Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We used in vivo microdialysis to determine the impact of a focal hypoxic-ischemic insult on striatal amino acid efflux in the immature brain. Microdialysis probes were inserted into the right striatum of postnatal day 7 rats. To induce hypoxic-ischemic injury, the right carotid artery was ligated and the animals were exposed to 8% oxygen for 2.5 hours (n = 22). Rats exposed to ligation alone (n = 10) or hypoxia alone (n = 8) and untreated controls (n = 17) were also studied. Two hours after probe insertion, a 30-minute baseline microdialysis sample was obtained. After arterial ligation, two additional baseline samples were collected. Five more samples were collected over the next 2.5 hours (in 8% oxygen or room air). Eight amino acids (glutamate, aspartate, taurine, glutamine, alanine, serine, glycine, and asparagine) were consistently detected in dialysates using a high-performance liquid chromatography assay with electrochemical detection. In untreated controls, amino acid efflux did not change over 4 hours. During hypoxia-ischemia, efflux values fluctuated widely, with marked intra-animal and interanimal variability. Efflux peaks for each amino acid were defined as values greater than the highest control mean value plus two standard deviations. Glutamate efflux peaks (greater than 7 pmol/min compared with 2 pmol/min at baseline) were detected in no controls and in eight hypoxic-ischemic rats (p = 0.006, Fisher's two-tailed exact test). Taurine efflux peaks (greater than 75 pmol/min compared with 10 pmol/min for controls at baseline) were detected in 10 hypoxic-ischemic rats and one control (p = 0.01) and in seven of the eight animals in which glutamate efflux peaks occurred (p = 0.006).(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1991 Jul
PMID:Effects of perinatal stroke on striatal amino acid efflux in rats studied with in vivo microdialysis. 185 13

Genetical differences in changes in blood pressure (BP) were chronologically investigated during pregnancy in stroke-prone spontaneously hypertensive rats (SHRSP), Wistar-Kyoto rats (WKY) and Sprague-Dawley (SD) rats. Especially, the early stages were carefully studied. Maternal conditions in SHRSP were modified by the treatments with NaCl and taurine, respectively. BP in SHRSP and WKY rose significantly at the early stage of pregnancy compared to prepregnancy levels (SHRSP; 208 +/- 2 mmHg vs 197 +/- 5 mmHg, WKY; 133 +/- 2 mmHg vs 126 +/- 1 mmHg) (p less than 0.05). In contrast, no such changes were observed in SD rats. Differences in 24-hour urinary epinephrine excretion before and during pregnancy ran parallel with such BP changes among these strains. NaCl-loaded SHRSP died during pregnancy with severe pathohistological changes in their kidneys and severe proteinuria. Taurine treatment had a marked prophylactic effect on these maternal pathological changes during pregnancy, resulting in better growth in offsprings. These results suggest that SHRSP could be one of the suitable animal models for the studies on toxemia of pregnancy and also suggest an important role of hypertensive genetical disposition in the development of toxemia of pregnancy.
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PMID:Stroke-prone spontaneously hypertensive rats as a model for toxemia of pregnancy and aggravating and preventive effects of maternal modifications during pregnancy on offspring's growth. 223 19

Cerebrospinal fluid (CSF) amino acid neurotransmitter concentrations in 23 patients with acute encephalitis were compared with those in patients with acute brain infarction, multiple sclerosis and controls. The concentration of glutamate was significantly higher in encephalitis (5.2+/-6.7 micromol/l) and stroke patients (9.6+/-14.2 micromol/l) than in MS patients (1.6+/-0.9 micromol/l) and controls (1.7+/-0.8 micromol/l; p < 0.001). The concentration of glycine was significantly higher in encephalitis (11.0+/-4.7 micromol/l) than in stroke (7.6+/-3.2 micromol/l) and MS patients (6.3+/-2.1 micromol/l) or controls (5.6+/-1.8 micromol/l; p < 0.002). Taurine levels were significantly lower in encephalitis patients than in the other groups (p = 0.04). The correlation of high glutamate levels with poor outcome was almost significant (Kendall tau 0.63, p = 0.06). Our observations suggest that exicitotoxic neurotransmission may play an important role in the series of events that lead to neuronal damage in encephalitis.
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PMID:Does glutamate mediate brain damage in acute encephalitis? 955 19

We previously reported that several markers on rat chromosome (Chr) 4 cosegregated with the occurrence of cerebral stroke and brain edema in stroke-prone spontaneously hypertensive rats (SHRSP). To obtain insights into the positional candidate genes for stroke susceptibility in this region, we mapped four genes, Taurine transporter (Tau), tumor necrosis factor receptor (Tnfr), GABA transporter (Gat1) and glucose transporter-3 (Glut3) genes, using newly developed simple sequence repeat (SSR) markers on rat Chr 4. We isolated the SSRs for the genes either by screening a rat genomic library or by searching the GenBank database. By linkage analysis using two sets of backcrosses, Gat1 and Tnfr were mapped in the region associated with stroke, while Taut was located distant from the region. The Glut3 locus was also assigned to rat Chr 4 using a rat x mouse hybrid clone panel. These results indicated that the Tnfr, Gat1 and Glut3 genes were good positional candidates for the stroke susceptibility in SHRSP, suggesting that further evaluation of these genes by functional studies could prove useful.
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PMID:Mapping of four simple sequence repeat (SSR) markers on rat chromosome 4. 1073 35

