AIM: To study the effects of neuregulin-1β (NRG-1β) on the nervous behavioral function, cerebral infarction volume, brain water content (BWC), neuroal apoptosis and aquaporin-4 (AQP-4) expression in astrocytes after cerebral ischemic reperfusion in mice. METHODS: Intraluminal thread methods were applied to establish the middle cerebral artery occlusion reperfusion (MCAO/R) model in mice. Neuregulin-1β (2 μg/kg) was injected into the internal carotid artery for treatment. The nervous behavioral function was evaluated by Bedersons test. The cerebral infarction volume was observed with tetrazolium chloride (TTC) staining. The BWC was measured by calculating the dry-wet weight ratio. The apoptotic positive cells were counted by immunofluorescence assay. The expression of AQP-4 was determined by immunohistochemical method. RESULTS: Nervous behavioral malfunction appeared in all the mice with left middle cerebral artery occlusion (MCAO) and/or reperfusion. The infarction focus showed in the ischemic hemisphere following the injury. The BWC, the numbers of neuroal apoptotic cells and AQP-4 expression in astrocytes were higher than those in sham control group. In MCAO/R+NRG-1β treatment group, the nervous behavioral function at ischemia 24 h significantly improved, the numbers of apoptotic positive cells reduced and the infarction volume decreased significantly than those in MCAO/R group (P<0.05). The BWC and AQP-4 expression in astrocytes showed no significant difference compared with MCAO/R group (P>0.05). In the reperfusion 22 h, 46 h and 70 h groups, the five indexes mentioned above were significantly different from those in the corresponding MCAO/R groups (P<0.05). CONCLUSION: NRG-1β might reduce cerebral edema and infarction volume, and improve the nervous behavioral function via down-regulating the expression of AQP-4 in astrocytes and inhibiting the neuronal apoptosis induced by ischemia reperfusion injury.

Objective To investigate the changes of cardiotrophin-1(CT-1) expression in rats with pressure overload-induced cardiac hypertrophy,and the effects of benazepril on this expression and the concerned cardiac hypertrophy.Methods The model of pressure overload was established by constriction of abdominal aorta and divided randomly into hypertrophied group(LVH,n=7) and benazepril intervention group(Ben,n=7,benazepril 1mg?kg~(-1)?d~(-1) orally)2 weeks later.A sham-operation group(Sham,n=7) served as control.Blood pressure and left ventricular mass index(LVMI) were investigated after 3 weeks' treatment.AngⅡ level in myocardium was measured by radioimmunoassay.The mRNA level of CT-1 was examined by RT-PCR.Results Compared with the sham group, blood pressure and LVMI in LVH group were increased significantly(P

Objective To investigate the changes of GP130 expression in rats with pressure overload-induced cardiac hypertrophy, and the effect of Benazepril on GP130 expression and the concerned cardiac hypertrophy. Methods Two weeks after the Wistar rat model of pressure overload was established by constriction of abdominal aorta, the survived rats were randomly divided into hypertrophy group (LVH, n=7) and Benazepril intervention group (Ben, n=7, 1 mg?kg -1 ?d -1 Benazepril orally for 3 weeks). A sham-operation group (Sham, n=7) was set up as control. Blood pressure and left ventricular mass index (LVMI) were investigated at 3th week after model establishment. AngⅡ level in myocardium was measured by radioimmunoassay. The protein level of GP130 in cardiomyocytes was determined by immunohistochemistry. Results As compared with the Sham group, blood pressure and LVMI increased significantly (P

Objective To evaluate the effects of exogenous adenovirus-mediated gene transfer of human apM1 gene (Ad-apM1) on malonaldehyde (MAD) and superoxide dismutase (SOD) levels in human umbilical vein endothelial cells (HUVEC). Methods HUVEC proliferation was measured by MTT after infection by AdapM1. Adiponetin protein level in cell culture medium of HUVEC cells infected with Ad-apM1 was detected by double antibody sandwich ELISA. The levels of MAD and SOD were measured by chromatometry. Results MTT assay showed that Ad-apMl had no effect on HUVEC proliferation. Human adiponectin protein levels in cell culture medium significantly increased after HUVEC was infected with Ad-apM1 for 24, 48, and 72 h, along with decreased MAD and increased SOD ( all P<0.05 ). MAD levels markedly increased and SOD levels decreased after HUVEC were incubated with 100 μmol/L H2O2 for 6, 12, and 24 h, and these reactions were reversed by AdapM1 transfection (all P<0.05 ). Conclusions HUVEC infected with Ad-apM1 effectively secrete human adiponectin. Ad-apM1 exerts antioxidation effect and antagonizes H2O2 -induced endothelial injury.

