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  • Articles  (235)
  • Springer Nature  (96)
  • Cell Press  (45)
  • Springer  (37)
  • American Society of Hematology  (34)
  • American Chemical Society  (23)
  • American Institute of Physics (AIP)
  • 2000-2004  (235)
  • Medicine  (213)
  • Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics  (22)
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  • Articles  (235)
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  • 1
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    Crystal Structure of Methylmalonyl-Coenzyme A Epimerase from P. shermanii (2001)
    Cell Press
    Details
    Publication Date: 2001-07-01
    Print ISSN: 0969-2126
    Electronic ISSN: 1878-4186
    Topics: Biology , Medicine
    Published by Cell Press
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  • 2
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    Water-Soluble, Core-Modified Porphyrins as Novel, Longer-Wavelength-Absorbing Sensitizers for Photodynamic Therapy. II. Effects of Core Heteroatoms andMeso-Substituents on Biological Activity (2002)
    American Chemical Society
    Details
    Publication Date: 2002-01-01
    Print ISSN: 0022-2623
    Electronic ISSN: 1520-4804
    Topics: Chemistry and Pharmacology , Medicine
    Published by American Chemical Society
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  • 3
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    T Cell Trafficking in Acute GVHD: In Vivo Bioluminescence Evaluation To Elucidate the Role of Different Lymphatic Organs. (2004)
    American Society of Hematology
    Details
    Publication Date: 2004-11-16
    Description: To study the complex pathophysiology of aGvHD in allogeneic hematopoietic cell transplantation (HCT) we transplanted transgenic luciferase expressing T cell populations into lethally irradiated HCT recipients (murine MHC major mismatch model, H-2q into H-2d). Tracking of light emitting donor T cells in living animals and detailed studies by multi color immunofluorescence microscopy (IFM) and FACS revealed the tight links of spatial and temporal evolution in this complex immune process. Donor derived T cells migrate to T cell areas in lymphoid tissues within a period of 12 hours. In the initial periods donor CD4+ T cells appear first with CD8+ T cell infiltration at later time points. Donor T cells start proliferating in lymphatic tissues on day 2 after transfer, as observed by BrdU stainings. Although alloreactive T cells are similarly activated in all lymphoid organs, they only up-regulate gut homing molecules after more than 5 cell divisions (CFSE proliferation analysis by FACS) in certain lymphoid organs (Peyer’s patches, mesenteric LN and spleen). Abruptly on day 4 after HCT, T cells migrate into intestinal sites. These findings strongly suggested, that specific priming sites are required for alloreactive T cells to induce a distinct type of tissue tropism in GvHD. In contrast to previous reports peformed without host conditioning, depletion of certain lymphoid organs (e.g. Peyer’s patches) before HCT or antibody blocking experiments did not control aGVHD. BLI showed, that anti-L-selectin or anti-MAdCAM-1 antibody treatment alone or in combination was effective in blocking donor T cell migration to lymph nodes and Peyer’s patches, while redirecting these cells to liver and spleen. Subsequently cells proliferated predominantly in the spleen until day 3 after HCT. Surprisingly we observed a full picture of gut infiltration on day 4 and skin involvement on day 5–6, similar in dynamics and strength to the aGvHD isotype control group. These findings demonstrated, that other lymphoid organs can functionally compensate for inducing gut and skin homing of alloreactive T cells. Of importance, we demonstrated that T cells that lacked homing molecules for secondary lymphoid organs had alloreactive properties in vitro, yet did not cause aGVHD in vivo. In summary, the activation of alloreactive T cells in specific sites throughout the body is complex and involves the acquisition of homing molecule expression. Transplantation of T cells with defined homing properties therefore, appears to be a promising alternative in conferring protective immunity early after HCT without the risk of aGvHD.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 4
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    Mae mediates MAP kinase phosphorylation of Ets transcription factors in Drosophila (2001)
    Springer Nature
    Details
