease consisting of both genetic and epigenetic changes. Although increasing evidence demonstrates that tumour progression entails chromatin-mediated changes such as DNA methylation, the role of histone variants in cancer initiation and progression currently remains unclear. Histone variants replace conventional histones within the nucleosome and confer unique biological functions to chromatin. Here we report that the histone variant macroH2A (mH2A) suppresses tumour progression of malignant melanoma. Loss of mH2A isoforms, histone variants generally associated with condensed chromatin and fine-tuning of developmental gene expression programs, is positively correlated with increasing malignant phenotype of melanoma cells in culture and human tissue samples. Knockdown of mH2A isoforms in melanoma cells of low malignancy results in significantly increased proliferation and migration in vitro and growth and metastasis in vivo. Restored expression of mH2A isoforms rescues these malignant phenotypes in vitro and in vivo. We demonstrate that the tumour-promoting function of mH2A loss is mediated, at least in part, through direct transcriptional upregulation of CDK8. Suppression of CDK8, a colorectal cancer oncogene, inhibits proliferation of melanoma cells, and knockdown of CDK8 in cells depleted of mH2A suppresses the proliferative advantage induced by mH2A loss. Moreover, a significant inverse correlation between mH2A and CDK8 expression levels exists in melanoma patient samples. Taken together, our results demonstrate that mH2A is a critical component of chromatin that suppresses the development of malignant melanoma, a highly intractable cutaneous neoplasm.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057940/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3057940/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kapoor, Avnish -- Goldberg, Matthew S -- Cumberland, Lara K -- Ratnakumar, Kajan -- Segura, Miguel F -- Emanuel, Patrick O -- Menendez, Silvia -- Vardabasso, Chiara -- Leroy, Gary -- Vidal, Claudia I -- Polsky, David -- Osman, Iman -- Garcia, Benjamin A -- Hernando, Eva -- Bernstein, Emily -- 5P30CA016087-27/CA/NCI NIH HHS/ -- CA109388/CA/NCI NIH HHS/ -- R21 CA150117/CA/NCI NIH HHS/ -- R21 CA150117-01/CA/NCI NIH HHS/ -- R21 CA150117-02/CA/NCI NIH HHS/ -- R21CA150117/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1105-9. doi: 10.1038/nature09590.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Mount Sinai School of Medicine, 1425 Madison Avenue, New York, New York 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179167" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cyclin-Dependent Kinase 8/*metabolism ; Disease Progression ; Gene Expression Profiling ; *Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; HCT116 Cells ; Histones/deficiency/genetics/*metabolism ; Humans ; Melanoma/*pathology/physiopathology ; Melanoma, Experimental ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neoplasm Metastasis/*pathology/physiopathology ; Rats ; Up-Regulation
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Clinical efficacy of a RAF inhibitor needs broad target blockade in BRAF-mutant melanoma (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-09-09
    Description: B-RAF is the most frequently mutated protein kinase in human cancers. The finding that oncogenic mutations in BRAF are common in melanoma, followed by the demonstration that these tumours are dependent on the RAF/MEK/ERK pathway, offered hope that inhibition of B-RAF kinase activity could benefit melanoma patients. Herein, we describe the structure-guided discovery of PLX4032 (RG7204), a potent inhibitor of oncogenic B-RAF kinase activity. Preclinical experiments demonstrated that PLX4032 selectively blocked the RAF/MEK/ERK pathway in BRAF mutant cells and caused regression of BRAF mutant xenografts. Toxicology studies confirmed a wide safety margin consistent with the high degree of selectivity, enabling Phase 1 clinical trials using a crystalline formulation of PLX4032 (ref. 5). In a subset of melanoma patients, pathway inhibition was monitored in paired biopsy specimens collected before treatment initiation and following two weeks of treatment. This analysis revealed substantial inhibition of ERK phosphorylation, yet clinical evaluation did not show tumour regressions. At higher drug exposures afforded by a new amorphous drug formulation, greater than 80% inhibition of ERK phosphorylation in the tumours of patients correlated with clinical response. Indeed, the Phase 1 clinical data revealed a remarkably high 81% response rate in metastatic melanoma patients treated at an oral dose of 960 mg twice daily. These data demonstrate that BRAF-mutant melanomas are highly dependent on B-RAF kinase activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2948082/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2948082/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bollag, Gideon -- Hirth, Peter -- Tsai, James -- Zhang, Jiazhong -- Ibrahim, Prabha N -- Cho, Hanna -- Spevak, Wayne -- Zhang, Chao -- Zhang, Ying -- Habets, Gaston -- Burton, Elizabeth A -- Wong, Bernice -- Tsang, Garson -- West, Brian L -- Powell, Ben -- Shellooe, Rafe -- Marimuthu, Adhirai -- Nguyen, Hoa -- Zhang, Kam Y J -- Artis, Dean R -- Schlessinger, Joseph -- Su, Fei -- Higgins, Brian -- Iyer, Raman -- D'Andrea, Kurt -- Koehler, Astrid -- Stumm, Michael -- Lin, Paul S -- Lee, Richard J -- Grippo, Joseph -- Puzanov, Igor -- Kim, Kevin B -- Ribas, Antoni -- McArthur, Grant A -- Sosman, Jeffrey A -- Chapman, Paul B -- Flaherty, Keith T -- Xu, Xiaowei -- Nathanson, Katherine L -- Nolop, Keith -- K24 CA097588/CA/NCI NIH HHS/ -- P50 CA093372/CA/NCI NIH HHS/ -- P50 CA093372-01/CA/NCI NIH HHS/ -- R01 CA118871/CA/NCI NIH HHS/ -- R01 CA118871-01A1/CA/NCI NIH HHS/ -- England -- Nature. 