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  • 1
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    Dynamics of Protein Kinases: Insights from Nuclear Magnetic Resonance (2015)
    American Chemical Society (ACS)
    Details
    Publication Date: 2015-03-25
    Description: Accounts of Chemical Research DOI: 10.1021/acs.accounts.5b00001
    Print ISSN: 0001-4842
    Electronic ISSN: 1520-4898
    Topics: Chemistry and Pharmacology
    Published by American Chemical Society (ACS)
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  • 2
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    Corrigendum: Endocrinization of FGF1 produces a neomorphic and potent insulin sensitizer (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suh, Jae Myoung -- Jonker, Johan W -- Ahmadian, Maryam -- Goetz, Regina -- Lackey, Denise -- Osborn, Olivia -- Huang, Zhifeng -- Liu, Weilin -- Yoshihara, Eiji -- van Dijk, Theo H -- Havinga, Rick -- Fan, Weiwei -- Yin, Yun-Qiang -- Yu, Ruth T -- Liddle, Christopher -- Atkins, Annette R -- Olefsky, Jerrold M -- Mohammadi, Moosa -- Downes, Michael -- Evans, Ronald M -- P01 HL088093/HL/NHLBI NIH HHS/ -- P42 ES010337/ES/NIEHS NIH HHS/ -- R01 DE013686/DE/NIDCR NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R24 DK090962/DK/NIDDK NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- England -- Nature. 2015 Apr 16;520(7547):388. doi: 10.1038/nature14304. Epub 2015 Mar 4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25739500" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Endocrinization of FGF1 produces a neomorphic and potent insulin sensitizer (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-07-22
    Description: Fibroblast growth factor 1 (FGF1) is an autocrine/paracrine regulator whose binding to heparan sulphate proteoglycans effectively precludes its circulation. Although FGF1 is known as a mitogenic factor, FGF1 knockout mice develop insulin resistance when stressed by a high-fat diet, suggesting a potential role in nutrient homeostasis. Here we show that parenteral delivery of a single dose of recombinant FGF1 (rFGF1) results in potent, insulin-dependent lowering of glucose levels in diabetic mice that is dose-dependent but does not lead to hypoglycaemia. Chronic pharmacological treatment with rFGF1 increases insulin-dependent glucose uptake in skeletal muscle and suppresses the hepatic production of glucose to achieve whole-body insulin sensitization. The sustained glucose lowering and insulin sensitization attributed to rFGF1 are not accompanied by the side effects of weight gain, liver steatosis and bone loss associated with current insulin-sensitizing therapies. We also show that the glucose-lowering activity of FGF1 can be dissociated from its mitogenic activity and is mediated predominantly via FGF receptor 1 signalling. Thus we have uncovered an unexpected, neomorphic insulin-sensitizing action for exogenous non-mitogenic human FGF1 with therapeutic potential for the treatment of insulin resistance and type 2 diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184286/" 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/PMC4184286/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suh, Jae Myoung -- Jonker, Johan W -- Ahmadian, Maryam -- Goetz, Regina -- Lackey, Denise -- Osborn, Olivia -- Huang, Zhifeng -- Liu, Weilin -- Yoshihara, Eiji -- van Dijk, Theo H -- Havinga, Rick -- Fan, Weiwei -- Yin, Yun-Qiang -- Yu, Ruth T -- Liddle, Christopher -- Atkins, Annette R -- Olefsky, Jerrold M -- Mohammadi, Moosa -- Downes, Michael -- Evans, Ronald M -- DE13686/DE/NIDCR NIH HHS/ -- DK-033651/DK/NIDDK NIH HHS/ -- DK-063491/DK/NIDDK NIH HHS/ -- DK-074868/DK/NIDDK NIH HHS/ -- DK057978/DK/NIDDK NIH HHS/ -- DK090962/DK/NIDDK NIH HHS/ -- ES010337/ES/NIEHS NIH HHS/ -- HL088093/HL/NHLBI NIH HHS/ -- HL105278/HL/NHLBI NIH HHS/ -- P01 DK054441/DK/NIDDK NIH HHS/ -- P01 DK074868/DK/NIDDK NIH HHS/ -- P01 HL088093/HL/NHLBI NIH HHS/ -- P01-DK054441-14A1/DK/NIDDK NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P42 ES010337/ES/NIEHS NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R24 DK090962/DK/NIDDK NIH HHS/ -- R37 DK033651/DK/NIDDK NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- T32 