    Publication Date: 2001-05-01
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 5
    Electronic Resource
    Electronic Resource
    A Method for Architecting Product Platforms (2000)
    Springer
    Research in engineering design 12 (2000), S. 61-72 
    Details
    ISSN: 1435-6066
    Keywords: Key words:Product families – Product platforms, Product portfolio architecture.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Technology
    Notes: Abstract: Consider a group of products sharing common parts and assemblies. The products in question we call a product family, and the common elements, the platform. In this paper, we present a method for designing product platforms and the derived family that takes into consideration both the technical performance requirements as well as the cost of the product family. The design of a platform-based product family is formulated as a general optimization problem in which the advantages of designing a common platform must be balanced against the constraints of the individual product variants and constraints of the family as a whole. This optimization approach forms the basis for a practical implementation as an interactive, team-based negotiation model for designing a family of interplanetary spacecraft based on a common platform. The approach is used to consider and specify different subsystems that could be made common to all the missions. It is also used to evaluate the impact of those platform design decisions on the performance of the product family, and thus be able to select from among feasible platform designs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001630050024
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  • 6
    Electronic Resource
    Electronic Resource
    Phosphatidylethanol stimulates calcium-dependent cytosolic phospholipase A2 activity of a macrophage cell line (RAW 264.7) (2000)
    Springer
    Journal of biomedical science 7 (2000), S. 311-316 
    Details
    ISSN: 1423-0127
    Keywords: Phosphatidylethanol ; Phosphatidic acid ; Ethanol ; Phospholipase A2, cytosolic ; Phospholipase D ; RAW 264.7 cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The synthesis of inflammation mediators produced from arachidonic acid is regulated primarily by the cellular concentration of free arachidonic acid. Since intracellular arachidonic acid is almost totally present as phospholipid esters, the concentration of intracellular arachidonic acid is primarily dependent on the balance between the release of arachidonic acid from membrane phospholipids and are uptake of arachidonic acid into membrane phospholipids. Cytosolic phospholipase A2 is a calcium-dependent enzyme that catalyzes the stimulus-coupled hydrolysis of arachidonic acid from membrane phospholipids. Following exposure of macrophages to various foreign or endogenous stimulants, cytosolic phospholipase A2 is activated. Treatment with these compounds may also stimulate phospholipase D activity, and, in the presence of ethanol, phospholipase D catalyzes the synthesis of phosphatidylethanol. A cell-free system was used to evaluate the effect of phosphatidylethanol on cytosolic phospholipase A2 activity. Phosphatidylethanol (0.5 µM) added to 1-stearoyl-2-[3H]-arachidonoyl-sn-glycero-3-phosphocholine vesicles stimulated cytosolic phospholipase A2 activity. However, high concentrations (20–100 µM) of phosphatidylethanol inhibited cytosolic phospholipase A2 activity. Phosphatidic acid, the normal phospholipase D product, also stimulated cytosolic phospholipase A2 activity at 0.5 µM, but had an inhibitory effect on cytosolic phospholipase A2 activity at concentrations of 50 and 100 µM. Ethanol (20–200 mM), the precursor of phosphatidylethanol, added directly to the assay did not alter cytosolic phospholipase A2 activity. These results suggest that phosphatidylethanol alters the physical properties of the substrate, and at lower concentrations of anionic phospholipids the substrate is more susceptible to hydrolysis. However, at high concentrations, phosphatidylethanol either reverses the alterations in physical properties of the substrate or phosphatidylethanol may be competing as the substrate. Both interactions may result in lower cytosolic phospholipase A2 activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253250
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  • 7
    Electronic Resource
    Electronic Resource
    Three-dimensional model of human TIP30, a coactivator for HIV-1 Tat-activated transcription, and CC3, a protein associated with metastasis suppression (2000)
