Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe two families with heterozygous plasminogen deficiency. In the first the patient was a 27 year-old female who suffered an acute episode of ischemic cerebrovascular disease affecting the left temporal lobe documented by arteriographic, gammagraphic and CAT studies. She had no family history of thrombotic conditions. In the other family the propositus was a 31 year-old man with spontaneous deep venous thrombosis in the left leg. His father was also symptomatic, with a history of recurrent thrombotic complications after predisposing factors, that included multiple venous thrombosis and a pulmonary embolism. Laboratory data showed normal hemostasis test results. Antigenic and functional levels of protein C, protein S and antithrombin III were within normal limits. The only abnormality found was decreased plasminogen activity in plasma; antigenic and functional levels were reduced to about half-normal levels. In both cases crossed immunoelectrophoresis revealed a normal migration pattern of plasminogen. Thus, we conclude that our patients were carriers of congenital hypoplasminogenemia or familial type I plasminogen deficiency, due to decreased synthesis. We also reported on fibrinolytic response to infusion of DDAVP, a synthetic analogue of the antidiuretic hormone. Fibrinolytic activity was normal in basal conditions as well as in response to DDAVP infusion.
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PMID:[Plasminogen deficiencies in 2 Spanish families. Response to the administration of DDAVP]. 236 94

To investigate the role of nitric oxide (NO) and its interaction with oxygen radicals in fever, we injected conscious rabbits intravenously (i.v.) with 1 microgram/kg bacterial lipopolysaccharide (LPS) and measured body temperatures, and circulatory and respiratory parameters. We estimated plasma levels of antidiuretic hormone (ADH); nitrate as a measure of NO metabolism under aerobic conditions; prostaglandin E2 (PGE2) and prostaglandin PGF2 alpha (PGF2 alpha); and tumor necrosis factor alpha (TNF alpha). We studied the effects of LPS before and after treatment with oxygen radical scavengers superoxide dismutase and catalase (SOD/CAT), before and after treatment with NG-monomethyl-L-arginine (L-NMMA), a specific blocker of nitric oxide synthase (NOS), before and after treatment with methylene blue (MB). N-methyl-D-aspartate (NMDA) receptors were blocked with ketamine. LPS increased core temperature by 1.1 +/- 0.1 degree C within 3 h, associated with a rapid increase of plasma TNF alpha, PGE2 and PGF2 alpha, and a fall of nitrate. The decrease of nitrate following LPS was augmented in rabbits pretreated with SOD/CAT, associated with a rise of core temperature of 1.6 +/- 0.1 degree C within 3 h. The lowest levels of nitrate were observed in rabbits pretreated with L-NMMA, associated with a rise of core temperature of 3.0 +/- 0.1 degree C within 3 h. Treating the same rabbits with a continuous i.v. infusion of 5 mg/kg/h MB, starting 30 min before injection of LPS, caused an immediate increase in nitrate and completely prevented fever. The rise of TNF alpha and ADH after LPS, however, was not significantly different from the control fever, and plasma PGE2 levels were nearly twice as elevated. MB also prevented fever in NMMA-treated rabbits, but only as long as nitrate levels remained elevated. MB induced an immediate rise of core temperature in ketamine-treated rabbits. We conclude that an undisturbed or elevated synthesis of NO in the central nervous system prevents fever, possibly via positive feedback action of NO on presynaptic glutaminergic neurons.
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PMID:Antipyretic role of nitric oxide during endotoxin-induced fever in rabbits. 950 19

The oxytocin (OT) and vasopressin (VP) expressing magnocellular neurons in the hypothalamic-neurohypophysial system (HNS) have been the most studied of all the neuroendocrine cell-types. Despite this, our understanding of the mechanisms that underly the cell-specific expression of the peptide genes in these neurons has remained obscure. Part of the reason for this may be related to the close apposition of the OT and VP genes in the chromosomal locus, the genes being separated by as little as 3.5 kb in the mouse, and their interactions which are critical for cell-specific expression of the genes. Recent studies using intact rat OT and VP constructs in transgenic mice, and rat and mouse VP genes with CAT inserts in exon III as reporters in transgenic rats and mice, respectively, have suggested the presence of cell-specific enhancer elements in the 3' downstream (intergenic region, IGR) region of the VP gene. Evidence in favor of this view is presented from transgenic mouse studies on the expression of mouse OT- and VP-CAT gene constructs. Oxytocin and vasopressin phenotypes in the magnocellular neuronal population have traditionally been assessed by either immunocytochemical or in situ hybridization histochemical methods leading to the view that these genes are never coexpressed. However, more sensitive methods show that most OT cells also express some VP mRNA, and most VP cells contain some OT mRNA. A third phenotype containing equivalent levels of both OT and VP mRNA can also be found under some conditions, thereby complicating our analysis of cell-specificity. A continuing problem hindering studies of the regulation of OT and VP gene expression in neurons, is the absence of an appropriate cell line to examine these issues. We have found that stationary slice-explant cultures allow for excellent preservation of highly differentiated magnocellular neurons in long-term culture, and that these cultures can be used for physiological and pharmacological studies and analysis of gene expression.
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PMID:Cell-specific gene expression in oxytocin and vasopressin magnocellular neurons. 1002 82

Corticotropin-releasing factor (CRF) is the key regulator of the hypothalamic-pituitary-adrenal axis. CRF neurons cannot be distinguished morphologically from other neuroendocrine neurons in the paraventricular nucleus of the hypothalamus (PVH) without immunostaining. Thus, we generated a knock-in mouse that expresses modified yellow fluorescent protein (Venus) in CRF neurons (CRF-Venus), and yet its expression is driven by the CRF promoter and responds to changes in the interior milieu. In CRF-Venus, Venus-expressing neurons were distributed in brain regions harboring CRF neurons, including the PVH. The majority of Venus-expressing neurons overlapped with CRF-expressing neurons in the PVH, but many neurons expressed only Venus or CRF in a physiological glucocorticoid condition. After glucocorticoid deprivation, however, Venus expression intensified, and most Venus neurons coexpressed CRF. Conversely, Venus expression was suppressed by excess glucocorticoids. Expression of copeptin, a peptide encoded within the vasopressin gene, was induced in PVH-Venus neurons by glucocorticoid deprivation and suppressed by glucocorticoid administration. Thus, Venus neurons recapitulated glucocorticoid-dependent vasopressin expression in PVH-CRF neurons. Noradrenaline increased the frequency of glutamate-dependent excitatory postsynaptic currents recorded from Venus-expressing neurons in the voltage clamp mode. In addition, the CRF-iCre knock-in mouse was crossed with a CAG-CAT-EGFP reporter mouse to yield the Tg(CAG-CAT-EGFP/wt);CRF(iCre/wt) (EGFP/CRF-iCre) mouse, in which enhanced green fluorescent protein (EGFP) is driven by the CAG promoter. EGFP was expressed more constitutively in the PVH of EGFP/CRF-iCre mice. Thus, CRF-Venus may have an advantage for monitoring dynamic changes in CRF neurons and CRF networks in different glucocorticoid states.
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PMID:Visualization of corticotropin-releasing factor neurons by fluorescent proteins in the mouse brain and characterization of labeled neurons in the paraventricular nucleus of the hypothalamus. 2505 91