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  • Articles  (124)
  • Rats  (124)
  • 2020-2022
  • 1990-1994
  • 1985-1989  (124)
  • 1950-1954
  • 1985  (124)
  • Computer Science  (124)
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  • Articles  (124)
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  • 2020-2022
  • 1990-1994
  • 1985-1989  (124)
  • 1950-1954
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  • 1
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    Diazepam-binding inhibitor: a neuropeptide located in selected neuronal populations of rat brain (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-12
    Description: An endogenous polypeptide of rat brain has been identified that is capable of displacing 1,4-benzodiazepines and the esters of the 3-carboxylic acid derivatives of beta-carbolines from their specific synaptic binding sites. This polypeptide was termed diazepam-binding inhibitor (DBI). Previous studies have shown that DBI injected intraventricularly in rodents elicits "proconflict" responses and antagonizes the "anticonflict" action of benzodiazepines. An antiserum to this peptide, directed toward an immunodeterminant near its amino terminus, makes it possible to detect, measure, and study the neuronal location of this peptide in rat brain. In the rat cerebral cortex, DBI immunoreactivity is located in neurons that are not GABAergic (GABA, gamma-aminobutyric acid); in the cerebellum and hippocampus, however, it might be present also in GABAergic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alho, H -- Costa, E -- Ferrero, P -- Fujimoto, M -- Cosenza-Murphy, D -- Guidotti, A -- New York, N.Y. -- Science. 1985 Jul 12;229(4709):179-82.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3892688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Cerebellum/analysis ; Cerebral Cortex/analysis ; Colchicine/pharmacology ; Diazepam Binding Inhibitor ; Hippocampus/analysis ; Histocytochemistry ; Hypothalamus/analysis ; Immune Sera ; Immunologic Techniques ; Nerve Tissue Proteins/*analysis/immunology ; Radioimmunoassay ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Induction of the intermediate pituitary by stress: synthesis and release of a nonopioid form of beta-endorphin (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-25
    Description: beta-Endorphin in the intermediate lobe of the pituitary gland is posttranslationally modified to produce opioid inactive peptides. Whether these are metabolites or biologically relevant products has not been known. It was found that repeated stress induces increased biosynthesis and release of beta-endorphin-like substances from the intermediate lobe of rats and that opioid-inactive N-acetylated beta-endorphin-(1-31) is selectively made and liberated. The possible role of this nonopioid product and the selective release of peptide forms are discussed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akil, H -- Shiomi, H -- Matthews, J -- New York, N.Y. -- Science. 1985 Jan 25;227(4685):424-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3155575" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatography, High Pressure Liquid ; Endorphins/*biosynthesis/blood ; Half-Life ; Kinetics ; Melanocyte-Stimulating Hormones/biosynthesis/blood ; Pituitary Gland/*metabolism ; Rats ; Stress, Physiological/*metabolism ; beta-Endorphin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Brain dopamine and serotonin receptor sites revealed by digital subtraction autoradiography (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-03
    Description: Autoradiography combined with image analysis permitted quantitative visualization of dopamine (D2) and serotonin (S2) binding sites in rat brain. Forebrain sections were incubated with tritiated spiroperidol alone or with tritiated spiroperidol plus unlabeled compounds that saturated the D2 or S2 sites. By subtracting the digitized image of an autoradiograph derived from the latter sections from that of the former, the D2 or S2 sites were specifically revealed. The resulting quantitative images demonstrate the differing anatomical distributions of these sites. The D2 site is largely restricted to the striatal complex (caudate-putamen, nucleus accumbens septi, and olfactory tubercle), whereas the S2 site is enriched in layer 5 of motor cortex, the perirhinal and cingulate cortices, and the claustrum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altar, C A -- O'Neil, S -- Walter, R J Jr -- Marshall, J F -- AG 00538/AG/NIA NIH HHS/ -- AG00096/AG/NIA NIH HHS/ -- NS 20122/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 May 3;228(4699):597-600.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2580352" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography/*methods ; Brain/physiology/*radionuclide imaging ; Butaclamol/metabolism ; Computers ; Ketanserin ; Piperidines/metabolism ; Radiographic Image Enhancement/methods ; Rats ; Receptors, Dopamine/*physiology ; Receptors, Serotonin/*physiology ; Spiperone/metabolism ; Sulpiride/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Expression in brain of a messenger RNA encoding a novel neuropeptide homologous to calcitonin gene-related peptide (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-13
    Description: As a consequence of alternative RNA processing events, a single rat gene can generate messenger RNA's (mRNA's) encoding either calcitonin or a neuropeptide referred to as alpha-type calcitonin gene-related peptide (alpha-CGRP). An mRNA product of a related gene has been identified in rat brain and thyroid encoding the protein precursor of a peptide differing from alpha-CGRP by only a single amino acid. The RNA encoding this peptide, which is referred to as beta-CGRP, appears to be the only mature transcript of the beta-CGRP gene. Hybridization histochemistry reveals a similar distribution of alpha- and beta-CGRP mRNA's, but their relative levels of expression vary in different cranial nerve nuclei. Thus beta-CGRP is a new member of a family of related genes with potential functions in regulating the transduction of sensory and motor information.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amara, S G -- Arriza, J L -- Leff, S E -- Swanson, L W -- Evans, R M -- Rosenfeld, M G -- New York, N.Y. -- Science. 1985 Sep 13;229(4718):1094-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2994212" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Brain Chemistry ; Calcitonin Gene-Related Peptide ; DNA/analysis ; DNA Restriction Enzymes/metabolism ; Gene Expression Regulation ; Nerve Tissue Proteins/*genetics ; RNA, Messenger/*analysis ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Two distinct populations of calcium channels in a clonal line of pituitary cells (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-04
    Description: The whole-cell variant of the patch clamp technique was used to study calcium channels in GH3 cells. Two distinct populations of calcium channels, first recognized from their closing kinetics, were observed. The slowly closing channels are activated in a relatively negative voltage range and are inactivated within 100 milliseconds. They conduct barium and calcium about equally well. The fast closing channels are activated at more positive voltages, are not inactivated during a 100-millisecond pulse, conduct barium in preference to calcium, and are activated slightly more rapidly than the slowly closing channels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Armstrong, C M -- Matteson, D R -- New York, N.Y. -- Science. 1985 Jan 4;227(4682):65-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2578071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Barium/metabolism ; Calcium/*metabolism ; Clone Cells ; Electrophysiology ; Ion Channels/metabolism/*physiology ; Kinetics ; Membrane Potentials ; Pituitary Gland/*cytology/metabolism ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Identification of the protein encoded by the E6 transforming gene of bovine papillomavirus (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-25
    Description: Papillomaviruses (PV) contain several conserved genes that may encode nonstructural proteins; however, none of these predicted gene products have been identified. Papillomavirus E6 genes are retained and expressed as RNA in PV-associated human and animal carcinomas and cell lines. This suggests that the E6 gene product may be important in the maintenance of the malignant phenotype. The E6 open reading frame of the bovine papillomavirus (BPV) genome has been identified as one of two BPV genes that can independently transform mouse cells in vitro. A polypeptide encoded by this region of BPV was produced in a bacterial expression vector and used to raise antisera. The antisera specifically immunoprecipitated the predicted 15.5-kilodalton BPV E6 protein from cells transformed by the E6 gene. The E6 protein was identified in both the nuclear and membrane fractions of these transformed cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Androphy, E J -- Schiller, J T -- Lowy, D R -- 5-F32-CA-07237/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 25;230(4724):442-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996134" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bovine papillomavirus 1/*genetics ; Cell Line ; Cell Transformation, Viral ; *Genes, Viral ; Mice ; Oncogenes ; Papillomaviridae/*genetics ; RNA, Messenger/genetics ; Rabbits ; Rats ; Tumor Virus Infections/genetics ; Viral Proteins/*genetics/isolation & purification
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    A neuroendocrine marker in tissues of the immune system (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-04
    Description: Antibodies to chromogranin, a secretory protein marker for the diffuse neuroendocrine system, were used to analyze rat lymphoreticular tissues by means of immunochemistry and immunohistochemistry. Chromogranin-positive cells were present in spleen, lymph node, thymus, and fetal liver. When these organs were gently dispersed and separated on a Ficoll gradient, the chromogranin-immunoreactive cells became enriched in the dense red-cell pellets. The unexpected distribution of these neuroendocrine cells in all immunologically relevant structures suggests that they may link the nervous and immunological systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Angeletti, R H -- Hickey, W F -- K07-NS00889/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 4;230(4721):89-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3898368" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Chromogranins/*analysis ; Electrophoresis, Polyacrylamide Gel ; Histocytochemistry ; Immunosorbent Techniques ; Lymphoid Tissue/*analysis ; Mononuclear Phagocyte System/*analysis ; Nerve Tissue Proteins/*analysis ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Induced expression of the glucocorticoid receptor in the rat intermediate pituitary lobe (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-19
    Description: Synthesis and release of pro-opiomelanocortin-derived peptides are under differential regulation in the anterior and intermediate lobes of the pituitary. Glucocorticoids inhibit synthesis of pro-opiomelanocortin-related peptides in the anterior lobe but not in the intermediate lobe. These two lobes are also characterized by differences in neural innervation and blood flow, both of which may represent routes of access for regulatory factors (the intermediate lobe is avascular). Immunoreactive glucocorticoid receptor, which can be demonstrated in many tissues, is absent from the intermediate lobe. Immunocytochemistry was used to demonstrate the presence of immunoreactive glucocorticoid receptor in the intermediate lobe after pituitary stalk transection, neurointermediate lobe grafts to kidney capsule, or monolayer culture of neurointermediate pituitary cells. This appearance of the glucocorticoid receptor is presumably a consequence of removal of intermediate pituitary cells from neural influences that may be responsible for inhibiting their expression under normal conditions in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Antakly, T -- Sasaki, A -- Liotta, A S -- Palkovits, M -- Krieger, D T -- NSO2893/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):277-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3892690" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Immunoenzyme Techniques ; Immunoglobulin G/immunology ; Male ; Melanocyte-Stimulating Hormones/physiology ; Pituitary Gland/analysis/*metabolism/surgery ; Pituitary Gland, Anterior/analysis/metabolism ; Rabbits/immunology ; Rats ; Rats, Inbred F344 ; Receptors, Glucocorticoid/*biosynthesis/genetics ; Receptors, Steroid/*biosynthesis ; Serotonin/analysis
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Reversibility of progression of the transformed phenotype in Ad5-transformed rat embryo cells (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-31
    Description: The carcinogenic process is extremely complex and is affected by diverse environmental and host factors. The mechanism for the gradual development of the transformed phenotype (a process termed "progression") was studied in type 5 adenovirus (Ad5)-transformed rat embryo cells. Progression was not correlated with major changes in the pattern of integration of viral DNA sequences. Instead, it was associated with an increased methylation of integrated viral sequences other than those corresponding to the E1 transforming genes of Ad5. A single exposure of progressed cells to the demethylating agent 5-azacytidine (Aza) resulted in a stable reversion to the unprogressed state of the original parental clone. A further selection of cells after growth in agar allowed the isolation of Aza-treated clones that had regained the progressed phenotype. These observations indicate that progression is a reversible process and suggest that progression may be associated with changes in the state of methylation of one or more specific genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Babiss, L E -- Zimmer, S G -- Fisher, P B -- CA-33434/CA/NCI NIH HHS/ -- CA-35675/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 31;228(4703):1099-101.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2581317" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/*genetics ; Animals ; Azacitidine/*pharmacology ; Cell Division ; Cell Transformation, Viral/*drug effects ; Cells, Cultured ; DNA, Neoplasm/genetics ; DNA, Viral/genetics ; Gene Expression Regulation ; Genes, Viral ; *Methylation ; Mice ; Neoplasms, Experimental/*pathology ; Rats ; Rats, Inbred Strains/embryology ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 10
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    Trigeminal-taste interaction in palatability processing (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-10
    Description: Peripheral transection of the sensory branches of the trigeminal nerve in rats unbalanced palatability, selectively reducing the ingestive actions elicited by preferred tastes but leaving unchanged the aversive actions elicited by unpreferred tastes. The reduction in the number of positive ingestive actions occurred even though the capacity to emit these actions remained unimpaired. These findings show that there is an interaction between somatosensation and gustation in the processing of palatability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berridge, K C -- Fentress, J C -- New York, N.Y. -- Science. 1985 May 10;228(4700):747-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3992242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Food Preferences ; Humans ; Male ; Rats ; Rats, Inbred Strains ; Taste/*physiology ; Tongue/physiology ; Trigeminal Nerve/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Biosynthesis and secretion of proatrial natriuretic factor by cultured rat cardiocytes (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-12-06
    Description: Rat atrial natriuretic factor (ANF) is translated as a 152-amino acid precursor preproANF. PreproANF is converted to the 126-amino acid proANF, the storage form of ANF in the atria. ANF isolated from the blood is approximately 25 amino acids long. It is demonstrated here that rat cardiocytes in culture store and secrete proANF. Incubation of proANF with serum produced a smaller ANF peptide. PreproANF seems to be processed to proANF in the atria, and proANF appears to be released into the blood, where it is converted by a protease to a smaller peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloch, K D -- Scott, J A -- Zisfein, J B -- Fallon, J T -- Margolies, M N -- Seidman, C E -- Matsueda, G R -- Homcy, C J -- Graham, R M -- Seidman, J G -- 1R23CA33570/CA/NCI NIH HHS/ -- HL07208/HL/NHLBI NIH HHS/ -- HL26215/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1168-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2933808" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Atrial Natriuretic Factor/*biosynthesis/genetics/secretion ; Autoradiography ; Cells, Cultured ; Electrophoresis, Polyacrylamide Gel ; Heart/physiology ; Immune Sera/immunology ; Myocardium/*cytology/metabolism ; Protein Precursors/*biosynthesis/genetics/secretion ; RNA, Messenger/genetics ; Rabbits/immunology ; Rats
    Print ISSN: 0036-8075
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  • 12
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    Selective extraction of small and large molecules from the cerebrospinal fluid by Purkinje neurons (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-19
    Description: Cerebellar Purkinje neurons accumulated propidium iodide, granular blue, and horseradish peroxidase conjugated to wheat germ agglutinin but not unconjugated horseradish peroxidase, bisbenzimide, or Evans blue when these compounds were infused into the lateral cerebral ventricles of awake, unrestrained rats. Accumulation of propidium iodide by Purkinje neurons of the vermis was associated with a reproducible behavioral abnormality characterized by truncal tremor, ataxia, and nystagmus. Both the accumulation of propidium iodide in Purkinje cells and the behavioral abnormality were prevented by prior intracerebroventricular administration of ouabain or colchicine, drugs that block neuronal transport processes. The ability of cerebellar Purkinje neurons to extract small and large molecules from the cerebrospinal fluid has important implications for their physiology and pathology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borges, L F -- Elliott, P J -- Gill, R -- Iversen, S D -- Iversen, L L -- New York, N.Y. -- Science. 1985 Apr 19;228(4697):346-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2580350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bisbenzimidazole/metabolism ; Cerebrospinal Fluid/*physiology ; Dendrites/physiology ; Evans Blue/metabolism ; Horseradish Peroxidase/metabolism ; Humans ; Male ; Propidium/metabolism/pharmacology ; Purkinje Cells/*metabolism/physiology ; Rats ; Rats, Inbred Strains ; Tremor/chemically induced/physiopathology
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  • 13
