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  • Rats, Inbred Strains  (30)
  • American Association for the Advancement of Science (AAAS)  (30)
  • American Association for the Advancement of Science
  • American Chemical Society
  • Blackwell Publishing Ltd
  • 1985-1989  (30)
  • 1980-1984
  • 1965-1969
  • 1985  (30)
  • 1967
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (30)
  • American Association for the Advancement of Science
  • American Chemical Society
  • Blackwell Publishing Ltd
Years
  • 1985-1989  (30)
  • 1980-1984
  • 1965-1969
Year
  • 1
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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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  • 2
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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
    Print ISSN: 0036-8075
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  • 3
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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
    Print ISSN: 0036-8075
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  • 4
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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
    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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    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
    Print ISSN: 0036-8075
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  • 6
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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)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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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)
    Details
    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
    Print ISSN: 0036-8075
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  • 8
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    Endogenous anticonvulsant substance in rat cerebrospinal fluid after a generalized seizure (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
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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)
    Details
    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
    Print ISSN: 0036-8075
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  • 10
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    Regional myocardial substrate uptake in hypertensive rats: a quantitative autoradiographic measurement (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 11
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    Distribution of enkephalin immunoreactivity in germinative cells of developing rat cerebellum (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 12
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    Plasticity of hippocampal circuitry in Alzheimer's disease (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 13
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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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  • 14
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    Platelet-mediated cholesterol accumulation in cultured aortic smooth muscle cells (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 15
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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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  • 16
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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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  • 17
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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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  • 18
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    Glucocorticoids potentiate ischemic injury to neurons: therapeutic implications (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 19
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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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  • 20
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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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  • 21
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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)
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    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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  • 22
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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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  • 23
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    Vasopressin-stimulated release of atriopeptin: endocrine antagonists in fluid homeostasis (1985)
    American Association for the Advancement of Science (AAAS)
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    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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  • 24
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    Loss of M2 muscarine receptors in the cerebral cortex in Alzheimer's disease and experimental cholinergic denervation (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-05-31
    Description: Cerebral cortex samples from patients with Alzheimer's disease and from rats after experimental cholinergic denervation of the cerebral cortex exhibited reductions in the presynaptic marker choline acetyltransferase activity and in the number of M2 muscarine receptors, with no change in the number of M1 receptors. These results are in keeping with evidence that M2 receptors function in cholinergic nerve terminals to regulate the release of acetylcholine, whereas M1 receptors are located on postsynaptic cells and facilitate cellular excitation. New M1-selective agonists and M2-selective antagonists directed at post- or presynaptic sites deserve consideration as potential agents for the treatment of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mash, D C -- Flynn, D D -- Potter, L T -- HLO-7188/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 31;228(4703):1115-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3992249" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Alzheimer Disease/*metabolism ; Animals ; Cerebral Cortex/*metabolism ; Choline O-Acetyltransferase/*metabolism ; Cholinergic Fibers/physiology ; Denervation ; Humans ; Male ; Oxotremorine ; Quinuclidinyl Benzilate ; Rats ; Rats, Inbred Strains ; Receptors, Muscarinic/*metabolism ; Synaptic Membranes/*metabolism
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  • 25
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    Methionine and leucine enkephalin in rat neurohypophysis: different responses to osmotic stimuli and T2 toxin (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-05-03
    Description: Specific radioimmunoassays were used to measure the effects of hypertonic saline (salt loading), water deprivation, and trichothecene mycotoxin (T2 toxin) on the content of methionine enkephalin (ME), leucine enkephalin (LE), alpha-neoendorphin, dynorphin A, dynorphin B, vasopressin, and oxytocin in the rat posterior pituitary. Concentrations of vasopressin and oxytocin decreased in response to both osmotic stimuli and treatment with T2 toxin, but the decrease was greater with osmotic stimulations. Similarly, concentrations of LE and dynorphin-related peptides declined after salt loading and water deprivation; LE concentrations also decreased after treatment with T2 toxin. The concentration of ME decreased after water deprivation, did not change after salt loading, and increased after T2 toxin treatment. The differentiating effects of these stimuli on the content of immunoreactive LE and ME are consistent with the hypothesis that LE and ME may be localized in separate populations of nerve endings with different roles in the posterior pituitary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zamir, N -- Zamir, D -- Eiden, L E -- Palkovits, M -- Brownstein, M J -- Eskay, R L -- Weber, E -- Faden, A I -- Feuerstein, G -- New York, N.Y. -- Science. 1985 May 3;228(4699):606-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2858918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dynorphins/analogs & derivatives/analysis ; Endorphins/analysis ; Enkephalin, Leucine/*analysis ; Enkephalin, Methionine/*analysis ; Male ; Osmosis ; Oxytocin/analysis ; Pituitary Gland, Posterior/*analysis/drug effects ; Protein Precursors/analysis ; Rats ; Rats, Inbred Strains ; Saline Solution, Hypertonic ; Sesquiterpenes/*pharmacology ; T-2 Toxin/*pharmacology ; Vasopressins/analysis ; Water Deprivation