2010 Sep 30;467(7315):596-9. doi: 10.1038/nature09454.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plexxikon Inc., 91 Bolivar Drive, Berkeley, California 94710, USA. gbollag@plexxikon.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20823850" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Dogs ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/metabolism ; Humans ; Indoles/administration & dosage/adverse effects/chemistry/*therapeutic use ; MAP Kinase Signaling System/drug effects ; Macaca fascicularis ; Melanoma/*drug therapy/*enzymology/genetics/pathology ; Models, Molecular ; Mutant Proteins/antagonists & inhibitors/chemistry/genetics/metabolism ; Mutation/*genetics ; Neoplasm Metastasis ; Phosphorylation/drug effects ; Positron-Emission Tomography ; Proto-Oncogene Proteins B-raf/*antagonists & ; inhibitors/chemistry/genetics/metabolism ; Rats ; Substrate Specificity ; Sulfonamides/administration & dosage/adverse effects/chemistry/*therapeutic use ; Xenograft Model Antitumor Assays
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    Bold claims for optogenetics (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-11-26
    Description: In a recent Letter to Nature, Lee and colleagues combined optogenetic stimulation with functional magnetic resonance imaging (ofMRI) to examine the relationship between pyramidal-cell spiking and the blood oxygenation level dependent (BOLD) signal. To do so, they injected an adeno-associated viral vector into the primary motor cortex (M1) of adult rats to drive the expression of channelrhodopsin (ChR2) in cortical projection neurons, thus making them sensitive to light. The authors then used combined light stimulation and functional magnetic resonance imaging (fMRI) to examine the effects of selective activation of the light-sensitive pyramidal cells on the BOLD signal, as well as to probe the value of this methodology for mapping brain connectivity. They found that excitation of these neurons induced positive BOLD signals both in the injected M1 region and in remote target thalamic nuclei receiving direct projections from that region, and concluded that ofMRI reliably links positive BOLD signals with increased local neuronal excitation. However, their analysis neglects the almost immediate activation of other circuits that could lead to the generation of BOLD signals through local perisynaptic rather than spiking activity. Their experiments therefore do not pin down the identity of the specific neuronal signals that give rise to the BOLD signal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Logothetis, Nikos K -- England -- Nature. 2010 Nov 25;468(7323):E3-4; discussion E4-5. doi: 10.1038/nature09532.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute for Biological Cybernetics, Tuebingen, Germany. nikos.logothetis@tuebingen.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21107378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Magnetic Resonance Imaging ; Motor Cortex/physiology ; Neurons/physiology ; Oxygen/blood ; Photic Stimulation ; Pyramidal Cells/*metabolism ; Rats ; Research/standards ; Rhodopsin/metabolism ; *Signal Transduction
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    Microenvironmental reprogramming of thymic epithelial cells to skin multipotent stem cells (2010)
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    Publication Date: 2010-08-21
    Description: The thymus develops from the third pharyngeal pouch of the anterior gut and provides the necessary environment for thymopoiesis (the process by which thymocytes differentiate into mature T lymphocytes) and the establishment and maintenance of self-tolerance. It contains thymic epithelial cells (TECs) that form a complex three-dimensional network organized in cortical and medullary compartments, the organization of which is notably different from simple or stratified epithelia. TECs have an essential role in the generation of self-tolerant thymocytes through expression of the autoimmune regulator Aire, but the mechanisms involved in the specification and maintenance of TECs remain unclear. Despite the different embryological origins of thymus and skin (endodermal and ectodermal, respectively), some cells of the thymic medulla express stratified-epithelium markers, interpreted as promiscuous gene expression. Here we show that the thymus of the rat contains a population of clonogenic TECs that can be extensively cultured while conserving the capacity to integrate in a thymic epithelial network and to express major histocompatibility complex class II (MHC II) molecules and Aire. These cells can irreversibly adopt the fate of hair follicle multipotent stem cells when exposed to an inductive skin microenvironment; this change in fate is correlated with robust changes in gene expression. Hence, microenvironmental cues are sufficient here to re-direct epithelial cell fate, allowing crossing of primitive germ layer boundaries and an increase in potency.