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    Stereoscopic images in confocal (tandem scanning) microscopy (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-12-13
    Description: Stereoscopic pair images with parallel projection geometry are obtained by through-focusing along two inclined axes while recording two (summed and stacked) images with a microscope with a very shallow depth of field. The two stack images sample the same depth slice of translucent or reflective specimens. The method will work most conveniently with a tandem scanning microscope (a direct-view, confocal scanning optical microscope). This is a direct method for recording stereo images that can be used to the limit of resolution in optical microscopy. It demonstrates a previously unrealized advantage of confocal optical microscopy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyde, A -- New York, N.Y. -- Science. 1985 Dec 13;230(4731):1270-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4071051" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone and Bones/anatomy & histology ; Cerebellum/anatomy & histology ; Mice ; Microscopy/*methods ; Rats ; Spinal Cord/anatomy & histology
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  • 14
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    Prolactin stimulation of maternal behavior in female rats (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-02-15
    Description: Inexperienced, hypophysectomized female rats treated with steroids were used in experiments to investigate the roles of the pituitary gland and prolactin in the expression of maternal behavior. Administration of ovine prolactin or treatment with ectopic pituitary grafts, which release prolactin into the circulation, stimulated maternal care in these females toward rat young. Steroid treatment alone, while stimulating maternal behavior in rats with intact pituitary glands, did not facilitate maternal responsiveness in hypophysectomized females. These findings indicate a stimulatory behavioral role for pituitary prolactin in the establishment of maternal care and suggest that exposure to prolactin during pregnancy helps to stimulate the immediate onset of maternal behavior at parturition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bridges, R S -- DiBiase, R -- Loundes, D D -- Doherty, P C -- HD 06333/HD/NICHD NIH HHS/ -- HD19789/HD/NICHD NIH HHS/ -- P 30-HD 06645/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 15;227(4688):782-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3969568" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Estradiol/pharmacology ; Female ; Hypophysectomy ; *Maternal Behavior ; Progesterone/pharmacology ; Prolactin/*physiology ; Rats
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  • 15
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    Hormonal control of the anatomical specificity of motoneuron-to-muscle innervation in rats (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-15
    Description: Motoneurons of the spinal nucleus of the bulbocavernosus innervate bulbocavernosus muscles in male rats. Adult female rats normally lack both the spinal nucleus and its target muscles. Prenatal treatment of females with testosterone propionate resulted in adults having, like males, both the spinal nucleus and its target muscles. However, prenatal treatment with dihydrotestosterone propionate preserves the muscles but not the motoneurons. This paradoxical condition might result from (i) bulbocavernosus muscles without innervation; (ii) muscles innervated by morphologically unrecognizable motoneurons; (iii) muscles innervated by a very few spinal nucleus cells, each innervating many bulbocavernosus fibers; or (iv) muscles innervated by motoneurons outside their normal anatomical locus in the spinal nucleus. The results of retrograde marker injections into the bulbocavernosus muscles of females treated with androgen refute the first three possibilities and confirm the last: the different androgen treatments result in anatomically distinct spinal motor nuclei innervating bulbocavernosus muscles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breedlove, S M -- NS19790/NS/NINDS NIH HHS/ -- RR07006/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1357-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dihydrotestosterone/analogs & derivatives/pharmacology ; Female ; Male ; Motor Neurons/anatomy & histology/drug effects/*physiology ; Muscles/drug effects/*innervation ; Pregnancy ; Rats ; Rats, Inbred Strains ; Sex Differentiation/drug effects ; Testosterone/*pharmacology
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  • 16
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    Association of crossover points with topoisomerase I cleavage sites: a model for nonhomologous recombination (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-22
    Description: Nonhomologous DNA recombination is frequently observed in somatic cells upon the introduction of DNA into cells or in chromosomal events involving sequences already stably carried by the genome. In this report, the DNA sequences at the crossover points for excision of SV40 from chromosomes were shown to be associated with eukaryotic topoisomerase I cleavage sites in vitro. The precise location of the cleavage sites relative to the crossover points has suggested a general model for nonhomologous recombination mediated by topoisomerase I.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bullock, P -- Champoux, J J -- Botchan, M -- CA 30490/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Nov 22;230(4728):954-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2997924" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; Cell Transformation, Viral ; Chromatin/ultrastructure ; Chromosome Mapping ; DNA Topoisomerases, Type I/*metabolism ; Rats ; *Recombination, Genetic ; Simian virus 40/*genetics
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  • 17
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    Imaging elemental distribution and ion transport in cultured cells with ion microscopy (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-28
    Description: Both elemental distribution and ion transport in cultured cells have been imaged by ion microscopy. Morphological and chemical information was obtained with a spatial resolution of approximately 0.5 micron for sodium, potassium, calcium, and magnesium in freeze-fixed, cryofractured, and freeze-dried normal rat kidney cells and Chinese hamster ovary cells. Ion transport was successfully demonstrated by imaging Na+-K+ fluxes after the inhibition of Na+- and K+ -dependent adenosine triphosphatase with ouabain. This method allows measurements of elemental (isotopic) distribution to be related to cell morphology, thereby providing the means for studying ion distribution and ion transport under different physiological, pathological, and toxicological conditions in cell culture systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandra, S -- Morrison, G H -- R01GM24314/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 28;228(4707):1543-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990033" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/analysis ; Cell Line ; Cells, Cultured ; Cricetinae ; Elements/*analysis ; Female ; Freeze Fracturing ; Kidney/*ultrastructure ; Magnesium/analysis ; Microscopy/methods ; Ouabain/pharmacology ; Ovary/*ultrastructure ; Potassium/analysis ; Rats ; Sodium/analysis ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors ; Tissue Distribution
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  • 18
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    Activated proto-onc genes: sufficient or necessary for cancer? (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-10
    Description: Proto-onc genes are normal cellular genes that are related to the transforming (onc) genes of retroviruses. Because of this relationship these genes are now widely believed to be potential cancer genes. In some tumors, proto-onc genes are mutated or expressed more than in normal cells. Under these conditions, proto-onc genes are hypothesized to be active cancer genes in one of two possible ways: The one gene-one cancer hypothesis suggests that one activated proto-onc gene is sufficient to cause cancer. The multigene-one cancer hypothesis suggests that an activated proto-onc gene is a necessary but not a sufficient cause of cancer. However, mutated or transcriptionally activated proto-onc genes are not consistently associated with the tumors in which they are occasionally found and do not transform primary cells. Further, no set of an activated proto-onc gene and a complementary cancer gene with transforming function has yet been isolated from a tumor. Thus, there is still no proof that activated proto-onc genes are sufficient or even necessary to cause cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duesberg, P H -- CA 11426/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 10;228(4700):669-77.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3992240" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/metabolism ; Chickens ; DNA, Neoplasm/genetics ; Genes, Viral ; Humans ; Kirsten murine sarcoma virus/genetics ; Lymphoma/genetics ; Melanoma/genetics ; Mice ; Mutation ; Neoplasms/etiology/*genetics ; *Oncogenes ; Plasmacytoma/genetics ; Rats ; Retroviridae/genetics ; Sarcoma, Experimental/genetics ; Transduction, Genetic ; Translocation, Genetic ; Tumor Virus Infections/genetics
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  • 19
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    Cell-specific expression of the rat insulin gene: evidence for role of two distinct 5' flanking elements (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-22
    Description: The 5' flanking DNA of the rat insulin I gene contains sequences controlling cell-specific expression. Analysis of this region by replacement of specific portions with nondiscriminatory control elements from viral systems shows that a transcriptional enhancer is located in the distal portion of the 5' flanking DNA; its position has been mapped by deletion analysis. Additional experiments suggest that another distinct regulatory element is located more proximal to the transcription start site. The activity of both elements is restricted to pancreatic B cells. The combinatorial effect of multiple control elements could explain the cell-specific expression of insulin genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edlund, T -- Walker, M D -- Barr, P J -- Rutter, W J -- AM 21344/AM/NIADDK NIH HHS/ -- GM 28520/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Nov 22;230(4728):912-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3904002" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyltransferases/genetics ; Animals ; Cell Differentiation ; Chloramphenicol O-Acetyltransferase ; Chromosome Mapping ; Enhancer Elements, Genetic ; *Gene Expression Regulation ; Genetic Vectors ; Insulin/*genetics ; Islets of Langerhans/*physiology ; Plasmids ; Promoter Regions, Genetic ; Rats ; Transcription, Genetic
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  • 20
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    Transovarial transmission of murine typhus rickettsiae in Xenopsylla cheopis fleas (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-02-01
    Description: It has been generally accepted that infected fleas do not pass on Rickettsia mooseri, or indeed any other known pathogen, to their progeny. It is reported here that such transovarial transmission does occur in laboratory-infected Xenopsylla cheopis fleas. By means of the direct fluorescent antibody test, Rickettsia mooseri was observed in cells of the hemolymph of infected fleas. As many as 11 percent of the adults and 2.9 percent of the larvae of the generation reared therefrom, had demonstrable rickettsiae. Moreover, batches of the F1 fleas were capable of transmitting the infection to more than 18 percent of the rats they infested. The data support the contention that Xenopsylla cheopis fleas play an important role in the maintenance of murine typhus in rats in nature.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farhang-Azad, A -- Traub, R -- Baqar, S -- AI-04242/AI/NIAID NIH HHS/ -- AI-17828/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 1;227(4686):543-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3966162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Hemolymph/microbiology ; Insect Vectors/*physiology ; Male ; Ovary/microbiology ; Rats ; Rickettsia/*physiology ; Siphonaptera/*microbiology ; Typhus, Endemic Flea-Borne/microbiology/*transmission
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  • 21
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    Vitamin E reversal of the effect of extracellular calcium on chemically induced toxicity in hepatocytes (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-02-15
    Description: Isolated rat hepatocytes were incubated in the presence or absence of extracellular calcium and alpha-tocopherol succinate with three different toxic chemicals; namely, adriamycin in combination with 1,3-bis(2-chloroethyl)-1-nitrosourea, ethyl methanesulfonate, and the calcium ionophore A23187. In the absence of extracellular calcium these three compounds were far more toxic to the cells than in its presence. The addition of vitamin E to calcium-free medium, however, protected hepatocytes against toxic injury, whereas cells incubated in medium containing calcium were not protected. Hepatocyte viability during each toxic insult correlated well with the cellular alpha-tocopherol content but not with the presence or absence of extracellular calcium. These results suggest that cellular alpha-tocopherol maintains the viability of the cell during a toxic insult and that the presence or absence of vitamin E in the incubation medium probably explains the conflicting reports on the role of extracellular calcium in toxic cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fariss, M W -- Pascoe, G A -- Reed, D J -- ES01978/ES/NIEHS NIH HHS/ -- ES07060/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 15;227(4688):751-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3918345" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcimycin/toxicity ; Calcium/*physiology ; Carmustine/toxicity ; Cell Survival/*drug effects ; Cells, Cultured ; Doxorubicin/toxicity ; Ethyl Methanesulfonate/toxicity ; Liver/cytology/*drug effects ; Male ; Rats ; Rats, Inbred Strains ; Vitamin E/*physiology
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  • 22
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    Interaction of calcitonin and calcitonin gene-related peptide at receptor sites in target tissues (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-15
    Description: Discrete receptor sites for calcitonin (CT) and calcitonin gene-related peptide (CGRP) were found in the nervous system and in peripheral tissues. Each peptide was capable of cross-reacting with the specific receptor of the other. In contrast to CT receptors, CGRP receptors were not linked to adenylate cyclase. However, CGRP could stimulate adenylate cyclase in CT target tissues apparently by interacting with CT receptors. The relative abilities of CGRP and mammalian CT to inhibit CT binding suggest that CGRP could serve as an endogenous ligand for CT receptors in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goltzman, D -- Mitchell, J -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1343-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2983422" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Adrenal Glands/metabolism ; Animals ; Bone and Bones/metabolism ; Brain/metabolism ; Calcitonin/*metabolism ; Calcitonin Gene-Related Peptide ; Kidney/metabolism ; Male ; Nerve Tissue Proteins/*metabolism ; Pituitary Gland/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Calcitonin ; Receptors, Cell Surface/*metabolism ; Spinal Cord/metabolism
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  • 23
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    Interleukin-1 stimulation of astroglial proliferation after brain injury (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-26
    Description: The interleukins, which have a regulatory role in immune function, may also mediate inflammation associated with injury to the brain. In experiments to determine the effect of these peptide hormones on glial cell proliferation in culture, interleukin-1 was a potent mitogen for astroglia but had no effect on oligodendroglia. Interleukin-2 did not alter the growth of either type of glial cell. Activity similar to that of interleukin-1 was detected in brains of adult rats 10 days after the brains had been injured. These findings suggest that interleukin-1, released by inflammatory cells, may promote the formation of scars by astroglia in the damaged mammalian brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giulian, D -- Lachman, L B -- EY04915/EY/NEI NIH HHS/ -- R01CA38043/CA/NCI NIH HHS/ -- RR5511/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Apr 26;228(4698):497-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3872478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Astrocytes/*pathology ; Brain Injuries/*pathology ; Cells, Cultured ; Chromatography, High Pressure Liquid/methods ; Chromatography, Ion Exchange/methods ; Interleukin-1/isolation & purification/*physiology ; Interleukin-2/physiology ; Isoelectric Focusing ; *Mitogens ; Oligodendroglia/pathology ; Rats
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  • 24
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    Atrotoxin: a specific agonist for calcium currents in heart (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-12
    Description: A specific label for voltage-dependent calcium channels is essential for the isolation and purification of the membrane protein that constitutes the calcium channel and for a better understanding of its function. A fraction of Crotalus atrox that increases voltage-dependent calcium currents in single, dispersed guinea pig ventricular cells was isolated. In the doses used, neither sodium nor potassium currents were changed. The fraction was active in the absence of detectable phospholipase or protease activity, and the active component, designated atrotoxin, produced its effect rapidly and reversibly. The effect was produced by extracellular but not intracellular application of the agent. The increase in Ca2+ current was blocked by the Ca2+ channel blockers cobalt and nitrendipine. The active fraction completely blocked specific [3H]nitrendipine binding to guinea pig ventricular membrane preparations. The inhibition of nitrendipine binding by atrotoxin was apparently via an allosteric mechanism. Thus atrotoxin was shown to bind to the Ca2+ channel and to act as a specific Ca2+ channel agonist.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hamilton, S L -- Yatani, A -- Hawkes, M J -- Redding, K -- Brown, A M -- 1R01 HL3293S/HL/NHLBI NIH HHS/ -- 1R01-HL33662-01/HL/NHLBI NIH HHS/ -- 5R01-HL25145-05/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Jul 12;229(4709):182-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3160111" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Calcium/*metabolism ; Cell Membrane/metabolism ; Crotalid Venoms/*pharmacology ; Dose-Response Relationship, Drug ; Guinea Pigs ; In Vitro Techniques ; Molecular Weight ; Myocardium/*metabolism ; Nifedipine/analogs & derivatives/metabolism ; Nitrendipine ; Potassium/metabolism ; Rats ; Sodium/metabolism