Taurine is known to play a major role in volume regulation in astrocytic swelling associated with stroke and brain trauma. Apart from brain edema, the severity of brain injury is related to the levels of inflammatory cytokines such as tumor necrosis factor alpha (TNFalpha). TNFalpha had been shown to be closely associated with brain edema formation since the neutralization of TNFalpha reduced brain edema. Considering taurine has osmoregulatory functions in astrocytes, experiments were performed to study the effects of TNFalpha on taurine uptake in cultured astrocytes. Astrocytes exposed to 20 ng/ml of TNFalpha for 48 h showed a 91% increase in taurine uptake and significant increase was observed after 24 h exposure. This cytokine caused neither significant changes in cell volume nor taurine release. The increased in taurine uptake induced by TNFalpha was unlikely resulted from the modification of Na(+) movement because TNFalpha decreased tyrosine uptake, Na(+)-dependent transport system. In contrast to TNFalpha, interferon-gamma (IFNgamma) did not significantly affect taurine uptake. Taken together, our results did not support a suggestion that TNFalpha affects cell volume regulation via modulating taurine uptake in astrocytes. Increasing lines of evidence have demonstrated that taurine has anti-inflammatory and anti-oxidative effects, these findings therefore suggested that the increase in taurine uptake might be an adaptive response or a tool for astrocytes against oxidative stress.
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PMID:Effects of tumor necrosis factor alpha on taurine uptake in cultured rat astrocytes. 1109 84

Taurine is present in high concentrations in mammalian tissues and has been implicated in cardiovascular control mechanisms. The aim of the present study was to evaluate the ability of taurine to attenuate salt-induced elevations in blood pressure and markers of damage to the kidney and cardiovascular system in stroke prone spontaneously hypertensive rats (SPSHR). Male SPSHR (6 weeks old) were placed on high salt diets that contained 1% (w/w) NaCl added to their normal chow for 84 days and then were switched to 3% added NaCl for the remaining 63 days of the study. SPSHR was given 1.5% taurine in the drinking water (n = 8), a taurine free diet (n = 8) or normal chow (n = 8). A final control group (n = 6) was not given high salt diets. High salt diets caused an acceleration in the development of hypertension in all groups. Taurine supplementation reduced ventricular hypertrophy and decreased urinary excretion of protein and creatinine. The taurine free diet did not alter serum or urinary excretion of taurine, but did result in elevated urinary nitrogen excretion, increased serum cholesterol levels, and impaired performance in a spatial learning task. Alterations in dietary taurine intake did not alter urinary or serum electrolytes (Na+, K+), but taurine supplementation did attenuate a rise in serum calcium seen with the high salt diets. Urinary excretion (microg/24h) of epinephrine and dopamine was significantly reduced in SPSHR given 1% NaCl in the diet, but this effect was not seen in SPSHR on taurine free or supplemented diets. Taurine supplementation showed cardioprotective and renoprotective effects in SPSHR given high salt diets.
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PMID:Effects of high salt diets and taurine on the development of hypertension in the stroke-prone spontaneously hypertensive rat. 1114 Mar 67

1. Taurine supplementation attenuated the development of hypertension and stroke in stroke-prone spontaneously hypertensive rats (SHRSP). 2. WHO-CARDIAC (Cardiovascular Diseases Alimentary Comparison) study revealed wide differences in 24-h urinary taurine excretion, which were inversely associated with age-adjusted mortality rates of coronary heart diseases (CHD). 3. Hypercholesterolemia as well as arterial fat deposition related to the cause of CHD was attenuated by dietary taurine supplementation in SHRSP on high-fat cholesterol diet. 4. Taurine affected the gene expression of 7alpha-hydroxylase and thus regulated serum cholesterol level through the control of the rate limiting step of cholesterol excretion into bile acids. 5. Taurine attenuated atherogenesis due to the control of oxidative stress through the inhibition of the production of oxidative LDL and to its scavenger effect on hypochlorous acid (HOCl) from leucocytes and macrophages. 6. Taurine may act as an immunomodulator of cytokine production, which is involved in atherogenesis.
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PMID:Fish and lifestyle-related disease prevention: experimental and epidemiological evidence for anti-atherogenic potential of taurine. 1564 78

