Objective To evaluate the correlation between serum uric acid with cognitive disorder after acute cere?bral infarction by prospective study. Methods Four hundred consecutively enrolled patients of acute cerebral infarction were divided into no cognitive impairment group and cognitive impairment group according to the assess of Montreal Cog?nitive Assessment (MoCA). Univariate analysises were conducted in the potential risk factors of cognitive impairment in?cluding age, sex, smoking, alcohol, hypertension, diabetes, dyslipidemia, level of education, infarction in key parts, atrial fibrillation, serum uric acid, blood homocysteine between two groups. The statistically significant indicators in univariate analysises were used as independent variables and the scores of MoCA were used as the dependent variable to conduct multiple linear regression analysis. The assessment on the risk of cognitive impairment after cerebral infarction were con?ducted according to serum uric acid, sex, age and TOAST classification further. Results Serum uric acid was indepen?dent risk factors of cognitive disorder after acute cerebral infarction. The risk of cognitive disorder after acute cerebral in?farction was significantly increased in patients with high level of serum uric acid than with normal level and the relative risk was 1.35,95%CI(1.098,1.660). Especially for the young, male or patients with cerebral infarction in classification of small artery occlusion, the risk increased further, and the relative risk was 1.513, 95%CI(1.092, 2.096)1.412, 95%CI (1.125, 1.771)and 1.464, 95%CI(1.128, 1.900)respectively. Conclusion Exaltation of Serum uric acid was indepen?dent risk factor of cognitive disorder after acute cerebral infarction. The risk of cognitive disorder after acute cerebral in?farction was significantly increased in patients with high level of serum uric acid than with normal level, and especially for the young, male and patients with cerebral infarction in classification of small artery occlusion, the risk increased fur?ther.

The lack of effective in vitro infection model for hepatitis E virus (HEV) has greatly hindered the quantitative analysis of neutralizing titers of anti-HEV antibodies and human sera, thus impeding further studies of HEV-stimulated antibody responses and the immunological mechanisms. In order to improve this situation, the infection of HepG2 cells that are inefficient for HEV replication was continuously monitored until the viral load reached the limit of detection on day 13, the results of which confirmed the feasibility of using this cell line to establish the infection model. Then, neutralization assays of five anti-HEV murine monoclonal antibodies and serum samples collected from four HEV vaccine recipients (collected before and after vaccination) were performed by 96 multi-channel parallel infections, nucleic acid extraction, and qPCR. The results showed that the cell model can be applied for quantitative evaluation of the neutralizing capacity of different antibodies and antiserum samples from HEV vaccine recipients. In this study, we have successfully established a high-throughput in vitro HEV replication model, which will prove to be useful for the evaluation of HEV vaccines and studies of HEV epitopes.
Animals ; Antibodies, Viral ; analysis ; immunology ; Hepatitis Antibodies ; analysis ; immunology ; Hepatitis E ; immunology ; virology ; Hepatitis E virus ; chemistry ; immunology ; physiology ; High-Throughput Screening Assays ; methods ; Humans ; Mice ; Mice, Inbred BALB C ; Neutralization Tests ; methods ; Virus Replication

OBJECTIVE To study the effects of Zigui yichong formula on premature ovarian insufficiency （POI） in mice through glycolysis metabolic pathway. METHODS Eighty SPF C57BL/6N female mice were divided into normal group， model group， Zigui yichong formula group （14.175 g/kg）， Zigui yichong formula+2-deoxy-D-arabino-hexose （2-DG） group （Zigui yichong formula 14.175 g/kg + glycolysis inhibitor 2-DG 100 mg/kg）， with 20 mice in each group. Except for the normal group， POI model mice were induced by intraperitoneal administration of cyclophosphamide in the other groups. After the model was successfully established， each group was given corresponding drugs. HE staining was employed to observe the pathomorphological changes in ovarian tissue and to count follicles at all developmental stages； radioimmunoassay was conducted to measure the serum levels of estradiol （E2）， anti-Müllerian hormone （AMH）， and follicle-stimulating hormone （FSH）； TUNEL assay was employed to detect apoptosis in ovarian granulosa cells of mice； the activities of hexokinase （HK）， pyruvate kinase （PK） and lactate dehydrogenase （LDH） were detected by colorimetry； Western blot and real-time fluorescence quantitative PCR were employed to analyze the protein and mRNA expressions of B-cell lymphoma-2 （Bcl-2）， Bcl-2 associated X protein （Bax）， caspase-3， HK2， pyruvate kinase M2 （PKM2）， and lactate dehydrogenase A （LDHA）. RESULTS Compared with model group， the number of primordial follicles， growing follicles， antral follicles and granulosa cells were increased significantly（P＜0.05）， and granulosa cells arranged neatly， but the number of atretic follicles and granulosa cells apoptosis were decreased significantly in Zigui yichong formula group （P＜0.05）； the serum levels of E2 and AMH， the activities of HK， PK and LDH， protein and mRNA expressions of Bcl-2， HK2， PKM2 and LDHA were increased significantly （P＜0.05）； the serum levels of FSH， the protein and mRNA expressions of Bax and caspase-3， Bax/Bcl-2 ratio were decreased significantly （P＜0.05）. 2-DG could reverse the improvement effects of Zigui yichong formula on the above indexes of POI model mice. CONCLUSIONS Zigui yichong formula may inhibit the apoptosis of ovarian granulosa cells， reduce follicle atresia and improve ovarian reserve function by promoting glycolysis levels in POI model mice.