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonfanti, Paola -- Claudinot, Stephanie -- Amici, Alessandro W -- Farley, Alison -- Blackburn, C Clare -- Barrandon, Yann -- England -- Nature. 2010 Aug 19;466(7309):978-82. doi: 10.1038/nature09269.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Stem Cell Dynamics, School of Life Sciences, Ecole Polytechnique Federale de Lausanne (EPFL), 1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20725041" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Culture Techniques ; *Cell Dedifferentiation ; Cell Lineage/physiology ; *Cell Transdifferentiation ; Cells, Cultured ; *Cellular Reprogramming ; Clone Cells/cytology/metabolism ; Epithelial Cells/*cytology/metabolism ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Hair Follicle/cytology ; Histocompatibility Antigens Class II/metabolism ; Male ; Mice ; Multipotent Stem Cells/*cytology/metabolism ; Rats ; Rats, Sprague-Dawley ; Skin/*cytology/embryology ; Thymus Gland/*cytology/embryology ; Transcription Factors/metabolism
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    Pericytes are required for blood-brain barrier integrity during embryogenesis (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-10-15
    Description: Vascular endothelial cells in the central nervous system (CNS) form a barrier that restricts the movement of molecules and ions between the blood and the brain. This blood-brain barrier (BBB) is crucial to ensure proper neuronal function and protect the CNS from injury and disease. Transplantation studies have demonstrated that the BBB is not intrinsic to the endothelial cells, but is induced by interactions with the neural cells. Owing to the close spatial relationship between astrocytes and endothelial cells, it has been hypothesized that astrocytes induce this critical barrier postnatally, but the timing of BBB formation has been controversial. Here we demonstrate that the barrier is formed during embryogenesis as endothelial cells invade the CNS and pericytes are recruited to the nascent vessels, over a week before astrocyte generation. Analysing mice with null and hypomorphic alleles of Pdgfrb, which have defects in pericyte generation, we demonstrate that pericytes are necessary for the formation of the BBB, and that absolute pericyte coverage determines relative vascular permeability. We demonstrate that pericytes regulate functional aspects of the BBB, including the formation of tight junctions and vesicle trafficking in CNS endothelial cells. Pericytes do not induce BBB-specific gene expression in CNS endothelial cells, but inhibit the expression of molecules that increase vascular permeability and CNS immune cell infiltration. These data indicate that pericyte-endothelial cell interactions are critical to regulate the BBB during development, and disruption of these interactions may lead to BBB dysfunction and neuroinflammation during CNS injury and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3241506/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3241506/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daneman, Richard -- Zhou, Lu -- Kebede, Amanuel A -- Barres, Ben A -- R01 NS045621/NS/NINDS NIH HHS/ -- R01 NS045621-04/NS/NINDS NIH HHS/ -- R01-NS045621/NS/NINDS NIH HHS/ -- England -- Nature. 2010 Nov 25;468(7323):562-6. doi: 10.1038/nature09513. Epub 2010 Oct 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UCSF Department of Anatomy, 513 Parnassus Avenue, HSW1301, San Francisco, California 94143-0452, USA. Richard.daneman@ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20944625" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood-Brain Barrier/*cytology/*embryology/ultrastructure ; Cells, Cultured ; Central Nervous System/blood supply/cytology/*embryology ; Gene Expression Regulation, Developmental ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Pericytes/*metabolism ; Rats ; Rats, Sprague-Dawley
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    Beta2-adrenergic receptor redistribution in heart failure changes cAMP compartmentation (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-02-27
    Description: The beta1- and beta2-adrenergic receptors (betaARs) on the surface of cardiomyocytes mediate distinct effects on cardiac function and the development of heart failure by regulating production of the second messenger cyclic adenosine monophosphate (cAMP). The spatial localization in cardiomyocytes of these betaARs, which are coupled to heterotrimeric guanine nucleotide-binding proteins (G proteins), and the functional implications of their localization have been unclear. We combined nanoscale live-cell scanning ion conductance and fluorescence resonance energy transfer microscopy techniques and found that, in cardiomyocytes from healthy adult rats and mice, spatially confined beta2AR-induced cAMP signals are localized exclusively to the deep transverse tubules, whereas functional beta1ARs are distributed across the entire cell surface. In cardiomyocytes derived from a rat model of chronic heart failure, beta2ARs were redistributed from the transverse tubules to the cell crest, which led to diffuse receptor-mediated cAMP signaling. Thus, the redistribution of beta(2)ARs in heart failure changes compartmentation of cAMP and might contribute to the failing myocardial phenotype.