hydrocephalus/protease

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Thrombin disrupts vascular endothelial-cadherin and leads to hydrocephalus via protease-activated receptors-1 pathway.

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Previous studies indicated that intraventricular injection of thrombin would induce hydrocephalus. But how thrombin works in this process remains unclear. Since cadherin plays a critical role in hydrocephalus, we aimed to explore the mechanisms of how thrombin acted on choroid plexus

Variably protease-sensitive prionopathy: a novel disease of the prion protein.

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Variably protease-sensitive prionopathy (VPSPr) is a novel disease involving the prion protein (PrP) that has clinical similarities with non-Alzheimer's dementias especially frontotemporal dementia, diffuse Lewis body disease, and normal pressure hydrocephalus. VPSPr can be distinguished from

Hydrocephalus after intraventricular hemorrhage: the role of thrombin.

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Previous studies demonstrated that thrombin is an important factor in brain injury after intracerebral hemorrhage. This study investigated the effect of thrombin on hydrocephalus development in a rat intraventricular hemorrhage (IVH) model. There were three parts in this study. First, male

Teratogenic effects of combined use of anti-kidney serum and E-64 in the rat.

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The teratogenic effects of rabbit anti-rat-kidney serum (AKS) combined with E-64 (a thiol protease inhibitor) were examined. Wistar rats were injected with 10 or 20 mg/kg of E-64 on days 9 and 10 of gestation, and with a subteratogenic dose (1 ml/kg) of AKS on day 9 or day 10. The most common

The teratogenic effects of E-64 on rat embryogenesis.

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To examine the effects of E-64 (a thiol protease inhibitor) on the development of rat embryos, pregnant Wistar rats were injected with 10-30 mg/kg of E-64 intra-peritoneally on days 9 and 10 of gestation. On day 21, the rats were killed and the fetuses were examined for malformations. When 30 mg/kg

Reexamination of the role of ubiquitin-like modifier ISG15 in the phenotype of UBP43-deficient mice.

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UBP43/USP18 was described as a specific protease that removes conjugated ubiquitin-like modifier ISG15 from target proteins. The severe phenotype of UBP43(-/-) mice characterized by premature death, brain cell injury, and deregulated STAT1 signaling was ascribed to an enhanced conjugation of ISG15.

Should we use the serum vaspin level for the diagnosis and/or prognosis of subarachnoid hemorrhage?

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BACKGROUND We aimed to investigate whether vaspin, a member of the serine protease family, could be used as a marker for the severity and prognosis of subarachnoid hemorrhage (SAH). METHODS Fifty-two consecutive patients (mean age, 51.46±3.2 years; 61.5% male) admitted to the emergency service of

Advances in adjuvant therapy against acute bacterial meningitis.

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Death and co-morbidity derived from acute bacterial meningitis remain unacceptably high and are mainly related to immune-mediated cerebral dysfunction. Cerebral edema, hydrocephalus and ischaemic cerebrovascular events are severe complications that eventually occur following the activation of a

Development of adjunctive therapies for bacterial meningitis and lessons from knockout mice.

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Bacterial meningitis is a medical emergency and is optimally managed in an intensive care environment. Despite the use of antibiotics, the prognosis of this disease is poor because of central nervous system complications such as brain edema formation, cerebrovascular alterations, intracranial

Reversible posterior leukoencephalopathy syndrome in a patient with thrombotic thrombocytopenic purpura.

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Thrombotic thrombocytopenic purpura (TTP) is an autoimmune disorder characterised by fever, microangiopathic haemolytic anaemia, renal insufficiency, and thrombocytopenia. Neurological involvement, a prominent component of TTP, is characterised by a variety of brain lesions which include reversible

Staphylococcus aureus sarA regulates inflammation and colonization during central nervous system biofilm formation.

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Infection is a frequent and serious complication following the treatment of hydrocephalus with CSF shunts, with limited therapeutic options because of biofilm formation along the catheter surface. Here we evaluated the possibility that the sarA regulatory locus engenders S. aureus more resistant to

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