DK007494/DK/NIDDK NIH HHS/ -- T32-DK-007494/DK/NIDDK NIH HHS/ -- U54 HD012303/HD/NICHD NIH HHS/ -- U54-HD-012303-25/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Sep 18;513(7518):436-9. doi: 10.1038/nature13540. Epub 2014 Jul 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA [2]. ; 1] Center for Liver, Digestive and Metabolic Diseases, Departments of Pediatrics and Laboratory Medicine, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands [2]. ; Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA. ; Department of Medicine, Division of Endocrinology and Metabolism, University of California at San Diego, La Jolla, California 92093, USA. ; 1] Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA [2] School of Pharmacy, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China. ; Center for Liver, Digestive and Metabolic Diseases, Departments of Pediatrics and Laboratory Medicine, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands. ; The Storr Liver Unit, Westmead Millennium Institute and University of Sydney, Westmead Hospital, Westmead, New South Wales 2145, Australia. ; 1] Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA [2] Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Body Weight/drug effects ; Diabetes Mellitus, Experimental/drug therapy/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Diet, High-Fat ; Dose-Response Relationship, Drug ; Fibroblast Growth Factor 1/administration & dosage/adverse effects/*pharmacology ; Glucose/*metabolism ; Glucose Tolerance Test ; Humans ; Insulin/*metabolism ; Insulin Resistance ; Liver/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mitogens/pharmacology ; Muscle, Skeletal/drug effects/metabolism ; Receptor, Fibroblast Growth Factor, Type 1/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Regulation of circadian behaviour and metabolism by REV-ERB-alpha and REV-ERB-beta (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-03-31
    Description: The circadian clock acts at the genomic level to coordinate internal behavioural and physiological rhythms via the CLOCK-BMAL1 transcriptional heterodimer. Although the nuclear receptors REV-ERB-alpha and REV-ERB-beta have been proposed to form an accessory feedback loop that contributes to clock function, their precise roles and importance remain unresolved. To establish their regulatory potential, we determined the genome-wide cis-acting targets (cistromes) of both REV-ERB isoforms in murine liver, which revealed shared recognition at over 50% of their total DNA binding sites and extensive overlap with the master circadian regulator BMAL1. Although REV-ERB-alpha has been shown to regulate Bmal1 expression directly, our cistromic analysis reveals a more profound connection between BMAL1 and the REV-ERB-alpha and REV-ERB-beta genomic regulatory circuits than was previously suspected. Genes within the intersection of the BMAL1, REV-ERB-alpha and REV-ERB-beta cistromes are highly enriched for both clock and metabolic functions. As predicted by the cistromic analysis, dual depletion of Rev-erb-alpha and Rev-erb-beta function by creating double-knockout mice profoundly disrupted circadian expression of core circadian clock and lipid homeostatic gene networks. As a result, double-knockout mice show markedly altered circadian wheel-running behaviour and deregulated lipid metabolism. These data now unite REV-ERB-alpha and REV-ERB-beta with PER, CRY and other components of the principal feedback loop that drives circadian expression and indicate a more integral mechanism for the coordination of circadian rhythm and metabolism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367514/" 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/PMC3367514/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cho, Han -- Zhao, Xuan -- Hatori, Megumi -- Yu, Ruth T -- Barish, Grant D -- Lam, Michael T -- Chong, Ling-Wa -- DiTacchio, Luciano -- Atkins, Annette R -- Glass, Christopher K -- Liddle, Christopher -- Auwerx, Johan -- Downes, Michael -- Panda, Satchidananda -- Evans, Ronald M -- DK057978/DK/NIDDK NIH HHS/ -- DK062434/DK/NIDDK NIH HHS/ -- DK090962/DK/NIDDK NIH HHS/ -- DK091618/DK/NIDDK NIH HHS/ -- HL105278/HL/NHLBI NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R01 DK091618/DK/NIDDK NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R01 HL105278-21/HL/NHLBI NIH HHS/ -- R24 DK090962/DK/NIDDK NIH HHS/ -- R24 DK090962-02/DK/NIDDK NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- R37 DK057978-34/DK/NIDDK NIH HHS/ -- T32 HL007770/HL/NHLBI NIH HHS/ -- T32 HL007770-15/HL/NHLBI NIH HHS/ -- T32-HL007770/HL/NHLBI NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-10/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Mar 29;485(7396):123-7. doi: 10.1038/nature11048.