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)

The utility of the Clock Drawing Test (CDT) in localizing lesions has not been thoroughly examined to date. In the present study, six scoring systems (Freedman et al., 1994; Ishiai, Sugishita, Ichikawa, Gono, & Watabiki, 1993; Mendez, Ala, & Underwood, 1992; Rouleau, Salmon, Butters, Kennedy, & McGuife, 1992; Sunderland et al., 1989; Tuokko, Hadjistavropoulos, Miller, & Beattie, 1992; Watson, Arfken, & Birge, 1993; Wolf-Klein, Silverstone, Levy, & Brod, 1989) were used to assess clock drawings by 76 stroke patients and 71 normal controls. Significant differences were found between normals and stroke patients on all scoring systems for both quantitative and qualitative features of the CDT. Quantitative indices were not helpful in differentiating between various stroke groups (left versus right versus bilateral stroke; cortical versus subcortical stroke; anterior versus posterior stroke). Qualitative features were helpful in lateralizing lesion site and differentiating subcortical from cortical groups. Correlational analyses revealed that CDT performance was related to visuospatial processing and measures commonly used in cognitive screening.
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PMID:Quantitative and qualitative performance of stroke versus normal elderly on six clock drawing systems. 1459 Jun 33

The solute carrier family 1 (SLC1) is composed of five high affinity glutamate transporters, which exhibit the properties of the previously described system XAG-, as well as two Na+-dependent neutral amino acid transporters with characteristics of the so-called "ASC" (alanine, serine and cysteine). The SLC1 family members are structurally similar, with almost identical hydropathy profiles and predicted membrane topologies. The transporters have eight transmembrane domains and a structure reminiscent of a pore loop between the seventh and eighth domains [Neuron 21 (1998) 623]. However, each of these transporters exhibits distinct functional properties. Glutamate transporters mediate transport of L-Glu, L-Asp and D-Asp, accompanied by the cotransport of 3 Na+ and one 1 H+, and the countertransport of 1 K+, whereas ASC transporters mediate Na+-dependent exchange of small neutral amino acids such as Ala, Ser, Cys and Thr. Given the high concentrating capacity provided by the unique ion coupling pattern of glutamate transporters, they play crucial roles in protecting neurons against glutamate excitotoxicity in the central nervous system (CNS). The regulation and manipulation of their function is a critical issue in the pathogenesis and treatment of CNS disorders involving glutamate excitotoxicity. Loss of function of the glial glutamate transporter GLT1 (SLC1A2) has been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), resulting in damage of adjacent motor neurons. The importance of glial glutamate transporters in protecting neurons from extracellular glutamate was further demonstrated in studies of the slc1A2 glutamate transporter knockout mouse. The findings suggest that therapeutic upregulation of GLT1 may be beneficial in a variety of pathological conditions. Selective inhibition of the neuronal glutamate transporter EAAC1 (SLC1A1) but not the glial glutamate transporters may be of therapeutic interest, allowing blockage of glutamate exit from neurons due to "reversed glutamate transport" of EAAC1, which will occur during pathological conditions, such as during ischemia after a stroke.
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PMID:The glutamate and neutral amino acid transporter family: physiological and pharmacological implications. 1461 54

Microdialysis coupled to liquid chromatography (LC) has proven to be a valuable in vivo sampling technique for studying neurotransmitter changes in normal and ischaemic brain. However, few analytical methods have described the simultaneous determination of amino acids, relevant in stroke research, together with the nitric-oxide-related compound citrulline. Therefore, we developed a gradient LC method for the quantitative simultaneous determination of aspartate, glutamate, serine, glutamine, arginine, taurine, alanine and citrulline in dialysates of rat brain using narrowbore LC with o-phthalaldehyde-2-mercaptoethanol pre-column derivatisation and fluorescence detection. The proposed method is a thoroughly validated, fully automated and robust LC method for the determination of amino acids in a wide concentration range. The method was applied for the determination of amino acids and the citrulline/arginine ratio in the Et-1 model for focal cerebral ischaemia.
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PMID:Determination of amino acids associated with cerebral ischaemia in rat brain microdialysates using narrowbore liquid chromatography and fluorescence detection. 1584 40

