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)

Three major cytokines, namely, tumor necrosis factor (TNF-alpha), interleukin (IL)-1, and IL-6 are produced by cultured brain cells after various stimuli such as ischemia. Neurones, astrocytes, microglia and oligodendrocytes can produce inflammatory mediators, and cytokine receptors are expressed constitutionally throughout the Central Nervous System (CNS), albeit at low levels. Cytokines are involved in virtually every facet of stroke and they have numerous pro-inflammatory and pro-coagulant effects on endothelium. TNF-alpha expression after stroke stimulates expression of tissue factor and adhesion molecules for leukocytes, release of interleukin-1 (IL-1), nitric oxide, factor VIII/von Willebrand factor, platelet-activating factor and endothelin, suppression of the thrombomodulin-protein C-protein S system, reduction of tissue-plasminogen activator and release of plasminogen activator inhibitor-1. Research into the actions of IL-1beta in the brain initially focused on its role in host defence responses to systemic disease. IL-1beta can also elicit an array of responses which could either inhibit, exacerbate or induce neuronal damage and death. IL-6 can be induced by a variety of molecules including IL-1, TNF-alpha, transforming growth factor-beta and prostaglandins (PGs), and many other mediators such as b-amyloid, interferon-g (IFNg) and IL-4 can potentiate these primary inducers, highlighting the complex nature of IL-6 modulation. Several studies reported that plasma levels of TNF-alpha and IL-6 are associated with prognosis after ischemic stroke and our group showed that plasma levels of cytokines such as TNF-alpha, IL-1beta are different in every diagnostic subtype of ischemic stroke, and how plasma levels of some immunoinflammatory markers and thrombotic-phybrinolitic markers are predictive of acute ischemic stroke diagnosis in the acute setting.
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PMID:Inflammatory cytokines in acute ischemic stroke. 1907 34

There are few reports on valproic acid related to thrombophilia. Thrombophilic risk factors were investigated in 21 children (age range, 1-13 years) diagnosed with epilepsy and newly treated with valproic acid monotherapy. None of the children had been previously treated with any anticonvulsant agent. Before starting valproic acid therapy, homocysteine, lipoprotein(a), factor VIII, factor IX, protein C, protein S, antithrombin III levels, and activated protein C resistance levels were evaluated in all patients, with repeat evaluation after 9 months or 1 year of the therapy. Thrombosis gene mutations (factor V Leiden and prothrombin G20210A) were also evaluated in all patients before therapy. There was statistically significant elevation in lipoprotein(a) levels and reduction in fibrinogen levels after treatment. Reduction in protein C levels and elevation in homocysteine levels were also observed, but without statistical significance. Before therapy, no thrombotic event had occurred, despite thrombotic risk factors in some patients. Valproic acid can increase lipoprotein(a) and decrease fibrinogen, which may increase the risk of stroke or other thrombotic events. No clinical adverse effects resulted from changes in the levels or activity of thrombophilic factors associated with valproic acid treatment. Thus, routine investigation of factors implicated in thrombosis prior to initiation of valproic acid is not warranted for all patients. Nonetheless, caution is advised when initiating valproic acid treatment in children who have had prior stroke or thrombotic events.
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PMID:Thrombophilic risk factors in epileptic children treated with valproic Acid. 1952 Feb 86

Stroke is common in children with sickle cell anemia, but is rarely attributed to the traditional causes of stroke identified in other children. An 11-year-old girl with sickle cell anemia presented with severe headache and was found to have recurrent bilateral multifocal strokes in a cardioembolic pattern. Evaluation revealed the presence of a patent foramen ovale, antiphospholipid antibodies, and elevations in factor VIII and lipoprotein(a). Sickle cell anemia is itself a hypercoagulable state with potential for increased right heart pressures, both of which predispose to paradoxical embolization via right-to-left intracardiac shunting of emboli, thus causing stroke. The present case suggests that the more traditional etiologies for pediatric stroke may also cause stroke in children with sickle cell anemia.
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PMID:Stroke in sickle cell anemia: alternative etiologies. 1958 61

