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  • Cell & Developmental Biology  (15)
  • Engineering General  (13)
  • Biochemistry  (5)
  • 2020-2022
  • 1990-1994  (33)
  • 11
    Electronic Resource
    Electronic Resource
    Free vibration analysis and shape optimization of prismatic folded plates and shells with circular curved planform (1994)
    Chichester [u.a.] : Wiley-Blackwell
    International Journal for Numerical Methods in Engineering 37 (1994), S. 1713-1739 
    Details
    ISSN: 0029-5981
    Keywords: Engineering ; Engineering General
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Mathematics , Technology
    Notes: This paper deals with the elastic free vibration analysis and structural shape optimization of prismatic folded plate and shell structures with circular curved planform. The structures are supported on diaphragms at two opposite edges. The basic formulation of a family of curved variable thickness C(0) Mindlin-Reissner finite strips is presented. The accuracy and performance of these newly developed strips are explored through a series of examples including annular plate sectors, a box girder bridge and a cylinder with an interior longitudinal plate. Numerical results obtained are compared with results from other sources. The whole shape optimization process is carried out by integrating finite strip analysis, cubic spline shape and thickness definition, sensitivity analysis and mathematical programming. The objective is either the maximization of the fundamental frequency or the minimization of volume by changing the shape or thickness variation of the cross-section of the structure with constraints on the volume or natural frequencies. Several examples are included to illustrate and highlight various features of the optimization, including annular sector plates, a curved box girder bridge and a cylinder shell segment with curved pianform.
    Additional Material: 16 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/nme.1620371006
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  • 12
    Electronic Resource
    Electronic Resource
    Finite element formulation for a baffled, fluid-loaded, finite cylindrical shell (1994)
    Chichester [u.a.] : Wiley-Blackwell
    International Journal for Numerical Methods in Engineering 37 (1994), S. 2971-2985 
    Details
    ISSN: 0029-5981
    Keywords: Engineering ; Engineering General
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Mathematics , Technology
    Notes: A new method for obtaining the response of a baffled, fluid-loaded, finite cylindrical shell using the finite element method is presented. The Galerkin finite element formulation for this problem utilizes a Neumann Green's function representation of the pressure loading on the shell. By representing the pressure loading in this manner, only the structure need be discretized. Both C0 and C1 finite element discretizations of the shell are considered. The finite element results are compared with the analytic solutions of the fluid-loaded cylinder which are obtained using an expansion of the displacement in terms of the in vacuo modes of the Naghdi-Cooper and Flügge shell theories.
    Additional Material: 11 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/nme.1620371708
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  • 13
    Electronic Resource
    Electronic Resource
    Plasminogen activators and inhibitors in the neuromuscular system: III. The serpin protease nexin I is synthesized by muscle and localized at neuromuscular synapses (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 147 (1991), S. 76-86 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Recent studies suggest that the nature of events leading to the formation, maintenance, and elimination of synapses may be regulated by cascade-type, locally expressed proteases and protease inhibitors acting on adhesive extracellular matrix components. We have identified a molecule in conditioned medium of murine skeletal muscle cells that in molecular weight, target protease inhibition, heparin-binding and cross-reactivity with authenic antisera is similar to the human serine proteinase inhibitor, protease nexin I. Protease nexin I is a 43-50 kDa glycoprotein of the serpin superfamily (arg-serpin class). Purified anti-protease nexin I antibody (anti-47 kDa) stains adult mouse skeletal muscle in discrete foci that precisely superimpose on synaptic neuromuscular junctions. Protease nexin I appears in patches on surfaces of cultured mouse skeletal myotubes, but not on myoblasts. These patches co-localize with acetylcholine receptor clusters and acetylcholinesterase staining during cellular maturation in culture. Evidence that protease nexin I is a synaptic, extracellular antigen is particularly intriguing since it has been shown to be identical, in structure and activity, with a factor released by glial cells, called glia-derived nexin that stimulates mouse neuroblastoma cell neurite outgrowth and inhibits granule cell migration Protease nexin I inhibits both tumor cell and myoblast plasminogen activator-mediated destruction of extracellular matrix. Thus, such observations as presented in this report provide further evidence for involvement of cascade proteolytic systems, and their post-translational regulation by specific serpins, in the remodeling that occurs in synapse formation and elimination.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041470111