The alanine (A) to threonine (T) substitution at codon 54 of the intestinal fatty acid-binding protein 2 (FABP2) has been associated with dyslipidaemia and other characteristics of the metabolic syndrome, which in turn is a risk factor for cerebrovascular disease. The aim of this study was to investigate whether the A54T polymorphism in the FABP2 gene is associated with internal carotid artery (ICA) stenosis in stroke patients. Swedish subjects initially diagnosed with acute cerebrovascular disease (n=196) that had been assessed with ultrasound of the carotid arteries were identified and grouped depending on whether a stenosis was found. The subjects were genotyped for the A54T polymorphism using a PCR-RFLP method. In a multivariate logistic-regression analysis, where known risk factors for atherosclerosis were fixed (diabetes, systolic blood pressure, age and smoking), having the FABP2 T allele was a significant risk factor for ICA stenosis (odds ratio 2.9; 95% confidence interval, 1.1-7.7; p = 0.04) together with diabetes (odds ratio 4.9; 95% confidence interval, 1.8-14; p < 0.01). Age, smoking and blood pressure did not reach statistical significance. In conclusion, our result supports the hypothesis that the FABP2 A54T polymorphism is associated with ICA stenosis.
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PMID:Genetic variation of the intestinal fatty acid-binding protein 2 gene in carotid atherosclerosis. 1601 94

Rho-associated kinases (ROCKs), the immediate downstream targets of RhoA, are ubiquitously expressed serine-threonine protein kinases that are involved in diverse cellular functions, including smooth muscle contraction, actin cytoskeleton organization, cell adhesion and motility, and gene expression. Recent studies have shown that ROCKs may play a pivotal role in cardiovascular diseases such as vasospastic angina, ischemic stroke, and heart failure. Indeed, inhibition of ROCKs by statins or other selective inhibitors leads to the upregulation and activation of endothelial nitric oxide synthase (eNOS) and reduction of vascular inflammation and atherosclerosis. Thus inhibition of ROCKs may contribute to some of the cholesterol-independent beneficial effects of statin therapy. Currently, two ROCK isoforms have been identified, ROCK1 and ROCK2. Because ROCK inhibitors are nonselective with respect to ROCK1 and ROCK2 and also, in some cases, may be nonspecific with respect to other ROCK-related kinases such as myristolated alanine-rich C kinase substrate (MARCKS), protein kinase A, and protein kinase C, the precise role of ROCKs in cardiovascular disease remains unknown. However, with the recent development of ROCK1- and ROCK2-knockout mice, further dissection of ROCK signaling pathways is now possible. Herein we review what is known about the physiological role of ROCKs in the cardiovascular system and speculate about how inhibition of ROCKs could provide cardiovascular benefits.
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PMID:Physiological role of ROCKs in the cardiovascular system. 1646 61

The threonine (Thr) for alanine (Ala) codon 54 polymorphism of the fatty acid binding protein (FABP) 2 gene, when compared to the wild type, is associated with dyslipidemia. Since dyslipidemia is common in diabetes and is associated with increased cardiovascular risk, we tested the hypothesis that Thr-54 is associated with increased cardiovascular risk in patients with diabetes. The secondary prevention veterans affairs HDL intervention trial (VA-HIT) was carried out in patients with dyslipidemia. The DNA of trial participants (n=776) was screened for the Thr-54 polymorphism and cardiovascular endpoints were monitored. The polymorphism was detected in 370 (47.7%). For first occurrence of the primary endpoint [myocardial infarction (MI) or coronary heart disease (CHD) death] the hazard ratio (HR) and confidence intervals (Cox proportional hazards model) was 2.5 (1.2, 5.3) p=.02 in diabetic carriers of Thr-54 versus carriers without diabetes or fasting glucose >7 mmol/L. For the expanded endpoint (stroke, MI or CHD death), the corresponding HR was 3.0 (1.4, 5.4) p=.0003 and for the stroke alone the corresponding HR was 3.5 (1.4-8.9) p=.01. The higher cumulative incidence of the expanded endpoint in diabetic participants carrying the FABP2 polymorphism versus non-diabetic carriers was consistently present throughout the 5 years of the study (p=.0002). We conclude that based on the VA-HIT data, the Thr-54 polymorphism of the FABP2 gene is associated with a 2-3.5-fold increase in cardiovascular risk in dyslipidemic men with diabetes compared to their non-diabetic counterparts.
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PMID:Codon 54 polymorphism of the fatty acid binding protein (FABP) 2 gene is associated with increased cardiovascular risk in the dyslipidemic diabetic participants of the Veterans Affairs HDL intervention trial (VA-HIT). 1694 73

