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inositol/pendarahan
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Defective signal transduction through the thromboxane A2 receptor in a patient with a mild bleeding disorder: deficiency of the inositol 1,4,5-triphosphate formation despite normal G-protein activation.
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We describe an 11-year-old girl with a mild bleeding disorder since early childhood. The disorder was characterized by a prolonged bleeding time, and the patient's platelets showed defective aggregation responses to thromboxane A2 (TXA2) mimetic U46619 and arachidonic acid. In contrast, the
Subarachnoid hemorrhage induces Na+/myo-inositol cotransporter in the rat brain.
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Neurons and glial cells respond to extracellular hyperosmolarity by accumulating small organic solutes, called "osmolytes." Na+/myo-inositol is one of the major organic osmolytes in the brain and Na+/myo-inositol cotransporter (SMIT) regulates extracellular Na+/myo-inositol content. Subarachnoid
Effect of inositol, lecithin, vitamins (B12 with choline and E), and iodinated casein on induced fatty liver-hemorrhagic syndrome in laying chickens.
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Egg production, liver lipid, and liver hemorrhagic score were not significantly altered by diets that contained inositol (at 1 or 2 g./kg. diet) and fed ad libitum, or force-fed to S.C. White Leghorn hens to produce fatty liver-hemorrhagic syndrome (FLHS). FLHS was not prevented by lecithin,
Intracerebral hemorrhage upregulates Na(+)/myo-inositol cotransporter in the rat brain.
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We examined the expression of Na(+)/myo-inositol cotransporter (SMIT) in the rat brain after intrastriatal hemorrhage. The expression of SMIT messenger RNA (mRNA) increased around hematoma 3 days after hemorrhage and it returned to control level as hematoma was absorbed. The expression of SMIT mRNA
MicroRNA-23b alleviates neuroinflammation and brain injury in intracerebral hemorrhage by targeting inositol polyphosphate multikinase.
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Neuroinflammation plays a critical role in the pathogenesis of intracerebral hemorrhage (ICH), contributing to detrimental brain injury and neurological function deficits. MicroRNA-23b (miR-23b) exerts anti-inflammatory effects in many diseases and is downregulated in patients with ICH. This study
Severe Trauma and Hemorrhage Leads to Platelet Dysfunction and Changes in Cyclic Nucleotides In The Rat.
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Pathogenetic analysis of three cases with a bleeding disorder characterized by defective platelet aggregation induced by Ca2+ ionophores.
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We report three cases of platelet dysfunction characterized by defective Ca2+ ionophore-induced platelet aggregation without impaired production of thromboxane A2 (TXA2). The patients had mild to moderate bleeding tendencies, and their platelet aggregation and secretion induced by ADP, collagen,
Defective signal transduction induced by thromboxane A2 in a patient with a mild bleeding disorder: impaired phospholipase C activation despite normal phospholipase A2 activation.
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A patient with a mild bleeding disorder whose platelets responded defectively to thromboxane A2 (TXA2) was identified, and the mechanism of this dysfunction was analyzed. The platelets were defective in shape change, aggregation, and release reaction in response to synthetic TXA2 mimetic (STA2).
A haemorrhagic platelet disorder associated with altered stimulus-response coupling and abnormal membrane phospholipid composition.
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Haemorrhagic diatheses due to platelet function defects are a heterogenous and poorly understood group of conditions. We report the investigation of a female with a lifelong history of epistaxes, haemarthroses, menorrhagia and persistent iron-deficiency anaemia. Although platelet numbers and
Sevoflurane postconditioning improves the spatial learning and memory impairments induced by hemorrhagic shock and resuscitation through suppressing IRE1α-caspase-12-mediated endoplasmic reticulum stress pathway.
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Severe hemorrhagic shock induces cognitive dysfunction by promoting cell death mediated by activating endoplasmic reticulum (ER) stress. Sevoflurane postconditioning prevents neuronal apoptosis against cerebral ischemia/reperfusion injury. It is unknown if this protective effect on hemorrhagic shock
Cytosolic free calcium elevation in vascular smooth muscle cells induced by cerebrospinal fluid from patients with subarachnoid hemorrhage--biochemical nature of the calcium-mobilizing factor.
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The present study was undertaken to characterize the biochemical nature of the factor in cerebrospinal fluid (CSF) from patients with subarachnoid hemorrhage (SAH) that induces a transient elevation of cytosolic free calcium in cultured vascular smooth muscle cells. Cell-free CSF collected from
Blood Metabolomic Predictors of 1-Year Outcome in Subarachnoid Hemorrhage.
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BACKGROUND
Delayed neurological deficit (DND) is the most important cause of morbidity and mortality in patients with subarachnoid hemorrhage (SAH) whose aneurysms have been secured. However, the methods currently used to predict the development of DND, such as trans-cranial Doppler or levels
The mechanisms of energy crisis in human astrocytes after subarachnoid hemorrhage.
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BACKGROUND
Calcium (Ca2+) is a cofactor of multiple cellular processes. The mechanisms that lead to elevated cytosolic Ca2+ concentration are unclear.
OBJECTIVE
To illuminate how bloody cerebrospinal fluid (bCSF) from patients with intraventricular hemorrhage causes cell death of cultured human
Correlation Between Altered DNA Methylation of Intergenic Regions of ITPR3 and Development of Delayed Cerebral Ischemia in Patients with Subarachnoid Hemorrhage.
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Gene expression profiles of patients with cerebral hematoma following spontaneous intracerebral hemorrhage.
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The present study aimed to investigate the gene functions and expression profiles in perihematomal (PH) brain regions following spontaneous intracerebral hemorrhage. The gene expression profiles were downloaded from the Gene Expression Omnibus database under accession number GSE24265, which includes
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