Functional vision is the visual ability of patients with visual disorders when they participate in or complete daily activities, through early evaluation and targeted treatment, the improvement of disease prognosis can be realized. In this paper, the concept of functional vision was introduced, the evaluation content, scoring method and application status of functional vision evaluation tools for patients with visual disorders were described, and the analysis and comparison of the characteristics and shortcomings of each evaluation tool were carried out.Thus providing appropriate functional vision evaluation tools for medical staff in China and providing reference for improving the quality of functional vision evaluation for patients with visual disorders.

Objective:To analyze the longitudinal characteristics of CD4 +T lymphocytes (CD4) among the adult HIV/AIDS on antiretroviral therapy (ART) and the related factors. Methods:A retrospective cohort of adult HIV/AIDS starting ART in Dehong Dai and Jingpo Autonomous Prefecture (Dehong) in 2007-2016 was followed up to December 31, 2018. Group-based trajectory models were utilized to identify CD4 subgroups based on immune recovery (whether and when CD4 reached the average level of >500 cells/μl). The demographics and information at ART baseline were described, and the related factors were analyzed with polytomous logistic regression. The SAS 9.4 software was used for statistical analysis.Results:A total of 7 605 adults with HIV/AIDS were included, of which the median ( P 25, P 75) age at ART were 36 (30,43) years old, 61.0% were male, 42.5% were Han nationality, and 60.8% with the education of primary school or below. The follow-up duration M ( P 25, P 75) was 6.1 (4.1,8.1) years. HIV/AIDS in Dehong showed four CD4 trajectory subgroups from low to high: below the average level, primary recovery to a normal level, full recovery to a moderate level, and normal steady level, accounting for 34.4%, 39.8%, 20.6%, and 5.2%, respectively. When compared with corresponding control groups, age <35 years at ART, female, education of middle school or above, sexual transmission, no opportunistic infection, CD4 ≥200 cells/μl, baseline regimen with tenofovir (TDF) and time from HIV diagnosis to ART <1 year were the related factors facilitating the higher CD4 subgroups. Conclusions:The various CD4 immune recoveries of HIV/AIDS were changing patterns after ART. Starting ART with a high CD4 level was beneficial to CD4 recovery to normal level during the follow-up period. Early initiation of ART and exceptional attention to CD4 immune recovery should be encouraged after the ART.

Objective:To explore the effects and mechanisms of bortezomib on the proliferation and apoptosis of acute T lymphocyte leukemia cell line Jurkat.Methods:MTT assay was used to test the influence of bortezomib on the proliferation of Jurkat cells.Flow cytometry was used to detect the influence of bortezomib on apoptosis of Jurkat cells.Real-time quantitative polymerase reaction(RT-PCR) was used to detect the effects of bortezomib on the expression of Bax, Bcl-2 and Cox-2 genes in Jurkat cells.Results:The inhibition rates of 5ng/mL, 10ng/mL, 20ng/mL and 40ng/mL bortezomib on Jurkat cells at 24h were (13.23±0.71)%, (39.53±0.95)%, (53.07±1.12)%, (60.43±0.75)%, respectively, and the inhibition rates at 48h were (25.20±0.96)%, (52.80±1.30)%, (60.67±0.64)%, (75.10±1.35)%, respectively.The inhibitory rates of proliferation of Jurkat cells at 72h were (38.37±0.93)%, (60.94±0.85)%, (73.83±5.08)%, (88.37±1.55)%, respectively.The inhibitory rates of proliferation of Jurkat cells increased with the increase of drug concentration and the prolongation of action time, and the differences were statistically significant( F=1 602.202, 1 085.089, 181.034, all P<0.05). Bortezomib (5ng/mL, 10ng/mL, 20ng/mL and 40ng/mL) treatment for 24h, 48h and 72h, the apoptosis rate of Jurkat cells increased with the increase of drug concentration and the prolongation of action time, the differences were statistically significant( F=1 288.571, 223.378, 251.175, all P<0.05). The expression of Bax mRNA in Jurkat cells increased with the increase of drug concentration and time( F=258.446, 518.929, 276.764, all P<0.05). The Bcl-2 mRNA and Cox-2 mRNA expression levels decreased with the increase of drug concentration and the prolongation of action time( FBcl-2 mRNA=236.848, 264.849, 343.968, FCox-2 mRNA=679.404, 1288.681, 1541.850, all P<0.05). Conclusion:Bortezomib can inhibit the proliferation and induce apoptosis of Jurkat cells.Bortezomib can increase the expression of Bax mRNA and decrease the expression of Bcl-2 and Cox-2 mRNA, which may be the molecular mechanism of bortezomib to promote apoptosis.

