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diacylglycerol/крварење
Врската е зачувана во таблата со исечоци
Страница 1 од 44 резултати
Protein kinase C has two different major roles in lattice compaction enhanced by cerebrospinal fluid from patients with subarachnoid hemorrhage.
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OBJECTIVE
Compaction of extracellular matrix (ECM) lattices by cultured fibroblasts was accelerated by cerebrospinal fluid (CSF) from patients with subarachnoid hemorrhage (SAH). The rate of acceleration was significantly related to the clinical grade of vasospasm. However, the mechanism remains
Mannheimia ovis sp. nov., Isolated from Dead Sheep with Hemorrhagic Pneumonia
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Two Gram-stain-negative, facultatively anaerobic bacteria, designated ZY170218T and ZY180512, were isolated from lungs of dead sheep with hemorrhagic pneumonia in Yunnan Province, China and their taxonomic positions were studied by a polyphasic approach. The two isolates grew optimally at
Human CalDAG-GEFI deficiency increases bleeding and delays αIIbβ3 activation.
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Affinity regulation of integrin αIIbβ3 for fibrinogen by inside-out signaling plays a critical role in hemostasis. Calcium and diacylglycerol (DAG)-regulated guanine nucleotide exchange factor I (CalDAG-GEFI) was identified as a Rap1-activating molecule, and its role in inside-out αIIbβ3 activation
Acute ischaemic and delayed ischaemic neurological deficits as the causes of bad grading in aneurysmal subarachnoid haemorrhage.
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When subarachnoid haemorrhage (SAH) occurs, intracranial pressure (ICP) rises which heralds a series of symptoms termed acute ischaemic neurological deficits (AINDs). At the same time, free radicals are generated, and because of deficient scavenging mechanisms in the cerebrospinal fluid (CSF), these
A Diacylglycerol Kinase Inhibitor, R-59-022, Blocks Filovirus Internalization in Host Cells.
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Filoviruses, such as Ebola virus (EBOV) and Marburg virus, are causative agents of unpredictable outbreaks of severe hemorrhagic fevers in humans and non-human primates. For infection, filoviral particles need to be internalized and delivered to intracellular vesicles containing cathepsin proteases
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
Antioxidant therapy against cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
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1. Approximately one-third of the morbidity and mortality due to aneurysmal subarachnoid hemorrhage (SAH) is caused by delayed ischemic neurological deficit (DIND) due to cerebral vasospasm. 2. Compared to prolonged arterial constriction in other parts of the body, cerebral vasospasm is
Diacylglycerol kinase ζ is a negative regulator of GPVI-mediated platelet activation.
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Diacylglycerol kinases (DGKs) are a family of enzymes that convert diacylglycerol (DAG) into phosphatidic acid (PA). The ζ isoform of DGK (DGKζ) has been reported to inhibit T-cell responsiveness by downregulating intracellular levels of DAG. However, its role in platelet function remains undefined.
Protein kinase C and diacylglycerol content in basilar arteries during experimental cerebral vasospasm in the dog.
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Sixteen dogs were entered into a study of the double subarachnoid hemorrhage (SAH) model of cerebral vasospasm. Six animals were sacrificed 72 hours after the first experimental SAH, and the remaining 10 animals were killed 72 hours after the second experimental SAH; ten additional animals served as
Calcium-diacylglycerol guanine nucleotide exchange factor I gene mutations associated with loss of function in canine platelets.
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Calcium-Diacylglycerol Guanine Nucleotide Exchange Factor I (CalDAG-GEFI) has been implicated in platelet aggregation signaling in CalDAG-GEFI knockouts. Functional mutations were identified in the gene encoding for CalDAG-GEFI in 3 dog breeds. Affected dogs experienced epistaxis, gingival bleeding,
Expanded repertoire of RASGRP2 variants responsible for platelet dysfunction and severe bleeding.
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Heritable platelet function disorders (PFDs) are genetically heterogeneous and poorly characterized. Pathogenic variants in RASGRP2, which encodes calcium and diacylglycerol-regulated guanine exchange factor I (CalDAG-GEFI), have been reported previously in 3 pedigrees with bleeding and reduced
Evidence for a role for Galphai1 in mediating weak agonist-induced platelet aggregation in human platelets: reduced Galphai1 expression and defective Gi signaling in the platelets of a patient with a chronic bleeding disorder.
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We have examined platelet functional responses and characterized a novel signaling defect in the platelets of a patient suffering from a chronic bleeding disorder. Platelet aggregation responses stimulated by weak agonists such as adenosine diphosphate (ADP) and adrenaline were severely impaired. In
Possible mechanism to induce protein kinase C-dependent arterial smooth muscle contraction after subarachnoid haemorrhage.
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A possible mechanism for the induction of protein kinase C (PKC)-dependent vascular contraction independent to the increase of intracellular Ca++ was investigated in the pathogenesis of cerebral vasospasm in the double subarachnoid haemorrhage (SAH) model. The level of 1,2-diacylglycerol (DAG),
Mechanism of inhibition of Shiga-toxigenic Escherichia coli SubAB cytotoxicity by steroids and diacylglycerol analogues.
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Shiga toxigenic Escherichia coli (STEC) are responsible for a worldwide foodborne disease, which is characterized by severe bloody diarrhea and hemolytic uremic syndrome (HUS). Subtilase cytotoxin (SubAB) is a novel AB5 toxin, which is produced by Locus for Enterocyte Effacement (LEE)-negative STEC.
Inflammation induces hemorrhage in thrombocytopenia.
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The role of platelets in hemostasis is to produce a plug to arrest bleeding. During thrombocytopenia, spontaneous bleeding is seen in some patients but not in others; the reason for this is unknown. Here, we subjected thrombocytopenic mice to models of dermatitis, stroke, and lung inflammation. The
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