@article{AdamDimitrijevicSchartl1993,
  author    = {Adam, Dieter and Dimitrijevic, Nicola and Schartl, Manfred},
  title     = {Tumor suppression in Xiphophorus by an accidentally acquired promoter},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61630},
  year      = {1993},
  abstract  = {Melanoma formation in the teleost Xiphophorus is caused by a dominant genetic locus, Tu. This locus includes the Xmrk oncogene, which encodes a receptor tyrosine kinase. Tumor induction is. suppressed in wild-type fish by a tumor suppressor locus, R. Molecular genetic analyses revealed that the Tu locus emerged by nonhomologaus recombination of the Xmrk proto-oncogene with a previously uncharacterized sequence, D. This event generated an additional copy of Xmrk with a new promoter. Suppression of the new Xmrk promoter by R in parental fish and its deregulation in hybrids explain the genetics of melanoma formation in Xiphophorus.},
  subject      = {Physiologische Chemie},
  language  = {en}
}
@article{AdamAhrweilerSahaMoelleretal.1993,
  author    = {Adam, W. and Ahrweiler, M. and Saha-M{\"o}ller, C. R. and Sauter, M. and Sch{\"o}nberger, A. and Epe, B. and M{\"u}ller, E. and Schiffmann, D. and Stopper, Helga and Wild, D.},
  title     = {Genotoxicity studies of benzofuran dioxetanes and epoxides with isolated DNA, bacteria and mammalian cells},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-63420},
  year      = {1993},
  abstract  = {1.2-Dioxetanes, very reactive and high energy molecules. are involved as labile intermediates in dioxygenase- activated aerobic metabolism and in physiological processes. Various toxico1ogica1 tests reveal that dioxetanes are indeed genotoxic. In supercoiled DNA of bacteriophage PM2 they induce endonucleasesensitive sites, most of them are FPG protein-sensitive base modifications (8-hydroxyguanine, fonnamidopyrimidines). Pyrimidinedimersand sites ofbase loss (AP sites) which were probed by UV endonuclease and exonuclease 111 are minor lesions in this system. While the alky1-substituted dioxetanes do not show any significant mutagenic activity in different Salmonella typhimurium strains, heteroarene dioxetanes such as benzofuran and furocoumarin dioxetanes are strongly mutagenic in S. typhimurium strain TA I 00. DNA adducts formed with an intermediary alkyJating agent appear to be responsible for the mutagenic activity of benzofuran dioxetane. We assume that the benzofuran epoxides, generated in situ from benzofuran dioxetanes by deoxygenation are the ultimate mutagens of the latter. since benzofuran epoxides are highly mutagenic in the S. typhimurium strain TAIOO and they form DNA adducts. as detected by the 212Ppostlabelling technique. Our results imply that the type of D NA darnage promoted by dioxetanes is dependent on the structural feature of dioxetanes. Furthermore, the direct photochemical DNA darnage by energy transfer. i.e., pyrimidine dimers, plays a minor role in the genotoxicity of dioxetanes. Instead, photooxidation dominates in isolated DNA. while radical darnage and alkylation prevail in the cellular system.},
  subject      = {Toxikologie},
  language  = {en}
}
@article{AdamiDragstedEnigetal.1993,
  author    = {Adami, Hans-Olov and Dragsted, Lars and Enig, Bent and Hansen, Jens and Haraldsd{\´o}ttir, J{\´o}hanna and Hill, Michael J. and Holm, Lars Erik and Knudsen, Ib and Larsen, Jens-Jorgen and Lutz, Werner K. and Osler, Merete and Overvad, Kim and Sabroe, Svend and Sanner, Tore and Strube, Michael and Sorensen, Thorkild I. A. and Thorling, Eivind B.},
  title     = {Report from the working group on diet and cancer.},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-71601},
  year      = {1993},
  abstract  = {No abstract available.},
  subject      = {Krebs <Medizin>},
  language  = {en}
}
@article{AguzziWagnerNetzeretal.1993,
  author    = {Aguzzi, A. and Wagner, E. F. and Netzer, K. O. and Bothe, K. and Anhauser, I. and Rethwilm, Axel},
  title     = {Human foamy virus proteins accumulate in neurons and induce multinucleated giant cells in the brain of transgenic mice},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47356},