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nikolaev, Viacheslav O -- Moshkov, Alexey -- Lyon, Alexander R -- Miragoli, Michele -- Novak, Pavel -- Paur, Helen -- Lohse, Martin J -- Korchev, Yuri E -- Harding, Sian E -- Gorelik, Julia -- 084064/Wellcome Trust/United Kingdom -- BB/D020875/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0500373/Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1653-7. doi: 10.1126/science.1185988. Epub 2010 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiac Medicine, National Heart and Lung Institute, Imperial College London, Dovehouse Street, London SW3 6LY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20185685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Membrane/*metabolism/ultrastructure ; Chronic Disease ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cytosol/metabolism ; Fluorescence Resonance Energy Transfer ; Heart Failure/*metabolism/*pathology ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Microscopy/methods ; Myocytes, Cardiac/*metabolism/ultrastructure ; Rats ; Rats, Sprague-Dawley ; Receptors, Adrenergic, beta-1/genetics/metabolism ; Receptors, Adrenergic, beta-2/genetics/*metabolism ; Sarcolemma/*metabolism/ultrastructure ; Signal Transduction
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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    Role of secondary sensory cortices in emotional memory storage and retrieval in rats (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-08-07
    Description: Visual, acoustic, and olfactory stimuli associated with a highly charged emotional situation take on the affective qualities of that situation. Where the emotional meaning of a given sensory experience is stored is a matter of debate. We found that excitotoxic lesions of auditory, visual, or olfactory secondary sensory cortices impaired remote, but not recent, fear memories in rats. Amnesia was modality-specific and not due to an interference with sensory or emotional processes. In these sites, memory persistence was dependent on ongoing protein kinase Mzeta activity and was associated with an increased activity of layers II-IV, thus suggesting a synaptic strengthening of corticocortical connections. Lesions of the same areas left intact the memory of sensory stimuli not associated with any emotional charge. We propose that secondary sensory cortices support memory storage and retrieval of sensory stimuli that have acquired a behavioral salience with the experience.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sacco, Tiziana -- Sacchetti, Benedetto -- New York, N.Y. -- Science. 2010 Aug 6;329(5992):649-56. doi: 10.1126/science.1183165.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, University of Turin, Corso Raffaello 30, I-10125 Turin, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20689011" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Amnesia/physiopathology ; Amygdala/physiology ; Animals ; Auditory Cortex/*physiology ; Conditioning (Psychology) ; Early Growth Response Protein 1/genetics/metabolism ; *Emotions ; *Fear ; Habituation, Psychophysiologic ; Male ; Memory/*physiology ; Odors ; Olfactory Pathways/*physiology ; Photic Stimulation ; Protein Kinase C/antagonists & inhibitors/metabolism ; Rats ; Rats, Wistar ; Synapses/physiology ; Visual Cortex/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Molecular identity of dendritic voltage-gated sodium channels (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-15
    Description: Active invasion of the dendritic tree by action potentials (APs) generated in the axon is essential for associative synaptic plasticity and neuronal ensemble formation. In cortical pyramidal cells (PCs), this AP back-propagation is supported by dendritic voltage-gated Na+ (Nav) channels, whose molecular identity is unknown. Using a highly sensitive electron microscopic immunogold technique, we revealed the presence of the Nav1.6 subunit in hippocampal CA1 PC proximal and distal dendrites. Here, the subunit density is lower by a factor of 35 to 80 than that found in axon initial segments. A gradual decrease in Nav1.6 density along the proximodistal axis of the dendritic tree was also detected without any labeling in dendritic spines. Our results reveal the characteristic subcellular distribution of the Nav1.6 subunit, identifying this molecule as a key substrate enabling dendritic excitability.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546315/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546315/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lorincz, Andrea -- Nusser, Zoltan -- 083484/Wellcome Trust/United Kingdom -- 090197/Wellcome Trust/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 May 14;328(5980):906-9. doi: 10.1126/science.1187958.