Papillary thyroid microcarcinoma (PTMC) is a subtype of papillary thyroid cancer,and there are many debates about its treatments,including extent of thyroidectomy,necessity of prophylactic central-neck nodal dissection,risk-benefit ratio of thyroid-stimulating hormone suppression and indications of observation therapy,et al.The epidemiology and treatment programs of thyroid PTMC were reviewed in this article.

Objective:To investigate the effects of miR-497 on cytobiology behaviors of papillary thyroid carcinoma (PTC) by targetingly regulating the expression of Yes-associated protein 1 (YAP1) .Methods:Human TPC-1 cells were divided into control group, miR-497 group, si-YAP1 group and miR-497+si-YAP1 group. The liposome transfection was conducted by LipofectamineTM3000. The targeted relationship between miR-497 and YAP1 was validated by Luciferase Reporter Assay. The cell proliferation activity in each group was detected by MTT method. The apoptosis rates were analyzed by flow cytometry. The number of invasion cells was detected by Transwell. The cell migration rates were detected by scratch assay. The expression of Cyclin D1, matrix metalloproteinase 2 (MMP-2) , MMP-9, matrix metalloproteinase inhibitor-1 (TIMP-1) and activated caspase 3 (cleaved Caspase-3) was detected by Western blot. SPSS 22.0 was used to analyze data, and normally distributed measurement data were expressed as ( ± s) . One-way ANOVA was analyzed for the difference between multiple groups, and SNK-q were analyzed for the difference between two groups. Results:Compared with the control group, the expression of YAP1 mRNA and protein was decreased in miR-497 group and si-YAP1 group ( q=14.682, 14.597; 23.743, 23.571; P<0.05) , cell proliferation activity, number of invasion cells and migration rate were decreased ( q=4.724, 4.568, 3.841; 4.216, 3.952, 3.274; P<0.05) , apoptosis rate was increased ( q=3.783; 4.336; P<0.05) , expression of CyclinD1, MMP-2, MMP-9 and cleared Caspase-3 proteins was decreased ( q=5.823, 5.981, 6.036, 6.485; 5.934, 6.110, 6.573, 6.614; P<0.05) , and expression of TIMP-1 protein was increased ( q=6.071; 6.148; P<0.05) . Compared with si-YAP1 group, miR-497 level was increased in miR-497+si-YAP1 group ( q=14.726, P<0.05) , the expression of YAP1 mRNA and protein was decreased ( q=3.089, 3.126; P<0.05) , cell proliferation activity, number of invasion cells and migration rate were decreased ( q=2.654, 2.537, 2.246; P<0.05) , apoptosis rate was increased ( q=2.875, P<0.05) , expression of CyclinD1, MMP-2, MMP-9 and cleared Caspase-3 proteins was decreased ( q=4.371, 4.365, 4.383, 4.368; P<0.05) , and expression of TIMP-1 protein was increased ( q=4.275, P<0.05) . Conclusion:MiR-497 can negatively targetingly regulate the expression of YAP1, inhibit proliferation, invasion and migration of TPC-1 cells.

Objective To investigate expression,significance and relationship of IMP3 and CD44v6 protein in papillary thyroid carcinoma.Methods Immunohistochemical method was used to investigate the expression of IMP3 and CD44v6 protein in 30 cases PTC(10 follicular variant of papillary carcinoma cases,20 conventional papillary thyroid carcinoma cases),20 PTC with lymph node metastasis cases,20 benign tissues of thyroid cases.Quantitative analysis of the detection was conducted by Biosens Digital Imaging System vl.6 (professional image analysis software),and the target integral optical density (IOD) was used for the judgement parameter.Results IMP3 and CD44v6 expression in the PTC is higher than in benign group,the difference was statistically significant (P ＜ 0.05) ; IMP3 and CD44v6 expression in PTC with lymph node metastasis was higher than without lymph node metastasis in the organization to express,the difference was statistically significant (P ＜ 0.05) ; There was a positive correlation between IMP3 and CD44v6 expression and metastasis in PTC (r =0.903,P ＜ 0.05).Conclusions The expression of IMP3 and CD44v6 protein was closely correlated with the invasion and metastasis of PTC.IMP3 and CD44v6 protein might be considered as molecular markers for PTC.

