hemorrhage/phosphatase

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Treatment with sodium orthovanadate reduces blood-brain barrier disruption via phosphatase and tensin homolog deleted on chromosome 10 (PTEN) phosphorylation in experimental subarachnoid hemorrhage.

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Attenuation of blood-brain barrier (BBB) disruption is one of the therapeutic candidates for treatment of subarachnoid hemorrhage (SAH). In this study, the protective effect of sodium orthovanadate (SOV) on BBB disruption was investigated in SAH using the endovascular perforation model. Fifty-five

The presence of an extractable substance in the CSF of humans with cerebral vasospasm after subarachnoid haemorrhage that correlates with phosphatase inhibition.

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The cellular events leading to cerebral vasospasm after subarachnoid haemorrhage are poorly understood, although an increase in smooth muscle myosin light chain phosphorylation has been observed. This study set out to determine if phosphatase inhibition may be involved in the pathological

Tyrosine phosphatase inhibition attenuates early brain injury after subarachnoid hemorrhage in rats.

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OBJECTIVE Sodium orthovanadate (SOV) is a representative tyrosine phosphatase inhibitor and has been shown to ameliorate neuronal injury in cerebral ischemia. We hypothesized that tyrosine phosphatase inhibition by SOV might attenuate early brain injury after subarachnoid hemorrhage (SAH) in this

Intestinal alkaline phosphatase: role in the depressed gut lipid transport after trauma-hemorrhagic shock.

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Although studies have indicated that the gut lipid absorptive capacity is impaired after trauma and hemorrhagic shock, the mechanism responsible for this remains unknown. The aim of this study, therefore, was to determine whether intestinal alkaline phosphatase (IAP) plays any role in the depressed

Regulation of liver and kidney glucose-6-phosphatase gene expression in hemorrhage and resuscitation.

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The authors have recently demonstrated that increased gene expression of glucose-6-phosphatase (Glu-6-Pase) in hemorrhagic hypotension (HH) and following lactated Ringer's resuscitation (LR) is associated with a decrease in insulin and an increase in corticosterone concentrations. OBJECTIVE To

Glucose-6-phosphatase gene expression and activity are modulated in hemorrhagic shock: evidence for a new heat-sensitive activator.

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Decreased hepatic fructose 2,6-bisphosphate levels were observed in the early phase of hemorrhagic shock. The lower sugar bisphosphatae level was a result of increased phosphoenolpyruvate levels and decreased glucose-6-phosphate and fructose-6-phosphate levels. The decreased glucose-6-phosphate

Acid phosphatase activity of cerebrospinal fluid cells in leptomeningeal haemorrhage.

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One hundred and twenty samples of haemorrhagic spinal fluid were examined by acid phosphatase staining. This enzyme activity starts to appear in mono-histiocytic cells 2 days after bleeding and increases up to the 5th day. After 1 week the activity decreases rapidly. Similar results are found in

Alterations in hepatic 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase and glucose-6-phosphatase gene expression after hemorrhagic hypotension and resuscitation.

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The mRNA abundance of several hepatic glycolytic and gluconeogenic enzymes and blood hormone concentrations were determined in hemorrhagic hypotension-induced rats before and after resuscitation with lactated Ringer's. Northern blot analysis of total liver RNA after 30 min of hemorrhage showed

MiR-21-5p/dual-specificity phosphatase 8 signalling mediates the anti-inflammatory effect of haem oxygenase-1 in aged intracerebral haemorrhage rats.

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Intracerebral haemorrhage (ICH) is a severe neurological disorder caused by bleeding within the brain tissue. Inflammation has been implicated in ICH pathogenesis and is a potential therapeutic target for ICH. Haemin, an activator of haem oxygenase-1 (HO-1), rapidly increases HO-1 protein expression

Neuroprotective Effect of Protein Phosphatase 2A/Tristetraprolin Following Subarachnoid Hemorrhage in Rats.

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Early brain injury (EBI) following subarachnoid hemorrhage (SAH) can lead to inflammation and neuronal dysfunction. There is a need for effective strategies to mitigate these effects and improve the outcome of patients who experience SAH. The mRNA-destabilizing protein tristetraprolin (TTP) is an

Serum Alkaline Phosphatase Level is Associated with Angiographic Vasospasm, Delayed Cerebral Ischemia-Caused Clinical Deterioration, and Functional Outcome After Aneurysmal Subarachnoid Hemorrhage.

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Alkaline phosphatase (ALP) has been implicated to be associated with poor outcome in ischemic stroke patients, yet its role in aneurysmal subarachnoid hemorrhage (aSAH) patients is unknown. The current study aimed to investigate the on-admission and short-term variation trend of ALP

Alkaline phosphatase histochemical staining in the study of germinal matrix hemorrhage and brain vascular morphology in a very-low-birth-weight neonate.

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We evaluated the utility of alkaline phosphatase (AP) histochemical staining for studying intraparenchymal vascular morphology in the brain of a 31-wk-gestation (1480 g) neonate who died of respiratory insufficiency after 23 h. In this baby, afferent cerebral vessels (arteries, arterioles, and

Increased Serum Alkaline Phosphatase as a Predictor of Symptomatic Hemorrhagic Transformation in Ischemic Stroke Patients with Atrial Fibrillation and/or Rheumatic Heart Disease.

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OBJECTIVE Elevated alkaline phosphatase (ALP) is considered as a marker of liver function in clinical practice. Furthermore, it has been identified that liver function can contribute to hemorrhagic transformation (HT). However, whether ALP levels play a role in HT after stroke remains an open

Tyrosine phosphatase inhibition induces loss of blood-brain barrier integrity by matrix metalloproteinase-dependent and -independent pathways.

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Tight junctions between endothelial cells of brain capillaries form the structural basis of the blood-brain barrier (BBB), which controls the exchange of molecules between blood and CNS. Regulation of cellular barrier permeability is a vital and complex process involving intracellular signalling and

[Definitive survival after experimental irreversible hemorrhagic shock. Roles of metabolic correction and oral treatment by neomycin. Development of acid phosphatases].

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