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  • 25
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    Synthesis and evaluation of a prototypal artificial red cell (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-12-06
    Description: A new process allows microencapsulation of purified human hemoglobin and 2,3-diphosphoglycerate to form neohemocytes. The microcapsule membrane is composed of phospholipids and cholesterol. Neohemocytes are substantially smaller than erythrocytes, contain 15.1 grams per decaliter of hemoglobin, and have a P50 value (the partial pressure of oxygen at which the hemoglobin is half-saturated) of 24.0 torr. All rats given 50-percent exchange transfusions survived with only limited evidence of reversible toxicity. Normal serum glutamate-pyruvate-transaminase values at 1, 7, and 30 days after transfusion were consistent with minimal hepatotoxicity. The concentration of blood urea-nitrogen was elevated by 35 percent after 1 day but returned to normal by day 7. However, histopathology revealed normal kidneys on day 1 as well as on days 7 and 30. Neohemocytes cleared from the circulation of transfused rats with an apparent half-life of 5.8 hours.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hunt, C A -- Burnette, R R -- MacGregor, R D -- Strubbe, A E -- Lau, D T -- Taylor, N -- Kiwada, H -- R01-GM-24612/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1165-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4071041" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine Transaminase/blood ; Animals ; Aspartate Aminotransferases/blood ; Bilirubin/blood ; Blood Substitutes/adverse effects/*metabolism ; Blood Transfusion ; Blood Urea Nitrogen ; Creatinine/blood ; Disseminated Intravascular Coagulation/etiology ; Hematocrit ; Hemoglobins/metabolism ; Humans ; Microscopy, Electron ; Oxygen/metabolism ; Rats
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  • 26
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    Choline acetyltransferase activity in striatum of neonatal rats increased by nerve growth factor (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-07-19
    Description: Some neurodegenerative disorders may be caused by abnormal synthesis or utilization of trophic molecules required to support neuronal survival. A test of this hypothesis requires that trophic agents specific for the affected neurons be identified. Cholinergic neurons in the corpus striatum of neonatal rats were found to respond to intracerebroventricular administration of nerve growth factor with prominent, dose-dependent, selective increases in choline acetyltransferase activity. Cholinergic neurons in the basal forebrain also respond to nerve growth factor in this way. These actions of nerve growth factor may indicate its involvement in the normal function of forebrain cholinergic neurons as well as in neurodegenerative disorders involving such cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mobley, W C -- Rutkowski, J L -- Tennekoon, G I -- Buchanan, K -- Johnston, M V -- ES07094/ES/NIEHS NIH HHS/ -- NS00603/NS/NINDS NIH HHS/ -- NS17642/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):284-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2861660" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/physiology ; Alzheimer Disease/metabolism ; Animals ; Animals, Newborn/metabolism ; Brain/drug effects/enzymology ; Choline O-Acetyltransferase/*metabolism ; Corpus Striatum/cytology/drug effects/*enzymology ; Dose-Response Relationship, Drug ; Glutamate Decarboxylase/metabolism ; Humans ; Huntington Disease/metabolism ; Nerve Growth Factors/*pharmacology/physiology ; Neurons/enzymology/physiology ; Rats ; Rats, Inbred Strains ; Tyrosine 3-Monooxygenase/metabolism
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  • 27
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    Parkinson's disease: an environmental cause? (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-07-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):257-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3925554" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Animals ; Haplorhini ; Humans ; Mice ; Parkinson Disease/*etiology ; Parkinson Disease, Secondary/chemically induced ; Pesticides/adverse effects ; Pyridines/adverse effects/metabolism ; Quebec ; Rats ; Substantia Nigra/drug effects
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  • 28
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    Molecular clocks scrutinized (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-05-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewin, R -- New York, N.Y. -- Science. 1985 May 3;228(4699):571.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3983640" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Biological Clocks ; DNA/metabolism ; Humans ; Mice ; Rats
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  • 29
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    Brain "identifier sequence" is not restricted to brain: similar abundance in nuclear RNA of other organs (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-20
    Description: A repeated 82 base pair sequence in genomic DNA of the rat was previously proposed as being a control element governing brain (neuron) specific genetic expression. This intronic sequence, termed the brain "identifier" (ID), is complementary to small RNA species localized in brain cytoplasm, and it was thought to be represented specifically in RNA produced by brain nuclei in vitro. The RNA blot analyses of total nuclear and polyadenylated heterogeneous nuclear RNA described in the present report show that this ID sequence is also present in the liver and kidney in abundances similar to those in the brain. This repeated sequence is not, therefore, restricted to transcripts produced in the brain as suggested from previous transcriptional "runoff" experiments. Measurements on rat and mouse nuclear RNA indicate that the abundance of ID sequence transcript is roughly proportional to the number of copies of this repeat in the respective genomes. This suggests a rather random genomic location and transcription of this sequence. From these results it seems improbable that the ID sequence functions as a transcriptional-level control element in genes expressed specifically in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Owens, G P -- Chaudhari, N -- Hahn, W E -- NS10813/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 20;229(4719):1263-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2412293" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Brain Chemistry ; Cloning, Molecular ; *Genes ; Kidney/analysis ; Liver/analysis ; Mice ; Neural Crest/analysis ; Nucleic Acid Hybridization ; RNA/*analysis ; Rats ; Transcription, Genetic
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    Geometrical differences among homologous neurons in mammals (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-04-19
    Description: The dendritic arbors of sympathetic neurons in different species of mammals vary systematically: the superior cervical ganglion cells of smaller mammals have fewer and less extensive dendrites than the homologous neurons in larger animals. This difference in dendritic complexity according to body size is reflected in the convergence of ganglionic innervation; the ganglion cells of progressively larger mammals are innervated by progressively more axons. These relations have implications both for the function of homologous neural systems in animals of different sizes and for the regulation of neuronal geometry during development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Purves, D -- Lichtman, J W -- NS 11699/NS/NINDS NIH HHS/ -- NS 18629/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 19;228(4697):298-302.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3983631" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/ultrastructure ; Body Constitution ; Cricetinae ; Dendrites/ultrastructure ; Ganglia, Spinal/ultrastructure ; Guinea Pigs ; Mice ; Neurons/physiology/*ultrastructure ; Rabbits ; Rats ; Species Specificity
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    trans-4-Hydroxy-2-hexenal: a reactive metabolite from the macrocyclic pyrrolizidine alkaloid senecionine (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-08-02
    Description: The toxicity of macrocyclic pyrrolizidine alkaloids in the livers of man and animals has been attributed to the formation of reactive pyrroles from dihydropyrrolizines. Now a novel metabolite, trans-4-hydroxy-2-hexenal, has been isolated from the macrocyclic pyrrolizidine alkaloid senecionine, in an in vitro hepatic microsomal system. Other alkenals such as trans-4-hydroxy-2-nonenal have previously been isolated from microsomal systems when treated with halogenated hydrocarbons or subjected to lipid peroxidation. The in vivo pathology caused by trans-4-hydroxy-2-hexenal appears to be identical to that previously attributed to reactive pyrroles. There are similarities between the toxic effects of this alkenal and those of centrilobular hepatotoxins such as CCl4 and other alkenals formed during lipid peroxidation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Segall, H J -- Wilson, D W -- Dallas, J L -- Haddon, W F -- ES-03343/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 2;229(4712):472-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4012327" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehydes/*metabolism/toxicity ; Animals ; Biotransformation ; Drug-Induced Liver Injury ; In Vitro Techniques ; Injections, Intravenous ; Lipid Peroxides/biosynthesis ; Liver Diseases/pathology ; Mice ; Microsomes, Liver/metabolism ; Necrosis/chemically induced ; Portal Vein ; Pyrrolizidine Alkaloids/*metabolism/toxicity ; Rats
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    Monoclonal antibody-directed radioimmunoassay detects cytochrome P-450 in human placenta and lymphocytes (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-26
    Description: A multiplicity of cytochromes P-450 is responsible for the detoxification and activation of xenobiotics such as drugs and carcinogens. Individual differences in sensitivity to these agents may reside in the cytochrome P-450 phenotype. A monoclonal antibody-directed radioimmunoassay was developed that detects epitope-specific cytochromes P-450 in human placentas and peripheral lymphocytes. Placentas from women who smoked cigarettes contained greater amounts of cytochrome P-450 with the monoclonal antibody-specific epitope than placentas from nonsmokers. The amount of this cytochrome P-450 in human peripheral lymphocytes increased after treatment of the mitogenized lymphocytes with the cytochrome P-450 inducer benz[a]anthracene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, B J -- Gelboin, H V -- Park, S S -- Tsokos, G C -- Friedman, F K -- New York, N.Y. -- Science. 1985 Apr 26;228(4698):490-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2580351" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal ; Antibody Specificity ; Aryl Hydrocarbon Hydroxylases/metabolism ; Benz(a)Anthracenes/pharmacology ; Cytochrome P-450 Enzyme System/*analysis/immunology ; Enzyme Induction/drug effects ; Epitopes/immunology ; Humans ; Lymphocytes/*enzymology ; Methylcholanthrene/pharmacology ; Microsomes/enzymology ; Microsomes, Liver/enzymology ; Placenta/*enzymology ; Radioimmunoassay/methods ; Rats
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    Androgens and prenatal alcohol exposure (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sparber, S B -- New York, N.Y. -- Science. 1985 Jul 12;229(4709):195-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4012317" target="_blank"〉PubMed〈/a〉
    Keywords: Androgens/*metabolism ; Animals ; Ethanol/*pharmacology ; Female ; Fetus/*drug effects ; Pregnancy ; Rats ; Sexual Behavior, Animal/*drug effects
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    Direct evidence that endogenous GM1 ganglioside can mediate thymocyte proliferation (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-12-13
    Description: The B subunit of cholera toxin, which is multivalent and binds exclusively to a specific ganglioside, GM1, was mitogenic for rat thymocytes. When exposed to the B subunit, the cells proliferated, as measured by 3H-labeled thymidine incorporation. Mitogenesis depended on the direct interaction of the B subunit with GM1 on the surface of the cells. This demonstrates that endogenous plasma membrane gangliosides can mediate proliferation in lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Spiegel, S -- Fishman, P H -- Weber, R J -- New York, N.Y. -- Science. 1985 Dec 13;230(4731):1285-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2999979" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Animals ; Antigen-Antibody Reactions ; Cholera Toxin/immunology/*pharmacology ; Cyclic AMP/physiology ; Enzyme Activation/drug effects ; G(M1) Ganglioside/*physiology ; Lymphocyte Activation/drug effects ; Macromolecular Substances ; *Mitogens ; Rats ; T-Lymphocytes/*physiology
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    A strong influence of serotonin axons on beta-adrenergic receptors in rat brain (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-10-18
    Description: The role of serotonin axons in modulating the norepinephrine neurotransmission system in rat brain was investigated. Selective lesions of the forebrain serotonergic system were made by injecting 5,7-dihydroxytryptamine into the midbrain raphe nuclei. Four to six weeks after the lesion, the uptake of 3H-labeled serotonin in the frontal cortex and the hippocampus was reduced by more than 90 percent, while neither the uptake of 3H-labeled norepinephrine nor the content of norepinephrine was affected in either tissue. The number of beta-adrenergic receptors, as measured by radioligand binding with 3H-labeled dihydroalprenolol, was increased in the frontal cortex and hippocampus of rats with lesions. Similarly, specific lesions of central serotonin axons produced by systemically administered p-chloramphetamine resulted in an increase in the binding of 3H-labeled dihydroalprenolol to beta-adrenergic receptors and in the production of adenosine 3',5'-monophosphate in response to isoproterenol. These results indicate that serotonin axons may regulate beta-adrenergic receptor number and function in brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stockmeier, C A -- Martino, A M -- Kellar, K J -- MH08982/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):323-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996132" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cerebral Cortex/*metabolism ; Clonidine/analogs & derivatives/metabolism ; Dihydroalprenolol/metabolism ; Hippocampus/*metabolism ; Kinetics ; Male ; Norepinephrine/metabolism ; Prazosin/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic, beta/*metabolism ; Serotonin/*physiology
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    Acquisition by innervated cardiac myocytes of a pertussis toxin-specific regulatory protein linked to the alpha 1-receptor (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-11
    Description: During development, the chronotropic response of rat ventricular myocardium to alpha 1-adrenergic stimulation changes from positive to negative. The alpha 1-agonist phenylephrine increases the rate of contraction of neonatal rat myocytes cultured alone but decreases the rate of contraction when the myocytes are cultured with functional sympathetic neurons. The developmental induction of the inhibitory myocardial response to alpha 1-adrenergic stimulation in intact ventricle and in cultured myocytes was shown to coincide with the functional acquisition of a substrate for pertussis toxin. A 41-kilodalton protein from myocytes cultured with sympathetic neurons and from adult rat myocardium showed, respectively, 2.2- and 16-fold increases in pertussis toxin-associated ADP-ribosylation (ADP, adenosine diphosphate) as compared to controls. In nerve-muscle cultures, inhibition of the actions of this protein by pertussis toxin-specific ADP-ribosylation reversed the mature inhibitory alpha 1-adrenergic response to an immature stimulatory pattern. The results suggest that innervation is associated with the appearance of a functional pertussis toxin substrate by which the alpha 1-adrenergic response becomes linked to a decrease in automaticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steinberg, S F -- Drugge, E D -- Bilezikian, J P -- Robinson, R B -- AM-01186/AM/NIADDK NIH HHS/ -- HL-20859/HL/NHLBI NIH HHS/ -- HL-28958/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 11;230(4722):186-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2994230" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate/metabolism ; Animals ; Bacterial Toxins/*pharmacology ; Chickens ; Cyclic AMP/metabolism ; Heart/*drug effects/growth & development/innervation ; Myocardium/*cytology/metabolism ; Pertussis Toxin ; Phenylephrine/pharmacology ; Propranolol/pharmacology ; Rats ; Receptors, Adrenergic, alpha/*drug effects ; Virulence Factors, Bordetella
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    Reversal of oncogenesis by the expression of a major histocompatibility complex class I gene (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-05
    Description: The classical transplantation antigens (the major histocompatibility complex class I antigens) play a key role in host defense against cells expressing foreign antigens. Several naturally occurring tumors and virally transformed cells show an overall suppression of these surface antigens. Since the class I molecules are required in the presentation of neoantigens on tumor cells to the cytotoxic T lymphocytes, their absence from the cell surface may lead to the escape of these tumors from immunosurveillance. To test this possibility, a functional class I gene was transfected into human adenovirus 12-transformed mouse cells that do not express detectable levels of class I antigens; the transformants were tested for expression of the transfected gene and for changes in oncogenicity. The expression of a single class I gene, introduced by DNA-mediated gene transfer into highly tumorigenic adenovirus 12-transformed cells, was sufficient to abrogate the oncogenicity of these cells. This finding has important implications for the regulation of the malignant phenotype in certain tumors and for the potential modulation of oncogenicity through derepression of the endogenous class I genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, K -- Isselbacher, K J -- Khoury, G -- Jay, G -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):26-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975631" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/immunology ; Cell Line ; Immunization ; *Major Histocompatibility Complex ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Neoplasm Transplantation ; Neoplasms, Experimental/genetics/*immunology ; Rats