Purpose: Cerebral ischemia-reperfusion (IR) injury is a severe secondary injury induced by reperfusion after stroke. Didymin has been reported to have a protective effect on intracerebral hemorrhage. However, the underlying mechanism of didymin on regulating cerebral IR injury remains largely unknown. Materials and Methods: A rat cerebral IR model and oxygen-glucose deprivation/reperfusion (OGD/R) model in PC12 cells were established. Hematoxylin and eosin (H&E) was used to detect the pathological changes in brain tissues, and TUNEL staining was performed to detect apoptosis of brain tissues. MTT and flow cytometry were used to measure the viability and apoptosis of PC12 cells. QRT-PCR and western blot were used to detect inflammation cytokines in PC12 cells. Western blot was used to measure the expression of PPAR-γ, RXRA, Bax, c-caspase-3, and Bcl-2. Results: Didymin pretreatment decreased apoptotic rates, reduced levels of Bax and c-caspase-3, and increased Bcl-2 level in vivo and in vitro. Additionally, didymin pretreatment increased viability and decreased the inflammation levels [interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and monocyte chemotactic protein (MCP)-1] of OGD/R treated PC12 cells. Moreover, didymin activated the peroxisome proliferator-activated receptors (PPAR) signaling pathway and increased the expression of PPAR-γ and RXRA in OGD/R treated PC12 cells. Inhibition of PPAR-γ eliminated the protective effect of didymin on OGD/R treated cells. Conclusion Didymin protected neuron cells against IR injury in vitro and in vivo by activation of the PPAR pathway. Didymin may be a candidate drug for IR treatment.

Objective: To observe the incidence of unreasonable use of high beam at nighttime among motor vehicle drivers, so as to provide the evidence for the prevention and control of road traffic injury. Methods: Four roads into city and five urban roads were selected in Yongkang of Zhejiang Province. An automatic recording system was used to collect the unreasonable use of high beam among motor vehicle drivers on the selected roads from 19:00 to 5:00 on Monday, Wednesday, Friday and Sunday during a week in July 2020. The regression tree model was used to analyze the relationship of the unreasonable use of high beam with road, time and traffic flow. Results: A total of 89 989 motor vehicles were observed, and 2 419 motor vehicle drivers had unreasonable use of high beam, with an incidence rate of 2.69%. The incidence rate of the unreasonable use of high beam was 3.14% in the roads into city, which was higher than 2.30% in the urban roads ( P<0.05 ). The incidence rates of the unreasonable use of high beam in the roads into city and in the urban roads were 5.15% and 2.90% on Wednesday, which were higher than those on Monday ( 2.89% and 2.34% ), Friday ( 2.90% and 1.92% ) and Sunday (2.06% and 2.12%). The highest incidence rate of the unreasonable use of high beam in the roads into city was 6.07% between 4:00 and 5:00, and in the urban roads was 4.50% between 2:00 and 3:00. The results of regression tree classification analysis showed that the highest incidence rate was 8.13% on the roads into city in the east, west and south directions, and on the urban roads in the east and north directions with less than 317 vehicles per hour on Wednesday. Conclusion It is more likely for motor vehicle drivers to use high beams unreasonably at nighttime on the roads into city with less traffic flow.

AIM:To explore the influence of exogenous hydrogen sulfide ( H2 S) on coagulation and fibrinoly-sis in ferric chloride ( FeCl3 )-induced mouse carotid artery thrombosis .METHODS: The mice were divided into sham control group, model group, different concentrations (12.5, 25 and 50μmol/kg) of sodium hydrosulfide (NaHS, H2S do-nor) groups and 30 mg/kg clopidogrel ( positive control ) group.Intraperitoneal injection of NaHS at different concentra-tions and oral administration of clopidogrel bisulfate were performed for 3 d prior to FeCl 3-induced carotid artery thrombo-sis.The frozen sections of the carotid artery were collected to perform HE staining , and the thrombus pattern and the chan-ges of vascular pathology were observed .The thrombus was weighed to calculate thrombosis inhibitory rate .Prothrombin time ( PT) , activated partial thromboplastin time ( APTT) , fibrinogen ( FIB) and fibrinogen degradation product ( FDP) in the mice were also measured by a coagulometer .The plasma levels of thromboxane B 2 ( TXB2 ) , 6-keto-prostaglandin F 1α(6-keto-PGF1α) and plasminogen activator inhibitor (PAI) were detected by ELISA.RESULTS: Compared with model group, NaHS dose-dependently inhibited the formation of carotid artery thrombus .NaHS treatment reduced the contents of TXB2 and PAI, and recovered 6-keto-PGF1αcontent in thrombosis model group .In NaHS treatment groups , 6-keto-PGF1α/TXB2 and thrombus weight was negatively correlated .NaHS treatment prolonged PT and APTT , reduced the content of FIB, but increased the level of FDP in thrombosis model group .CONCLUSION:Hydrogen sulfide prevents FeCl 3-induced carotid artery thrombosis by inhibiting coagulation and activating fibrinolysis .