cerebral hemorrhage/phosphatase

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[Experimental study on histochemical action of phosphatases and of nucleic acids on foci of cerebral hemorrhages].

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Risk factors for primary cerebral hemorrhage: a population-based study--the Stroke Registry of Dijon.

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Risk factors for primary cerebral hemorrhage remain uncertain. The population-based Stroke Registry of Dijon provides data on the risk factors. Among residents of Dijon (France), 130 cases of primary cerebral hemorrhage hospitalized from 1985 to 1992 were matched with 130 controls by age and sex.

Measurement of serum alkaline phosphatase isozyme I in brain-damaged patients.

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The authors measured alkaline phosphatase isozyme I (ALP-I) in sera of 24 brain-damaged patients and four with disorders other than brain damage. The study population comprised three patients with postresuscitation encephalopathy, four with ruptured cerebral aneurysms, 14 with acute subdural

[Essential thrombocythemia associated with subdural hematoma and postoperative intracerebral hemorrhage--a case report].

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A case of essential thrombocythemia (ET) associated with subdural hematoma and postoperative intracerebral hemorrhage was reported. A 57-year-old man had complained headache in the morning. Six hours later he was found unconsciousness and soon he was brought to our hospital. On admission he was

A Combined Proteomics and Bioinformatics Approach Reveals Novel Signaling Pathways and Molecular Targets After Intracerebral Hemorrhage.

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Intracerebral hemorrhage (ICH) is a non-traumatic cerebrovascular disorder with very high morbidity and mortality and regarded as one of the deadliest stroke subtypes. Notably, there is no effective treatment for ICH. Despite an overall increase in preclinical studies, the pathophysiology of ICH is

Tristetraprolin attenuates brain edema in a rat model of cerebral hemorrhage.

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We evaluated the protective effects of protein phosphatase 2A (PP2A)/tristetraprolin (TTP) against brain edema in a rat model of cerebral hemorrhage, bleeding in the brain that occurs in tissues and ventricles. TTP is a well-known mRNA-binding protein and essential regulatory molecule

HDAC10 alleviates inflammation after intracerebral hemorrhage via the PTPN22/NLRP3 pathway in rats.

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Pyrin domain-containing 3 inflammasome (NLRP3), a member of the NOD-like receptor family, has a crucial role in the inflammatory process that occurs during intracerebral hemorrhage (ICH)-induced injury. Histone deacetylase 10 (HDAC10) is a newly identified class II histone deacetylase involved in

PTEN Inhibition Protects Against Experimental Intracerebral Hemorrhage-Induced Brain Injury Through PTEN/E2F1/β-Catenin Pathway.

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Intracerebral hemorrhage (ICH) is a subtype of stroke with highest mortality and morbidity. We have previously demonstrated that dipotassium bisperoxo (picolinato) oxovanadate (V), (bpV[pic]) inhibits phosphatase and tensin homolog (PTEN) and activates extracellular signal-regulated kinase (ERK)1/2.

Elevated miR-29a Contributes to Axonal Outgrowth and Neurological Recovery After Intracerebral Hemorrhage via Targeting PTEN/PI3K/Akt Pathway

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Spontaneous intracerebral hemorrhage (ICH) is a clinical challenge with high disability and lacks an effective treatment. miR-29a strongly expressed in the brain has been implicated in various neurological disorders. In this study, we investigated the biological roles of miR-29a in axonal outgrowth

MicroRNA-181c provides neuroprotection in an intracerebral hemorrhage model.

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Apoptosis is an important factor during the early stage of intracerebral hemorrhage. MiR-181c plays a key regulatory role in apoptosis. However, whether miR-181c is involved in apoptosis of prophase cells after intracerebral hemorrhage remains unclear. Therefore, in vitro and in vivo experiments

Subclinical change of liver function could also provide a clue on prognosis for patients with spontaneous intracerebral hemorrhage.

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Whether subclinical change of liver function is associated with outcome of spontaneous intracerebral hemorrhage remains to be an open question. A total of 639 patients of spontaneous intracerebral hemorrhage within 7 days from stroke onset were finally enrolled. Liver function indicators, including

Hereditary cerebral hemorrhage with amyloidosis (Dutch): a model for congophilic plaque formation without neurofibrillary pathology.

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Plaque-like lesions and amyloid angiopathy were investigated in the frontal cerebral cortex of four patients with hereditary cerebral hemorrhage with amyloidosis (Dutch) (HCHWA-D), using immunohistochemical [antibodies to beta amyloid protein (A beta), beta protein precursor (beta PP),

Glycine confers neuroprotection through PTEN/AKT signal pathway in experimental intracerebral hemorrhage.

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Glycine has been shown to protect against ischemic stroke through various mechanisms. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) which antagonize Akt-dependent cell survival has been linked to neuronal damage. However, whether glycine has a neuroprotective property in

Regulatory T cells ameliorate intracerebral hemorrhage-induced inflammatory injury by modulating microglia/macrophage polarization through the IL-10/GSK3β/PTEN axis.

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Inflammation mediated by the peripheral infiltration of inflammatory cells plays an important role in intracerebral hemorrhage (ICH) induced secondary injury. Previous studies have indicated that regulatory T lymphocytes (Tregs) might reduce ICH-induced inflammation, but the precise mechanisms that

The p35/CDK5 signaling is regulated by p75NTR in neuronal apoptosis after intracerebral hemorrhage.

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The p75 neurotrophin receptor (p75NTR), a member of tumor necrosis factor receptor superfamily, involves in neuronal apoptosis after intracerebral hemorrhage (ICH). It has been previously demonstrated that phosphorylation of p35 is a crucial factor for fighting against the proapoptotic p25/CDK5

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