    Springer
    Cellular and molecular life sciences 57 (2000), S. 851-858 
    Details
    ISSN: 1420-9071
    Keywords: Key words. HIV-1; Tat; metastasis; TIP30; CC3.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Human TIP30 is a cofactor that specifically enhances human immunodeficiency virus-1 (HIV-1) Tat-activated transcription. The sequence of TIP30 is identical to that of CC3, a protein associated with metastasis suppression. TIP30/CC3 is a member of the short-chain dehydrogenases/reductases (SDR) family. Of the several experimentally determined SDR structures, Escherichia coli uridine diphosphate (UDP) galactose-4 epimerase is most similar to TIP30/CC3. Because the direct sequence similarity between TIP30/CC3 and E. coli UDP galactose-4 epimerase is low, we used the transitive nature of homology and employed two Aquifex aeolicus proteins as intermediaries in the homology modeling process. Comparison of our structural model with that of known SDRs reveals that TIP30/CC3 contains several well-conserved features, including a βαβ fold at the amino terminus, which we predict binds NADP(H). TIP30/CC3 contains characteristic motifs at the catalytic site of SDRs, including a serine, tyrosine, and lysine that are important in catalyzing hydride transfer between substrate and cofactor. We also predict that a unique 20-amino acid sequence found at the amino terminus is an α-helix. Because this region contains several positively and negatively charged amino acids, it may dock TIP30/CC3 to other proteins. Our structural model points to this α-helix and the SDR-like part of TIP30/CC3 for mutagenesis experiments to elucidate its role in HIV-1 Tat-activated transcription, metastasis suppression, and other cellular functions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000180050047
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  • 8
    Electronic Resource
    Electronic Resource
    The regulation of CoA-independent transacylation reactions in neuronal nuclei by lysophospholipid, free fatty acid, and lysophospholipase: The control of nuclear lyso platelet-activating factor metabolism (2000)
    Springer
    Molecular and cellular biochemistry 215 (2000), S. 135-144 
    Details
    ISSN: 1573-4919
    Keywords: transacylase ; platelet activating factor ; lysophospholipid ; lysophospholipase ; free fatty acid ; neuronal nuclei
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract CoA-independent transacylase activities generating alkylacylglycerophosphocholine (AAGPC) from alkylglycerophosphocholine (1-alkyl GPC) were considerably enriched in neuronal nuclei isolated from rabbit cerebral cortex. Specific nuclear transacylation activities were 13 times the corresponding microsomal values. Several lysophospholipids, notably 1-acyl glycerophosphocholine (1-acyl GPC), 1-alkenyl GPC and 1-alkenyl GPE (1-alkenyl glycerophosphoethanolamine) inhibited the transacylation of 1-alkyl GPC. The inhibitory effects of 1-acyl GPC were seen in the presence of MAFP (methyl arachidonoylfluorophosphonate) or free oleate, compounds that inhibit neuronal nuclear lysophospholipase. When neuronal nuclei were preincubated with 1-alkyl GPC, the radioactive AAGPC product served as donor in transacylation reactions, to generate 1-alkyl GPC. In these nuclear reactions, 1-palmitoyl GPE and 1-palmitoyl GPC appeared to be poor acceptor substrates, when compared with corresponding 1-alkyl and 1-alkenyl analogues. The presence of free oleate or MAFP in the reactions containing 1-acyl GPC boosted the release of 1-alkyl GPC from AAGPC. These observations are of particular relevance to brain ischemia in which lysophospholipid, free fatty acid, and platelet-activating factor (PAF) levels rise dramatically. PAF can be made by the nuclear acetylation of 1-alkyl GPC, which is formed by nuclear transacylation mechanisms. Yet transacylase also removes 1-alkyl GPC, and thus this enzyme activity can regulate 1-alkyl GPC availability. Our observations indicate that lysophospholipids promote the formation of 1-alkyl GPC from nuclear AAGPC via transacylation, while free fatty acid likely prolongs the lifetime of 1-acyl lysophospholipids substrates by lysophospholipase inhibition. Similarly, once 1-alkyl GPC is formed, other lysophospholipids effectively compete with this 1-alkyl analogue and reduce its conversion back to AAGPC by transacylation. Free oleate, in this case, sustains 1-acyl lysophospholipid inhibitors of 1-alkyl GPC transacylation. Thus the cycle of transacylation may favour 1-alkyl GPC formation during ischemia, increasing levels of 1-alkyl GPC for nuclear acetylation reactions and PAF formation. The nuclear generation of PAF is of considerable importance as PAF can play regulatory roles in transcription events associated with inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026535611654