We explored the possibility that hypoxia-inducible factor-1alpha (HIF-1alpha) might contribute to the therapeutic effect of neural stem cell (NSC) transplantation in cerebral ischemia. The relative efficacy of modified NSC to promote behavioral recovery was investigated in a rat model of stroke induced by a transient middle cerebral artery occlusion (MCAO). A recombinant adenovirus (Ad-HIF-1alpha) was engineered to express HIF-1alpha. Control NSC infected with control adenovirus (NSC-Ad), recombinant adenovirus Ad-HIF-1alpha, or NSC infected by Ad-HIF-1alpha (NSC-Ad-HIF-1alpha), were used for intraventricular transplantion into rat brain 24 hours after MCAO. Neurological deficits were assessed over 4 weeks using the modified neurological severity scale (NSS) score. Long-term in vivo expression of HIF-1alpha was demonstrated by Western blotting and immunocytochemistry, and derivatives of nestin-positive transplanted cells contributed to both neuronal (neurofilament-positive) and astroglial (glial fibrillary acidic protein-positive) lineages. All animals showed functional improvement. Improvement was accelerated in animals receiving either NSC-Ad or Ad-HIF-1alpha, while improvement at all times between 7 days and 28 days post MCAO was significantly greater in animals transplanted with NSC-Ad-HIF-1alpha than for other treated animals. NSC-Ad-HIF-1alpha cells also increased the number of factor VIII-positive cells in the region of ischemic injury, indicating that HIF-1alpha expression can promote angiogenesis. Gene-modified NSC expressing HIF-1alpha have therapeutic potential in ischemic stroke.
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PMID:Transplantation of neural stem cells expressing hypoxia-inducible factor-1alpha (HIF-1alpha) improves behavioral recovery in a rat stroke model. 1991 30

We are reporting a 36 year-old woman, gravid 3, para 1, aborta 2, who was 18 weeks pregnant and developed a sudden onset of motor aphasia and hemiparesis on the right side. On the initial visit to our hospital, the NIH stroke scale was 6, and the brain MRI revealed high intensity areas in the left insular cortex and the periventricular white matter with occlusion of the left middle cerebral artery (MCA) branches. We diagnosed her as having cerebral embolism, and treated with intravenous recombinant tissue plasminogen activator (rt-PA) with subsequent recanalization of the occuluded left MCA branches. Her motor aphasia and hemiparesis disappeared within a few hours of initiating the therapy. She received aspirin for four months and then heparin until delivery to prevent recurrence. She delivered a healthy term infant without any apparent complications. An 18-week pregnancy itself is not considered a risk factor of stroke, and we ruled out the possibilities of dysfibrinogenemia, homocysteinemia, hereditary or acquired deficiencies of protein C, protein S, and antithrombin III deficiencies, and antiphospholipid antibody syndrome. However, her plasma factor VIII level was significantly elevated to more than 200% (reference for 18-week pregnant woman: 151 +/- 44%), which may have led to her acquired activated protein C resistance or hypercoagulability. As safety of thrombolytic therapy with rt-PA during pregnancy has not been established, this therapy could be carefully used upon due consideration of risks and benefits for both mother and fetus.
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PMID:[Intravenous recombinant tissue plasminogen activator in an 18-week pregnant woman with embolic stroke]. 2053 80

Protein S is a vitamin K-dependent anticoagulant protein. It functions as a cofactor of activated protein C to inactivate activated factor V (FVa) and activated factor VIII (FVIIIa). Its deficiency is a rare condition and can lead to deep vein thrombosis, pulmonary embolism or stroke. It is often treated with long-term anti-coagulant therapy. Protein S deficiency may be hereditary or acquired; the latter is usually due to hepatic diseases or a vitamin K deficiency. Protein S deficiency manifests as an autosomal dominant trait; manifestations of thrombosis are observed in both heterozygous and homozygous genetic deficiencies of protein S. This case report is of DVT due to Protein S deficiency in a 53 year old male. Venous Doppler was used to diagnose DVT and free Protein S level measured by ELISA. IVC filter was placed on the third day of admission.
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PMID:Deep vein thrombosis in protein S deficiency. 2118 Feb 23

This study aimed to investigate the maternal, pre- and perinatal, and prothrombotic factors with congenital hemiparesis due to presumed perinatal stroke (PPS). Prothrombotic risk factors including protein C and S, antithrombin III, lipoprotein (a), homocystein, factor VIII levels; anticardiolipin antibodies and lupus anticoagulant; methylenetetrahydrofolate reductase mutations, factor V Leiden, prothrombin G20210A mutations were investigated. Arterial ischemic stroke was detected in 60% and periventricular venous infarction in 40%. At least one prothrombotic risk factor was present in 69%, two in 17%, and three or more in 8.5% of cases. The most common combination was methylenetetrahydrofolate reductase C677T and factor V Leiden heterozygosity. The etiology and pathogenesis of PPS is still unclear. According to this study, most of the patients with PPS might have one or more prothrombotic risk factors and certain prenatal risk factors including intrauterine growth retardation, twin gestation and preeclampsia might be related to PPS.
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PMID:Etiological analysis of presumed perinatal stroke. 2156 29