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  • 14
    Electronic Resource
    Electronic Resource
    Na+/H+ antiporter gene expression increases during retinoic acid-induced granulocytic differentiation of HL60 cells (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 151 (1992), S. 361-366 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: During differentiation of human leukemic HL60 cells into granulocytes, sustained increases in intracellular pH and Na+/H+ antiporter activity have been observed. In the present study we report that retinoic acid (RA)-induced granulocytic differentiation of HL60 cells causes an ∼18-fold increase in the steady-state mRNA levels for the Na+/H+ antiporter. This was due to an increase in the rate of Na+/H+ antiporter gene transcription as measured by nuclear run-on analysis. Antiporter protein synthesis increased by seven-fold during RA-induced granulocytic differentiation of HL60 cells as measured by immunoprecipitation of 35S-methionine-labeled proteins with the RP1-c28 Na+/H+ antiporter antibody. No increase in antiporter mRNA was observed in response to etretinate, an analogue of retinoic acid, which did not induce differentiation. Thus, Na+/H+ antiporter gene expression is associated with RA-induced granulocytic differentiation of HL60 cells. The present findings and our previous data (Rao et al., 1991) demonstrate that Na+/H+ antiporter gene expression is a generalized feature of HL60 cell differentiation. © 1992 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041510217
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  • 15
    Electronic Resource
    Electronic Resource
    Plasminogen activators and their inhibitors in the neuromuscular system: I. Developmental regulation of plasminogen activator isoforms during in vitro myogenesis in two cell lines (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 144 (1990), S. 262-271 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Plasminogen activators (PAs), were estimated qualitatively and quantitatively in two different clonal murine skeletal muscle cell lines. Both cell lines produced the two major types of PAs found in mammalian cells, urokinase-type (uPA) and tissue type (tPA). These two lines are models for the study of myogenesis in vitro, but differ in several growth and differentiation characteristics. Because of their possible involvement in these characteristics we assayed the expression of PAs in both cell systems during development in culture. Utilizing fibrin zymography two isoforms of tPA were detected. One co-migrated with human tPA at 75 kd and another may represent a tPA:inhibitor complex at 105 Kd. Several isoenzymes of uPA were detected and these changed depending on whether cell homogenates or conditioned medium was analyzed and whether myogenic cells were at single-cell myoblast or multi-nucleated myotube stage. Species-specific antisera to mouse uPA identified 4 uPA bands in muscle cell medium and 5 in cell layers. Antigenic uPA bands also varied depending on stage of myogenesis. Quantitative amidolytic studies using chromogenic substrates showed that maximal PA activity, both uPA and tPA, occurred at the time of myoblast fusion. Furthermore, uPA activity in membranes increased during myogenesis, while both uPA and tPA in medium decreased after fusion. These studies indicate that muscle PA expression is developmentally regulated and may correlate with growth and differentiation in skeletal muscle.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041440212
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  • 16
    Electronic Resource
    Electronic Resource