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    Neurotrophic factors (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-07-19
    Description: In addition to nerve growth factor (NGF), many proteins present in soluble tissue extracts and in the extracellular matrix influence the survival and development of cultured neurons. The structure, synthesis, and mechanism of action of NGF as a neurotrophic factor are considered along with the experiments on the new putative trophic molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thoenen, H -- Edgar, D -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):238-42.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2409599" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; Cell Survival ; Cells, Cultured ; Chick Embryo ; Chickens ; Cyclic AMP/physiology ; DNA/genetics ; Extracellular Matrix/physiology ; Humans ; Ion Channels/physiology ; Male ; Mice ; Molecular Weight ; Myocardium/cytology ; Nerve Growth Factors/genetics/isolation & purification/*physiology ; Neurons/physiology ; Protein Precursors/genetics ; RNA, Messenger/metabolism ; Rats ; Receptors, Cell Surface/physiology ; Receptors, Nerve Growth Factor ; Sympathetic Nervous System/cytology
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    Endogenous anticonvulsant substance in rat cerebrospinal fluid after a generalized seizure (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-05-31
    Description: Cerebrospinal fluid taken from rats subjected to electroshock-induced seizures and injected into the cerebral ventricles of rats that had not been shocked increased the seizure threshold of the recipients. The anticonvulsant activity of the donor cerebrospinal fluid was antagonized by opioid antagonists and enhanced by peptidase inhibitors. These results suggest the existence of an endogenous anticonvulsant substance in rat cerebrospinal fluid, possibly opioid in nature, which is activated as a consequence of a seizure and which may play a critical role in postseizure inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tortella, F C -- Long, J B -- New York, N.Y. -- Science. 1985 May 31;228(4703):1106-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2986292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticonvulsants/*cerebrospinal fluid ; Electroshock ; Enkephalin, Leucine/analogs & derivatives/pharmacology ; Male ; Naloxone/pharmacology ; Narcotic Antagonists/pharmacology ; Peptide Hydrolases ; Rats ; Rats, Inbred Strains ; Receptors, Opioid/drug effects ; Receptors, Opioid, delta ; Seizures/*cerebrospinal fluid
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    Protection against lethal hyperoxia by tracheal insufflation of erythrocytes: role of red cell glutathione (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-02-15
    Description: Intact erythrocytes placed into the tracheobronchial tree of hyperoxic rats dramatically improved their chances for survival. Over 70 percent of the animals so treated survived more than 12 days during continuous exposure to 95 percent oxygen, whereas all of the control animals died within 96 hours. Lungs from erythrocyte-protected rats showed almost none of the morphologic damage suffered by untreated animals. Erythrocytes containing cyanomethemoglobin were as beneficial as normal erythrocytes, but cells in which glutathione was partially blocked were significantly less protective. Analogous results were obtained in vitro: 51Cr-labeled target cells released 70 to 90 percent of their label when exposed briefly to hydrogen peroxide or to toxic oxygen species generated by phorbol ester-stimulated neutrophils. Addition of intact erythrocytes decreased release by approximately 75 percent, but significantly less than this if red blood cell glutathione was partially blocked. These results suggest that insufflated erythrocytes, through their recyclable glutathione, protect rats from toxic oxygen species engendered by hyperoxia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Asbeck, B S -- Hoidal, J -- Vercellotti, G M -- Schwartz, B A -- Moldow, C F -- Jacob, H S -- HL 19725/HL/NHLBI NIH HHS/ -- HL07062/HL/NHLBI NIH HHS/ -- HL28935/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 15;227(4688):756-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2982213" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Erythrocyte Transfusion ; Glutathione/*administration & dosage/blood ; Lung/*drug effects ; Male ; Oxygen/*toxicity ; Rats ; Superoxides/toxicity ; Trachea
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    HTLV x-gene product: requirement for the env methionine initiation codon (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-06-28
    Description: The human T-cell leukemia viruses (HTLV) are replication-competent retroviruses whose genomes contain gag, pol, and env genes as well as a fourth gene, termed x, which is believed to be the transforming gene of HTLV. The product of the x gene is now shown to be encoded by a 2.1-kilobase messenger RNA derived by splicing of at least two introns. By means of S1 nuclease mapping of this RNA and nucleic acid sequence analysis of a complementary DNA clone, the complete primary structure of the x-gene product has been determined. It is encoded by sequences containing the env initiation codon and one nucleotide of the next codon spliced to the major open reading frame of the HTLV-I and HTLV-II x gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wachsman, W -- Golde, D W -- Temple, P A -- Orr, E C -- Clark, S C -- Chen, I S -- CA 30388/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- CA 38597/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jun 28;228(4707):1534-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990032" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Transformation, Viral ; Codon ; Deltaretrovirus/*genetics ; Electrophoresis, Polyacrylamide Gel ; Humans ; Methionine/*genetics ; Rats ; Viral Proteins/*analysis
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    Distinct monoamine oxidase A and B populations in primate brain (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-11
    Description: Monoclonal antibodies specific for monoamine oxidase (MAO) A and MAO B, respectively, were used to localize these enzymes in primate brain. The reagents recognized different populations of neurons: those that recognized MAO A were located in cell groups containing catecholamines, including the substantia nigra, nucleus locus coeruleus, nucleus subcoeruleus, and the periventricular region of the hypothalamus, whereas those that recognized MAO B were observed in serotonin regions, including the nucleus raphe dorsalis and nucleus centralis superior. These data illustrate the physiological independence of MAO A and B and show that neurons may be specialized for their degradative as well as their synthetic functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westlund, K N -- Denney, R M -- Kochersperger, L M -- Rose, R M -- Abell, C W -- MH34757/MH/NIMH NIH HHS/ -- NS07309/NS/NINDS NIH HHS/ -- NS19543/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Oct 11;230(4722):181-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3875898" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Animals ; Antibodies, Monoclonal/immunology ; Brain/drug effects/*enzymology ; Brain Stem/enzymology ; Humans ; Macaca fascicularis ; Mice/immunology ; Monoamine Oxidase/immunology/*metabolism ; Neurons/enzymology ; Paraventricular Hypothalamic Nucleus/enzymology ; Pyridines/pharmacology ; Raphe Nuclei/enzymology ; Rats ; Serotonin/physiology ; Substantia Nigra/enzymology
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    Hypoglycemia-induced neuronal damage prevented by an N-methyl-D-aspartate antagonist (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-11-08
    Description: The possibility that neuronal damage due to hypoglycemia is induced by agonists acting on the N-methyl-D-aspartate (NMDA) receptor was investigated in the rat caudate nucleus. Local injections of an NMDA receptor antagonist, 2-amino-7-phosphonoheptanoic acid, were performed before induction of 30 minutes of reversible, insulin-induced, hypoglycemic coma. Neuronal necrosis in these animals after 1 week of recovery was reduced 90 percent compared to that in saline-injected animals. The results suggest that hypoglycemic neuronal damage is induced by NMDA receptor agonists, such as the excitatory amino acids or related compounds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wieloch, T -- New York, N.Y. -- Science. 1985 Nov 8;230(4726):681-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996146" target="_blank"〉PubMed〈/a〉
    Keywords: *2-Amino-5-phosphonovalerate/*analogs & derivatives ; Amino Acids/*pharmacology ; Animals ; Aspartic Acid/*analogs & derivatives/antagonists & inhibitors ; Caudate Nucleus/cytology ; Electroencephalography ; Hypoglycemia/*metabolism/pathology ; Male ; N-Methylaspartate ; Necrosis ; Neurons/*drug effects/metabolism/pathology ; Rats ; Rats, Inbred Strains ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/metabolism
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    Transformation of human bronchial epithelial cells transfected by Harvey ras oncogene (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-08
    Description: Transfection of normal human bronchial epithelial (NHBE) cells with a plasmid carrying the ras oncogene of Harvey murine sarcoma virus (v-Ha ras) changed the growth requirements, terminal differentiation, and tumorigenicity of the recipient cells. One of the cell lines isolated after transfection (TBE-1) was studied extensively and shown to contain v-Ha ras DNA. Total cellular RNA from TBE-1 cells hybridized to v-Ha ras structural gene fragment probes five to eight times more than RNA from parental NHBE cells. The TBE-1 cells expressed phosphorylated v-Ha ras polypeptide p21, showed a reduced requirement for growth-factor supplements, and became aneuploid as an early cellular response to v-Ha ras expression. As the transfectants acquire an indefinite life-span and anchorage independence they became transplantable tumor cells and showed many phenotypic changes suggesting a pleiotropic mechanism for the role of Ha ras in human carcinogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yoakum, G H -- Lechner, J F -- Gabrielson, E W -- Korba, B E -- Malan-Shibley, L -- Willey, J C -- Valerio, M G -- Shamsuddin, A M -- Trump, B F -- Harris, C C -- New York, N.Y. -- Science. 1985 Mar 8;227(4691):1174-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975607" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bronchi/*cytology/microbiology ; Carcinoma, Bronchogenic/genetics ; Cell Line ; Cell Transformation, Neoplastic/metabolism ; *Cell Transformation, Viral ; Culture Media ; DNA, Neoplasm/genetics ; Epithelial Cells ; Epithelium/microbiology ; Humans ; Lung Neoplasms/genetics ; Mice ; Mice, Nude ; Nucleic Acid Hybridization ; *Oncogenes ; Rats ; *Transfection
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  • 45
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    Regional myocardial substrate uptake in hypertensive rats: a quantitative autoradiographic measurement (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-22
    Description: Severe hypertension causes global and regional changes in myocardial perfusion and substrate utilization. Regional perfusion and fatty acid utilization were evaluated by dual-tracer autoradiography in normotensive and hypertensive rats of the Dahl strain. The regional distributions of perfusion and fatty acid utilization were homogeneous in normotensive rats. Severe hypertension was associated with a homogeneous pattern of regional perfusion, but fatty acid utilization was focally decreased in the free wall of the left ventricle. The decrease in fatty acid uptake was associated with a concomitant increase in glucose utilization. These findings suggest that severe hypertension is associated with uniform myocardial perfusion and focal alterations in the substrates used for the performance of myocardial work.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yonekura, Y -- Brill, A B -- Som, P -- Yamamoto, K -- Srivastava, S C -- Iwai, J -- Elmaleh, D R -- Livni, E -- Strauss, H W -- Goodman, M M -- HL29636/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1494-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975623" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Deoxyglucose/analogs & derivatives/metabolism ; Endocardium/metabolism ; Fatty Acids/*metabolism ; Fluorodeoxyglucose F18 ; Glucose/*metabolism ; Heart Septum/metabolism ; Hypertension/*metabolism ; Myocardium/*metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred Strains ; Tissue Distribution
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  • 46
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    Distribution of enkephalin immunoreactivity in germinative cells of developing rat cerebellum (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-01
    Description: The cellular distribution of enkephalin, an endogenous opioid, in the developing rat cerebellum was determined by immunocytochemistry. Methionine and leucine enkephalin were concentrated in the external germinal layer, a matrix of proliferative cells; staining was confined to the cortical cytoplasm. Enkephalin was not detected by immunocytochemistry in differentiated neural cells. These results indicate that endogenous opioids are involved specifically in early phases of nervous system development, particularly cell proliferation and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zagon, I S -- Rhodes, R E -- McLaughlin, P J -- NS-20500/NS/NINDS NIH HHS/ -- NS-20623/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 1;227(4690):1049-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3883485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cerebellum/cytology/*growth & development/physiology ; Enkephalin, Leucine/immunology/physiology ; Enkephalin, Methionine/immunology/physiology ; Enkephalins/immunology/*physiology ; Fluorescent Antibody Technique ; Rats ; Rats, Inbred Strains
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  • 47
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    Superinduction of c-fos by nerve growth factor in the presence of peripherally active benzodiazepines (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-20
    Description: Alterations in proto-oncogene expression after stimulation of rat pheochromocytoma (PC12) cells by nerve growth factor (NGF) have been investigated. A specific stimulation of c-fos messenger RNA and protein was detected 30 minutes after treatment. This induction was enhanced more than 100-fold in the presence of peripherally active benzodiazepines. The effect was specific as very little change was observed in the levels of c-rasHa, c-rasKi, c-myc, and N-myc messenger RNA's. Under the conditions used here, NGF treatment ultimately results in neurite outgrowth, with a reduction or cessation of cell division. Thus, stimulation of the c-fos gene in this system appeared to be associated with differentiation and not with cellular proliferation. The effect of benzodiazepines was stereospecific and represents a novel action of these compounds at the level of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Curran, T -- Morgan, J I -- New York, N.Y. -- Science. 1985 Sep 20;229(4719):1265-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4035354" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzodiazepines/*pharmacology ; Cell Line ; Cell Transformation, Neoplastic/drug effects ; Gene Expression Regulation/*drug effects ; Nerve Growth Factors/*pharmacology ; *Oncogenes ; Pheochromocytoma/genetics/metabolism ; RNA, Messenger/biosynthesis ; Rats
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    A potent nonpeptide cholecystokinin antagonist selective for peripheral tissues isolated from Aspergillus alliaceus (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-10-11
    Description: A new, competitive, nonpeptide cholecystokinin (CCK) antagonist, asperlicin, was isolated from the fungus Aspergillus alliaceus. The compound has 300 to 400 times the affinity for pancreatic, ileal, and gallbladder CCK receptors than proglumide, a standard agent of this class. Moreover, asperlicin is highly selective for peripheral CCK receptors relative to brain CCK and gastrin receptors. Since asperlicin also exhibits long-lasting CCK antagonist activity in vivo, it should provide a valuable tool for investigating the physiological and pharmacological actions of CCK.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, R S -- Lotti, V J -- Monaghan, R L -- Birnbaum, J -- Stapley, E O -- Goetz, M A -- Albers-Schonberg, G -- Patchett, A A -- Liesch, J M -- Hensens, O D -- New York, N.Y. -- Science. 1985 Oct 11;230(4722):177-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2994227" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspergillus/*metabolism ; Benzodiazepinones/*isolation & purification/pharmacology ; Chemical Phenomena ; Chemistry ; Cholecystokinin/*antagonists & inhibitors/pharmacology/physiology ; Dose-Response Relationship, Drug ; Gallbladder/drug effects ; Guinea Pigs ; Ileum/drug effects ; Pancreas/drug effects ; Rats ; Receptors, Cell Surface/drug effects ; Receptors, Cholecystokinin
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    Atrial natriuretic factor ameliorates chronic metabolic alkalosis by increasing glomerular filtration (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-09-27
    Description: The kidney maintains the elevated plasma concentration of bicarbonate that occurs in chronic metabolic alkalosis. A reduction in the glomerular filtration rate (GFR) can maintain the filtered bicarbonate load at a normal level so that a normal rate of bicarbonate reabsorption suffices to prevent urinary excretion of this anion. It is also possible that bicarbonate reabsorption might increase so as to maintain the alkalosis if GFR were not reduced. To examine this latter possibility, atrial natriuretic factor was used in alkalotic rats to restore a more normal GFR and to increase the amount of bicarbonate filtered by the glomerulus. Proximal bicarbonate reabsorption remained relatively static. Higher than normal amounts of bicarbonate were then delivered out of the proximal tubule, bicarbonate appeared in the urine, and the plasma concentration of bicarbonate fell. A reduction in GFR is thus necessary for the maintenance of chronic metabolic alkalosis. Normalizing GFR induces bicarbonaturia and initiates repair of the alkalosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cogan, M G -- 1-K08-AM 01015/AM/NIADDK NIH HHS/ -- AM-27045/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 27;229(4720):1405-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2930899" target="_blank"〉PubMed〈/a〉
