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Acute cerebral infarction is a common type of ischemic stroke, causing brain dysfunction in patients with high morbidity and disability. With the changes in people's diet, lifestyle patterns and population aging, the incidence of acute cerebral infarction has increased year by year, which has become an important cause of disability and death in middle-aged and elderly patients. Therefore, it is of great significance to society and individuals to carry out in-depth research on new ideas for the treatment of cerebral infarction and to reduce the disability and mortality of patients.Acute cerebral infarction leads to damage of the corticospinal tract, which can cause severe limb paralysis, seriously affecting the patients' prognosis and daily activities, and imposing a heavy burden on the patients' family and society.According to current research, TK plays a neuroprotective role in ischemic and hypoxic brain cells, and promotes the survival of nerve cells and improves the prognosis of patients with clinical ischemic stroke. Kallikrein is a human urokininogenase, which has been proven to be effective in acute ischemic stroke. Kallikrein can selectively dilate the arterioles in the ischemic area through the kallikrein-kinin system (KKS), reduce the infarct size, increase the density of blood vessels around the infarct, improve collateral circulation, and significantly improve the symptoms of neurological deficits in patients. However, to date, there is no direct evidence that Kallikrein can mediate neuroprotection and regeneration under conditions of ischemic injury.
In this study, the investigators used primary cortical neuronal cells of CD-1 mice treated with ischemia and hypoxia, C57 black mice with MCAO, and patients with clinical acute ischemic stroke to try to prove the effect of Kallikrein's direct evidence on neuroprotection and regeneration of acute ischemic injury.
The investigators collected 80 patients with acute cerebral infarction from July 2007 to March 2019 in the Department of Neurology, Second Hospital of Hebei Medical University. They were randomly divided into Kallikrein+standard treatment group and standard treatment group. And both groups were treated for 14 ± 5 days. Blood samples were collected from patients within 3 days of onset and after 14±5 days of treatment. Serum nerve growth markers NEFH, MBP, and VEGF were detected by ELISA, and two diffusion tensor imaging (DTI) scans were performed. Growth markers and imaging indicators FA and ADC values were used to evaluate the effect of Kallikrein on motor function recovery in clinical patients.
Second hospital of hebei medical university
The Second Hospital of Hebei Medical University
Published on BioPortfolio: 2019-09-30T07:06:55-0400
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Activated form of factor XII. In the initial event in the intrinsic pathway of blood coagulation, kallikrein (with cofactor HIGH MOLECULAR WEIGHT KININOGEN) cleaves factor XII to XIIa. Factor XIIa is then further cleaved by kallikrein, plasmin, and trypsin to yield smaller factor XII fragments (Hageman-Factor fragments). These fragments increase the activity of prekallikrein to kallikrein but decrease the procoagulant activity of factor XII.
Restoration of functions to the maximum degree possible in a person or persons suffering from a stroke.
Sudden death from overwork, most often as a result of acute CARDIOVASCULAR STROKE.
Proteolytic enzymes from the serine endopeptidase family found in normal blood and urine. Specifically, Kallikreins are potent vasodilators and hypotensives and increase vascular permeability and affect smooth muscle. They act as infertility agents in men. Three forms are recognized, PLASMA KALLIKREIN (EC 220.127.116.11), TISSUE KALLIKREIN (EC 18.104.22.168), and PROSTATE-SPECIFIC ANTIGEN (EC 22.214.171.124).
Stroke caused by lacunar infarction or other small vessel diseases of the brain. It features hemiparesis (see PARESIS), hemisensory, or hemisensory motor loss.
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