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular Neurophysiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary. lorincz@koki.hu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466935" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/chemistry/physiology ; CA1 Region, Hippocampal/*chemistry/physiology/ultrastructure ; Cell Membrane/chemistry ; Dendrites/*chemistry/physiology/ultrastructure ; Dendritic Spines/chemistry ; Fluorescent Antibody Technique ; Freeze Fracturing ; Immunohistochemistry ; Ion Channel Gating ; Male ; Microscopy, Immunoelectron ; NAV1.1 Voltage-Gated Sodium Channel ; NAV1.6 Voltage-Gated Sodium Channel ; Nerve Tissue Proteins/analysis ; Ranvier's Nodes/chemistry ; Rats ; Rats, Wistar ; Sodium Channels/*analysis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Transition to addiction is associated with a persistent impairment in synaptic plasticity (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-06-26
    Description: Chronic exposure to drugs of abuse induces countless modifications in brain physiology. However, the neurobiological adaptations specifically associated with the transition to addiction are unknown. Cocaine self-administration rapidly suppresses long-term depression (LTD), an important form of synaptic plasticity in the nucleus accumbens. Using a rat model of addiction, we found that animals that progressively develop the behavioral hallmarks of addiction have permanently impaired LTD, whereas LTD is progressively recovered in nonaddicted rats maintaining a controlled drug intake. By making drug seeking consistently resistant to modulation by environmental contingencies and consequently more and more inflexible, a persistently impaired LTD could mediate the transition to addiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kasanetz, Fernando -- Deroche-Gamonet, Veronique -- Berson, Nadege -- Balado, Eric -- Lafourcade, Mathieu -- Manzoni, Olivier -- Piazza, Pier Vincenzo -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1709-12. doi: 10.1126/science.1187801.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉INSERM U862, NeuroCentre Magendie, 147 Rue Leo Saignat, 33077, Bordeaux Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20576893" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive ; Cocaine/administration & dosage ; Cocaine-Related Disorders/*physiopathology ; Disease Models, Animal ; Glutamic Acid/metabolism ; *Long-Term Synaptic Depression ; Nucleus Accumbens/*physiopathology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Self Administration ; Synaptic Transmission
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    Astrocytes control breathing through pH-dependent release of ATP (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-07-22
    Description: Astrocytes provide structural and metabolic support for neuronal networks, but direct evidence demonstrating their active role in complex behaviors is limited. Central respiratory chemosensitivity is an essential mechanism that, via regulation of breathing, maintains constant levels of blood and brain pH and partial pressure of CO2. We found that astrocytes of the brainstem chemoreceptor areas are highly chemosensitive. They responded to physiological decreases in pH with vigorous elevations in intracellular Ca2+ and release of adenosine triphosphate (ATP). ATP propagated astrocytic Ca2+ excitation, activated chemoreceptor neurons, and induced adaptive increases in breathing. Mimicking pH-evoked Ca2+ responses by means of optogenetic stimulation of astrocytes expressing channelrhodopsin-2 activated chemoreceptor neurons via an ATP-dependent mechanism and triggered robust respiratory responses in vivo. This demonstrates a potentially crucial role for brain glial cells in mediating a fundamental physiological reflex.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160742/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160742/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gourine, Alexander V -- Kasymov, Vitaliy -- Marina, Nephtali -- Tang, Feige -- Figueiredo, Melina F -- Lane, Samantha -- Teschemacher, Anja G -- Spyer, K Michael -- Deisseroth, Karl -- Kasparov, Sergey -- 079040/Wellcome Trust/United Kingdom -- PG/09/064/27886/British Heart Foundation/United Kingdom -- British Heart Foundation/United Kingdom -- New York, N.Y. -- Science. 2010 Jul 30;329(5991):571-5. doi: 10.1126/science.1190721. Epub 2010 Jul 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience, Physiology, and Pharmacology, University College London, London WC1E 6BT, UK. a.gourine@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20647426" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Astrocytes/*physiology ; Brain Stem/cytology/*physiology ; Calcium/metabolism ; Carbon Dioxide/analysis/blood ; Cells, Cultured ; Chemoreceptor Cells/*physiology ; Exocytosis ; Gap Junctions/metabolism ; Hydrogen-Ion Concentration ; In Vitro Techniques ; Light ; Medulla Oblongata/cytology/*physiology ; Membrane Potentials ; Rats ; Rats, Sprague-Dawley ; Receptors, Purinergic P2/metabolism ; *Respiration ; Rhodopsin/genetics/metabolism
    Print ISSN: 0036-8075
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    Sfrp5 is an anti-inflammatory adipokine that modulates metabolic dysfunction in obesity (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-06-19