    Keywords: Alkalosis/*drug therapy/physiopathology ; Animals ; Atrial Natriuretic Factor ; Bicarbonates/urine ; Chlorides/urine ; Extracellular Space/drug effects ; Glomerular Filtration Rate/*drug effects ; Kidney/drug effects/physiopathology ; Muscle Proteins/*pharmacology/therapeutic use ; Nephrons/drug effects/physiology ; Rats
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    Alzheimer's disease: a biologist's perspectives (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-12-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Finch, C E -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4071039" target="_blank"〉PubMed〈/a〉
    Keywords: *Alzheimer Disease/genetics/pathology ; Animals ; Humans ; Rats
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    Immunocytochemical detection of acetylcholine in the rat central nervous system (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-05
    Description: A specific antibody to acetylcholine was raised and used as a marker for cholinergic neurons in the rat central nervous system. The acetylcholine conjugate was obtained by a two-step immunogen synthesis procedure. An enzyme-linked immunosorbent assay was used to test the specificity and affinity of the antibody in vitro; the results indicated high affinity. A chemical perfusion mixture of allyl alcohol and glutaraldehyde was used to fix the acetylcholine in the nervous tissue. Peroxidase-antiperoxidase immunocytochemistry showed many acetylcholine-immunoreactive cells and fibers in sections from the medial septum region.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geffard, M -- McRae-Degueurce, A -- Souan, M L -- New York, N.Y. -- Science. 1985 Jul 5;229(4708):77-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3892687" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*immunology/metabolism ; Animals ; Antibody Specificity ; Brain/*anatomy & histology ; Brain Mapping ; Cholinergic Fibers/*anatomy & histology ; Immunoenzyme Techniques ; Male ; Rats
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    Plasticity of hippocampal circuitry in Alzheimer's disease (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-12-06
    Description: Two markers of neuronal plasticity were used to compare the response of the human central nervous system to neuronal loss resulting from Alzheimer's disease with the response of rats to a similar neuronal loss induced by lesions. In rats that had received lesions of the entorhinal cortex, axon sprouting of commissural and associational fibers into the denervated molecular layer of the dentate gyrus was paralleled by a spread in the distribution of tritiated kainic acid-binding sites. A similar expansion of kainic acid receptor distribution was observed in hippocampal samples obtained postmortem from patients with Alzheimer's disease. An enhancement of acetylcholinesterase activity in the dentate gyrus molecular layer, indicative of septal afferent sprouting, was also observed in those patients with a minimal loss of cholinergic neurons. These results are evidence that the central nervous system is capable of a plastic response in Alzheimer's disease. Adaptive growth responses occur along with the degenerative events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geddes, J W -- Monaghan, D T -- Cotman, C W -- Lott, I T -- Kim, R C -- Chui, H C -- AG00538/AG/NIA NIH HHS/ -- MH 19691/MH/NIMH NIH HHS/ -- P50AG5142/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1179-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4071042" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/metabolism ; Alzheimer Disease/*pathology ; Animals ; Hippocampus/enzymology/*pathology ; Humans ; Kainic Acid/metabolism ; Male ; *Neuronal Plasticity ; Neurons/pathology ; Rats ; Rats, Inbred Strains
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    Transcription of class III genes activated by viral immediate early proteins (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-10-25
    Description: The adenovirus EIA and pseudorabies virus immediate early (IE) proteins induce transcription from transfected viral and nonviral genes transcribed by RNA polymerase II (class II genes). These proteins have now been shown also to activate transcription of transfected genes transcribed by RNA polymerase III (class III genes). As previously observed for class II genes, this stimulation of class III gene transcription was much greater for transfected genes than for the major endogenous cellular class III genes. Extracts made from cell lines stably expressing a transfected pseudorabies virus IE gene were 10 to 20 times more active in the in vitro transcription of exogenously added class III genes than extracts of the parental cell line. These results indicate that the E1A and IE proteins stimulate the expression of class III genes by a mechanism similar to the mechanism for stimulation of class II gene transcription by these proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gaynor, R B -- Feldman, L T -- Berk, A J -- CA 25235/CA/NCI NIH HHS/ -- CA 30981/CA/NCI NIH HHS/ -- CA 32737/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 25;230(4724):447-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996135" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Drosophila/genetics ; *Genes, Viral ; HeLa Cells ; Herpesvirus 1, Suid/genetics ; Humans ; RNA, Transfer/genetics ; Rabbits ; Rats ; *Transcription, Genetic ; Viral Proteins/*genetics
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  • 54
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    Alignment of rat cardionatrin sequences with the preprocardionatrin sequence from complementary DNA (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-04-19
    Description: Mammalian atria contain peptides that promote the excretion of salt and water from the kidney. When rat atrial tissue is extracted under conditions known to inhibit proteolysis, four natriuretic peptides, cardionatrins I to IV, are consistently isolated. These peptides derive from a common precursor, preprocardionatrin, of 152 amino acids, whose sequence was determined by DNA sequencing of a complementary DNA clone. Amino acid sequencing located the start points of cardionatrins I, III, and IV in the overall sequence. Cardionatrin IV most closely resembles procardionatrin because it begins immediately after the signal sequence at residue 25. Cardionatrin III begins at residue 73, and cardionatrin I, sequenced previously, begins at residue 123. Compositional analysis indicated that each of these cardionatrins extends up to tyrosine at position 150 but lacks the terminal two arginine residues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flynn, T G -- Davies, P L -- Kennedy, B P -- de Bold, M L -- de Bold, A J -- New York, N.Y. -- Science. 1985 Apr 19;228(4697):323-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3157217" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Atrial Function ; Atrial Natriuretic Factor ; Base Sequence ; Chromatography, High Pressure Liquid ; DNA/*genetics ; Electrophoresis, Polyacrylamide Gel ; Molecular Sequence Data ; Muscle Proteins/*genetics/isolation & purification ; *Peptide Fragments ; Protein Precursors/*genetics/isolation & purification ; Rats
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    Peroxisomal defects in neonatal-onset and X-linked adrenoleukodystrophies (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-01-04
    Description: Accumulation of very long chain fatty acids in X-linked and neonatal forms of adrenoleukodystrophy (ALD) appears to be a consequence of deficient peroxisomal oxidation of very long chain fatty acids. Peroxisomes were readily identified in liver biopsies taken from a patient having the X-linked disorder. However, in liver biopsies from a patient having neonatal-onset ALD, hepatocellular peroxisomes were greatly reduced in size and number, and sedimentable catalase was markedly diminished. The presence of increased concentrations of serum pipecolic acid and the bile acid intermediate, trihydroxycoprostanic acid, in the neonatal ALD patient are associated with a generalized diminution of peroxisomal activities that was not observed in the patient with X-linked ALD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goldfischer, S -- Collins, J -- Rapin, I -- Coltoff-Schiller, B -- Chang, C H -- Nigro, M -- Black, V H -- Javitt, N B -- Moser, H W -- Lazarow, P B -- AG-01468/AG/NIA NIH HHS/ -- AM-17702/AM/NIADDK NIH HHS/ -- N5-03356/PHS HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Jan 4;227(4682):67-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3964959" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenoleukodystrophy/genetics/metabolism/*pathology ; Adult ; Animals ; Bile Acids and Salts/metabolism ; Catalase/metabolism ; Child ; Child, Preschool ; Diffuse Cerebral Sclerosis of Schilder/*pathology ; Female ; Humans ; Liver/pathology ; Male ; Microbodies/*pathology ; Oxidation-Reduction ; Pipecolic Acids/blood ; Rats ; *X Chromosome
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    The insulin receptor contains a calmodulin-binding domain (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-11-15
    Description: Substantial evidence suggests that calcium has a pivotal role in regulating the initial events through which insulin alters plasma membrane metabolism. Because binding of insulin to its receptor represents the initial site of insulin action in the plasma membrane, studies were undertaken to determine whether the insulin receptor is a calmodulin-binding protein. Preparations enriched in the insulin receptor and calmodulin-binding proteins were isolated from detergent-solubilized rat adipocyte membranes by chromatography with wheat germ agglutinin agarose and calmodulin-conjugated Sepharose, respectively. Substantial purification of a manganese-dependent, insulin-sensitive phosphoprotein of 95K identified as the beta subunit of the insulin receptor was accomplished. Binding and photocovalent cross-linking of iodine-125-labeled calmodulin to these affinity-purified preparations and to isolated plasma membranes, followed by immunoadsorption with insulin receptor antibodies bound to protein A Sepharose, resulted in significant purification of a binding complex of 110K to 140K. These results indicate that the adipocyte insulin receptor or a polypeptide closely associated with the receptor is a calmodulin-binding protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graves, C B -- Goewert, R R -- McDonald, J M -- AM-25897/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1985 Nov 15;230(4727):827-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3904001" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/cytology ; Animals ; Calmodulin/metabolism ; Calmodulin-Binding Proteins/isolation & purification/*metabolism ; Cell Membrane/metabolism ; Insulin/metabolism ; Phosphorylation ; Rats ; Receptor, Insulin/isolation & purification/*metabolism
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  • 57
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    Effect of vanadate on elevated blood glucose and depressed cardiac performance of diabetic rats (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-22
    Description: The trace element vanadium has an unclear biological function. Vanadate, an oxidized form of vanadium, appears to have an insulin-like action. The effect of vanadate on blood glucose and cardiac performance was assessed in female Wistar rats 6 weeks after they were made diabetic with streptozotocin. When vanadate was administered for a 4-week period to the diabetic rats, their blood glucose was not significantly different from that of nondiabetic controls despite a low serum insulin. In contrast, blood glucose was increased about threefold in the diabetic rats that were not treated with vanadate; these rats also had low insulin levels. Cardiac performance was depressed in the untreated diabetic animals, but the cardiac performance of the vanadate-treated diabetic animals was not significantly different from that of nondiabetic controls. Thus vanadate controlled the high blood glucose and prevented the decline in cardiac performance due to diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heyliger, C E -- Tahiliani, A G -- McNeill, J H -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1474-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3156405" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/*analysis ; Calcium-Transporting ATPases/antagonists & inhibitors ; Diabetes Mellitus, Experimental/blood/*physiopathology ; Drinking ; Female ; Insulin/blood ; Myocardial Contraction/*drug effects ; Myocardium/enzymology ; Rats ; Rats, Inbred Strains ; Sarcoplasmic Reticulum/enzymology ; Vanadates ; Vanadium/*pharmacology
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    Stimulation of bone resorption in vitro by synthetic transforming growth factor-alpha (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-05-24
    Description: Experiments were conducted to test the hypothesis that tumor-derived transforming growth factor-alpha (TGF-alpha) is responsible for the increased bone resorption and hypercalcemia seen in some malignant diseases. Homogeneous synthetic TGF-alpha prepared by the solid-phase synthesis method stimulated bone resorption directly in vitro in a concentration-dependent manner. Incubation times of 72 hours or more were required to stimulate resorption, which is similar to the time course of bone resorption by epidermal growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ibbotson, K J -- Twardzik, D R -- D'Souza, S M -- Hargreaves, W R -- Todaro, G J -- Mundy, G R -- AM-28149/AM/NIADDK NIH HHS/ -- CA-29537/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 24;228(4702):1007-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3859011" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Resorption/*drug effects ; Bone and Bones/drug effects ; Dose-Response Relationship, Drug ; History, 20th Century ; Kinetics ; Molecular Weight ; Organ Culture Techniques ; Peptides/chemical synthesis/*pharmacology ; Rats ; Transforming Growth Factors
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    Immunohistochemical localization in the rat brain of the precursor for thyrotropin-releasing hormone (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-09-13
    Description: A rabbit antiserum to a peptide sequence present in the precursor for thyrotropin-releasing hormone (proTRH), deduced from cloned amphibian-skin complementary DNA, was raised by immunization with the synthetic decapeptide Cys-Lys-Arg-Gln-His-Pro-Gly-Lys-Arg-Cys (proTRH-SH). Immunohistochemical studies on rat brain tissue showed staining of neuronal perikarya in the parvicellular division of the paraventricular nucleus of the hypothalamus and the raphe complex of the medulla, identical to that already described for thyrotropin-releasing hormone (TRH). Immunostaining was abolished by preincubation with proTRH-SH (10(-6)M) but not TRH (10(-5)M). Both TRH precursor and TRH were located in neurons of the paraventricular nucleus. However, in contrast to the findings for TRH, no staining was observed in axon terminals of the median eminence. These results suggest that a TRH precursor analogous to that reported in frog skin is present in the rat brain and that TRH in the mammalian central nervous system is a product of ribosomal biosynthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jackson, I M -- Wu, P -- Lechan, R M -- AM 34540/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 13;229(4718):1097-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3929378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/analysis ; *Brain Chemistry ; DNA/analysis ; Histocytochemistry ; Immunoenzyme Techniques ; Neurons/analysis ; Paraventricular Hypothalamic Nucleus/analysis ; Protein Precursors/*analysis ; Pyrrolidonecarboxylic Acid/analogs & derivatives ; Rats ; Thyrotropin-Releasing Hormone/*analysis
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    Sequence homology between certain viral proteins and proteins related to encephalomyelitis and neuritis (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-07-19
    Description: Post-infectious or post-vaccinal demyelinating encephalomyelitis and neuritis may be due to immunological cross-reactions evoked by specific viral antigenic determinants (epitopes) that are homologous to regions in the target myelins of the central and peripheral nervous systems. Such homologies have been found by computer searches in which decapeptides in two human myelin proteins were compared with proteins of viruses known to infect humans. These viruses include measles, Epstein-Barr, influenza A and B, and others that cause upper respiratory infections. Several regions identified in myelin basic protein and P2 protein can be related to experimental allergic encephalomyelitis or neuritis in laboratory animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jahnke, U -- Fischer, E H -- Alvord, E C Jr -- AM07902/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):282-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2409602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chickens ; Encephalomyelitis/etiology/immunology/*metabolism ; Epitopes ; Guinea Pigs ; Haplorhini ; Humans ; Measles/metabolism ; Myelin Basic Protein/genetics ; Myelin P2 Protein ; Neuritis/etiology/immunology/*metabolism ; Rabbits ; Rats ; Rats, Inbred Lew ; Viral Proteins/*genetics ; Viral Vaccines/adverse effects/immunology
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    Insulin mediators from rat skeletal muscle have differential effects on insulin-sensitive pathways of intact adipocytes (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-02-01
    Description: The effects of partially purified insulin-generated mediators from rat skeletal muscle were compared to those of insulin on intact adipocytes. Insulin and insulin mediator stimulated both pyruvate dehydrogenase and glycogen synthase activity of intact adipocytes. In contrast, insulin stimulated glucose oxidation and 3-O-methylglucose transport, whereas insulin-generated mediators had no effect. Insulin-generated mediators cannot account for all the pleiotropic effects of insulin, especially membrane-controlled processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jarett, L -- Wong, E H -- Macaulay, S L -- Smith, J A -- AM19525/AM/NIADDK NIH HHS/ -- AM28144/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 1;227(4686):533-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3917578" target="_blank"〉PubMed〈/a〉
    Keywords: 3-O-Methylglucose ; Adipose Tissue/cytology/drug effects/enzymology/*metabolism ; Animals ; Biological Transport/drug effects ; Glucose/metabolism ; Glycogen Synthase/metabolism ; In Vitro Techniques ; *Inositol Phosphates ; Insulin/*pharmacology ; Methylglucosides/metabolism ; Muscles/analysis ; Oxidation-Reduction ; *Polysaccharides ; Pyruvate Dehydrogenase Complex/metabolism ; Rats ; Receptor, Insulin/*pharmacology
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    Digestive adaptations for fueling the cost of endothermy (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-04-12
