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  • Articles  (6)
  • Cell & Developmental Biology  (3)
  • Life and Medical Sciences  (3)
  • Humans  (2)
  • 65N30  (1)
  • Life Sciences (General)
  • 2000-2004
  • 1990-1994  (6)
  • 1935-1939
  • 1994  (4)
  • 1992  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Boundary Lagrange multipliers in finite element methods: Error analysis in natural norms (1992)
    Springer
    Numerische Mathematik 62 (1992), S. 1-15 
    Details
    ISSN: 0945-3245
    Keywords: 65N30
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics
    Notes: Summary A finite element procedure for circumventing the Babuška-Brezzi condition in mixed formulations with Lagrange multipliers defined on the boundary is presented. Residual terms constructed from the Euler-Lagrange equations are added to the classical Galerkin formulation in order to attain coercivity in a mesh-dependent norm. Convergence is proven for the primal variable and the multiplier in the natural mesh-independent norm of the problem, generalizing results of a previous paper.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01396217
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  • 2
    Electronic Resource
    Electronic Resource
    Cell cycle arrest by prostaglandin A1 at the G1/S phase interface with up-regulation of oncogenes in S-49 cyc- cells (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 54 (1994), S. 265-272 
    Details
    ISSN: 0730-2312
    Keywords: DNA synthesis ; cAMP ; cell growth inhibition ; lymphoma ; PGA1 ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Our previous studies have implied that prostaglandins inhibit cell growth independent of cAMP. Recent reports, however, have suggested that prostaglandin arrest of the cell cycle may be mediated through protein kinase A. In this report, in order to eliminate the role of c-AMP in prostaglandin mediated cell cycle arrest, we use the-49 lymphoma variant (cyc-) cells that lack adenylate cyclase activity. We demonstrate that dimethyl prostaglandin A1 (dmPGA1) inhibits DNA synthesis and cell growth in cyc- cells. DNA synthesis is inhibited 42% by dmPGA1 (50 μM) despite the fact that this cell line lacks cellular components needed for cAMP generation. The ability to decrease DNA synthesis depends upon the specific prostaglandin structure with the most effective form possessing the α,β unsaturated ketone ring. Dimethyl PGA1 is most effective in inhibiting DNA synthesis in cyc- cells, with prostaglandins PGE1 and PGB1 being less potent inhibitors of DNA synthesis. DmPGE2 caused a significant stimulation of DNA synthesis. S-49 cyc- variant cells exposed to (30-50 μm) dmPGA1, arrested in the G1 phase of the cell cycle within 24 h. This growth arrest was reversed when the prostaglandin was removed from the cultured cells; growth resumed within hours showing that this treatment is not toxic. The S-49 cyc- cells were chosen not only for their lack of adenylate cyclase activity, but also because their cell cycle has been extensively studied and time requirements for G1, S, G2, and M phases are known. Within hours after prostaglandin removal the cells resume active DNA synthesis, and cell number doubles within 15 h suggesting rapid entry into S-phase DNA synthesis from the G1 cell cycle block. The S-49 cyc- cells are known to have a G1/S boundary through M phase transition time of 14.8 h, making the location of the prostaglandin cell cycle arrest at or very near the G1/S interface. The oncogenes, c-fos and c-myc which are normally expressed during G1 in proliferating cells have a 2-3 fold enhanced expression in prostaglandin G1 arrested cells. These data using the S-49 variants demonstrate that dmPGA1 inhibits DNA synthesis and arrests the cell cycle independent of cAMP-mediated effects. The prostaglandin arrested cells maintain the gene expression of a G1 synchronous cell which suggests a unique molecular mechanism for prostaglandin action in arresting cell growth. These properties indicate that this compound may be an effective tool to study molecular mechanisms of regulation of the cell cycle.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240540302
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  • 3
    Electronic Resource
    Electronic Resource
    E.coli hemolysin interactions with prokaryotic and eukaryotic cell membranes (1992)
    New York, NY : Wiley-Blackwell
    BioEssays 14 (1992), S. 519-525 
    Details
    ISSN: 0265-9247
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The hemolysin toxin (HlyA) is secreted across both the cytoplasmic and outer membranes of pathogenic Escherichia coli and forms membrane pores in cells of the host immune system, causing cell dysfunction and death. The processes underlying the interaction of HlyA with the bacterial and mammalian cell membranes are remarkable. Secretion of HlyA occurs without a periplasmic intermediate and is directed by an uncleaved C-terminal targetting signal and the HlyB and HlyD translocator proteins, the former being a member of a transporter superfamily central to import and export of a wide range of substrates by prokaryotic and eukaryotic cells. The separate process by which HlyA is targetted to mammalian cell membranes is dependent upon fatty acylation of a non-toxic precursor, proHlyA. This is achieved by a novel mechanism directed by the activator protein HlyC, which binds to an internal proHlyA recognition sequence and provides specificity for the transfer of fatty acid from cellular acyl carrier protein.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bies.950140804
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  • 4
    Electronic Resource
    Electronic Resource
    The prion mystery. Prion diseases of humans and animals (1993). Edited by S. B. PRUSINER, J. COLLINGE, J. POWELL AND B. ANDERTON. Ellis Horwood, Chichester, England. xxvi+583pp. $80.ISBN 0-13-720327-6 (1994)
    New York, NY : Wiley-Blackwell
    BioEssays 16 (1994), S. 445-445 
    Details
    ISSN: 0265-9247
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bies.950160614
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  • 5
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    Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-29
    Description: Rasmussen's encephalitis is a progressive childhood disease of unknown cause characterized by severe epilepsy, hemiplegia, dementia, and inflammation of the brain. During efforts to raise antibodies to recombinant glutamate receptors (GluRs), behaviors typical of seizures and histopathologic features mimicking Rasmussen's encephalitis were found in two rabbits immunized with GluR3 protein. A correlation was found between the presence of Rasmussen's encephalitis and serum antibodies to GluR3 detected by protein immunoblot analysis and by immunoreactivity to transfected cells expressing GluR3. Repeated plasma exchanges in one seriously ill child transiently reduced serum titers of GluR3 antibodies, decreased seizure frequency, and improved neurologic function. Thus, GluR3 is an autoantigen in Rasmussen's encephalitis, and an autoimmune process may underlie this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogers, S W -- Andrews, P I -- Gahring, L C -- Whisenand, T -- Cauley, K -- Crain, B -- Hughes, T E -- Heinemann, S F -- McNamara, J O -- NS17771/NS/NINDS NIH HHS/ -- NS28709/NS/NINDS NIH HHS/ -- NS30990R29/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 29;265(5172):648-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salt Lake City Geriatric Research Education and Clinical Center, Veterans Affairs Medical Center, UT.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8036512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Specificity ; Autoantibodies/blood/*immunology ; Brain/pathology ; Cell Line ; Child ; Disease Models, Animal ; Encephalitis/complications/*immunology/pathology/therapy ; Female ; Humans ; Male ; Plasma Exchange ; Rabbits ; Receptors, Glutamate/*immunology ; Recombinant Fusion Proteins/immunology ; Seizures/etiology/immunology
    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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  • 6
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    Infectious disease surveillance: a crumbling foundation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berkelman, R L -- Bryan, R T -- Osterholm, M T -- LeDuc, J W -- Hughes, J M -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):368-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153621" target="_blank"〉PubMed〈/a〉
    Keywords: Centers for Disease Control and Prevention (U.S.) ; Communicable Disease Control ; Communicable Diseases/*epidemiology ; *Disease Outbreaks ; Epidemiologic Methods ; Humans ; *Population Surveillance ; United States ; World Health Organization
    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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