Over 800 different missense mutations in the low density lipoprotein (LDL) receptor gene (LDLR) have been identified in patients with familial hypercholesterolaemia (FH). Only two of them, including the Alanine to Threonine change at position 370 (A370T), have been discovered in FH patients but do not cause FH. The frequency of the 370T allele has been reported worldwide to be between 0.022 and 0.070, with no clear association with high cholesterol levels or risk for coronary heart disease (CHD) and stroke. To explore this relationship in more detail we have determined this genotype in 2,659 healthy middle-aged (50-61 years) men participating in the prospective Second Northwick Park Heart Study, with 236 CHD and 67 stroke incident events. The genotype distribution was in Hardy-Weinberg equilibrium and in the no-event group the frequency of 370T was 0.046 (95% CI 0.040-0.052). Overall, there was no significant association of the 370T allele with any measured plasma lipid trait, and there was no difference in genotype distribution or allele frequency between the no-event and CHD (0.059; 95% CI 0.040-0.085) or stroke (0.037; 95% CI 0.012-0.085) groups ( p= 0.18 and 0.65, respectively). There was evidence for significant interaction ( p= 0.006) between body mass index (BMI) and genotype on CHD risk, with 370A homozygotes showing the expected higher CHD risk for those with higher BMI, whilst risk for 370T allele carriers was highest in men in the lowest tertile of BMI. The explanation for this association is unclear, and may simply be chance. Thus, these data confirm the absence of a significant impact of the A370T polymorphism on LDL receptor function, at least as measured by the effect on plasma lipid levels and CHD risk.
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PMID:The A370T variant (StuI polymorphism) in the LDL receptor gene is not associated with plasma lipid levels or cardiovascular risk in UK men. 1704 44

Peroxisome proliferator-activated receptor (PPAR)-gamma2 has important effects to insulin sensitivity, atherosclerosis, inflammation and endothelial cell function. Through these effects, PPAR-gamma2 might be involved with the ischemic stroke in type 2 diabetes. To determine the role of PPAR-gamma2 in genetic susceptibility to ischemic stroke in type 2 diabetes, we genotyped 302 ischemic stroke patients, 283 healthy controls and 141 type 2 diabetic patients without ischemic stroke (diabetes duration >10 years) for PPAR-gamma2 Pro12Ala polymorphism by polymerase chain reaction-restriction fragment length polymorphism methods. PPAR-gamma2 Pro/Ala genotype were lower in ischemic stroke patients than those observed in the control group (4.0% vs. 9.9%, OR=0.38, P=0.0046), and it were associated with the incidence of ischemic stroke in the multivariate analysis (OR=0.43, P=0.025). Genotypic analysis revealed that ischemic stroke patients with type 2 diabetes displayed a great lower prevalence of the Pro/Ala genotype (2.3%) than controls (9.9%) (OR=0.21, P=0.0047). And Pro/Ala genotype of type 2 diabetes patients with ischemic stroke were lower than type 2 diabetes patients without ischemic stroke (2.3% vs. 8.5%, OR=0.25, P=0.0321), however the significant association with ischemic stroke was not detected in the multivariate analysis (OR=0.27, P=0.051). These results suggest that the Pro/Ala genotype of PPAR-gamma2 Pro12Ala polymorphism may be associated with reduced risk for ischemic stroke, and the possibility that it might have a protective effect for ischemic stroke with type 2 diabetes.
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PMID:Peroxisome proliferator-activated receptor-gamma2 Pro12Ala polymorphism is associated with reduced risk for ischemic stroke with type 2 diabetes. 1708 28

