Ischemic stroke causes varying degrees of cognitive impairment, and its incidence is very high. Early diagnosis of cognitive impairment may provide the best intervention treatment opportunity, and slow disease progression. Therefore, it has attracted more and more attention. This article reviews the advances in etiology, pathogenesis, risk factors, diagnosis, prevention and treatment of cognitive impairment after ischemic stroke.

Objective To compare the clinical efficacies of transverse insertion of a thick needle into point Shendao(GV11) versus conventional acupuncture in treating facial neuritis of different durations.Method Two hundred and twenty patients meeting the inclusion criteria were randomly allocated to thick needle and tradition groups. The two groups separately received corresponding treatment in addition to oral administration of Western medicine. The therapeutic effects were evaluated using the House-Brackmann rating scale and the Portmann's Simple Scale (RPA) for facial symptoms and compared after two courses of treatment.Result The therapeutic effect was better, posttreatment H-B rating scale score was lower and posttreatment RPA score was higher in the thick needle group than in the tradition group; there were statistically significant differences (P<0.05). Different durations of disease affected the therapeutic effect. In the thick needle group, the therapeutic effect was better in the patients in the early stage than in the middle and late stages; there was a statistically significant difference (P<0.05). The cure rate was higher in the patients in the early and middle stages in the thick needle group than in the tradition group; there was a statistically significant difference (P<0.05). Conclusion Transverse insertion of a thick needle into point Shendao has a definite therapeutic effect on facial neuritis. It is safe, easily performed and of an advantage over conventional acupuncture.

The effects of ATP-sensitive mitochondrial K(+) channel (mitoK(ATP)) on mitochondrial membrane potential (Δψm), cell proliferation and protein kinase C alpha (PKCα) expression in airway smooth muscle cells (ASMCs) were investigated. Thirty-six Sprague-Dawley (SD) rats were immunized with saline (controls) or ovalbumin (OVA) with alum (asthma models). ASMCs were cultured from the lung of control and asthma rats. ASMCs were treated with diazoxide (the potent activator of mitoK(ATP)) or 5-hydroxydencanote (5-HD, the inhibitor of mitoK(ATP)). Rhodamine-123 (R-123) was used to detect Δψm. The expression of PKCα protein was examined by using Western blotting, while PKCα mRNA expression was detected by using real-time PCR. The proliferation of ASMCs was measured by MTT assay and cell cycle analysis. In diazoxide-treated normal ASMCs, the R-123 fluorescence intensity, protein and mRNA levels of PKCα, MTT A values and percentage of cells in S phase were markedly increased as compared with untreated controls. The ratio of G(0)/G(1) cells was decreased (P<0.05) in diazoxide-treated ASMCs from normal rats. However, there were no significant differences between the ASMCs from healthy rats treated with 5-HD and the normal control group. In untreated and diazoxide-treated ASMCs of asthmatic rats, the R-123 fluorescence intensity, protein and mRNA levels of PKCα, MTT A values and the percentage of cells in S phase were increased in comparison to the normal control group. Furthermore, in comparison to ASMCs from asthmatic rats, these values were considerably increased in asthmatic group treated with diazoxide (P<0.05). After exposure to 5-HD for 24 h, these values were decreased as compared with asthma control group (P<0.05). In ASMCs of asthma, the signal transduction pathway of PKCα may be involved in cell proliferation, which is induced by the opening of mitoK(ATP) and the depolarization of Δψm.

Literatures on arrhythmia induced by acute organophosphorous pesticide poisoning published in domestic journals from 1979 to 2010 were searched. Total 3468 cases of acute organophosphorous poisoning were collected and analyzed. The average abnormal ECC rate was (53 ±15)%(35. 4% -68. 4% ) in acute organophosphorous poisoning, the most common ECG abnormalities were ST-T segment changes (26. 5% ) and sinus tachycardia (16. 6% ). The rate and severity of ECG abnormalities were increased with the severity of organophosphorous poisoning(x2 = 33. 253,P < 0. 01). The most common causes of death in acute organophosphorous poisoning were ventricular tachycardia and ventricular fibrillation (26.2%).