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22460952" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Clocks/drug effects/genetics ; Circadian Rhythm/genetics/*physiology ; Cryptochromes/deficiency/genetics/metabolism ; *Energy Metabolism/genetics ; Feedback, Physiological ; Gene Expression Regulation ; Gene Regulatory Networks/genetics ; Homeostasis/genetics ; *Lipid Metabolism/genetics ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Motor Activity/genetics/physiology ; Nuclear Receptor Subfamily 1, Group D, Member 1/deficiency/genetics/*metabolism ; Period Circadian Proteins/deficiency/genetics/metabolism ; Receptors, Cytoplasmic and Nuclear/deficiency/genetics/*metabolism ; Repressor Proteins/deficiency/genetics/*metabolism ; Transcriptome/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Depletion of fat-resident Treg cells prevents age-associated insulin resistance (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-11-19
    Description: Age-associated insulin resistance (IR) and obesity-associated IR are two physiologically distinct forms of adult-onset diabetes. While macrophage-driven inflammation is a core driver of obesity-associated IR, the underlying mechanisms of the obesity-independent yet highly prevalent age-associated IR are largely unexplored. Here we show, using comparative adipo-immune profiling in mice, that fat-resident regulatory T cells, termed fTreg cells, accumulate in adipose tissue as a function of age, but not obesity. Supporting the existence of two distinct mechanisms underlying IR, mice deficient in fTreg cells are protected against age-associated IR, yet remain susceptible to obesity-associated IR and metabolic disease. By contrast, selective depletion of fTreg cells via anti-ST2 antibody treatment increases adipose tissue insulin sensitivity. These findings establish that distinct immune cell populations within adipose tissue underlie ageing- and obesity-associated IR, and implicate fTreg cells as adipo-immune drivers and potential therapeutic targets in the treatment of age-associated IR.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4670283/" 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/PMC4670283/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bapat, Sagar P -- Myoung Suh, Jae -- Fang, Sungsoon -- Liu, Sihao -- Zhang, Yang -- Cheng, Albert -- Zhou, Carmen -- Liang, Yuqiong -- LeBlanc, Mathias -- Liddle, Christopher -- Atkins, Annette R -- Yu, Ruth T -- Downes, Michael -- Evans, Ronald M -- Zheng, Ye -- AI099295/AI/NIAID NIH HHS/ -- AI107027/AI/NIAID NIH HHS/ -- CA014195/CA/NCI NIH HHS/ -- DK057978/DK/NIDDK NIH HHS/ -- DK090962/DK/NIDDK NIH HHS/ -- ES010337/ES/NIEHS NIH HHS/ -- F30 DK096828/DK/NIDDK NIH HHS/ -- HL088093/HL/NHLBI NIH HHS/ -- HL105278/HL/NHLBI NIH HHS/ -- P01 HL088093/HL/NHLBI NIH HHS/ -- P42 ES010337/ES/NIEHS NIH HHS/ -- R01 AI107027/AI/NIAID NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R24 DK090962/DK/NIDDK NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- R56 AI099295/AI/NIAID NIH HHS/ -- T32 GM007198/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Dec 3;528(7580):137-41. doi: 10.1038/nature16151. Epub 2015 Nov 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunobiology and Microbial Pathogenesis Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Gene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Graduate School of Medical Science and Engineering, KAIST 34141, South Korea. ; Department of Biotechnology, College of Life Sciences, Sejong University, Seoul 143-747, South Korea. ; Storr Liver Centre, Westmead Millennium Institute, Sydney Medical School, University of Sydney, Sydney 2145, Australia. ; Howard Hughes Medical Institute, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26580014" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology/*immunology ; Aging/*immunology ; Animals ; Diabetes Mellitus, Type 2/metabolism ; Glucose/metabolism ; Inflammation/immunology/metabolism ; Insulin Resistance/*immunology ; Macrophages/immunology ; Male ; Metabolic Syndrome X/immunology/metabolism ; Mice ; Obesity/metabolism ; T-Lymphocytes, Regulatory/*cytology/*immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Electronic Resource