    Plasminogen activators and their inhibitors in the neuromuscular system: II. Serpins and serpin: Protease complex receptors increase during in vitro myogenesis (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 144 (1990), S. 272-279 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: In the course of studies on the regulation of plasminogen activator-mediated extracellular matrix degradation in muscle we found the presence of a factor, a cellular inhibitor of serine proteases having features similar to the serpin protease nexin I (PNI). This factor was present in the medium and at maximum concentration following fusion of skeletal muscle cells in culture. The ability of the PNI homologue in mouse muscle to inhibit ECM degradation by urokinase in myo-blast medium was compared to that of human PNI purified from human fibro-blasls. Stable (to SDS) 1:1 molar ratio complex formation between PNI and proteases, the proposed means by which these enzymes are regulated and removed, was also detected. Cell surface receptors for protease:PNI complexes, the specific binding sites for inactive complex internalization, were found on multinucleated myotubes, while little or no receptor activity was detected on myoblasts. These data suggest that developmental regulation of (a) increased PNI proteolytic inhibitory activity expression and (b) the appearance of protease:inhibitor complex receptors on muscle cell surfaces during myogenesis may constitute important regulatory features of muscle suface proteolytic activity. They complement previous studies of proteoglycan metabolism in muscle, which itself contains molecules capable of regulating the activity of myotube surface proteases.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041440213
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  • 17
    Electronic Resource
    Electronic Resource
    Angiotensin II-induced vascular smooth muscle cell hypertrophy: PDGF A-chain mediates the increase in cell size (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 154 (1993), S. 368-380 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: We report here that angiotensin II-mediated hypertrophy of vascular smooth muscle cells (VSMC) exhibits PDGF A-chain-and -pathways. Secretion of PDGF A-chain is required for the increase in cell size, but not for the increase in protein synthesis. Angiotensin II stimulates a hypertrophic growth response in VSMC characterized by increases in cell size and protein synthesis, but not cell number. Because angiotensin II-stimulated VSMC hypertrophy has been associated with increased PDGF A-chain expression, we studied its role in the hypertrophic response by inhibiting PDGF A-chain expression with hydrocortisone or anti-PDGF antibody. Hydrocortisone (1 μM for 48 h) inhibited basal protein synthesis by 47%, but angiotensin II-stimulated protein synthesis was enhanced (111% increase after hydrocortisone treatment vs. 25% increase in control). In contrast, hypertrophy, as measured by cell size, was completely inhibited. Although hydrocortisone had no effect on early growth signals stimulated by angiotensin II (e.g., activation of protein kinase C, stimulation of Na+/H+ exchange, and c-fos and c-myc expression), it significantly decreased angiotensin II-stimulated secretion of PDGF-like material into the medium from 0.4 to 0.1 ng/ml/24 h (p 〈 0.01). However, the time course for PDGF secretion (maximal at 16-24 h) was significantly slower than the time course for angiotensin II-stimulated protein synthesis (maximal at 4-12 h). To block the action of PDGF A-chain selectively, VSMC were treated with anti-PDGF A-chain antibody. The antibody completely inhibited the angiotensin II-stimulated increase in cell size, but it had no significant effect on protein synthesis at early times (〈8 h). These findings demonstrate two pathways involved in angiotensin II-stimulated VSMC hypertrophy: an increase in cell size dependent on PDGF A-chain and an increase in protein synthesis independent of PDGF A-chain. © 1993 Wiley-Liss, Inc.
    Additional Material: 12 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041540221
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  • 18
    Electronic Resource
    Electronic Resource
    Interleukin-3 inhibits cycloheximide of C-Jun mRNA in human monocytes: Possible role for a serine/threonine phosphatase (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 156 (1993), S. 560-566 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Cycloheximide is a strong inducer of the c-jun protooncogene mRNA at concentrations (≤50 ng/ml) that do not inhibit protein synthesis in human monocytes. This induction is transient lasting 30-60 min in contrast to the sustained induction obtained with concentrations that inhibit protein synthesis. The pluripotent colony stimulating factor interleukin-3 (IL-3) (10 ng/ml) is also a modest inducer of the c-jun gene in these cells; however, in combination with cycloheximide, IL-3 dramatically reduces the c-jun induction below levels induced by cycloheximide alone. This is a true inhibition and is not due to a change in temporal kinetics of induction because the suppression in the presence of IL-3 is observed at both 30 and 60 min after simultaneous addition of both IL-3 and cycloheximide. Preincubation of monocytes with 12.5 nM okadaic acid (a potent inhibitor of protein phosphatases 1 and 2A) and cycloheximide prior to addition of IL-3 restored the level of c-jun induction to that mediated by cycloheximide alone. This concentration of okadaic acid inhibited almost 70% of the phosphorylase phosphatase activity in monocyte lysates. These observations suggest that activation of protein serine/threonine phosphatase(s) underlies the ability of IL-3 to inhibit cycloheximide induction of c-jun in monocytes. © 1993 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041560315
