Objective To investigate the protective effect of 17?-estradiol (?E2) on cultured retinal neurons. Methods By using methods of the cultured retinal neurons, the effects of H 2O 2, ? E2, and tamoxifen, the estrogen receptor antagonist, on the cultured retinal neurons were observed. Results H 2O 2 significantly decreased cell viability in cultured retinal neurons in a dose- and time-dependent manner. When the retinal neurons were pretreated with ? E2 30 min prior to H 2O 2 treatment, cell viability was significantly increased (P

Objective To investigate the therapeutic effects of mesenchymal stem cells (MSCs) on N-methyl-N-nitrosourea (MNU)-induced retinal degeneration in C57BL mice.Methods Different doses of MNU (30 mg · kg-1,45 mg · kg-1,60 mg · kg-1,75 mg · kg-1 and 90 mg · kg-1) were injected to C57BL mice for 7 days.Then electroretinogram (ERG) detection and HE staining were performed to examine retinal electrophysiological function and morphological changes on day 1,day 3 and day 7 after MNU treatment,respectively.Then we could explore the optimum condition to establish stable animal model of retinitis pigmentosa.MSCs were transplanted to C57BL mice by intravitreal or tail intravenous injection.Then ERG detection and HE staining were performed to evaluate the effect of MSCs on retinitis pigmentosa induced by MNU.Results When compared with control group,30 mg · kg-1 and 45 mg · kg-1 MNU could cause mild retinal damage in morphology and function in mice;while 60 mg · kg-1 and above dose of MNU induced serious retinal damage,leading to decreased ERG amplitude of the retina (all P ＜ 0.001) and outer nuclear layer (ONL) thickness (all P ＜ 0.001).On day 1 and day 3 after single dose of 60 mg · kg-1 MNU injection,ERG amplitude of the retina was decreased,and outer nuclear layer thickness became thin;while the retinal damage was serious badly in morphological structure on day 7,with the ERG amplitude extinguished (all P ＜ 0.001),ONL thickness thin (all P ＜ 0.001) and internal and external nuclear layer fusion.When compared with MNU alone treatment group,following injection of 60 mg · kg-1 MNU for 1 day MSCs were transplanted to C57BL mice by intravitreal or tail intravenous injection,and the amplitude of ERG and retinal ONL thickness were increased on day 7 after MSCs transplantation (all P ＜ 0.001).Conclusion MSCs transplantation has a certain therapeutic effect on MNU-induced retinitis pigmentosa in C57BL mice.

Objective To observe the effects of methionine enkephalin (M-Enk) on migration of macrophages from mice with impaired liver and its immunomodulatory mechanisms. MethodsLiver of mice was impaired by feeding CCl4 and macrophage migration inhibitory factor (MMIF) was produced by Con A-stimulated spleen lympho- cytes. Inhibition of macrophage migration was measured in reaction system by adding M-Enk. Results Migration of macrophages in both liver-impaired and control group were suppressed by MMIF, but the suppression might be re- versed by adding 1 μmol/L M-Enk (P＜0. 05). M-Enk could significantly inhibit in vitro both of the combination of MMIF with macrophages and production of MMIF from lymphocytes (P＜0. 01). Macrophages from liver-imparied group showed a higher sensitivity compared to the control group (P＜0. 05). ConclusionThe study suggests that opi- oid peptieds play an important role in the modulation of the immune response under stress as liver impairment.

Objective To study the characteristics of skinfold thickness of Han adults in Jiangsu province . Methods The skinfold thicknesses of facial , subscapular , suprailiac , biceps , triceps and calf on 311 urban adults ( 157 males and 154 females) and 421 rural adults ( 213 males and 208 females ) of Han were investigated in Huaian city of Jiangsu province .Results The thickness of skinfold of urban females were thicker than that of urban males .Rural adults were the same .Han adults of Jiangsu showed the most significant differences between urban areas and rural areas .The values of six skinfold thicknesses of Jiangsu urban adults have positive correlation with age .Conclusion Han adults of Jiangsu show the most significant differences between genders .