Thrombosis contributes to morbidity and mortality in neonates following cardiac surgery. Alterations in hemostatic factors following cardiac surgery have been described, but there is no data correlating these changes with risk of thrombosis in neonates. The aim of this study is to predict thrombosis in neonates undergoing cardiac surgery by assessment of a panel of hypercoagulability markers. Neonates undergoing cardiac surgery were enrolled preoperatively and prospectively followed. Preoperative hypercoagulability panel testing included thrombin generation assay (TGA), immunoassays for antithrombin III, protein C, protein S, factor VIII, thrombin-activatable fibrinolytic inhibitor (TAFI), plasminogen activator inhibitor-1 (PAI-1), and cardiolipin antibody. Postoperative thrombosis was defined by clinical events (shunt thrombosis, limb ischemia, and stroke) or imaging (intravascular or intracardiac thrombus). Risk factors for thrombosis were assessed. One hundred neonates were enrolled in the study over a two-year period. The incidence of postoperative in-hospital thrombosis was 20%. The only significant clinical risk factor associated with thrombosis was the single ventricle physiology. Hypercoagulability factors associated with increased risk of thrombosis by univariate analysis were elevated PAI-1, TAFI, and TGA, and presence of anticardiolipin antibodies. Multivariable logistic regression analysis demonstrated that elevated PAI-1 (P = 0.015), TAFI (P = 0.028), and TGA (P = 0.007) were independent predictors of thrombosis. Hypercoagulability panel testing may help identify neonates at high risk for thrombosis following cardiac surgery. Future studies are warranted to determine if high risk patients benefit from targeted anticoagulation therapies.
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PMID:Hypercoagulability panel testing predicts thrombosis in neonates undergoing cardiac surgery. 2412 21

Arterial cerebral ischaemia has been described in different diseases of the thyroid. Likewise, cerebral venous thrombosis (CVT) has been reported in association with hyperthyroidism. However, the association of arterial and venous cerebral ischaemic events in patients with hyperthyroidism has not been previously described. We report the case of a patient with thyrotoxicosis who presented initially with an arterial ischaemic stroke complicated by a concomitant CVT, ultimately treated with decompressive craniectomy. Laboratory results revealed elevated factor VIII coagulant activity and a positive lupus anticoagulant IgG. In conclusion, CVT and arterial ischaemic events can happen concomitantly in patients with hyperthyroidism. Although there is insufficient evidence to prove that a hypercoagulability state in hyperthyroidism predisposes to cerebral ischaemia, the presence of antiphospholipid antibodies and other hypercoagulability studies should be performed in patients with thyrotoxicosis and ischaemic events.
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PMID:An unusual association between acute ischaemic stroke and cerebral venous thrombosis with thyrotoxic state. 2431 16

It has been well known for many years that the ABO blood group has a major influence on hemostasis, through its influence on von Willebrand factor and, consequently, factor VIII plasma levels. Although the relationship between non-O blood type and the risk of venous thromboembolism is nowadays also well established, the association with arterial thrombotic events (i.e., myocardial infarction [MI] and ischemic stroke) is less well characterized. To elucidate the latter issue, we have conducted a systematic review and meta-analysis of the existing literature. After an electronic search strategy using MEDLINE and EMBASE and a manual review of abstract books of the International Society on Thrombosis and Haemostasis and of reference lists of all retrieved articles, 28 studies were finally included in our systematic review. The prevalence of non-O blood group was significantly higher in patients with MI (pooled odds ratio [OR]: 1.28, 95% confidence interval [CI]: 1.17-1.40; p < 0.001) and ischemic stroke (pooled OR: 1.17, 95% CI: 1.01-1.35; p = 0.03) than in controls. The restriction of the analysis to high quality studies only confirmed the association with MI (pooled OR: 1.17, 95% CI: 1.03-1.32) but not with ischemic stroke (pooled OR: 1.28, 95% CI: 0.94-1.74). In conclusion, the results of our meta-analysis confirm the existing literature evidence of a weak association between non-O blood group and vascular arterial thrombosis, in particular myocardial ischemia.
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PMID:ABO blood group and vascular disease: an update. 2717 4


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