Objective To investigate the mechanism of cigarette smoke promotes non-small cell lung cancer (NSCLC) NCI-H520 cell line proliferation mediated by macrophages with method of blocking NFκB-p65 pathway by RNAi.Methods To co-culture NCI-H520 cells with primary macrophages or U937 cell line,the Transwell Inserts system was used in cell co-culture model.NFκB activation was confirmed by electrophoretic mobility shift assay (EMSA) and Western blot analysis.U937 cells were transfected with NFκB-p65 shRNA plasmid to abrogate the NFκB activation,by BrdU ELISA,the effect of cigarette smoke extract (CSE) promoted NCI-H520 cells proliferation were assessed,inflammatory factors TNF and IL-6 expressions were analysed by ELISA.Results Exposure of CSE enhanced NFκB-p65 nuclcus translocation and activated the NFκB pathway.CSE did not promote NCI-H520 cells proliferation alone (P ＞ 0.05),but after 4 days coincubation with macrophages,the proliferation of NCI-H520 cells was significantly increased (P ＜0.01),addition of CSE to the co-culture much more enhanced this effect (P ＜ 0.01).After NFκB-p65 was blocked by RNAi,it significantly reduced NFκB-p65 protein expression and inhibited NFκB activation in U937 p65-cells,and markedly inhibited U937 cells induced proliferation of NCI-H520 cells and IL-6,TNF secretion (P ＜ 0.01).Conclusion Cigarette smoke promotes NCI-H520 cells proliferation mediated by macrophages.Blockade of NFκB pathway with RNAi in macrophages can reduced cigarette smoke induced inflammatory factors secretion in macrophages,and significantly inhibit cigarette smoke promoted tumor proliferation.

Objective To explore the genotype distribution of lipoprotein lipase gene polymorphism at Ser447Stop locus and its possible association with metabolic syndrome and dietary intakes. Method Ser447Stop polymorphism was determined by PCR-PFLP method in 222 adults with MS and 222 normal adults as control. Their physical examination,dietary investigation and levels of biochemical profile,including BG,TG,TC and HDL-C were analyzed. Results (1) The genotype frequencies of Ser447Stop SS,SX and XX were 85.6%,13.3% and 1.1% respectively,which were in agreement with Hardy-Weinberg equilibrium. There was no significant difference in frequencies of genotypes or allele between MS and the control,and between male and female. (2) After adjusting age and gender,the levels of serum TG were significantly different among three genotype groups,the highest in SS genotype and the lowest in XX genotype. (3) After adjusting age,gender and body mass index,the intakes of protein and carbohydrate were significantly different among three genotype groups. (4) There was significantly different in negative correlation between the intakes of protein and serum TG levels after adjusting age,gender and body mass index. Conclusion Lipoprotein lipase gene polymorphism influenced serum TG levels,while associated with protein intakes. It might contribute to the predisposition in metabolic syndrome response to dietary intervention.

Adult ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Cyclophosphamide ; therapeutic use ; Cystadenocarcinoma, Papillary ; pathology ; Dactinomycin ; therapeutic use ; Diagnosis, Differential ; Ependymoma ; drug therapy ; metabolism ; pathology ; surgery ; Female ; Follow-Up Studies ; Glial Fibrillary Acidic Protein ; metabolism ; Humans ; Hysterectomy ; Ovarian Neoplasms ; drug therapy ; metabolism ; pathology ; surgery ; Ovariectomy ; Teratoma ; pathology ; Vimentin ; metabolism ; Vincristine ; therapeutic use

Objective To study the effect of balloon dilatation therapy on dysphagia caused by cricopharyn- geal achalasia.Methods Ten cases of dysphagia were diagnosed as cricopharyngeal achalasia by videofluoroscopic swallowing study(VFSS).A 14~* urethral catheter was inserted into the esophagus and an amount of water was injec- ted into the balloon of the urethral catheter to make it turgid.Then the catheter was pulled upwards and passed through the stricture of esophagus to dilatate the cricopbarygeus muscle.Meanwhile,low frequency electrical stimula- tion was used and combined with functional training of the organs related to deglutition and ingestion.The results be- fore and after the treatment were evaluated.Results After 19.7 times of dilatation therapy,the content of water in- jected into the balloon was increased from 2.65?0.91 ml to 8.20?0.92 ml.Cricopharyngeal achalasia was alle- viated significantly(P

Objective To investigate the impact of 1,25(OH)2D3 on histological changes and activation of STAT3 in BLM?induced pulmonary fibrosis mice. Methods 30 male C57BL/6 mice were randomly divided into control group ,BLM group and BLM+VD group. Mice in BLM group and BLM+VD group received intratracheal injection of BLM(3 U/kg). Control group were intratracheally injected equal volume of sterile saline. From the first day after the surgery,mice in BLM+VD group received intraperitoneal injection of VD (5μg/kg·d). After 21 days, H&E and Masson′s trichrome staining were carried out. Aschroft score were used to evaluate histological changes in lungs. IL?6,IL?4 and INF?γin BALF were assessed by Elisa. p?STAT3,α?SMA and Collagen I were detected by western blot (WB) and immunohistochemistry. Results Fibrosis score and level of α?SMA,Collagen I in BLM group were significantly higher than that in control group (P < 0.05). However ,treatment with VD effectively at?tenuated fibrosis (P<0.05). IL?6 and IL?4 increased while INF?γwas decreased in BALF of BLM group (P<0.05). VD could ameliorate these changes. Upregulation and neuclear translocation of p?STAT3 were observed in BLM group,while VD intervention could inhibit phosphorylation of STAT3. Conclusions VD attenuate BLM?induced pulmonary fibrosis and regulate inflammatory cytokines probably by blocking STAT3 activation.