AIM:To investigate the molecular mechanism of Xijiao Dihuang decoction combined with Yinqiao powder (XDY) in treating viral pneumonia, and the effects of XDY on TNF-α-induced permeability in pulmonary microvascular endothelial cells (PMVEC) and the role of PKC-SSeCKS pathway involved.METHODS:The electric conductivity method was used to detect transendothelial electrical resistance (TER) of primarily cultured PMVEC on Transwell chamber at different time points to determine the permeability of PMVEC.After pretreatment for 24 h, the activity of PKC, TER, and the expression of SSeCKS at mRNA and protein levels were detected.Laser scanning confocal microscopy was used to observe the location of SSeCKS and construction of F-actin in PMVEC.RESULTS:The permeability of PMVECs induced by TNF-α reached the peak at 24 h.Compared with control group, the TER in TNF-α group was decreased, and the activity of PKC was increased.Compared with TNF-α group, the activity of PKC in TNF-α with PKC inhibitor group and TNF-α with XDY group was decreased, while the TER was increased, without difference from control group.Compared with control group, the mRNA expression of SSeCKS and phospho-SSeCKS was increased in PMVEC of TNF-α group, but decreased in TNF-α with XDY group compared with TNF-α group.In control group, F-actin was mainly located around the nucleus and at cytoplasmic borders of PMVEC, forming the dense peripheral bundle, and SSeCKS was evenly scattered in the cell.In TNF-α group, the dense peripheral bundle of F-actin surrounding the cells almost disappeared, and SSeCKS was concentrated around the nucleus.Compared with TNF-α group, the distribution and the structure of F-actin and SSeCKS nearly returned to normal in TNF-α with XDY group.CONCLUSION:XDY inhibits the activation of PKC signaling pathway in PMVEC caused by TNF-α to reduce the mRNA expression of SSeCKS and the phosphorylation of SSeCKS, thus preventing the deformation of endothelial cells and reducing the permeability of PMVEC.

An electrochemical L-lactate biosensor was fabricated by combining Platinum nanoparticles (Pt-nano) with multi-walled carbon nanotubes(MWCNTs).L-lactate oxidase(LOD) was immobilized on the surface of the glassy carbon electrode (GCE) modified with MWCNTs and Pt-nano.The surface of resulting LOD/MWCNTs/Pt-nano electrode was covered by a thin layer of sol-gel to avoid the loss of LOD and to improve the anti-interference ability.The cyclic voltammetric results indicated that MWCNTs/Pt-nano catalyst displayed a higher performance than MWCNTs.Under the optimized conditions, i.e., applied potential of 0.5 V, pH 6.4, 25 ℃, the proposed biosensor's determination range was 0.2-2.0 mmol/L, response time was within 5 s, and the sensitivity was 6.36 (A/(mmol/L).It still kept 90% activity after 4 weeks.The fabricated biosensor had practically good selectivity against interferences.The results for whole blood samples analyzed by the present biosensor showed a good agreement with those analyzed by spectrophotometric method.

Objective: To understand the survival time and influencing factors of HIV/AIDS cases in Gansu province from 1997 to 2018. Methods: A retrospective cohort study was conducted to analyze the AIDS epidemic data of Gansu from 1997 to 2018 collected from the National HIV/AIDS information system. Life-span table were used to calculate survival rate, Kaplan-Meier method was used to draw the survival curves and calculate the average survival time, the Cox proportional hazard regression model were used to analyze the risk factors for death for HIV/AIDS cases. Results: Among 6 813 HIV/AIDS cases, 715 (10.5%) died, and the average survival time was 195.9 months (95%CI: 189.7-202.2). The survival rates of 12 months, 60 months, 120 months and 180 months were 91.5%, 86.1%, 79.9% and 73.8%, respectively. Cox proportional hazard regression model showed that the risk factors for death in the HIV/AIDS cases were age (≥51 years old vs. ≤25 years old, HR=1.906, 95%CI: 1.353-2.685), transmission route (blood borne and others transmission vs. heterosexual transmission, HR=1.593, 95%CI: 1.226-2.069), detection way (hospital admission detection, blood transfusion and preoperative examination vs. entry-exit health examination, pre-marital examination and physical examination of recruits, HR=5.113, 95%CI: 2.083-12.547), disease phase (AIDS phase vs. HIV infection phase: HR=4.012, 95%CI: 3.401-4.732), baseline CD₄ count (no CD₄ detected vs. CD₄ count ≥350/μl, HR=5.446, 95%CI: 3.835-7.732), antiretroviral therapy (receiving no antiretroviral therapy vs. receiving antiretroviral therapy, HR=12.019, 95%CI: 9.861-14.648). Conclusions The average survival time of HIV/AIDS cases was above 16 years in Gansu during 1997 to 2018. Death risk of HIV/AIDS cases might be increased by age ≥51 years, hospital admission detection, blood transfusion and preoperative examination, AIDS phase of disease phase, no baseline CD₄ detected and no receiving antiretroviral therapy. It is necessary to conduct early HIV test, diagnosis and antiretroviral treatment and increase antiretroviral treatment rates and CD₄ testing rate to improve the survival of HIV/AIDS cases.