    Description: Little is known about the digestive adaptations that enable mammals to sustain metabolic rates an order of magnitude higher than those of reptiles. Comparison of several features of digestion in mammals and lizards of similar size eating the same diet revealed that mammals processed food ten times faster and with the same or greater extraction efficiency. Transport kinetics and rates of nutrient absorption normalized to the quantity of intestinal tissue were similar in these two classes of vertebrates. The main basis for faster absorption in mammals is their much greater intestinal surface area.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Karasov, W H -- Diamond, J M -- AM17328/AM/NIADDK NIH HHS/ -- GM14772/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 12;228(4696):202-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975638" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport ; *Body Temperature ; Diet ; *Digestion ; Eating ; Glucose/metabolism ; Intestines/anatomy & histology/physiology ; Lizards/physiology ; Mice ; Proline/metabolism ; Rats
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    Insertion mutagenesis of embryonal carcinoma cells by retroviruses (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-05-03
    Description: Mutagenesis was studied in cultured F9 embryonal carcinoma cells infected with a variant of Moloney murine leukemia virus. Proviral insertion induced the inactivation of the hypoxanthine phosphoribosyltransferase locus, and the virus was used to isolate the mutated genes rapidly. Mutagenesis by these methods may be useful for the genetic dissection of the various mammalian cell phenotypes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉King, W -- Patel, M D -- Lobel, L I -- Goff, S P -- Nguyen-Huu, M C -- New York, N.Y. -- Science. 1985 May 3;228(4699):554-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3838595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Line ; DNA/genetics ; DNA, Neoplasm/genetics ; DNA, Recombinant/metabolism ; DNA, Viral/genetics ; Mice ; Moloney murine leukemia virus/physiology ; *Mutation ; Nucleic Acid Hybridization ; Rats ; Retroviridae/*physiology ; Teratoma/*genetics/microbiology
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    High-affinity uptake of serotonin into immunocytochemically identified astrocytes (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-05-17
    Description: Primary cultures of astrocytes from neonatal rat brain were incubated with tritiated serotonin. After fixation they were stained by immunofluorescence for the astrocyte-specific marker glial fibrillary acidic protein and processed for autoradiography. Silver grain density was increased over cells positive for glial fibrillary acidic protein and was reduced to background levels when sodium was omitted from the medium or the specific inhibitors of serotonin uptake fluoxetine and chlorimipramine were present. The results indicate that mammalian astrocytes can take up serotonin by a sodium-dependent, high-affinity system previously thought to be the exclusive property of serotonergic nerve endings.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimelberg, H K -- Katz, D M -- NS 19492/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 May 17;228(4701):889-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3890180" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/analysis/drug effects/*metabolism ; Autoradiography ; Biological Transport ; Cells, Cultured ; Clomipramine/pharmacology ; Fluorescent Antibody Technique ; Fluoxetine/pharmacology ; Glial Fibrillary Acidic Protein/analysis ; Rats ; Serotonin/*metabolism ; Sodium/pharmacology
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    Cytosolic-free calcium transients in cultured vascular smooth muscle cells: microfluorometric measurements (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-08-09
    Description: Microfluorometric recordings were made of changes in the concentration of cytosolic-free calcium in cultured rat vascular smooth muscle cells treated with quin 2, an intracellularly trapped dye, under several conditions. Nitroglycerin decreased calcium in both the presence and absence of extracellular calcium and strongly and progressively decreased the extent of transient increases in calcium induced by repeated applications of caffeine in the absence of extracellular calcium. Therefore nitroglycerin probably decreases cytosolic-free calcium by accelerating the extrusion of calcium through the sarcolemmal membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kobayashi, S -- Kanaide, H -- Nakamura, M -- New York, N.Y. -- Science. 1985 Aug 9;229(4713):553-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3927484" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Animals ; Aorta ; Caffeine/pharmacology ; Calcium/*metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytosol/metabolism ; Fluorescent Antibody Technique ; Fluorescent Dyes ; Microscopy, Fluorescence ; Muscle, Smooth, Vascular/drug effects/*metabolism ; Nitroglycerin/pharmacology ; Photomicrography ; Potassium/pharmacology ; Rats
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    Why do people get fat? (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kolata, G -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1327-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975619" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/physiopathology ; Animals ; Diet ; Eating ; Female ; Humans ; Male ; Obesity/*etiology/physiopathology ; Rats
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    Hypertension in the recently weaned Dahl salt-sensitive rat despite a diet deficient in sodium chloride (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-11-15
    Description: The Dahl rat is used as a model of hypertension that is "sensitive" to dietary salt (sodium chloride, NaCl). When dietary salt is supplemented in the Dahl rat, the arterial blood pressure of the "salt-sensitive" strain (S) becomes much greater than that of the "salt-resistant" strain (R). It has been widely reported that arterial blood pressure of the young Dahl S rat is not greater than that of the young Dahl R rat before dietary salt is supplemented. In the present study, however, mean arterial pressure directly measured in unanesthetized, unrestrained S rats was greater than in R rats, both when they had been recently weaned and for at least 10 weeks thereafter, despite their having been fed a diet frankly deficient in salt. In weanling S rats, the ratio of heart weight to body weight was also significantly greater than that in weanling R rats, suggesting that the greater blood pressure in the S rat causes cardiac hypertrophy. Thus, biologic differences demonstrated between the S rat and the R rat after weaning, including the phenomenon of salt-sensitivity, could be a consequence of, or be dependent on, an already extant difference in arterial blood pressure between the two strains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kurtz, T W -- Morris, R C Jr -- HL01490-01/HL/NHLBI NIH HHS/ -- R01-AM32631-01/AM/NIADDK NIH HHS/ -- RR-00079/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1985 Nov 15;230(4727):808-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4059913" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Pressure ; Blood Pressure Determination ; *Diet, Sodium-Restricted ; Female ; Femoral Artery/physiology ; Hypertension/*physiopathology ; Rats ; Rats, Inbred Strains/*physiology ; Sodium Chloride/metabolism ; Weaning
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    Platelet-mediated cholesterol accumulation in cultured aortic smooth muscle cells (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-08
    Description: Cholesterol accumulates within smooth muscle cells and macrophages in atherosclerotic lesions, thereby contributing to the progressive enlargement of these lesions. The mechanism of this cellular accumulation of cholesterol is not known. The possibility that platelets may have a role in the cellular cholesterol accumulation that occurs during atherogenesis was investigated. Incubation of thrombin-activated washed rat platelets (or platelet-free supernatants prepared from thrombin-activated platelets) with cultured rat aortic smooth muscle cells induced cholesteryl ester lipid droplet accumulation within the smooth muscle cells. No cholesteryl ester lipid droplets accumulated when smooth muscle cells were incubated with unactivated platelets. Smooth muscle cell lipid droplet accumulation occurred in the absence of serum lipoproteins and was not inhibited by mevinolin, a drug that blocks cholesterol synthesis. These findings suggest that activated platelets may release cholesterol, which can be accumulated by cells and stored as lipid droplets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kruth, H S -- New York, N.Y. -- Science. 1985 Mar 8;227(4691):1243-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/physiopathology ; Arteriosclerosis/*physiopathology ; Blood Platelets/*physiology ; Cells, Cultured ; Cholesterol/*physiology ; Male ; Muscle, Smooth, Vascular/*cytology/physiopathology ; Platelet Aggregation ; Rats ; Rats, Inbred Strains ; Thrombin/physiology
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    Reexamination of glucose-6-phosphatase activity in the brain in vivo: no evidence for a futile cycle (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-07-05
    Description: Glucose-6-phosphatase activity in the rat brain in vivo was estimated by measuring the differential loss of tritium and carbon-14 from the glucose pool labeled by a mixture of [2-3H]glucose and [U-14C]glucose. The results provide no evidence of significant dephosphorylation of glucose-6-phosphate and do not support the hypothesis of a futile cycle involving glucose-6-phosphatase activity in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, T -- Lucignani, G -- Atlas, S -- Crane, A M -- Dienel, G A -- Sokoloff, L -- New York, N.Y. -- Science. 1985 Jul 5;229(4708):60-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Glucose/metabolism ; Glucose-6-Phosphatase/*metabolism ; Glucosephosphates/*metabolism ; Glycolysis ; Male ; Rats ; Rats, Inbred Strains
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    Androgens prevent normally occurring cell death in a sexually dimorphic spinal nucleus (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-08-16
    Description: The spinal nucleus of the bulbocavernosus (SNB) contains many more motoneurons in adult male rats than in females. Androgens establish this sex difference during a critical perinatal period, which coincides with normally occurring cell death in the SNB region. Sex differences in SNB motoneuron number arise primarily because motoneuron loss is greater in females than in males during the early postnatal period. Perinatal androgen treatment in females attenuates cell death in the SNB region, reducing motoneuron loss to levels typical of males. The results suggest that steroid hormones determine sex differences in neuron number by regulating normally occurring cell death and that the timing of this cell death may therefore define critical periods for steroid effects on neuron number.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nordeen, E J -- Nordeen, K W -- Sengelaub, D R -- Arnold, A P -- HD06478-02/HD/NICHD NIH HHS/ -- HD15021/HD/NICHD NIH HHS/ -- NS07355-01/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Aug 16;229(4714):671-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4023706" target="_blank"〉PubMed〈/a〉
    Keywords: Androgens/*pharmacology ; Animals ; Cell Survival/drug effects ; Female ; Male ; Motor Neurons/*physiology ; Penis/innervation ; Rats ; *Sex Characteristics
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    Blood-brain barrier: endogenous modulation by adrenal-cortical function (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-29
    Description: The blood-brain barrier restricts the passage of molecules from the blood to the brain. The permeability of the barrier to iodine-125-labeled bovine serum albumin was examined in rats that had undergone adrenalectomy, adrenal demedullation, and corticosterone replacement. Adrenalectomy, but not adrenal demedullation, increased the permeability of brain tissue to the isotopically labeled macromolecule; corticosterone replacement reversed this effect. These results indicate that the blood-brain barrier may be hormonally regulated; that is, the pituitary-adrenal axis may physiologically modulate the permeability of the brain microvasculature to macromolecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Long, J B -- Holaday, J W -- New York, N.Y. -- Science. 1985 Mar 29;227(4694):1580-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975627" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/*physiology ; Adrenal Medulla/physiology ; Adrenalectomy ; Animals ; Blood Pressure ; *Blood-Brain Barrier ; Central Nervous System/physiology ; Corticosterone/blood/physiology ; Male ; Pituitary-Adrenal System/physiology ; Rats ; Rats, Inbred Strains ; Serum Albumin, Bovine/metabolism
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    Retinal S antigen identified as the 48K protein regulating light-dependent phosphodiesterase in rods (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-17
    Description: Retinal S antigen chromatographically purified from whole retina, induces experimental autoimmune uveoretinitis in laboratory animals. The 48K protein, a soluble protein found in rod outer segments, is purified through its specific binding to photoexcited rhodopsin and is involved in the quenching of light-induced guanosine 3',5'-monophosphate-phosphodiesterase activity. Biochemical, immunological, functional, and pathological tests showed that retinal S antigen and the 48K protein are identical.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfister, C -- Chabre, M -- Plouet, J -- Tuyen, V V -- De Kozak, Y -- Faure, J P -- Kuhn, H -- New York, N.Y. -- Science. 1985 May 17;228(4701):891-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2988124" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-GMP Phosphodiesterases/*metabolism ; Animals ; *Antigens/isolation & purification ; Arrestin ; Autoimmune Diseases/etiology ; Cattle ; Eye Proteins/immunology/isolation & purification/pharmacology ; Light ; Molecular Weight ; Photoreceptor Cells/*enzymology ; Rats ; Retina/analysis/*immunology ; Rod Cell Outer Segment/analysis/immunology ; Uveitis/etiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 73
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    Ascorbic acid and the behavioral response to haloperidol: implications for the action of antipsychotic drugs (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-25
    Description: Haloperidol, a widely used antipsychotic drug, was tested for its ability to block the behavioral response to amphetamine and to elicit catalepsy in rats treated with saline or ascorbic acid (1000 milligrams per kilogram of body weight). By itself, ascorbic acid failed to exert significant behavioral effects, but it enhanced the antiamphetamine and cataleptogenic effects of haloperidol (0.1 or 0.5 milligrams per kilogram). These results, combined with a growing body of biochemical evidence, suggest that ascorbic acid plays an important role in modulating the behavioral effects of haloperidol and related antipsychotic drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rebec, G V -- Centore, J M -- White, L K -- Alloway, K D -- DA 02451/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 25;227(4685):438-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4038426" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ascorbic Acid/*pharmacology ; Behavior, Animal/*drug effects ; Catalepsy/chemically induced ; Dextroamphetamine/pharmacology ; Drug Synergism ; Haloperidol/*pharmacology ; Humans ; Male ; Motor Activity/drug effects ; Rats ; Rats, Inbred Strains ; Receptors, Dopamine/metabolism
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  • 74
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    A role for glycosylation of the alpha subunit in transduction of biological signal in glycoprotein hormones (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-05
    Description: The biological properties of recombinants of glycoprotein hormones in which the alpha and beta subunits were differentially deglycosylated have been investigated. Specific deglycosylation of the alpha subunit generated a recombinant that had more receptor-binding activity but did not produce hormone response in the target cells. The deglycosylated alpha + beta recombinant was also an antagonist of the action of the native hormone. Thus, the carbohydrates in the alpha subunit play a dominant role in the transduction of the hormone signal into the cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sairam, M R -- Bhargavi, G N -- New York, N.Y. -- Science. 1985 Jul 5;229(4708):65-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990039" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclic AMP/metabolism ; Female ; Follicle Stimulating Hormone/*physiology ; Glycoproteins/*physiology ; Leydig Cells/physiology ; Luteinizing Hormone/*physiology ; Male ; Ovary/physiology ; Rats ; Receptors, Cell Surface/*physiology ; Receptors, FSH ; Receptors, LH ; Seminiferous Tubules/physiology ; Sheep ; Structure-Activity Relationship ; Swine
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  • 75
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    The neu gene: an erbB-homologous gene distinct from and unlinked to the gene encoding the EGF receptor (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-06
    Description: The neu oncogene, identified in ethylnitrosourea-induced rat neuroglioblastomas, had strong homology with the erbB gene that encodes the epidermal growth factor receptor. This homology was limited to the region of erbB encoding the tyrosine kinase domain. It was concluded that the neu gene is a distinct novel gene, as it is not coamplified with sequences encoding the EGF receptor in the genome of the A431 tumor line and it maps to human chromosome 17.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schechter, A L -- Hung, M C -- Vaidyanathan, L -- Weinberg, R A -- Yang-Feng, T L -- Francke, U -- Ullrich, A -- Coussens, L -- CA 39964-01/CA/NCI NIH HHS/ -- GM 26105/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 6;229(4717):976-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2992090" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*genetics ; Chromosome Mapping ; Chromosomes, Human, 16-18 ; DNA, Neoplasm/*genetics ; Genes ; Genetic Linkage ; Humans ; Neoplasm Proteins/*genetics ; Neuroblastoma/genetics ; Neuroglia ; *Oncogenes ; Rats ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/*genetics
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  • 76
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    Glucocorticoids potentiate ischemic injury to neurons: therapeutic implications (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-09-27
