Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We experienced a case with sudden unexpected death caused by rupture of an intracranial aneurysm, which was confirmed by autopsy. Depending on this case, we reported the significance of the cerebellar tonsillar herniation on the cause of sudden death of ruptured cerebral aneurysm. A 58-year-old man was admitted to us for treatment of subarachnoid hemorrhage (SAH). The CT scanning showed diffuse SAH in the whole cistern. Cerebral angiography on admission revealed an aneurysm at the bifurcation of the left middle cerebral artery in association with bleb like configuration. The aneurysmal neck was clipped on the day of admission. The postoperative course was uneventful. In the early morning of postoperative 23rd day, he was found being expired. To clarify the cause of death, an autopsy was done, disclosing diffuse SAH in association with tonsillar herniation more marked on the left. Thus, the distortion of the spinomedullary junction due to asymmetrical herniation was considered to be responsible for unexpected sudden death in this case. Examination of the major cerebral artery disclosed a ruptured anterior communicating artery aneurysm.
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PMID:[The significance of the cerebellar tonsillar herniation on the cause of sudden death of ruptured cerebral aneurysm]. 962 66

Reports of Ask-Upmark kidney, initially described as a congenital defect in renal development, are uncommon. We report a case with the features of bilateral asymmetrical segmental atrophy in a patient with childhood-onset hypertension. As an adult, she developed cerebral, celiac, and renal artery aneurysms. She underwent successful clipping of the cerebral aneurysm and renal artery repair with preservation of renal function. Novel radiologic techniques make possible the noninvasive diagnosis of segmental atrophy and its complications.
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PMID:Ask-Upmark kidney associated with renal and extrarenal arterial aneurysms. 1019 35

Many uncertain and inconsistent etiologies of cerebral aneurysmal rupture including a wide spectrum of factors have been reported. Our recent observation discloses the potential new factor of cerebral aneurysm rupture with cerebral venous pressure gradient. We retrospectively reviewed 52 cases treated with coil embolization with or without cerebral aneurysmal rupture. Seventeen males and 30 females were recruited in this study. Quantitative color-coded cerebral angiography was performed during coil therapeutic procedures to measure cerebral venous circulation. Ruptured cases had shorter and symmetrical cerebral venous circulation time (P <0.05). In addition, an asymmetrical venous outflow pattern was critical for aneurysmal rupture. Non-ruptured cases tended to have slower and asymmetrical cerebral venous circulation compared with rupture cases. Symmetrical and shorter cerebral venous circulation in the dysplasia venous outlet may be a potential new factor for cerebral aneurysm rupture.
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PMID:Intracranial venous hemodynamics and rupture of cerebral aneurysm. 2548 94

Physiologically, neurovascular coupling (NVC) matches focal increases in neuronal activity with local arteriolar dilation. Astrocytes participate in NVC by sensing increased neurotransmission and releasing vasoactive agents (e.g., K(+)) from perivascular endfeet surrounding parenchymal arterioles. Previously, we demonstrated an increase in the amplitude of spontaneous Ca(2+) events in astrocyte endfeet and inversion of NVC from vasodilation to vasoconstriction in brain slices obtained from subarachnoid hemorrhage (SAH) model rats. However, the role of spontaneous astrocyte Ca(2+) signaling in determining the polarity of the NVC response remains unclear. Here, we used two-photon imaging of Fluo-4-loaded rat brain slices to determine whether altered endfoot Ca(2+) signaling underlies SAH-induced inversion of NVC. We report a time-dependent emergence of endfoot high-amplitude Ca(2+) signals (eHACSs) after SAH that were not observed in endfeet from unoperated animals. Furthermore, the percentage of endfeet with eHACSs varied with time and paralleled the development of inversion of NVC. Endfeet with eHACSs were present only around arterioles exhibiting inversion of NVC. Importantly, depletion of intracellular Ca(2+) stores using cyclopiazonic acid abolished SAH-induced eHACSs and restored arteriolar dilation in SAH brain slices to two mediators of NVC (a rise in endfoot Ca(2+) and elevation of extracellular K(+)). These data indicate a causal link between SAH-induced eHACSs and inversion of NVC. Ultrastructural examination using transmission electron microscopy indicated that a similar proportion of endfeet exhibiting eHACSs also exhibited asymmetrical enlargement. Our results demonstrate that subarachnoid blood causes a delayed increase in the amplitude of spontaneous intracellular Ca(2+) release events leading to inversion of NVC. Significance statement: Aneurysmal subarachnoid hemorrhage (SAH)--strokes involving cerebral aneurysm rupture and release of blood onto the brain surface--are associated with high rates of morbidity and mortality. A common complication observed after SAH is the development of delayed cerebral ischemia at sites often remote from the site of rupture. Here, we provide evidence that SAH-induced changes in astrocyte Ca(2+) signaling lead to a switch in the polarity of the neurovascular coupling response from vasodilation to vasoconstriction. Thus, after SAH, signaling events that normally lead to vasodilation and enhanced delivery of blood to active brain regions cause vasoconstriction that would limit cerebral blood flow. These findings identify astrocytes as a key player in SAH-induced decreased cortical blood flow.
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PMID:Astrocyte Ca2+ Signaling Drives Inversion of Neurovascular Coupling after Subarachnoid Hemorrhage. 2642 85