Host genetic, environmental and viral factors are classified as three categories that determine clinical outcomes of hepatitis B virus (HBV) infection. The objective of this study was to detect the associations between polymorphisms rs346473 and rs346482 in Rho GTPase-activating protein 24 (ARHGAP24) gene and disease progression of HBV infection in Han Chinese population. These two SNPs were found by our DNA pooling using Affymetrix Genome-Wide Human Mapping SNP6.0 Array in HBV carriers, and verified by using TaqMan 7900HT Sequence Detection System with 758 progressed HBV carriers versus 300 asymptomatic HBV carriers (AsC) in a discovery phase and 971 progressed HBV carriers versus 328 AsC in a replication phase. Multivariable logistic regression revealed that individuals with genotype TT at variant rs346473 displayed remarkable correlations with disease progression of HBV infection both in the discovery phase (OR, 2.693; 95% CI, 1.928-3.760; P=6.2×10(-9); additive model) and the replication phase (OR, 1.490; 95% CI, 1.104-2.012; P=9.0×10(-3); additive model). These two SNPs were in strong linkage disequilibrium with D'=0.99 and r (2)=0.951, and haplotype TT disclosed an increased susceptibility to HBV progression (OR, 1.980; 95% CI, 1.538-2.545; P=8.1×10(-8)). These findings suggest that polymorphism rs346473 in the ARHGAP24 gene might be a part of the genetic variants underlying the susceptibility of HBV carriers to disease progression.

As terminally differentiated cells, neurons undergo aging with specific patterns.Understanding the characteristics of neural cell senescence and associated aging models is helpful to select appropriate models for the study of nervous system senescence.

Background: Insulin resistance (IR) is the key pathological basis of many metabolic disorders. Lack of asialoglycoprotein receptor 1 (ASGR1) decreased the serum lipid levels and reduced the risk of coronary artery disease. However, whether ASGR1 also participates in the regulatory network of insulin sensitivity and glucose metabolism remains unknown. Methods: The constructed ASGR1 knockout mice and ASGR1-/- HepG2 cell lines were used to establish the animal model of metabolic syndrome and the IR cell model by high-fat diet (HFD) or drug induction, respectively. Then we evaluated the glucose metabolism and insulin signaling in vivo and in vitro. Results: ASGR1 deficiency ameliorated systemic IR in mice fed with HFD, evidenced by improved insulin intolerance, serum insulin, and homeostasis model assessment of IR index, mainly contributed from increased insulin signaling in the liver, but not in muscle or adipose tissues. Meanwhile, the insulin signal transduction was significantly enhanced in ASGR1-/- HepG2 cells. By transcriptome analyses and comparison, those differentially expressed genes between ASGR1 null and wild type were enriched in the insulin signal pathway, particularly in phosphoinositide 3-kinase-AKT signaling. Notably, ASGR1 deficiency significantly reduced hepatic gluconeogenesis and glycogenolysis. Conclusion The ASGR1 deficiency was consequentially linked with improved hepatic insulin sensitivity under metabolic stress, hepatic IR was the core factor of systemic IR, and overcoming hepatic IR significantly relieved the systemic IR. It suggests that ASGR1 is a potential intervention target for improving systemic IR in metabolic disorders.