  year      = {1993},
  abstract  = {Humanfoamy virus (HFV) is a retrovirus encoding structural genes and, like human immunodeficiency virus and human T ceU leukemia virus I, several anciUary reading frames collectively termed the belgenes. We have previously shown that HFV transgenic mice develop an encephalopathy with neuronal loss in hippocampus and cerebral cortex. We have now raised and characterized rabbit antisera to various recombinant portions of gag, pot, env, and bel-I, the viraltransactivator. Immunoreactivity for gag and bel-I was observed in nuclei and processes of hippocampal and cortical neurons before the onset of morphological lesions and correlated with the appearance of HFV mRNA. Astrocyte-derived multinucleated giant ceUs containing HFV proteins were present in the brain oftransgenic mice coexpressingfuU- length HFV genes but not in mice expressing truncated gag and env, suggesting that these genes contain afusogenic domain. Expression of fuU-length structural genes decreased the life expectancy oftransgenic mice, implying an a4Juvant rolefor these proteins in HFV-induced brain damage. (Am] Pathol 1993, 142:1061-1072)},
  subject      = {Molekularpathologie},
  language  = {en}
}
@article{ArbuznikovPlakhutin1993,
  author    = {Arbuznikov, Alexey V. and Plakhutin, A. B.},
  title     = {Symmetric vector coupling coefficients for atomic non-Roothaan states in the d\(^N\) configuration},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-47062},
  year      = {1993},
  abstract  = {No abstract available},
  language  = {en}
}
@article{ArchelosRoggenbuckSchneiderSchauliesetal.1993,
  author    = {Archelos, J. J. and Roggenbuck, K. and Schneider-Schaulies, J{\"u}rgen and Toyka, K. V. and Hartung, H. P.},
  title     = {Detection and quantification of antibodies to the extracellular domain of Po during experimental allergic neuritis},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54896},
  year      = {1993},
  abstract  = {Quantification of the peripheral nerve myelin glycoprotein PO and antibodies to PO is difficult due to insolubility of PO in physiological solutions. We have overcome this problern by using the water-soluble recombinant form of the extracellular domain of PO (PO-ED) and describe newly developed assays which allow detection and quantitation of PO and antibodies to PO, in serum and cerebraspinal fluid (CSF). These sensitive and specific assays based on the ELISA technique were used to study humoral immune responses to PO during experimental autoimmune ("allergic") neuritis (EAN). In order to establish these tests, monoclonal antiborlies to different epitopes of rodent and human PO-ED were produced. A two-antibody sandwich-ELISA allowing quantitation of PO Oower detection Iimit of 0.5 ngjml or 30 fmoljml) and an antibody-capture ELISA (lower detection Iimit 1 ng specific antibody jml) to detect antiborlies to PO in serum and CSF were developed. EAN was induced in rats by active immunization with bovine myelin or the neuritogenic protein P2 or by adoptive transfer using P2 specific CD4 positive T cells. Serum and CSF were assayed for the presence of PO-ED and antibodies to PO-ED or P2. Antibodies to PO-ED were detected during active myelin-induced EAN, but not during P2-induced or adaptive transfer EAN. The anti-PO-ED antibodies in the CSF showed a correJation with disease activity. In contrast, in the same model antibodies to P2 persisted long after the disease ceased. No soluble PO-Iike fragments could be found in serum or CSF during any of the three types of EAN. We conclude that PO may be a B-eeil epitope in EAN. These findings warrant a screen for antibodies to PO-ED in human immune neuropathies.},
  subject      = {Immunologie},
  language  = {en}
}
@article{ArchelosRoggenbuckSchneiderSchauliesetal.1993,
  author    = {Archelos, JJ and Roggenbuck, K. and Schneider-Schaulies, J{\"u}rgen and Linington, C. and Toyka, KV and Hartung, H.-P.},
