Neurological research
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Neurological research · Nov 2011
THR-18, a 18-mer peptide derived from PAI-1, is neuroprotective and improves thrombolysis by tPA in rat stroke models.
The thrombolytic treatment of stroke is limited by a narrow therapeutic time window and is associated with significant adverse side effects. To improve this situation, the modulation of tissue-type plasminogen activator (tPA) activity by a synthetic plasminogen activator inhibitor-1-derived 18-mer peptide (THR-18) was examined in two models of stroke in rats. ⋯ The results support the use of THR-18 together with tPA in the thrombolytic therapy of stroke, in order to achieve better patency, less tPA-induced damage, and possibly a widening of tPA therapeutic time window.
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Neurological research · Oct 2011
Complications and adverse events associated with Neuroform stent-assisted coiling of wide-neck intracranial aneurysms.
Successful experiences of the Neuroform stent-assisted coiling have been reported by many teams in endovascular neurosurgery centers throughout the world. However, most of the reported complications involved a limited number of patients. ⋯ Neuroform sent-assisted coiling of intracranial aneurysm is a safe technique with relatively low recanalization rate. The main cause of morbidity and mortality is thromboembolism. Long-term effect on parent artery should be observed carefully.
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Neurological research · Oct 2011
Comparative StudyAugmentation of endoplasmic reticulum stress in cerebral ischemia/reperfusion injury associated with comorbid type 2 diabetes.
Diabetes is one of the major risk factors for ischemic stroke and is reported to aggravate the ischemic brain damage in different experimental models as well as clinical situations. However, the mechanisms underlying the exacerbated ischemia/reperfusion (I/R) brain injury associated with comorbid diabetes are still not clear. This study investigated the role of endoplasmic reticulum (ER) stress in pathophysiology of aggravated I/R brain injury associated with diabetes. ⋯ Taken together, the current experimental findings demonstrate that diabetes exacerbates brain I/R injury which may be mediated through enhanced ER stress and cell death involving CHOP/GADD153 and caspase-12 activation.
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Neurological research · Oct 2011
Cerebral metabolism after early decompression craniotomy following controlled cortical impact injury in rats.
After traumatic brain injury, a cascade of metabolic changes promotes the development of secondary brain damage. In this study, we examined metabolic changes in rats in the acute stage after trauma. Furthermore, we investigated the effect of a very early decompression craniotomy on intracranial pressure (ICP) and on metabolic parameters. ⋯ In our model, thus we could detect a very early deterioration of glucose utilization and energy supply after trauma that recovered, due to the moderate intensity of the trauma, within 60 minutes without leading to ischemia in the peri-contusional region. Following decompression craniotomy, the increase of intracranial pressure could be reduced significantly. Any significant beneficial effects on metabolic changes, however, could not be proven in this very early stage after moderate CCII.
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Neurological research · Sep 2011
tPA contributes to impaired NMDA cerebrovasodilation after traumatic brain injury through activation of JNK MAPK.
N-methyl-D-aspartate (NMDA)-induced pial artery dilation (PAD) is reversed to vasoconstriction after fluid percussion brain injury (FPI). Tissue type plasminogen activator (tPA) is up-regulated and the tPA antagonist, EEIIMD, prevents impaired NMDA PAD after FPI. Mitogen-activated protein kinase (MAPK), a family of at least three kinases, ERK, p38, and JNK, is also up-regulated after traumatic brain injury (TBI). We hypothesize that tPA impairs NMDA-induced cerebrovasodilation after FPI in a MAPK isoform-dependent mechanism. ⋯ These data indicate that tPA contributes to impairment of NMDA-mediated cerebrovasodilation after FPI through JNK, while p38 may be protective. These data suggest that inhibition of the endogenous plasminogen activator system and JNK may improve cerebral hemodynamic outcome post-TBI.