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HDAC inhibitor valproic acid protects heart function through Foxm1 pathway after acute myocardial infarction.

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Epigenetic histone acetylation is a major event controlling cell functions, such as metabolism, differentiation and repair. Here, we aim to determine whether Valproic acid (VPA), a FDA approved inhibitor of histone deacetylation for bipolar disease, could protect heart against

Progressive encephalopathy with cerebral oedema and infarctions associated with valproate and diazepam overdose.

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Valproic Acid (VPA) in overdose is known to cause encephalopathy with or without cerebral odema, hyperammonaemia, hepatotoxicity, bone marrow suppression and non gap acidosis. Most of these conditions are reversible. We report a 45-year-old man who suffered permanent disability from the non

Neuroprotection by valproic Acid in mouse models of permanent and transient focal cerebral ischemia.

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Valproic acid (VPA) is a well-known anti-epileptic and mood stabilizing drug. A growing number of reports demonstrate that VPA is neuroprotective against various insults. Despite intensive efforts to develop new therapeutics for stroke over the past two decades, all treatments have thus far failed

Valproic acid ameliorates ischemic brain injury in hyperglycemic rats with permanent middle cerebral occlusion.

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Valproic acid (VPA) is widely used for the clinical treatment of epilepsy. Previous studies have demonstrated that VPA ameliorates brain injury following experimental stroke. However, the effect of VPA in stroke models featuring comorbid conditions has not been fully explored. In this study, we

Paclitaxel plus valproic acid versus paclitaxel alone as second- or third-line therapy for advanced gastric cancer: a randomized Phase II trial.

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BACKGROUND Weekly paclitaxel (wPTX) is the preferred second-line chemotherapy for gastric cancer in Japan. Histone deacetylase inhibitors have been shown to decrease proliferation through cell-cycle arrest, differentiation, and apoptosis in gastric cancer cells. One histone deacetylase inhibitor,

Valproic acid attenuates ischemia-reperfusion injury in the rat brain through inhibition of oxidative stress and inflammation.

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Valproic acid (VPA), widely used in clinical contexts for the treatment of seizures and bipolar mood disorder, has neuroprotective properties in cellular and animal models. However, the precise mechanisms underlying its neuroprotection against stroke remain unknown. In the present study, we explored

Profibrinolytic effect of the epigenetic modifier valproic acid in man.

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OBJECTIVE The aim of the study was to test if pharmacological intervention by valproic acid (VPA) treatment can modulate the fibrinolytic system in man, by means of increased acute release capacity of tissue plasminogen activator (t-PA) as well as an altered t-PA/Plasminogen activator inhibitor -1

Valproic acid enhances the effect of bone marrow-derived mononuclear cells in a rat ischemic stroke model.

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Bone marrow derived mononuclear cell (MNC) transplantation is a potential therapy for ischemic stroke. Here, we hypothesized that valproic acid (VPA) would modulate transplantation effects of MNCs in a rat ischemic stroke model. Male Sprague-Dawley rats were subjected to transient 90min middle

Valproic acid reduces brain damage induced by transient focal cerebral ischemia in rats: potential roles of histone deacetylase inhibition and heat shock protein induction.

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Growing evidence from in vitro studies supports that valproic acid (VPA), an anti-convulsant and mood-stabilizing drug, has neuroprotective effects. The present study investigated whether VPA reduces brain damage and improves functional outcome in a transient focal cerebral ischemia model of rats.

HDACi Valproic Acid (VPA) and Suberoylanilide Hydroxamic Acid (SAHA) Delay but Fail to Protect against Warm Hepatic Ischemia-Reperfusion Injury.

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BACKGROUND Histone deacetylases (HDAC) catalyze N-terminal deacetylation of lysine-residues on histones and multiple nuclear and cytoplasmic proteins. In various animal models, such as trauma/hemorrhagic shock, ischemic stroke or myocardial infarction, HDAC inhibitor (HDACi) application is cyto- and

Histone deacetylase inhibition enhances tissue plasminogen activator release capacity in atherosclerotic man.

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The expression of the tissue plasminogen activator (t-PA) gene appears to be under epigenetic control and can be affected by histone deacetylation inhibition. The study aimed to test if histone deacetalyase inhibitor treatment lead to increased t-PA release or reduced exhaustion in t-PA release in

Etiology of neonatal seizures and maintenance therapy use: a 10-year retrospective study at Toulouse Children's hospital.

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No guidelines exist concerning the maintenance antiepileptic drug to use after neonatal seizures. Practices vary from one hospital to another. The aim of this study was to investigate etiologies and to report on the use of maintenance antiepileptic therapy in our population of

[Clinical misdiagnosis analysis of valproate encephalopathy].

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OBJECTIVE To analyze the clinical and laboratory characteristics of postoperative patients of valproate encephalopathy (VHE), summarize the diagnostic and treatment experiences, discuss the reason of misdiagnosis and improve the level of early diagnosis. METHODS A total of 12 VHE patients diagnosed

[Cerebral venous thrombosis with familial antithrombin III deficiency].

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A case of cerebral venous thrombosis with familial antithrombin III (AT III) deficiency was reported and we discussed the anticoagulant therapy of cerebral venous thrombosis from the viewpoint of AT III. The patient, a 17-year-old boy, was admitted to our clinic with severe bifrontal headache,

Antiepileptic treatment in patients with early postischemic stroke seizures: a retrospective study.

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Early seizures caused by stroke are a common cause of epilepsy in adults. The protocol for treatment in such a case is not clear. Patients were studied retrospectively after early poststroke seizures. Two groups of patients were compared: one treated group included 35 patients who continued therapy

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