  title     = {Production and characterization of monoclonal antibodies to the extracellular domain of PO},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-54889},
  year      = {1993},
  abstract  = {Seven monoclonal antibodies were raised against the immunoglobulin-like extracellular domain of PO (POED), the major protein of peripheral nervous system myelin. Mice were immunized with purified recombinant rat PO-ED. After fusion, 7 clones (POI-P07) recognizing either recombinant, rat, mouse, or human PO-ED were selected by ELlS A and were characterized by Western blot, immunohistochemistry, and a competition assay. Antibodies belonged to the IgG or IgM class, and P04-P07, reacted with PO in fresh-frozen and paraffin-embedded sections of human or rat peripheral nerve, but not with myelin proteins of the central nervous system of either species. Epitope specificity of the antibodies was determined by a competition enzyme-linked immunosorbent assay (ELISA) and a direct ELlS A using short synthetic peptides spanning the entire extracellular domain of PO. These assays showed that POl and P02 exhibiting the same reaction pattern in Western blot and immunohistochemistry reacted with different distant epitopes of PO. Furthermore, the monoclonal antibodies P05 and P06 recognized 2 different epitopes in close proximity within the neuritogenic extracellular sequence of PO. This panel of monoclonal antibodies, each binding to a different epitope of the extracellular domain of PO, will be useful for in vitro and in vivo studies designed to explore the role of PO during myelination and in demyelinating diseases of the peripheral nervous system.},
  subject      = {Immunologie},
  language  = {en}
}
@article{BanachBuenemannHueseretal.1993,
  author    = {Banach, Katrin and B{\"u}nemann, Moritz and H{\"u}ser, J{\"o}rg and Pott, Lutz},
  title     = {Serum contains a potent factor that decreases \(\beta\)-adrenergic receptor-stimulated L-type Ca\(^{2+}\) current in cardiac myocytes},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-32027},
  year      = {1993},
  abstract  = {No abstract available},
  language  = {en}
}
@article{BarresSchmidSendtneretal.1993,
  author    = {Barres, B. A. and Schmid, R. and Sendtner, Michael and Raff, Martin C.},
  title     = {Multiple extracellular signals are required for long-term oligodendrocyte survival},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42644},
  year      = {1993},
  abstract  = {We showed previously that oligodendrocytes and their precursors require continuous signalling by protein trophic factors to avoid programmed cell death in culture. Here we show that three classes of such trophic factors promote oligodendrocyte survival in vitro: (1) insulin and insulin-like growth factors (IGFs), (2) neurotrophins, particularly neurotrophin-3 (NT -3), and (3) ciliary-neurotrophic factor (CNTF), leukemia inhibitory factor (LIF) and interleukin 6 (IL-6). A single factor, or combinations of factors within the same class, promote only short-term survival of oligodendrocytes and their precursors, while combinations of factors from different classes promote survival additively. Long-term survival of oligodendrocytes in vitro requires at least one factor from each class, suggesting that multiple signals may be required for long-term oligodendrocyte survival in vivo. We also show that CNTF promotes oligodendrocyte survival in vivo, that platelet-derived growth factor (PDGF) can promote the survival of oligodendrocyte precursors in vitro by acting on a novel, very high affinity PDGF receptor, and that, in addition to its effect on survival, NT-3 is a potent mitogen for oligodendrocyte precursor cells.},
  language  = {en}
}
@article{BaunachMaurerHahnetal.1993,
  author    = {Baunach, Gerald and Maurer, Bernd and Hahn, Heidi and Kranz, Manuela and Rethwilm, Axel},
  title     = {Functional analysis of human foamy virus accessory reading frames},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61398},
  year      = {1993},
  abstract  = {No abstract available},
  subject      = {Virologie},
  language  = {en}
}