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  • 26
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    Leukotrienes as mediators in tissue trauma (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-10-18
    Description: A significant increase in the production of cysteinyl leukotrienes was observed after mechanical or thermal trauma in the anesthesized rat. The amount of biliary N-acetyl-leukotriene E4, which represents a suitable indicator for blood plasma leukotrienes, was used as a measure of leukotriene generation. Cysteinyl leukotrienes were rapidly eliminated from blood plasma into bile where N-acetyl-leukotriene E4 was the major metabolite. Leukotrienes were at a much lower concentration in blood plasma than in bile and differed in the pattern of metabolites. The detected amounts of leukotrienes were sufficient to induce known phenomena associated with trauma, such as tissue edema and circulatory and respiratory dysfunction. Increased leukotriene generation appears to play an important role in the pathophysiology of tissue trauma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denzlinger, C -- Rapp, S -- Hagmann, W -- Keppler, D -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):330-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4048937" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta, Abdominal/injuries ; Bile/metabolism ; Bile Ducts/surgery ; Burns/physiopathology ; Female ; Fractures, Bone/physiopathology ; Half-Life ; Kinetics ; Rats ; Rats, Inbred Strains ; SRS-A/*biosynthesis/blood ; Tritium ; Wounds and Injuries/*physiopathology
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  • 27
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    Targeted modulation of acute inflammation (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-01-11
    Description: Localized inflammation of the lungs was induced with the neutrophil chemoattractant, N-formylmethionylleucylphenylalanine (FMLP) in combination with magnetically responsive albumin microspheres, a drug carrier that provides efficient, extremely rapid localization in tissue. Intravenous targeting to rat lungs was accomplished by means of an external thoracic magnet. This caused progressive local accumulation of neutrophils, extravascular cell migration, and acute tissue injury. Microscopic findings favored chemotaxis as the principal mechanism of cell accumulation. This system provides a new experimental model for acute alveolar damage, a rapid in vivo assay for drugs that modulate neutrophil chemotaxis, and a new therapeutic approach to focusing inflammation in patients with chemotactic defects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ranney, D F -- CA15673/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 11;227(4683):182-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3966151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemotaxis, Leukocyte ; Disease Models, Animal ; Magnetics ; Microspheres ; N-Formylmethionine Leucyl-Phenylalanine/*pharmacology ; Pneumonia/*etiology/immunology ; Pulmonary Edema/etiology/immunology ; Rats ; Rats, Inbred Strains ; Serum Albumin
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  • 28
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    Abrupt induction of a membrane digestive enzyme by its intraintestinal substrate (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-04
    Description: The regulation of amino-oligopeptidase (AOP), an intestinal brush border hydrolase essential for the surface digestion of peptide nutrients, was examined in rats in vivo. Short-term (30-minute) intraintestinal perfusion of a tetrapeptide substrate, Gly-Leu-Gly-Gly, or a synthetic substrate, leucyl-beta-naphthylamide, induced a doubling in the incorporation of [3H]leucine into the AOP in association with intracellular membranes. The subsequent conversion of AOP from nascent to mature enzyme and its membrane-associated transport to the brush border occurred at normal rates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reisenauer, A M -- Gray, G M -- AM 07056/AM/NIADDK NIH HHS/ -- AM 11270/AM/NIADDK NIH HHS/ -- AM 15802/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Jan 4;227(4682):70-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3838079" target="_blank"〉PubMed〈/a〉
    Keywords: Aminopeptidases/*biosynthesis ; Animals ; *Antigens, CD13 ; Dietary Proteins/metabolism ; Digestion ; Endoplasmic Reticulum/metabolism ; Enzyme Induction ; Golgi Apparatus/metabolism ; Intestines/*enzymology ; Kinetics ; Leucine/analogs & derivatives/metabolism ; Male ; Microvilli/enzymology ; Oligopeptides/metabolism ; Rats ; Rats, Inbred Strains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 29
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    Response to ethanol reduced by past thiamine deficiency (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-15
    Description: Ethanol-induced intoxication and hypothermia were studied in rats approximately 7 months after severe thiamine deficiency, when treated rats appeared to have recovered their physical health. Previously induced thiamine deficiency without prior ethanol exposure significantly decreased the area under the curve plotted for the concentration of ethanol in blood and also decreased behavioral impairment and hypothermia due to ethanol exposure. Pathophysiologic changes resulting from thiamine deficiency may contribute to both the pharmacodynamic and pharmacokinetic tolerance to ethanol in chronic alcoholics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, P R -- Majchrowicz, E -- Tamborska, E -- Marietta, C -- Mukherjee, A B -- Eckardt, M J -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1365-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975622" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Amnestic Disorder/pathology ; Alcoholic Intoxication/physiopathology ; Animals ; Behavior, Animal/drug effects ; Body Temperature/drug effects ; Brain/pathology ; Ethanol/*pharmacology ; Female ; Humans ; Hypothermia/chemically induced ; Male ; Rats ; Rats, Inbred Strains ; Thiamine Deficiency/*physiopathology ; Wernicke Encephalopathy/pathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 30
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    Antigenic and genetic properties of viruses linked to hemorrhagic fever with renal syndrome (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-01
    Description: Hemorrhagic fever with renal syndrome (HFRS) comprises a variety of clinically similar diseases of viral etiology that are endemic to and sporadically epidemic throughout the Eurasian continent and Japan. Although HFRS has not been reported in North America, viruses that are antigenically similar to HFRS agents were recently isolated from rodents in the United States. Examination and comparison of eight representative isolates from endemic disease areas and from regions with no known associated HFRS indicate that these viruses represent a new and unique group that constitutes a separate genus in the Bunyaviridae family of animal viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmaljohn, C S -- Hasty, S E -- Dalrymple, J M -- LeDuc, J W -- Lee, H W -- von Bonsdorff, C H -- Brummer-Korvenkontio, M -- Vaheri, A -- Tsai, T F -- Regnery, H L -- New York, N.Y. -- Science. 1985 Mar 1;227(4690):1041-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2858126" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Viral/immunology ; Arvicolinae ; Base Sequence ; Bunyaviridae/genetics ; Hantavirus/genetics/*immunology ; Hemorrhagic Fever with Renal Syndrome/genetics/immunology/*microbiology ; Humans ; Korea ; Mice ; Muridae ; Neutralization Tests ; RNA Viruses/*immunology ; Radioimmunoassay ; Rats ; Rats, Inbred Strains ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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