    Description: Adipose tissue secretes proteins referred to as adipokines, many of which promote inflammation and disrupt glucose homeostasis. Here we show that secreted frizzled-related protein 5 (Sfrp5), a protein previously linked to the Wnt signaling pathway, is an anti-inflammatory adipokine whose expression is perturbed in models of obesity and type 2 diabetes. Sfrp5-deficient mice fed a high-calorie diet developed severe glucose intolerance and hepatic steatosis, and their adipose tissue showed an accumulation of activated macrophages that was associated with activation of the c-Jun N-terminal kinase signaling pathway. Adenovirus-mediated delivery of Sfrp5 to mouse models of obesity ameliorated glucose intolerance and hepatic steatosis. Thus, in the setting of obesity, Sfrp5 secretion by adipocytes exerts salutary effects on metabolic dysfunction by controlling inflammatory cells within adipose tissue.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3132938/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3132938/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ouchi, Noriyuki -- Higuchi, Akiko -- Ohashi, Koji -- Oshima, Yuichi -- Gokce, Noyan -- Shibata, Rei -- Akasaki, Yuichi -- Shimono, Akihiko -- Walsh, Kenneth -- AG15052/AG/NIA NIH HHS/ -- AG34972/AG/NIA NIH HHS/ -- HL81587/HL/NHLBI NIH HHS/ -- HL86785/HL/NHLBI NIH HHS/ -- P01 HL081587/HL/NHLBI NIH HHS/ -- P01 HL081587-05/HL/NHLBI NIH HHS/ -- R01 AG015052/AG/NIA NIH HHS/ -- R01 AG015052-06/AG/NIA NIH HHS/ -- R01 AG034972/AG/NIA NIH HHS/ -- R01 AG034972-03/AG/NIA NIH HHS/ -- R01 HL086785/HL/NHLBI NIH HHS/ -- R01 HL086785-19/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Jul 23;329(5990):454-7. doi: 10.1126/science.1188280. Epub 2010 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Cardiology and Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany Street, W611, Boston, MA 02118, USA. nouchi@bu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20558665" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3-L1 Cells ; Adipocytes/*metabolism/pathology ; Adipokines/genetics/*metabolism ; Adipose Tissue/*metabolism/pathology ; Animals ; Dietary Fats/administration & dosage ; Dietary Sucrose/administration & dosage ; Fatty Liver/pathology/therapy ; Genetic Vectors ; Glucose/metabolism ; Humans ; Inflammation ; Insulin/metabolism ; Insulin Resistance ; Intercellular Signaling Peptides and Proteins/genetics/*metabolism ; Macrophages/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mitogen-Activated Protein Kinase 8/genetics/metabolism ; Obesity/*metabolism/pathology ; Phosphorylation ; Rats ; Rats, Zucker ; Signal Transduction ; Wnt Proteins/metabolism
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    Alpha-synuclein promotes SNARE-complex assembly in vivo and in vitro (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-08-28
    Description: Presynaptic nerve terminals release neurotransmitters repeatedly, often at high frequency, and in relative isolation from neuronal cell bodies. Repeated release requires cycles of soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-complex assembly and disassembly, with continuous generation of reactive SNARE-protein intermediates. Although many forms of neurodegeneration initiate presynaptically, only few pathogenic mechanisms are known, and the functions of presynaptic proteins linked to neurodegeneration, such as alpha-synuclein, remain unclear. Here, we show that maintenance of continuous presynaptic SNARE-complex assembly required a nonclassical chaperone activity mediated by synucleins. Specifically, alpha-synuclein directly bound to the SNARE-protein synaptobrevin-2/vesicle-associated membrane protein 2 (VAMP2) and promoted SNARE-complex assembly. Moreover, triple-knockout mice lacking synucleins developed age-dependent neurological impairments, exhibited decreased SNARE-complex assembly, and died prematurely. Thus, synucleins may function to sustain normal SNARE-complex assembly in a presynaptic terminal during aging.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235365/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235365/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burre, Jacqueline -- Sharma, Manu -- Tsetsenis, Theodoros -- Buchman, Vladimir -- Etherton, Mark R -- Sudhof, Thomas C -- 075615/Wellcome Trust/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1663-7. doi: 10.1126/science.1195227. Epub 2010 Aug 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, and Howard Hughes Medical Institute, Stanford University, 1050 Arastradero Road, Palo Alto, CA 94304-5543, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798282" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Animals ; Cell Line ; Cells, Cultured ; HSP40 Heat-Shock Proteins/metabolism ; Humans ; Membrane Fusion ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Nerve Degeneration/*metabolism ; Neurons/*metabolism ; Presynaptic Terminals/*metabolism ; Protein Binding ; Rats ; Recombinant Fusion Proteins/metabolism ; SNARE Proteins/*metabolism ; Vesicle-Associated Membrane Protein 2/metabolism ; alpha-Synuclein/chemistry/genetics/*metabolism
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    FCHo proteins are nucleators of clathrin-mediated endocytosis (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-05-08