To investigate the neuroprotective effect of taurine and the involved mechanisms, middle cerebral artery occlusion (MCAO) was induced with suture for 2h in rat, and the brain tissue was then reperfused. The infarct volume and cerebral damage area were measured, respectively, with 2,3,5-triphenyltetrazolium chloride (TTC) staining and MRI. Nissl staining was used for histological observation, and immunohistochemistry and Western-blot analysis for detecting the activated caspase-3 expression. Both pre- (200mgkg(-1)) and post-treatment of taurine decreased the neurology deficit score, infarct volume and brain water content. Taurine post-treatment (67, 200 and 600mgkg(-1)) showed a dose-dependent neuroprotective effect. Taurine (200mgkg(-1)) significantly decreased neuronal loss in the cerebral cortex and hippocampus, and reduced the expression of caspase-3 as well. The neuroprotective effect of taurine was partly blunted by strychnine or bicuculline alone, and almost completely blocked by coapplication of both antagonists of glycine and GABA(A) receptors. It is suggested that taurine exerts a neuroprotective role on the brain when administered before or after MCAO. Such effect is possibly mediated by the activation of both GABA(A) receptors and strychnine-sensitive glycine receptors. Moreover, inhibition of caspase-3 expression is involved in this neuroprotective effect. These results imply a potential therapeutic use of taurine for stroke.
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PMID:Neuroprotective effect of taurine against focal cerebral ischemia in rats possibly mediated by activation of both GABAA and glycine receptors. 1738 36

Taurine neuroinhibitory features have suggested its potential for neuroprotection. The aim of the present study was to assess whether it prevents or counteracts brain ischemia and reperfusion-induced cell injury. Rat brain cortical slices were subjected to oxygen/glucose deprivation and reperfusion. Tissue damage was assessed by measuring the release of glutamate and lactate dehydrogenase (LDH) during reperfusion and by determining final tissue water gain, taken as an index of cell swelling. When added during the reperfusion period taurine did not significantly affect oxygen/glucose deprivation-induced LDH and glutamate release, while it antagonised tissue water gain in a concentration-dependent manner (IC(50)=46.5 microM). The latter effect was antagonised by 50% when a taurine transport inhibitor, 2-(guanidino)ethanesulphonic acid (GES), or a GABA(A) receptor antagonist, bicuculline, was added together with taurine, while it was completely abolished when both GES and bicuculline or the volume-sensitive outwardly rectifying (VSOR) Cl(-) channel blocker, 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB), was used. On the contrary, when present throughout the entire experiment, taurine significantly reduced oxygen/glucose deprivation-induced LDH and glutamate release with a maximal effect (45% reduction) between 5 and 20 mM. Taurine antagonised also tissue water gain according to a "U-shaped" concentration-response curve, which was significant within the range of 0.01-1.0 mM concentration. This effect was partially counteracted by GES as well as by bicuculline and fully reverted by NPPB. In conclusion, since brain edema is a major contributing factor to morbidity and mortality in stroke, the present findings give the rational basis for assessing taurine efficacy in reducing brain edema in vivo.
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PMID:Protection by taurine of rat brain cortical slices against oxygen glucose deprivation- and reoxygenation-induced damage. 1969 42

Taurine (T) was first noted as beneficial for stroke and cardiovascular diseases (CVD) prevention in genetic rat models, stroke-prone spontaneously hypertensive rats (SHRSP). The preventive mechanisms of T were ascribed to sympathetic modulation for reducing blood pressure (BP) and anti-inflammatory action. Recent epidemiological surveys revealed the involvement of inflammatory mediators in the pathogenesis of stroke and also atherosclerosis for which T was proven to be effective experimentally. Arterio-lipidosis prone rats, a substrain of SHRSP selectively bred for higher reactive hypercholesterolemia, quickly develop not only arterial fat deposition but also fatty liver which could be attenuated by dietary T supplementation. CARDIAC (CVD and Alimentary Comparison) Study was a WHO-coordinated multi-center epidemiological survey on diets and CVD risks and mortalities in 61 populations. Twenty-four-hour urinary (24U) T was inversely related significantly with coronary heart disease mortality. Higher 24U-T excreters had significantly lower body mass index, systolic and diastolic BP, total cholesterol (T-Cho), and atherogenic index (AI: T-Cho/high density lipoprotein-cholesterol) than lower T excreters. T effects on CVD risks were intensified in individuals whose 24U-T and -magnesium (M) excretions were higher. Furthermore, higher Na excreters with higher heart rate whose BP were significantly higher than those with lower heart rate were divided into two groups by the mean of 24U-T, high and low T excreters. Since the former showed significantly lower BP than the latter, T may beneficially affect salt-sensitive BP rise. Included among the typical 61 populations, were Guiyang, China or St. John's, Newfoundland, Canada where in which the means of both 24U-T and -M were high or low, respectively. The former and the latter had low and high CVD risks, respectively. Australian Aboriginals living at the coastal area in Victoria were supposed to eat T- and M-rich bush and sea foods and be free from CVD 200 years ago, but they presently have nearly the highest CVD risks indicating that T- and/or M-containing seafood, vegetables, fruits, nuts, milk, etc, similar to prehistoric hunters' and gatherers' food should be good for CVD prevention. The preventive effects of T, good for health and longevity, first noted experimentally, were also proven epidemiologically in humans.
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PMID:Taurine in health and diseases: consistent evidence from experimental and epidemiological studies. 2080 26


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