Aim To investigate the relationship between sleep deprivation and vascular aging,as well as the un-derlying mechanisms.Methods Male Sprague-Dawley rats were divided into control group,senescence group,sleep deprivation group,and sleep deprivation+senescence group,with 6 rats in each group.The modified level table method deprived rats of sleep duration.Senescence-associated β-galactosidase(SA-β-Gal)staining was used to detect the senes-cence status of rat vascular tissue.The mRNA and protein expression of tumor suppressor protein p53,silent information regulator 1(SIRT1)and clock gene cryptochrome 1(CRY1)was detected by real-time fluorescence quantification PCR(RT-qPCR),Western blot and immunohistochemistry.Results Compared with the control group,the intensity of SA-β-Gal staining was increased in the vascular tissues of the senescence group rats,the expression level of p53 was elevat-ed,the expression level of SIRT1 was decreased.Similar changes were observed in the sleep deprivation group and the sleep deprivation+senescence group,including intensified SA-β-Gal staining,elevated p53 levels,and reduced SIRT1 lev-els in vascular tissues.Additionally,compared with the control group,the sleep deprivation group showed reduced CRY1 levels in vascular tissues,while only CRY1 mRNA levels were reduced in the sleep deprivation+senescence group.Fur-thermore,compared with the senescence group,the sleep deprivation+senescence group exhibited intensified SA-β-Gal staining,increased p53 level,decreased SIRT1 level,and reduced CRY1 mRNA level in vascular tissues.Conclusion Sleep deprivation may promote the expression of vascular aging-related factors,potentially through the inhibition of CRY1 expression in vascular tissues.

Aim To investigate the relationship between sleep deprivation and vascular aging,as well as the un-derlying mechanisms.Methods Male Sprague-Dawley rats were divided into control group,senescence group,sleep deprivation group,and sleep deprivation+senescence group,with 6 rats in each group.The modified level table method deprived rats of sleep duration.Senescence-associated β-galactosidase(SA-β-Gal)staining was used to detect the senes-cence status of rat vascular tissue.The mRNA and protein expression of tumor suppressor protein p53,silent information regulator 1(SIRT1)and clock gene cryptochrome 1(CRY1)was detected by real-time fluorescence quantification PCR(RT-qPCR),Western blot and immunohistochemistry.Results Compared with the control group,the intensity of SA-β-Gal staining was increased in the vascular tissues of the senescence group rats,the expression level of p53 was elevat-ed,the expression level of SIRT1 was decreased.Similar changes were observed in the sleep deprivation group and the sleep deprivation+senescence group,including intensified SA-β-Gal staining,elevated p53 levels,and reduced SIRT1 lev-els in vascular tissues.Additionally,compared with the control group,the sleep deprivation group showed reduced CRY1 levels in vascular tissues,while only CRY1 mRNA levels were reduced in the sleep deprivation+senescence group.Fur-thermore,compared with the senescence group,the sleep deprivation+senescence group exhibited intensified SA-β-Gal staining,increased p53 level,decreased SIRT1 level,and reduced CRY1 mRNA level in vascular tissues.Conclusion Sleep deprivation may promote the expression of vascular aging-related factors,potentially through the inhibition of CRY1 expression in vascular tissues.

Objective To investigate the efficacy of sertraline and nimodipine in treatment of stroke depression. Meth-ods Selected diagnosed post-stroke depression in our hospital from January 2011 to January 2013 as observed object. 60 cases of stroke depression were randomly divided into observation group and control group of 30 patients, were treated nutrition brain cells, the control group received sertraline 50~100 mg, observation group added in the nimodip-ine 30 mg / time, 3 times a day, sertraline 50~100mg, the course were 8 weeks. Before and after treatment, HAMD-17 score, the clinical efficacy of adverse reactions after treatment were compared between two groups. Results Before treatment , differences HAMD-17 score of were not statistically significant ( P> 0 . 05 ) , After 2 weeks of treatment , HAMD-17 score the observation group and control group of was significantly lower than before treatment,(P<0.05). Af-ter 4 weeks of treatment, HAMD-17 score of the observation group and control group was significantly lower than be-fore treatment and after 2 weeks of treatment,the difference was significant(P <0.05). After 6 weeks of treatment , the HAMD-17 observation group and control group score reduced than before treatment and after 2 weeks of treatment , reduced significantly than after 4 weeks of treatment, the difference was significant(P <0.05). Total efficiency of obser-vation group was 93.33%, the total efficiency of the control group was 70.00%, the difference of the effect was signifi-cant between two groups(P < 0.05). No case occurred during the observation group therapy anorexia, dry mouth , rash , and its complication rate of 10 % of the observation group , the control group complication rate of 40.00%, the differ-ence was significant between two groups(P < 0.05). Conclusion Sertraline and nimodipine treatment stroke depression has good efficacy, and safety, and it is worthy of promotion and application.

Objective:To investigate the change and related factors of nitric oxide,nitric oxide synthase level and cerebral blood flow(CBF) in panic disorder.Methods:30 patients with panic disorder,30 patients with generalized anxiety disorder and 22 normal controls entered the study.Serum level of NO and NOS were assayed.Cerebral blood flow were measured with TCD.Results:The concentration of NO was significantly lower in panic disorder group in comparison with GAD group.There was no significant difference in NOS level between panic disorder group and the control group.Cerebral blood peak flow velocity in the left and right middle cerebral artery and mean cerebral blood flow velocity in the right middle cerebral artery were lower than normal control group and the difference were very significant.Cerebral blood peak flow velocity in the right vertebral artery was lower than those of GAD and NC group.The concentration of NO in panic disorder was correlated with HAMA score negatively.Cerebral blood peak flow velocity in the left middle cerebral artery was correlated with mean Cerebral blood flow velocity in the left middle cerebral artery,peak CBF velocity in the right middle cerebral artery and psychological anxiety positively and correlated to cerebral blood peak mean velocity in the right middle cerebral artery,peak CBF velocity in the right anterior cerebral artery,age and female negatively.Cerebral blood peak flow velocity in the right middle cerebral artery has positive correlation with mean cerebral blood flow velocity in the right middle cerebral artery and peak CBF locity in the right anterior cerebral artery and negative correlation with cerebral blood mean flow velocity in the right anterior cerebral artery. Mean cerebral blood flow velocity in the right middle cerebral artery was correlated to cerebral blood peak flow velocity in the right middle cerebral artery,mean cerebral blood flow velocity in the left middle cerebral artery,cerebral blood mean flow velocity in the right anterior cerebral artery and NO level positively and age,cerebral blood peak flow velocity in the left middle cerebral artery and cerebral blood peak flow velocity in the right anterior cerebral artery negatively.Cerebral blood peak flow velocity in the right vertebra artery has positive correlation with cerebral blood mean flow velocity in the right vertebra artery and cerebral blood mean flow velocity in the left middle cercbral artery and negative correlation with cerebral blood peak flow velocity in the left anterior cerebral artery and cerebral blood mean flow velocity in the right anterior cerebral artery.Conclusion:The change of NO and cerebral blood flow may be one of the neurobiological mechanisms in panic disorder.To assay the level of NO and measure cerebral blood flow might become approach of diagnosis for panic disorder.