    Description: Clathrin-mediated endocytosis, the major pathway for ligand internalization into eukaryotic cells, is thought to be initiated by the clustering of clathrin and adaptors around receptors destined for internalization. However, here we report that the membrane-sculpting F-BAR domain-containing Fer/Cip4 homology domain-only proteins 1 and 2 (FCHo1/2) were required for plasma membrane clathrin-coated vesicle (CCV) budding and marked sites of CCV formation. Changes in FCHo1/2 expression levels correlated directly with numbers of CCV budding events, ligand endocytosis, and synaptic vesicle marker recycling. FCHo1/2 proteins bound specifically to the plasma membrane and recruited the scaffold proteins eps15 and intersectin, which in turn engaged the adaptor complex AP2. The FCHo F-BAR membrane-bending activity was required, leading to the proposal that FCHo1/2 sculpt the initial bud site and recruit the clathrin machinery for CCV formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883440/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2883440/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Henne, William Mike -- Boucrot, Emmanuel -- Meinecke, Michael -- Evergren, Emma -- Vallis, Yvonne -- Mittal, Rohit -- McMahon, Harvey T -- MC_U105178795/Medical Research Council/United Kingdom -- U.1051.02.007(78795)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2010 Jun 4;328(5983):1281-4. doi: 10.1126/science.1188462. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Laboratory of Molecular Biology (MRC-LMB), Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448150" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex 2/metabolism ; Adaptor Proteins, Signal Transducing ; Adaptor Proteins, Vesicular Transport/metabolism ; Animals ; Calcium-Binding Proteins/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Clathrin/*metabolism ; Clathrin-Coated Vesicles/*metabolism ; *Endocytosis ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins ; Mice ; Models, Molecular ; Neurons/cytology/metabolism ; Phosphoproteins/metabolism ; Protein Multimerization ; Protein Structure, Tertiary ; Proteins/chemistry/*metabolism ; RNA Interference ; Rats ; Rats, Sprague-Dawley ; Recombinant Fusion Proteins/metabolism ; Synaptic Vesicles/metabolism
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    Medicine. Refugee receptors switch sides (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-03-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dorn, Gerald W 2nd -- R01 HL087871/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1586-7. doi: 10.1126/science.1188538.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. gdorn@wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339055" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Compartmentation ; Cell Membrane/*metabolism/ultrastructure ; Cyclic AMP/*metabolism ; Heart Failure/*metabolism/pathology/physiopathology ; Humans ; Membrane Microdomains/metabolism ; Mice ; Myocardial Contraction ; Myocytes, Cardiac/*metabolism/ultrastructure ; Rats ; Receptors, Adrenergic, beta-1/*metabolism ; Receptors, Adrenergic, beta-2/*metabolism ; Sarcolemma/metabolism/ultrastructure ; Signal Transduction
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    Neuroscience. Dendrites do it in sequences (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-10-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Destexhe, Alain -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1611-2. doi: 10.1126/science.1196743.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Unite de Neurosciences, Information & Complexite, CNRS, 91198 Gif-sur-Yvette, France. destexhe@unic.cnrs-gif.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929837" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cerebral Cortex/cytology/*physiology ; Dendrites/*physiology/ultrastructure ; Dendritic Spines/*physiology/ultrastructure ; Membrane Potentials ; Pyramidal Cells/*physiology/ultrastructure ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology
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  • 98
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    Neuroscience. Dedicated to memory? (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eichenbaum, Howard -- New York, N.Y. -- Science. 2010 Dec 3;330(6009):1331-2. doi: 10.1126/science.1199462.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Memory and Brain, Boston University, Boston, MA 02215, USA. hbe@bu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21127238" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Injuries/*physiopathology ; Brain Mapping ; Darkness ; Hippocampus/physiology ; *Memory ; Memory Disorders/*physiopathology ; Models, Neurological ; Neural Pathways/physiology ; Prefrontal Cortex/physiology ; Rats ; Sensory Deprivation ; Temporal Lobe/*injuries/*physiopathology
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  • 99
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    Axon extension occurs independently of centrosomal microtubule nucleation (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-01-09
