Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiologic and neurologic examinations, ultrasonic dopplerography were performed in 89 patients after operation of carotid endarterectomy. Period of observation was 6-182 months after operation (61 months on the average). Positive clinical effect (absence of disorders of cerebral circulation-DCC) was achieved in 91% of cases. The frequency of both repeated transitory ischemic attacks and the strokes was 9%, the best frequency being in patients with initially asymptomatic course. It was found that the degree of restenosis directly correlated with frequency of neurologic symptom development: there were no repeated DCC in normal state of the operated artery. Meanwhile DCC frequency was less than 4% in cases with the degree of restenosis less than 60% and was equal to 15.8% in more than 60% restenosis. DCC were more frequently found in occlusion of internal carotid artery. Rather favourable course of restenosis of carotid artery was also conditioned by low content of the plaques dangerous in terms of embolism. Progression of atherosclerotic damages in other parts of extracranial arteries promoted clinical manifestation of cerebral ischemia. Moreover, negative neurologic dynamics developed in 7% of the patients with restenosis less than 60%, and in 13.8% of cases with restenosis more than 60%. The conclusion was made about efficiency of carotid endarterectomy in patients with atherosclerotic damages of carotid arteries. For prevention of repeated DCC it is recommended both to perform conservative therapy after the operation and to examine dynamically the patients using ultrasonic dopplerography beginning 6 months after the operation.
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PMID:[Clinical course of restenosis after carotid endarterectomy]. 950 97

Changes in expression of neurorepair and neuroregenerative factors were examined after transient cerebral ischemia in relation to the effects of tissue plasminogen activator (tPA) and the free radical scavenger edaravone. Physiological saline or edaravone was injected twice during 90 min of transient middle cerebral artery occlusion (tMCAO) in rats, followed by the same saline or tPA at reperfusion. Sizes of the infarct and protein factors relating to neurorepair and neuroregeneration were examined at 4d after tMCAO. The protein factors examined were: a chondroitin sulfate proteoglycan neurocan, semaphorin type 3A (Sema3A), a myelin-associated glycoprotein receptor (Nogo receptor, Nogo-R), a synaptic regenerative factor (growth associated protein-43, GAP43), and a chemotropic factor netrin receptor (deleted in colorectal cancer, DCC). Two groups treated by edaravone only or edaravone plus tPA showed a reduction in infarct volume compared to the two groups treated by vehicle only or vehicle plus tPA. Immunohistochemistry and western blot analyses indicated that protein expression of neurocan, Sema3A, Nogo-R, GAP43, and DCC was decreased with tPA, but recovered with edaravone. Additive edaravone prevented the reductions of these five proteins induced by tPA. The present study demonstrates for the first time that exogenous tPA reduced protein factors involved in inhibiting and promoting axonal growth, but that edaravone ameliorated such damage in brain repair after acute ischemia.
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PMID:Modifying neurorepair and neuroregenerative factors with tPA and edaravone after transient middle cerebral artery occlusion in rat brain. 2222 36

As a secreted axon guidance molecule, Netrin-1 has been documented to be a neuroprotective factor, which can reduce infarct volume, promote angiogenesis and anti-apoptosis after stroke in rodents. However, its role in axonal regeneration and synaptic formation after cerebral ischemic injury, and the related underlying mechanisms remain blurred. In this study, we used Adeno-associated vectors carrying Netrin-1 gene (AAV-NT-1) to up-regulate the expression level of Netrin-1 in rats' brain after middle cerebral artery occlusion (MCAO). We found that the up-regulated level of Netrin-1 and its receptor DCC promoted axonal regeneration and synaptic formation; the overexpression of Netrin-1 activated the JNK1 signaling pathway; these effects were partially reduced when JNK1 signaling pathway was inhibited by SP600125 (JNK specific inhibitor). Taken together, these findings suggest that Netrin-1 can facilitate the synaptic formation and axonal regeneration via the JNK1 signaling pathway after cerebral ischemia, thus promoting the recovery of neural functions.
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PMID:Netrin-1 Promotes Synaptic Formation and Axonal Regeneration via JNK1/c-Jun Pathway after the Middle Cerebral Artery Occlusion. 2948 2