    Electronic Resource
    Constitutive expression and hormonal regulation of male sexually differentiated cytochromes P450 in primary cultured rat hepatocytes
    Amsterdam : Elsevier
    Archives of Biochemistry and Biophysics 298 (1992), S. 159-166 
    Details
    ISSN: 0003-9861
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0003-9861(92)90107-8
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  • 7
    Electronic Resource
    Electronic Resource
    Effect of actinomycin D on vitamin D-mediated uptake of45Ca by intestinal slices (1973)
    Springer
    Calcified tissue international 13 (1973), S. 187-196 
    Details
    ISSN: 1432-0827
    Keywords: Vitamin D ; Actinomycin D ; Calcium Absorption ; Intestinal Uptake of Calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Description / Table of Contents: Résumé La vitamine D augmente nettement l'absorption et le transfert du calcium dans le duodenum de rats en avitaminose D, alimentés avec des régimes pauvres ou riches en calcium. Des travaux antérieurs ont montré que l'actinomycine D freine l'action de la vitamine D, faible en calcium: des animaux, équilibrés en phosphore, ont été utilisés, ne permettant pas de savoir si l'actinomycine a un effet similaire chez des animaux soumis à un régime élevé en calcium, faible en phosphore. Avec un traitement combinant±de vitamine D et±d'actinomycine D, des fragments de duodénum ont été testés concernant l'absorption passive ou active de calciumin vitro. Le transfert du calcium à travers l'intestin vers le sang est mesuréin vivo. Concernant l'absorption intestinale, il n'y a pas d'interaction entre l'actinomycine D et la vitamine D chez des animaux soumis à des régimes de 1.20% Ca: 0,06% P pendant 20 jours avant le traitement. Chez les animaux soumis à 0.02% Ca: 0.3% P pendant la même période, l'actinomycine D diminue l'absorption de fragments d'intestinsin vitro, cependant avec la vitamine D, l'absorption de calcium est augmentée, bien qu'à un degré moindre en présence de l'antibiotique. La vitamine D tend à augmenter le transfert du calcium vers le sang des animaux soumis aux deux régions en présence ou en l'absence de l'actinomycine D.
    Abstract: Zusammenfassung Vitamin D bewirkt eine signifikante Erhöhung der Aufnahme und des Transportes von Calcium im Duodenum von D-Mangel-Ratten, deren Nahrung wenig oder viel Calcium enthielt. In früheren Arbeiten anderer Autoren, welche nachwiesen, daß Actinomycin D die Wirkung von Vitamin D blockierte, wurden Tiere verwendet, welche wenig Calcium, jedoch genügend Phosphor erhielten. Dabei wurde die Frage nicht berücksichtigt, ob Actinomycin D bei Tieren, die viel Calcium und wenig Phosphor in der Nahrung erhielten, eine ähnliche Wirkung hätte. In dieser Arbeit wurden ± Vitamin D und ±Actonomycin D kombiniert und Duodenumschnitte auf passive im Gegensatz zu aktiver Calciumaufnahmein vitro geprüft. Der Calciumtransport durch den Darm ins Blut wurdein vivo gemessen. In Bezug auf die intestinale Aufnahme bestand keine Wechselwirkung zwischen Actinomycin D und Vitamin D bei den Tieren, welche während 20 Tagen vor der Behandlung eine 1,2% Ca: 0,06% P-Diät erhalten hatten. Bei den Tieren, welche ebenfalls 20 Tage lang 0,02% Ca: 0,3% P erhalten hatten, verminderte Actinomycin D die Calciumaufnahme von Darmschnittenin vitro, aber wenn Vitamin D mitverabreicht wurde, erhöhte das Vitamin die Calciumaufnahme signifikant; die Erhöhung war in Anwesenheit des Antibiotikums etwas weniger ausgeprägt. Vitamin D führte zu eine Zunahme des Calciumtransports ins Blut und zwar bei beiden Diäten und mit oder ohne Actinomycin D.