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  • 9
    Electronic Resource
    Electronic Resource
    Pharmacology of Fluorinated Pyrimidines: Eniluracil (2000)
    Springer
    Investigational new drugs 18 (2000), S. 373-381 
    Details
    ISSN: 1573-0646
    Keywords: clinical pharmacology ; dihydropyrimdine dehydrogenase ; eniluracil ; oral 5-FU ; pharmacokinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract The pharmacological inactivation of dihydropyrimidine dehydrogenase (DPD)represents one strategy to improve 5-FU therapy, which historically hasbeen associated with unpredictable pharmacological behavior andtoxicity. This is principally due to high interpatientdifferences in the activity of DPD, the enzyme that mediates theinitial and rate-limiting step in 5-FU catabolism. Byinactivating DPD and suppressing the catabolism of 5-FU,eniluracil has dramatically altered the pharmacological profileof 5-FU. The maximum tolerated dose of oral 5-FU given with oraleniluracil (1.0 to 25 mg/m2) is substantially lower thanconventional 5-FU doses. In the presence of eniluracil,bioavailability of 5-FU has increased to approximately 100%, thehalf-life is prolonged to 4 to 6 hours, and systemic clearanceis reduced 〉 20-fold to values comparable the glomerularfiltration rate (46 to 58 mL/min/m2). Renal excretion(∼ 45% to 75%), instead of DPD-related catabolism, is theprincipal route of elimination of oral 5-FU given witheniluracil. Chronic daily administration of oral 5-FU 1.0mg/m2 twice daily with eniluracil 20 mg twice dailyproduces 5-FU steady-state concentrations (8–38 ng/mL) similarto those achieved with protracted intravenous administration onclinically relevant dose-schedules. On a daily × 5regimen, higher 5-FU AUC values are related to neutropenia,whereas elevated 5-FU AUC and steady-state concentrations arerelated to diarrhea when oral 5-FU is given daily with eniluracilon a chronic schedule. The pharmacokinetic behavior of oraleniluracil is similar to that for oral 5-FU. Administration ofeniluracil 10 to 20 mg twice daily completely inactivates DPDactivity both in peripheral blood mononuclear cells and incolorectal tumor tissue, and prolonged inhibition of DPD afterdiscontinuation of eniluracil treatment has been noted. In thepresence of eniluracil, oral administration of 5-FU is feasibleand variation in 5-FU exposure is reduced, with the anticipationof further reduction in variation as dosing guidelines based onrenal function are formulated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006453500629
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  • 10
    Electronic Resource
    Electronic Resource
    A thermodynamic muscle model and a chemical basis for A.V. Hill's muscle equation (2000)
    Springer
    Journal of muscle research and cell motility 21 (2000), S. 335-344 
    Details
    ISSN: 1573-2657
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Direct measurements of a relationship between force and actin–myosin biochemistry in muscle suggest that molecular forces in active muscle rapidly equilibrate among, not within, individual myosin crossbridges [Baker et al. (1999) Biophys J 77: 2657–2664]. This observation suggests a thermodynamic model of muscle contraction in which muscle, not an individual myosin crossbridge, is treated as a near-equilibrium system. The general approach can be applied to any ensemble of molecular motors that undergo a physicochemical step against a constant external potential. In this paper we apply the model to a simple two-state crossbridge scheme like that proposed by A.F. Huxley (1957) [Prog Biophys 7: 255–317], and we immediately obtain A.V. Hill's muscle equation. We show that this equation accurately describes steady-state muscle mechanics, biochemistry and energetics. This thermodynamic model provides a novel description of force-dependent actin–myosin kinetics in muscle and provides precise chemical expressions for myosin cooperativity, myosin duty ratios, the number of working strokes per ATP hydrolyzed, muscle efficiency, and energy transfer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005615925390
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