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Article in Chinese | WPRIM | ID: wpr-929851


Objective:To investigate the correlation between white matter hyperintensities (WMHs) and the outcomes after reperfusion therapy in patients with acute ischemic stroke (AIS).Methods:Patients with AIS treated with reperfusion therapy (intravenous thrombolysis, endovascular mechanical thrombectomy or bridging therapy) in the Stroke Center of Zhongshan Hospital of traditional Chinese Medicine from January 2014 to December 2019 were retrospectively enrolled. The clinical baseline data of the patients were collected. The Fazekas scale was used to evaluate the severity of WMHs according to the MRI images. At 90 d after discharge, the modified Rankin Scale was used to evaluate the outcomes. A score of ≤ 2 was defined as good outcome, and a score of >2 was defined as poor outcome. Binary multivariate logistic regression analysis was used to determine the independent risk factors for hemorrhagic transformation (HT), symptomatic intracranial hemorrhage (sICH), and poor outcomes. Results:A total of 676 patients with AIS treated with reperfusion therapy were enrolled. Among them, 506 patients (74.9%) were complicated with WMHs, and 80 (11.8%) had severe WMHs. One hundred and thirty-two patients (19.5%) had HT, 34 (5.0%) had sICH, and 306 (45.3%) had a poor outcome. Multivariate logistic regression analysis showed that severe WMHs was an independent risk factor for the occurrence of HT (odds ratio [ OR] 1.890, 95% confidence interval [ CI] 1.047-3.413; P=0.035) and poor outcomes ( OR 3.366, 95% CI 1.567-7.232; P=0.002) after reperfusion treatment in patients with AIS, but there was no independent correlation with sICH ( OR 8.403, 95% CI 0.891-79.294; P=0.063). Conclusion:Severe WMHs is an independent risk factor for the occurrence of HT and poor outcomes in patients with AIS after reperfusion treatment, but it has no independent correlation with sICH.

Article in Chinese | WPRIM | ID: wpr-863133


Reperfusion therapy has become a standard treatment for acute ischemic stroke, which can effectively improve the outcomes of patients and reduce the mortality. Some studies have found that reperfusion therapy may increase the incidence of post-stroke seizures and post-stroke epilepsy, but this view is still controversial. This article reviews the recent studies on reperfusion therapy and post-stroke seizures and post-stroke epilepsy.

Article in Chinese | WPRIM | ID: wpr-498803


It analyzed the definition, mechanism, characteristics of Mirror Visual Feedback and summarized the application of mirror visual feedback in recovering upper limb function after stroke patients at home and abroad, so as to provide evidences for the further research in China.

Article in English | WPRIM | ID: wpr-121104


In order to ensure normal body function, the human body is dependent on a tight control of its blood glucose levels. This is accomplished by a highly sophisticated network of various hormones and neuropeptides released mainly from the brain, pancreas, liver, intestine as well as adipose and muscle tissue. Within this network, the pancreas represents a key player by secreting the blood sugar-lowering hormone insulin and its opponent glucagon. However, disturbances in the interplay of the hormones and peptides involved may lead to metabolic disorders such as type 2 diabetes mellitus (T2DM) whose prevalence, comorbidities and medical costs take on a dramatic scale. Therefore, it is of utmost importance to uncover and understand the mechanisms underlying the various interactions to improve existing anti-diabetic therapies and drugs on the one hand and to develop new therapeutic approaches on the other. This review summarizes the interplay of the pancreas with various other organs and tissues that maintain glucose homeostasis. Furthermore, anti-diabetic drugs and their impact on signaling pathways underlying the network will be discussed.

Blood Glucose , Brain , Comorbidity , Diabetes Mellitus, Type 2 , Glucagon , Glucose , Hand , Homeostasis , Human Body , Insulin , Intestines , Liver , Neuropeptides , Pancreas , Peptides , Prevalence
Article in Chinese | WPRIM | ID: wpr-406537


AIM To elucidate the effect of rhynchophylline(Rhy) on carotid sinus baroreceptor activity (CBA). METHODS By recording sinus nerve afferent discharge activity with isolated carotid sinus perfusion, parameters of CBA, such as peak slope (PS), peak integral value (PIV), threshold pressure (TP) and saturation pressure (SP) were examined. ①Rhy 10, 50, and 100 μmol·L-1, dissolved in K-H solution, was perfused into isolated carotid sinus, then the effects of Rhy on parameters of CBA were observed while intrasinus pressure was altered in a stepwise manner. ②NG-nitro-L-arginine methyl ester (L-NAME) 10 mmol·L-1, tetraethylammonium (TEA) 1 mmol·L-1 and Bay K8644 500 nmol·L-1 were perfused into isolated carotid sinus, and effects of them on the response of carotid baroreceptor to Rhy were observed. RESULTS ① By perfusing the isolated carotid sinus with Rhy 10 μmol·L-1, PS decreased from (19.2±0.3)% to (18.2±0.1)%·kPa-1and the PIV decreased from (219.3±3.3)% to (199.1±3.8)%, while TP and SP increased from (8.2±0.3) to (9.1±0.1)kPa and (21.5±0.1) to (22.1±0.1)kPa, respectively. By perfusing with Rhy 50 and 100 μmol·L-1, the changes in PS, TP and SP were in concentration-dependent manner, and this indicated inhibitory effect of Rhy on CBA. ②Pretreatment with L-NAME 100 μmol·L-1 did not affect inhibitory action of Rhy 50 μmol·L-1 on CBA. ③Pretreatment with TEA 1 mmol·L-1 had no effect on inhibitory effect of Rhy 50 μmol·L-1 on CBA. ④Pretreatment with Bay K8644 500 nmol·L-1 could mostly attenuate effect of Rhy 50 μmol·L-1 on CBA. CONCLUSION Rhy inhibits CBA via blocking calcium influx in baroreceptor nerve ending.

Article in Chinese | WPRIM | ID: wpr-410034


AIM To study if cholecystokinin octapeptide (CCK-8) alter cardiovascular functions by its direct inhibitory effect on carotid sinus baroreceptor (CSB) activity. METHODS The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus. RESULTS ① CCK-8 0.1, 0.5 and 1.0 μmol·L-1 shifted FCCB to the right and downward, with a marked decrease in peak slope and peak integral value of carotid sinus nerve discharge in a concentration-dependent manner, indicating the inhibitory effect of CCK-8 on CSB activity. ② Pretreatment with proglumide (100 μmol·L-1), a nonselective CCK receptor antagonist, or Bay K8644 (0.5 μmol·L-1), an agonist of calcium channel, partially attenuated the inhibitory effect of CCK-8 (0.5 μmol·L-1) on CSB activity. Pretreatment with L-NAME (100 μmol·L-1), an inhibitor of NO synthase, did not affect the inhibitory action of CCK-8. CONCLUSION CCK-8 inhibits CSB activity, which may be mediated by activating CCK receptors in the carotid sinus area and thereby resulting in an inhibition of stretch-sensitive channels and decrease in Ca2+ influx.