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  • 19
    Electronic Resource
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    Phorbol dibutyrate-specific protein phosphorylation in brush border membranes of chicken enterocytes (1994)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 159 (1994), S. 347-355 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: We have demonstrated that phorbol esters such as phorbol dibutyrate (PhE) transiently inhibit Na/H exchange both in intact avian enterocytes and in brush border membrane (BBM) vesicles prepared from enterocytes treated with PhE (Chang et al., 1991, Am. J. Physiol. 260: C1264-C1272). Maximal inhibition occurs at 90 sec and values return to baseline by 15 mm. In this study we examined if PhE causes changes in BBM protein phosphorylation by two methods: (1) in situ phosphorylation in which intact cells prelabeled with 32Pi were treated with PhE; (2) in vitro phosphorylation in which BBM, isolated from untreated and PhE-treated enterocytes, were exposed to γ32P-ATP. In situ phosphorylation studies showed that, at 90 sec, PhE increases the phosphorylation of BBM proteins of Mr (pl): 150 (6.5), 89 (≈6.2), and 48 (≈6.1) kDa which declined to control values at 15 min, suggesting that these may be transport-related substrates. These labeled substrates were recovered in the detergent-insoluble fraction after extraction with 0.1% Triton X-100 overnight. Transient phosphorylation of a number of proteins was also observed when BBM prepared from control or PhE-treated cells were incubated with γ 32P-ATP ± 10 nM PhE, phosphatidyl serine, Ca2+, and/or exogenous protein kinase C (PKC). The in vitro phosphoproteins included both Triton-soluble and Triton-insoluble proteins. However, none of these proteins labeled in vitro coincided with those labeled in situ. The decline in phosphorylation with time can be accounted for by phosphatase action as these BBM possess a Ca-dependent phosphatase. In summary, we have demonstrated that the BBM possess PKC-specific substrates which can be visualized by in situ and in vitro phosphorylation. Treatment of intact enterocytes with PhE results in the phosphorylation of three detergent-insoluble proteins with a time course similar to that of PhE inhibition of Na/H transport. © 1994 wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041590218
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  • 20
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    Bethanechol inhibition of chicken intestinal brush border Na/H exchange: Role of protein kinase C and other calcium-dependent processes (1992)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 152 (1992), S. 362-371 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Bethanechol, a muscarinic agonist, inhibits the initial rate of amiloride-sensitive Na uptake by intact mucosa of avian small intestine as well as by isolated chicken villus enterocytes, an effect that is maximal at 90 seconds and reverses by 6 minutes. Bethanechol similarly decreases intracellular pH in isolated cells suspended in bicarbonate-free buffer in a time course similar to inhibition of enterocyte Na uptake, suggesting inhibition of Na/H exchange. In brush border membrane vesicles rapidly prepared from cells stimulated with bethanechol, proton-dependent 22Na uptake is transiently inhibited in a time course similar to inhibition of cell Na uptake. Bethanechol also stimulates transient translocation of protein kinase C from the cytosol to the particulate fraction, a portion of this activity translocating to the brush border membrane. To determine the calcium dependence of bethanechol's action, enterocytes were loaded with varying concentrations of the calcium buffering agent quin-2. Inhibition of cell Na uptake by the calcium ionophore ionomycin could be completely reversed by quin-2 buffering in a concentration-dependent manner. In contrast, quin-2 buffering had little or no effect on the inhibition of Na uptake caused by the protein kinase C activators phorbol esters and oleoylacetylglycerol. Bethanechol's inhibitory effects were partially, but not completely reversed by quin-2 buffering. These data suggest that the effects of bethanechol on chicken villus enterocyte brush border Na/H exchange are mediated by calcium-dependent process(es) as well as by protein kinase C. © 1992 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041520218
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