Ripe specimens of Ptychodera flava were collected at Paiko Peninsula, Oahu, Hawaii, USA, and the development from egg to tornaria larva was followed in the laboratory. To complete the series, large tornaria larvae were collected from the plankton off the nearby Ala Moana Beach, and followed through metamorphosis to a juvenile stage with four pairs of gill slits. Ciliary band development was examined by scanning electron microscopy, and the development of the serotonergic nervous system was followed by means of immunostaining. The development of the apical tuft and neotroch (circumoral/perioral ciliary band) and their subsequent degeneration accorded fully with previous descriptions. A perianal ciliary ring of separate cilia develops just after hatching. This later develops a midventral extension, the neurotroch, extending to the neotroch posterior to the mouth. The cilia of this ring apparently beat diaplectically, with the effective stroke in the clockwise direction when seen from behind. An additional ring of cilia develops several days later anterior to the perianal ring. This opisthotroch (called telotroch by previous authors) consists at first of separate cilia, but later they became organized as large compound cilia. The apical tuft disappears after about a week, the neotroch degenerates at the transition to the Agassiz stage, and the opisthotroch degenerates just after metamorphosis. The serotonergic nervous system of the fully grown tornaria consists of an apical ganglion with many perikarya, a paired lateral group of perikarya on the postoral ciliary band, and scattered perikarya along the opisthotroch. Serotonergic processes are found along the ciliary bands except for the ventral and perianal ciliary bands and are scattered along the epidermis. At the Spengel stage and at metamorphosis (Agassiz stage), the processes along the ciliary bands are concentrated in the three ciliated food grooves so as to form three separate nerves, and are retained on the proboscis at least until 2-3 gill slit stage. No serotonergic processes were found to extend from the proboscis to the collar region, and no serotonergic neurons were observed in the collar cord or in the ventral nerve cord. Our results therefore do not provide any clues as to the origin of the chordate neural tube relative to the dorsal-ventral orientation of the enteropneusts.
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PMID:Development of the enteropneust Ptychodera flava: ciliary bands and nervous system. 1746 31

Oral anticoagulant treatment for secondary prevention after cerebral ischaemia of presumed arterial origin is associated with a higher bleeding rate than cardioembolic stroke. This discrepancy is only partly explained by known bleeding risk factors. Haemostatic genetic variants and AB0 blood group may be involved. We performed a nested casecontrol study in patients with cerebral ischaemia of presumed arterial origin on anticoagulant treatment (International Normalized Ratio between 3.0-4.5). All 34 cases with non-fatal haemorrhage (10 intracranial and 24 extracranial) and 68 control patients on anticoagulant treatment without such a bleeding were selected from the SPIRIT study. AB0 blood group and 11 haemostatic genetic variants were investigated. The Thr312Ala variant of the alpha fibrinogen gene was associated with a decreased bleeding risk (odds ratio (OR) 0.3 for Ala/Ala and Thr/Ala versus Thr/Thr genotype; 95% CI 0.1-0.8). Factor V Leiden was associated with an increased bleeding risk (OR 11.6; 95% CI 1.3-103). The APOE2 allele (OR 0.5; 95% CI 0.2-1.7) and the Tyr204Phe variant in the factor XIII subunit A (OR 2.1; 0.9-5) had nonsignificant relationships with bleeding risk. AB0 blood group and 7 other genetic variants in coagulation factors II and XIII, vitamin K epoxide reductase complex, beta fibrinogen and apolipoprotein E were not related with the risk of haemorrhage. The Ala312Thr variant in the alpha fibrinogen gene is associated with a decreased and factor V Leiden with an increased bleeding risk in patients on anticoagulant treatment after cerebral ischaemia of presumed arterial origin.
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PMID:Haemostatic genetic variants, ABO blood group and bleeding risk during oral anticoagulant treatment after cerebral ischaemia of arterial origin. 1799 14


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