    Description: Sustained exposure to glucocorticoids, the adrenocortical stress hormones, is toxic to neurons, and such toxicity appears to play a role in neuron loss during aging. Previous work has shown that glucocorticoids compromise the capacity of neurons to survive a variety of metabolic insults. This report extends those observations by showing that ischemic injury to neurons in rat brain is also potentiated by exposure to high physiological titers of glucocorticoids and is attenuated by adrenalectomy. The synergy between ischemic and glucocorticoid brain injury was seen even when glucocorticoid levels were manipulated after the ischemic insult. Pharmacological interventions that diminish the adrenocortical stress response may improve neurological outcome from stroke or cardiac arrest.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapolsky, R M -- Pulsinelli, W A -- NS-03346/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 27;229(4720):1397-400.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4035356" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Animals ; Brain/cytology/drug effects ; Brain Ischemia/metabolism/*physiopathology ; Cerebral Cortex/drug effects ; Cerebrovascular Disorders/physiopathology ; Corpus Striatum/drug effects ; Glucocorticoids/*pharmacology ; Heart Arrest/physiopathology ; Hippocampus/drug effects ; Humans ; Male ; Neurons/*drug effects ; Rats ; Rats, Inbred Strains
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  • 77
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    Widespread distribution of brain dopamine receptors evidenced with [125I]iodosulpride, a highly selective ligand (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-10
    Description: The new benzamide derivative [125I]iodosulpride is a highly sensitive and selective ligand for D-2 dopamine receptors and displays a very low nonspecific binding to membrane or autoradiographic sections. On autoradiographic images, D-2 receptors are present not only in well-established dopaminergic areas but also, in a discrete manner, in a number of catecholaminergic regions in which the dopaminergic innervation is still unknown, imprecise, or controversial, as in the sensorimotor cerebral cortex or cerebellum. This widespread distribution suggests larger physiological and pathophysiological roles for cerebral dopamine receptors than was previously thought.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martres, M P -- Bouthenet, M L -- Sales, N -- Sokoloff, P -- Schwartz, J C -- New York, N.Y. -- Science. 1985 May 10;228(4700):752-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3838821" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Brain/*physiology ; Cerebellum/physiology ; Cerebral Cortex/physiology ; Hippocampus/physiology ; *Iodine Radioisotopes ; Ligands ; Motor Cortex/physiology ; Rats ; Receptors, Dopamine/metabolism/*physiology ; Sulpiride/*analogs & derivatives/metabolism
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  • 78
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    "Anxiety peptide" found in brain (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, J L -- New York, N.Y. -- Science. 1985 Feb 22;227(4689):934.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2982215" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/*physiology ; Brain/metabolism/physiology ; Diazepam Binding Inhibitor ; Humans ; Nerve Tissue Proteins/*isolation & purification/metabolism/physiology ; Rats ; Receptors, GABA-A/metabolism
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  • 79
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    Two types of somatostatin receptors differentiated by cyclic somatostatin analogs (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-04-26
    Description: Somatostatin receptors in rat brain, pituitary, and pancreas were labeled with two radioiodinated analogs of somatostatins 14 and 28. Two cyclic analogs of somatostatin, SMS201-995 and cyclo(Ala-Cys-Phe-D-Trp-Lys-Thr-Cys), showed biphasic displacement of binding to somatostatin receptors by these radioligands. In contrast, all other somatostatin analogs, including somatostatin-14, competed for the receptor sites with monophasic displacement of radioligand receptor binding. Thus two types of somatostatin receptors were identified. It was found that the pituitary and pancreas have predominantly one type of somatostatin receptor whereas the brain has both, and that different regions of the brain have various proportions of the two types. These findings suggest methods to characterize other types of somatostatin receptors subserving somatostatin's diverse physiological functions, including a potential role in cognitive function and extrapyramidal motor system control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tran, V T -- Beal, M F -- Martin, J B -- NS16367/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 26;228(4698):492-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2858917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding, Competitive ; Brain/metabolism ; Kinetics ; Pancreas/metabolism ; *Peptides, Cyclic ; Pituitary Gland/metabolism ; Radioligand Assay ; Rats ; Receptors, Cell Surface/*classification/metabolism ; Receptors, Somatostatin ; Somatostatin/*analogs & derivatives
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  • 80
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    Molecular cloning of the complementary DNA for human tumor necrosis factor (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-12
    Description: Tumor necrosis factor (TNF) is a soluble protein that causes damage to tumor cells but has no effect on normal cells. Human TNF was purified to apparent homogeneity as a 17.3-kilodalton protein from HL-60 leukemia cells and showed cytotoxic and cytostatic activities against various human tumor cell lines. The amino acid sequence was determined for the amino terminal end of the purified protein, and oligodeoxyribonucleotide probes were synthesized on the basis of this sequence. Complementary DNA (cDNA) encoding human TNF was cloned from induced HL-60 messenger RNA and was confirmed by hybrid-selection assay, direct expression in COS-7 cells, and nucleotide sequence analysis. The human TNF cDNA is 1585 base pairs in length and encodes a protein of 233 amino acids. The mature protein begins at residue 77, leaving a long leader sequence of 76 amino acids. Expression of high levels of human TNF in Escherichia coli was accomplished under control of the bacteriophage lambda PL promoter and gene N ribosome binding site.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, A M -- Creasey, A A -- Ladner, M B -- Lin, L S -- Strickler, J -- Van Arsdell, J N -- Yamamoto, R -- Mark, D F -- New York, N.Y. -- Science. 1985 Apr 12;228(4696):149-54.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3856324" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; Cells, Cultured ; *Cloning, Molecular ; DNA/*genetics ; DNA, Recombinant/metabolism ; Glycoproteins/*genetics/isolation & purification/pharmacology ; Humans ; Leukemia, Myeloid/metabolism ; Mice ; Mice, Nude ; Neoplasms, Experimental/drug therapy ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Rabbits ; Rats ; Tumor Necrosis Factor-alpha ; Xenopus
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  • 81
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    Atrial natriuretic factor: a hormone produced by the heart (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-11-15
    Description: Systematic studies on the significance of the secretory-like morphological characteristic of cardiac atrial muscle cells of mammals led to the finding that these cells produce a polypeptide hormone. This hormone, described in 1981 as atrial natriuretic factor (ANF), is diuretic (natriuretic), hypotensive, and has an inhibitory effect on renin and aldosterone secretion. Thus, ANF probably intervenes in the short- and long-term control of water and electrolyte balance and of blood pressure. Phylogenetically, ANF appears early, suggesting different functions for this peptide in accordance with each species' environment. Knowledge of the properties of the hormone should provide insights into the pathophysiology of important clinical entities and lead to the development of new pharmaceutical products.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Bold, A J -- New York, N.Y. -- Science. 1985 Nov 15;230(4727):767-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2932797" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amphibians ; Animals ; Atrial Function ; Atrial Natriuretic Factor/genetics/*physiology ; Birds ; Cattle ; Cytoplasmic Granules/ultrastructure ; Fishes ; Heart/*physiology ; Humans ; Microscopy, Electron ; Myocardium/cytology/ultrastructure ; Rats ; Reptiles ; Rodentia ; Sinoatrial Node/cytology/physiology
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  • 82
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    Monitoring the time course of cerebral deoxyglucose metabolism by 31P nuclear magnetic resonance spectroscopy (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-06-14
    Description: The phosphorylation of 2-deoxyglucose by the mammalian brain is used as an index of the brain's energy metabolism. The results of phosphorus-31 nuclear magnetic resonance (31P NMR) monitoring of conscious animals in vivo showed rapid phosphorylation of 2-deoxyglucose by brain tissue. The rate of phosphorylation as determined by 31P NMR was consistent with results achieved by tracer methods using carbon-14-labeled 2-deoxyglucose. However, the disappearance of 2-deoxyglucose-6-phosphate was shown to be faster than that reported by tracer studies and occurred without alterations of intracellular pH and energy homeostasis. These results were confirmed by gas chromatography and mass spectroscopy. It is postulated that 2-deoxyglucose may be metabolized in several ways, including dephosphorylation by a hexose phosphatase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deuel, R K -- Yue, G M -- Sherman, W R -- Schickner, D J -- Ackerman, J J -- AM-20579/AM/NIADDK NIH HHS/ -- GM-30331/GM/NIGMS NIH HHS/ -- RR 00954/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Jun 14;228(4705):1329-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4001946" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Deoxy Sugars/*metabolism ; Deoxyglucose/*metabolism ; Kinetics ; Magnetic Resonance Spectroscopy ; Phosphorylation ; Rats ; Rats, Inbred Strains
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  • 83
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    Colocalization of band 3 with ankyrin and spectrin at the basal membrane of intercalated cells in the rat kidney (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-12-13
    Description: An immunoreactive form of the anion channel protein of erythrocytes, band 3, has been identified in the rat kidney. It is found in the intercalated cells of the distal tubule and collecting ducts. Immunostaining specific for band 3 is confined to the basolateral plasma membrane of these cells, where this protein probably mediates the transport of bicarbonate across the tubular wall. Double-immunolabeling studies demonstrate that band 3 is colocalized with immunoreactive forms of ankyrin and spectrin along the basolateral plasma membrane. The polarized distribution of band 3 may be the result of the association of its cytoplasmic domain with ankyrin, which in turn links band 3 to spectrin and the cytoskeleton. These observations help to explain how the collecting ducts of the kidney can direct the transport of bicarbonate ions, thus maintaining the acid-base balance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drenckhahn, D -- Schluter, K -- Allen, D P -- Bennett, V -- K04 AM00926/AM/NIADDK NIH HHS/ -- R01 AM29808/AM/NIADDK NIH HHS/ -- R01 GM33996/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Dec 13;230(4731):1287-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2933809" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anion Exchange Protein 1, Erythrocyte/*metabolism ; Ankyrins ; Bicarbonates/*metabolism ; Cell Membrane/metabolism ; Fluorescent Antibody Technique ; Immunosorbent Techniques ; Kidney/metabolism/*ultrastructure ; Kidney Tubules, Collecting/metabolism/ultrastructure ; Kidney Tubules, Distal/metabolism/ultrastructure ; Macromolecular Substances ; Membrane Proteins/*metabolism ; Molecular Weight ; Rats ; Spectrin/*metabolism
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  • 84
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    Regional brain dopamine metabolism: a marker for the speed, direction, and posture of moving animals (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-07-05
    Description: Brain dopamine is necessary for normal movement. To determine whether there is a precise relation between the intensity of movement and changes in brain dopamine metabolism, the investigators ran rats on straight and circular treadmills at different speeds and with different body postures. Concentrations of dopamine and its metabolite 3,4-dihydroxyphenylacetic acid increased in the caudate and accumbens nuclei in direct relation to the speed and angular posture of the animals. Dopamine metabolism in the nucleus accumbens was more strongly linked to the speed and direction of movement, while in the caudate nucleus dopamine and 3,4-dihydroxyphenylacetic acid were affected most by posture and direction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freed, C R -- Yamamoto, B K -- K04-HL 00782/HL/NHLBI NIH HHS/ -- P50 NS 09199/NS/NINDS NIH HHS/ -- R01 NS 18639/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jul 5;229(4708):62-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4012312" target="_blank"〉PubMed〈/a〉
    Keywords: 3,4-Dihydroxyphenylacetic Acid/metabolism ; Animals ; Brain/*metabolism ; Caudate Nucleus/metabolism ; Dopamine/*metabolism ; Male ; *Motor Activity ; Nucleus Accumbens/metabolism ; *Posture ; Rats ; Rats, Inbred Strains
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  • 85
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    Tyrosine kinase receptor with extensive homology to EGF receptor shares chromosomal location with neu oncogene (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-12-06
    Description: A novel potential cell surface receptor of the tyrosine kinase gene family has been identified and characterized by molecular cloning. Its primary sequence is very similar to that of the human epidermal growth factor receptor and the v-erbB oncogene product; the chromosomal location of the gene for this protein is coincident with the neu oncogene, which suggests that the two genes may be identical.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coussens, L -- Yang-Feng, T L -- Liao, Y C -- Chen, E -- Gray, A -- McGrath, J -- Seeburg, P H -- Libermann, T A -- Schlessinger, J -- Francke, U -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1132-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2999974" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; *Chromosome Mapping ; Chromosomes, Human, 16-18 ; Chromosomes, Human, 6-12 and X ; DNA/genetics ; Fetus/metabolism ; Humans ; Nucleic Acid Hybridization ; *Oncogenes ; Rats ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/*genetics
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  • 86
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    Redesigning trypsin: alteration of substrate specificity (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-04-19
    Description: A general method for modifying eukaryotic genes by site-specific mutagenesis and subsequent expression in mammalian cells was developed to study the relation between structure and function of the proteolytic enzyme trypsin. Glycine residues at positions 216 and 226 in the binding cavity of trypsin were replaced by alanine residues, resulting in three trypsin mutants. Computer graphic analysis suggested that these substitutions would differentially affect arginine and lysine substrate binding of the enzyme. Although the mutant enzymes were reduced in catalytic rate, they showed enhanced substrate specificity relative to the native enzyme. This increased specificity was achieved by the unexpected differential effects on the catalytic activity toward arginine and lysine substrates. Mutants containing alanine at position 226 exhibited an altered conformation that may be converted to a trypsin-like structure upon binding of a substrate analog.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Craik, C S -- Largman, C -- Fletcher, T -- Roczniak, S -- Barr, P J -- Fletterick, R -- Rutter, W J -- AM26081/AM/NIADDK NIH HHS/ -- GM07216/GM/NIGMS NIH HHS/ -- GM28520/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 19;228(4697):291-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3838593" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; DNA/genetics ; Electrophoresis ; Mutation ; Rats ; Substrate Specificity ; Trypsin/biosynthesis/*genetics/metabolism ; Trypsinogen/metabolism
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  • 87
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    Detection of a cellular oncogene in spontaneous liver tumors of B6C3F1 mice (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-03
    Description: An active cellular oncogene was demonstrated in hepatocellular neoplasms arising spontaneously in 24-month-old B6C3F1 mice. DNA isolated from the tumorous tissue and transfected into NIH 3T3 cells showed an 82 percent (9 of 11 animals) frequency of foci induction. In contrast, DNA isolated from the surrounding nontumorous hepatic tissue from the same animals and DNA from other 24-month-old B6C3F1 mice without tumors did not cause transformation in the NIH 3T3 cell assay. This strain of mouse is used extensively in carcinogen bioassays, and the observed high frequency of transformation (82 percent, compared to 10 to 20 percent in humans) supports the concept that the B6C3F1 mouse is hypersusceptible to liver tumor development. It also emphasizes the need to further understand the mechanisms of oncogene activation in animals used for long-term studies of toxicity and oncogenicity before evaluating potential human risk.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fox, T R -- Watanabe, P G -- New York, N.Y. -- Science. 1985 May 3;228(4699):596-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3983645" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogens/pharmacology ; Cattle ; DNA, Neoplasm/genetics ; Humans ; Liver Neoplasms/chemically induced/*genetics ; Mice ; Mice, Inbred C3H ; *Oncogenes ; Rats
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  • 88
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    Promoting functional plasticity in the damaged nervous system (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-29