    Notes: Abstract Vitamin D significantly increases the uptake and transport of calcium in the duodenum of D-deficient rats fed either high or low calcium diets. In previous work by others showing that actinomycin D blocked the effect of vitamin D, low calcium: adequate phosphorus animals were used, leaving unanswered the question as to whether actinomycin D would have a similar effect in animals fed a high calcium: low phosphorus diet. With treatment combining ±vitamin D and ±actinomycin D, slices of duodenum were tested for passivevs. active uptake of calciumin vitro. The transport of calcium across the intestine into blood was measuredin vivo. With regard to intestinal uptake, there was no interaction between actinomycin D and vitamin D in animals fed 1.2% Ca: 0.06% P diet for 20 days before treatment. In those animals fed the 0.02% Ca: 0.3% P diet for the same period of time, actinomycin D reduced the uptake of intestinal slicesin vitro but, when combined with vitamin D, the vitamin significantly enhanced the uptake of calcium, though to a lesser extent, in the presence of the antibiotic. Vitamin D tended to increase the transport of calcium into blood of animals on both diets in the presence or absence of actinomycin D.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02015409
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  • 8
    Electronic Resource
    Electronic Resource
    Alteration of circulating antibody response of mice exposed to 9-GHz pulsed microwaves (1980)
    New York, NY [u.a.] : Wiley-Blackwell
    Bioelectromagnetics 1 (1980), S. 397-404 
    Details
    ISSN: 0197-8462
    Keywords: antibody response ; microwaves ; immunology ; 9-GHz pulsed radiation ; infectivity ; mouse ; Life and Medical Sciences ; Occupational Health and Environmental Toxicology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Physics
    Notes: A significant increase was observed in the circulating antibody titers of mice exposed to 9-GHz pulsed microwaves at an average power density of 10 mW/ cm2, two hours per day for five days compared with sham-irradiated animals. The mice were previously immunized with type III pneumococcal polysaccharide. Following irradiation, a portion of the immunized animals were challenged with virulent Streptococcus pneumoniae, type III. Ten days after challenge, mortality was essentially the same in the two groups, but during the ten day period, there was a noticeable increase in the survival time of the irradiated animals compared with the sham-irradiated animals, suggesting that the increased circulating antibody response afforded some degree of temporary protection to the animals.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bem.2250010406
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  • 9
    Electronic Resource
    Electronic Resource
    Circulating antibody response of mice exposed to 9-GHz pulsed microwave radiation (1986)
    New York, NY [u.a.] : Wiley-Blackwell
    Bioelectromagnetics 7 (1986), S. 91-94 
    Details
    ISSN: 0197-8462
    Keywords: microwaves ; immunology ; antibody response ; mice ; Life and Medical Sciences ; Occupational Health and Environmental Toxicology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Physics
    Notes: Female CD-1 mice immunized against the bacterium Streptococcus pneumoniae type III were exposed to 9-GHz pulsed microwaves (pulse repetition rate 970-1,000, pulse width 1.0 μs, peak power 1 W/cm2) at an average incident power density of 1 mW/cm2 (calculated SAR = 0.47 W/kg) for 2 h per day for 5 days. Circulating antibody titers for the microwave-exposed animals were not significantly different from those of the shamirradiated animals, and there were no differences in any of the hematological parameters analyzed, indicating that 9-GHz pulsed microwaves at 1 mW/cm2 do not alter the immune response of mice immunized against S pneumoniae.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bem.2250070110
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  • 10
    Electronic Resource
    Electronic Resource
    Effect of 9.6-GHz pulsed microwaves on the orb web spinning ability of the cross spider (Araneus diadematus) (1986)
    New York, NY [u.a.] : Wiley-Blackwell
    Bioelectromagnetics 7 (1986), S. 101-105 
    Details
    ISSN: 0197-8462
    Keywords: microwaves ; spider webs ; behavior ; 9.6-GHz pulsed radiation ; Life and Medical Sciences ; Occupational Health and Environmental Toxicology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Physics
    Notes: Eight cross spiders (Araneus diadematus) were exposed overnight (16 h) during web-building activity to pulsed 9.6-GHz microwaves at average power densities of 10, 1, and 0.1 mW/cm2 (estimated SARs 40, 4, and 0.4 mW/g). Under these conditions, 9.6-GHz pulsed microwaves did not affect the web-spinning ability of the cross spider.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bem.2250070112
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