    Description: Microtubules are polymeric protein structures and components of the cytoskeleton. Their dynamic polymerization is important for diverse cellular functions. The centrosome is the classical site of microtubule nucleation and is thought to be essential for axon growth and neuronal differentiation--processes that require microtubule assembly. We found that the centrosome loses its function as a microtubule organizing center during development of rodent hippocampal neurons. Axons still extended and regenerated through acentrosomal microtubule nucleation, and axons continued to grow after laser ablation of the centrosome in early neuronal development. Thus, decentralized microtubule assembly enables axon extension and regeneration, and, after axon initiation, acentrosomal microtubule nucleation arranges the cytoskeleton, which is the source of the sophisticated morphology of neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stiess, Michael -- Maghelli, Nicola -- Kapitein, Lukas C -- Gomis-Ruth, Susana -- Wilsch-Brauninger, Michaela -- Hoogenraad, Casper C -- Tolic-Norrelykke, Iva M -- Bradke, Frank -- New York, N.Y. -- Science. 2010 Feb 5;327(5966):704-7. doi: 10.1126/science.1182179. Epub 2010 Jan 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Independent Junior Research Group Axonal Growth and Regeneration, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 Martinsried, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20056854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/metabolism ; Axons/*physiology/ultrastructure ; Axotomy ; Centrosome/*physiology/ultrastructure ; Hippocampus/*cytology ; Mice ; Microtubule-Associated Proteins/metabolism ; Microtubules/*metabolism/ultrastructure ; Nerve Regeneration ; Neurogenesis ; Neurons/*physiology/ultrastructure ; Rats ; Tubulin/metabolism
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    Composition of isolated synaptic boutons reveals the amounts of vesicle trafficking proteins (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-05-31
    Description: Synaptic vesicle recycling has long served as a model for the general mechanisms of cellular trafficking. We used an integrative approach, combining quantitative immunoblotting and mass spectrometry to determine protein numbers; electron microscopy to measure organelle numbers, sizes, and positions; and super-resolution fluorescence microscopy to localize the proteins. Using these data, we generated a three-dimensional model of an "average" synapse, displaying 300,000 proteins in atomic detail. The copy numbers of proteins involved in the same step of synaptic vesicle recycling correlated closely. In contrast, copy numbers varied over more than three orders of magnitude between steps, from about 150 copies for the endosomal fusion proteins to more than 20,000 for the exocytotic ones.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilhelm, Benjamin G -- Mandad, Sunit -- Truckenbrodt, Sven -- Krohnert, Katharina -- Schafer, Christina -- Rammner, Burkhard -- Koo, Seong Joo -- Classen, Gala A -- Krauss, Michael -- Haucke, Volker -- Urlaub, Henning -- Rizzoli, Silvio O -- New York, N.Y. -- Science. 2014 May 30;344(6187):1023-8. doi: 10.1126/science.1252884.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuro- and Sensory Physiology, University of Gottingen Medical Center, European Neuroscience Institute, Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain, Gottingen, Germany. International Max Planck Research School Neurosciences, 37077 Gottingen, Germany. ; Bioanalytical Mass Spectrometry Group, Max-Planck-Institute for Biophysical Chemistry, 37077 Gottingen, Germany. ; Department of Neuro- and Sensory Physiology, University of Gottingen Medical Center, European Neuroscience Institute, Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain, Gottingen, Germany. International Max Planck Research School Molecular Biology, 37077 Gottingen, Germany. ; Department of Neuro- and Sensory Physiology, University of Gottingen Medical Center, European Neuroscience Institute, Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain, Gottingen, Germany. ; Leibniz Institut fur Molekulare Pharmakologie, Department of Molecular Pharmacology and Cell Biology, Robert-Rossle-Strasse 10, 13125 Berlin, Germany. ; Bioanalytical Mass Spectrometry Group, Max-Planck-Institute for Biophysical Chemistry, 37077 Gottingen, Germany. Bioanalytics, Department of Clinical Chemistry, University Medical Center Gottingen, 37075 Gottingen, Germany. ; Department of Neuro- and Sensory Physiology, University of Gottingen Medical Center, European Neuroscience Institute, Cluster of Excellence Nanoscale Microscopy and Molecular Physiology of the Brain, Gottingen, Germany. srizzol@gwdg.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24876496" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism/ultrastructure ; Exocytosis ; Imaging, Three-Dimensional ; Immunoblotting/methods ; Mass Spectrometry/methods ; Microscopy, Electron/methods ; Models, Neurological ; Presynaptic Terminals/chemistry/*metabolism/ultrastructure ; Protein Transport ; Rats ; Rats, Wistar ; Synaptic Vesicles/chemistry/*metabolism ; Synaptosomes/chemistry/*metabolism/ultrastructure ; Vesicular Transport Proteins/analysis/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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