    Description: Damage to the central and peripheral nervous system often produces lasting functional deficits. A major focus of neuroscience research has been to enhance functional restitution of the damaged nervous system and thereby produce recovery of behavioral or physiological processes. Promising procedures include surgical, physical, and chemical manipulations to reduce scar formation and minimize the disruption of support elements, administration of growth-stimulating substances, tissue grafts to bridge gaps in fiber pathways, and embryonic brain tissue grafts to provide new cells with the potential to generate fiber systems. Two elements are required for functional nervous system repair: (i) neurons with the capacity to extend processes must be present, and (ii) the regenerating neurites must find a continuous, unbroken pathway to appropriate targets through a supportive milieu.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freed, W J -- de Medinaceli, L -- Wyatt, R J -- New York, N.Y. -- Science. 1985 Mar 29;227(4694):1544-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975624" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Amphibians ; Animals ; Axons/physiology ; Cell Membrane/physiology ; Central Nervous System/embryology ; Gangliosides/physiology ; Glycoproteins/physiology ; Lampreys ; Nerve Growth Factors/physiology ; Nerve Regeneration ; *Neuronal Plasticity ; Neurosecretory Systems/physiology ; Peripheral Nerve Injuries ; Peripheral Nerves/physiology ; Rats ; Retina/physiology ; Spinal Cord Injuries/physiopathology ; *Trauma, Nervous System
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  • 89
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    Induction of DNA synthesis in cultured rat hepatocytes through stimulation of alpha 1 adrenoreceptor by norepinephrine (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-02-15
    Description: Addition of norepinephrine to primary cultures of adult rat hepatocytes stimulates the incorporation of [3H]thymidine in a dose-dependent manner. This effect has been observed in serum-free medium containing epidermal growth factor and insulin. Stimulation of DNA synthesis by norepinephrine was strongly antagonized by the alpha 1-adrenergic antagonist prazosin but not by an alpha 2 antagonist or by a beta-adrenergic blocker. The beta agonist isoproterenol did not stimulate significant DNA synthesis. These results indicate that catecholamines interact with the alpha 1 adrenoreceptor to stimulate DNA synthesis in hepatocytes. Since alpha 1 receptors are present in most cells, this receptor may be important in cell growth regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cruise, J L -- Houck, K A -- Michalopoulos, G K -- CA 35373/CA/NCI NIH HHS/ -- T32 GM07184/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 15;227(4688):749-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2982212" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; DNA/*biosynthesis ; Epidermal Growth Factor/pharmacology ; Female ; Insulin/pharmacology ; Liver/*cytology ; Liver Regeneration ; Norepinephrine/*physiology ; Prazosin/pharmacology ; Rats ; Receptors, Adrenergic, alpha/drug effects/*physiology ; Yohimbine/pharmacology
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  • 90
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    Circadian timing of cancer chemotherapy (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-05
    Description: Animal studies have indicated that the time of administration of adriamycin and cisplatin, two widely used anticancer drugs, has a profound effect on their toxicity. This effect in cancer chemotherapy was studied in 31 patients with advanced ovarian cancer. Patients received at least eight monthly courses of adriamycin that were followed 12 hours later by cisplatin, with adriamycin randomly administered at either 6 a.m. or 6 p.m. The results show that in the group receiving adriamycin in the evening and cisplatin in the morning (i) twice as many patients required reductions in dosage and delays in treatment, (ii) four times as many treatments had to be delayed, (iii) drug dosages had to be modified downward three times as often, and (iv) even with more dose attenuation and treatment delays, treatment complications were still about two times more common as in the group receiving adriamycin in the morning and cisplatin in the evening. These findings show that the circadian stage at which anticancer drugs are given to patients should be carefully considered.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hrushesky, W J -- 5M-01RR00400/RR/NCRR NIH HHS/ -- R01 CA 31635/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):73-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3883493" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*administration & dosage/adverse effects ; *Circadian Rhythm ; Cisplatin/administration & dosage/adverse effects ; Clinical Trials as Topic ; Doxorubicin/administration & dosage/adverse effects ; Drug Administration Schedule ; Female ; Humans ; Mice ; Neoplasms/*drug therapy ; Ovarian Neoplasms/drug therapy ; Random Allocation ; Rats
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  • 91
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    Interactions between the gonadal steroids and the immune system (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-18
    Description: The immune system is regulated by the gonadal steroids estrogen, androgen, and progesterone, but the circulating levels of these steroids can also be affected by immune system function. Such interactions appear to be mediated through the hypothalamic-pituitary-gonadal-thymic axis and depend on pituitary luteinizing hormone released by thymic factors under the control of the gonadal steroids.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grossman, C J -- New York, N.Y. -- Science. 1985 Jan 18;227(4684):257-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3871252" target="_blank"〉PubMed〈/a〉
    Keywords: Androgens/physiology ; Animals ; Antibody Formation ; Castration ; Cricetinae ; Estrogens/physiology ; Female ; Gonadal Steroid Hormones/*physiology ; Guinea Pigs ; Hypothalamo-Hypophyseal System/physiology ; *Immunity ; Male ; Mice ; Ovary/physiology ; Pregnancy ; Rabbits ; Rats ; T-Lymphocytes/physiology ; Testis/physiology ; Thymosin/physiology ; Thymus Gland/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 92
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    Enzymatic removal of bilirubin from blood: a potential treatment for neonatal jaundice (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-11-01
    Description: Current treatments for severe jaundice can result in major complications. Neonatal jaundice is caused by excessive accumulation of bilirubin in the blood. A small blood filter containing immobilized bilirubin oxidase was developed to reduce serum bilirubin concentrations. When human or rat blood was passed through the enzyme filter, more than 90 percent of the bilirubin was degraded in a single pass. This procedure may have important applications in the clinical treatment of neonatal jaundice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lavin, A -- Sung, C -- Klibanov, A M -- Langer, R -- New York, N.Y. -- Science. 1985 Nov 1;230(4725):543-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4048947" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bilirubin/*blood ; Blood ; Filtration ; Humans ; Jaundice, Neonatal/*blood/therapy ; Kinetics ; Methods ; Oxidoreductases/metabolism ; *Oxidoreductases Acting on CH-CH Group Donors ; Rats ; Sepharose
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  • 93
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    Gene transfer and expression of human phenylalanine hydroxylase (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-05
    Description: Phenylketonuria (PKU) is caused by a genetic deficiency of the enzyme phenylalanine hydroxylase (PAH). A full-length complementary DNA clone of human PAH was inserted into a eukaryotic expression vector and transferred into mouse NIH3T3 cells which do not normally express PAH. The transformed mouse cells expressed PAH messenger RNA, immunoreactive protein, and enzymatic activity that are characteristic of the normal human liver products, demonstrating that a single gene contains all of the necessary genetic information to code for functional PAH. These results support the use of the human PAH probe in prenatal diagnosis and detection of carriers, to provide new opportunities for the biochemical characterization of normal and mutant enzymes, and in the investigation of alternative genetic therapies for PKU.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ledley, F D -- Grenett, H E -- DiLella, A G -- Kwok, S C -- Woo, S L -- HD-06495/HD/NICHD NIH HHS/ -- HD-17711/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 5;228(4695):77-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3856322" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cloning, Molecular ; DNA, Recombinant/metabolism ; *Genetic Engineering ; Humans ; Mice ; Nucleic Acid Hybridization ; Phenylalanine Hydroxylase/*genetics ; Phenylketonurias/diagnosis/genetics ; Prenatal Diagnosis ; Rats
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  • 94
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    Molecular cloning of a gene sequence regulated by nerve growth factor (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-26
    Description: Nerve growth factor (NGF) is essential for the development and differentiation of sympathetic or sensory neurons. A complementary DNA was cloned that corresponds to a gene sequence induced more than 50-fold in a cultured target cell line of pheochromocytoma cells (PC12 cells) 5 hours after the addition of NGF. The induced messenger RNA encodes a 90,000-dalton polypeptide that may represent one of the primary events in NGF-induced differentiation of neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levi, A -- Eldridge, J D -- Paterson, B M -- New York, N.Y. -- Science. 1985 Jul 26;229(4711):393-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3839317" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Adrenal Gland Neoplasms/genetics ; Animals ; Base Sequence ; Cell Line ; Chickens ; *Cloning, Molecular ; DNA/genetics ; Gene Expression Regulation ; *Genes ; Nerve Growth Factors/*physiology ; Nucleic Acid Hybridization ; Pheochromocytoma/genetics ; RNA, Messenger/genetics ; Rabbits ; Rats
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  • 95
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    Inhibition of calcification of bioprosthetic heart valves by local controlled-release diphosphonate (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-12
    Description: Bioprostheses fabricated from porcine aortic valves are widely used to replace diseased heart valves. Calcification is the principal cause of the clinical failure of these devices. In the present study, inhibition of the calcification of bioprosthetic heart valve cusps implanted subcutaneously in rats was achieved through the adjacent implantation of controlled-release matrices containing the anticalcification agent ethanehydroxydiphosphonate dispersed in a copolymer of ethylene-vinyl acetate. Prevention of calcification was virtually complete, without the adverse effects of retarded bone and somatic growth that accompany systemic administration of ethanehydroxydiphosphonate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levy, R J -- Wolfrum, J -- Schoen, F J -- Hawley, M A -- Lund, S A -- Langer, R -- GM26698/GM/NIGMS NIH HHS/ -- HL20764/HL/NHLBI NIH HHS/ -- HL24463/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 12;228(4696):190-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3919445" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bioprosthesis ; Bone Development/drug effects ; Calcinosis/*prevention & control ; Delayed-Action Preparations ; Etidronic Acid/administration & dosage/adverse effects/*therapeutic use ; *Heart Valve Prosthesis ; Polyvinyls ; Rats
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  • 96
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    A specific 37,000-dalton protein that accumulates in regenerating but not in nonregenerating mammalian nerves (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-26
    Description: A 37-kilodalton protein is synthesized at higher rates in the peripheral and central nervous system of newborn rats than in adult animals. As a specific response to denervation, the synthesis of the 37-kilodalton protein is increased in the mature peripheral and central nervous system; however, this protein accumulates only in the peripheral nervous system. The differences in accumulation of the protein correlate with the apparent differences in the ability of peripheral and central axons to regenerate. The synthesis of the 37-kilodalton protein is inhibited when proper innervation or reinnervation is established.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, H W -- Gebicke-Harter, P J -- Hangen, D H -- Shooter, E M -- NS 04270/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 26;228(4698):499-501.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3983637" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn/physiology ; Axons/physiology ; Brain/physiology ; Central Nervous System/metabolism/*physiology ; Molecular Weight ; *Nerve Regeneration ; Nerve Tissue Proteins/*biosynthesis ; Optic Nerve/physiology ; Peripheral Nerves/metabolism/*physiology ; Photofluorography ; Rats ; Rats, Inbred Strains ; Sciatic Nerve/physiology ; Spinal Cord/physiology
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  • 97
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    Hypertension and sodium salts (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liebman, B F -- Langford, H G -- Whitescarver, S A -- Ott, C E -- Jackson, B -- Kurtz, T W -- Morris, R C Jr -- New York, N.Y. -- Science. 1985 Apr 19;228(4697):351-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3983634" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Pressure/drug effects ; Chlorides/metabolism ; Diet ; Humans ; Hypertension/*etiology ; Rats ; Rats, Inbred SHR ; Sodium/*metabolism ; Sodium Chloride/metabolism
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  • 98
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    The product of the c-fms proto-oncogene: a glycoprotein with associated tyrosine kinase activity (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-19
    Description: The c-fms proto-oncogene is a member of a gene family that has been implicated in tumorigenesis. Glycoproteins encoded by c-fms were identified in cat spleen cells by means of an immune-complex kinase assay performed with monoclonal antibodies to v-fms-coded epitopes. The major form of the normal cellular glycoprotein has an apparent molecular weight of 170,000 and, like the product of the viral oncogene, serves as a substrate for an associated tyrosine-specific protein kinase activity in vitro. The results suggest that the transforming glycoprotein specified by v-fms is a truncated form of a c-fms-coded growth factor receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rettenmier, C W -- Chen, J H -- Roussel, M F -- Sherr, C J -- 1 RO1 CA 38187/CA/NCI NIH HHS/ -- RR-05584-20/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 19;228(4697):320-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2580348" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Cats ; Glycoproteins/immunology/*metabolism ; Humans ; Mice ; Molecular Weight ; Neoplasm Proteins/immunology/*metabolism ; *Oncogenes ; Phosphorylation ; Protein Kinases/*metabolism ; Protein-Tyrosine Kinases ; RNA/metabolism ; Rats
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  • 99
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    Patterns of growth hormone-releasing factor and somatostatin secretion into the hypophysial-portal circulation of the rat (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-25
    Description: The interrelation between the secretion of two hypophysiotropic peptides, growth hormone-releasing factor (GRF) and somatostatin (SRIF), in the generation of episodic growth hormone (GH) secretion was inferred from direct measurements of immunoreactive GRF and immunoreactive SRIF concentrations in the hypophysial-portal plasma of the rat. Secretion of immunoreactive GRF was found to be episodic, with maximal concentrations present during periods of expected GH secretory episodes. Secretion of immunoreactive GRF was accompanied by a moderate reduction in portal plasma levels of immunoreactive SRIF. Passive immunoneutralization of SRIF was associated with increased concentrations of immunoreactive GRF in hypophysial-portal plasma. On the basis of these observations, it appears that each GH secretory episode is initiated by pulsatile secretion of immunoreactive GRF into the portal circulation, which is preceded by or is concurrent with a moderate reduction of inhibitory tone provided by portal immunoreactive SRIF. These experiments provide direct insights into central and adenohypophysial mechanisms by which GRF and SRIF interact to generate episodic secretion of GH.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plotsky, P M -- Vale, W -- AM26741/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 25;230(4724):461-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2864742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Growth Hormone/blood/physiology/secretion ; Growth Hormone-Releasing Hormone/blood/physiology/*secretion ; Immune Sera/immunology ; Male ; Pituitary Gland/blood supply/*physiology ; Pituitary Gland, Anterior/secretion ; Radioimmunoassay ; Rats ; Rats, Inbred Strains ; Sheep/immunology ; Somatostatin/blood/physiology/*secretion
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  • 100
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    Vasopressin-stimulated release of atriopeptin: endocrine antagonists in fluid homeostasis (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-26
    Description: Administration of pharmacological doses of arginine-vasopressin, related peptides, and other pressor agents induced a profound release of atriopeptin immunoreactivity into the circulation. The stimulated release of atriopeptin apparently was related to increased arterial blood pressure. Neither the nonpressor vasopressin analog 1-deamino-D-Arg8-vasopressin nor arginine-vasopressin in the presence of a specific pressor antagonist caused atriopeptin to be released into the circulation. Urine output was correlated with the level of atriopeptin released. Physiological levels of arginine-vasopressin suppress diuresis and produced vasoconstriction. Pharmacological levels of the hormone stimulated the cardiac endocrine system to release atriopeptin, which may cause diuresis and vasodilation to physiologically antagonize the effects of vasopressin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manning, P T -- Schwartz, D -- Katsube, N C -- Holmberg, S W -- Needleman, P -- New York, N.Y. -- Science. 1985 Jul 26;229(4711):395-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990050" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/pharmacology ; Angiotensin II/pharmacology ; Animals ; Arginine Vasopressin/*pharmacology ; *Atrial Function ; Blood Pressure/drug effects ; Deamino Arginine Vasopressin/pharmacology ; Dose-Response Relationship, Drug ; Male ; Muscle Proteins/*secretion ; Oxytocin/pharmacology ; Phenylephrine/pharmacology ; Rats ; Rats, Inbred Strains ; Urodynamics/drug effects ; Water-Electrolyte Balance/*drug effects
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