Chromosomal region maintenance 1 (CRM1) is associated with an adverse prognosis in glioma. We previously reported that CRM1 inhibition suppressed glioma cell proliferation both in vitro and in vivo. In this study, we investigated the role of CRM1 in the migration and invasion of glioma cells. S109, a novel reversible selective inhibitor of CRM1, was used to treat Human glioma U87 and U251 cells. Cell migration and invasion were evaluated by wound-healing and transwell invasion assays. The results showed that S109 significantly inhibited the migration and invasion of U87 and U251 cells. However, mutation of Cys528 in CRM1 abolished the inhibitory activity of S109 in glioma cells. Furthermore, we found that S109 treatment decreased the expression level and activity of MMP2 and reduced the level of phosphorylated STAT3 but not total STAT3. Therefore, the inhibition of migration and invasion induced by S109 may be associated with the downregulation of MMP2 activity and expression, and inactivation of the STAT3 signaling pathway. These results support our previous conclusion that inhibition of CRM1 is an attractive strategy for the treatment of glioma.

Chromosomal region maintenance 1 (CRM1) is associated with an adverse prognosis in glioma. We previously reported that CRM1 inhibition suppressed glioma cell proliferation both in vitro and in vivo. In this study, we investigated the role of CRM1 in the migration and invasion of glioma cells. S109, a novel reversible selective inhibitor of CRM1, was used to treat Human glioma U87 and U251 cells. Cell migration and invasion were evaluated by wound-healing and transwell invasion assays. The results showed that S109 significantly inhibited the migration and invasion of U87 and U251 cells. However, mutation of Cys528 in CRM1 abolished the inhibitory activity of S109 in glioma cells. Furthermore, we found that S109 treatment decreased the expression level and activity of MMP2 and reduced the level of phosphorylated STAT3 but not total STAT3. Therefore, the inhibition of migration and invasion induced by S109 may be associated with the downregulation of MMP2 activity and expression, and inactivation of the STAT3 signaling pathway. These results support our previous conclusion that inhibition of CRM1 is an attractive strategy for the treatment of glioma.

Objective:To investigate whether irradiated U251 glioma cells can induce bystander effects in unexposed neural stem cells (NSCs) thus affecting its proliferation, stemness and differentiation.Methods:The cells were divided into NSCs group, NSCs+ U251 group (co-cultured with U251) and NSCs+ IR U251 group (co-cultured with 10 Gy irradiated U251). Glioma cells and NSCs were co-cultured in a transwell insert set. Cell counting and neurosphere diameter measuring were carried out to evaluate the proliferation and neurosphere formation ability of NSCs. Immunofluorescence assay was performed to detect the expression of Nestin protein to evaluate the stemness maintenance of NSCs, and to measure the expression levels of Tuj1 and GFAP proteins, the number of neuronal dendrites, synaptic length, the number of glial protrusions, as well as the length of glial protrusions.Results:The number of NSCs cultured with irradiated U251 cells was obviously smaller than that of NSCs cultured with sham-irradiated U251 cells ( t=2.52, P<0.05). The neurosphere formation ability of NSCs and the percentage of Nestin positive NSCs after co-culture with irradiated U251 cells significantly reduced in comparison with those after co-culture with sham-irradiated U251 cells ( t=-3.50, P<0.05). The percentages and the extent of NSCs differentiating into neuronal cells and glial cells( t=6.09, P<0.05)decreased obviously after co-culture with irradiated U251 cells in comparison with those after co-culture with sham-irradiated U251 cells. Conclusions:Irradiated glioma cells can significantly inhibit the proliferation, stemness and differentiation of unexposed NSCs due to bystander effect.

OBJECTIVE: To construct a recombinant lentiviral expression vector pCDH-Daxx-EGFP to investigate the effect of Daxx on the proliferation of vascular smooth muscle cells (VSMCs). METHODS: The recombinant lentiviral expression vector pCDHDaxx-EGFP was constructed using PCR-based accurate synthesis method. After identification by sequencing and enzyme digestion, the recombinant lentiviral vector was contransfected into 293T cells with lentivirus packaging vector. The recombinant lentivirus particles were collected and purified to infect VSMCs, whose expression of Daxx was detected with Western boltting. The cells infected with the empty vector pCDH-EGFP or pCDH-Daxx-EGFP were incubated in serum-free medium or in the presence of angiotensin Ⅱ (AngⅡ). The cell viability was determined with MTT assay, and the cell cycle changes were analyzed with flow cytometry. The cell migration ability was assessed using a scratch wound healing assay. The expression of p-Akt protein in the cells was detected using Western blotting. RESULTS: Double enzyme digestion and sequencing confirmed successful construction of the recombinant plasmid. Compared with the cells infected with the empty vector, the cells infected with pCDH-Daxx-EGFP exhibited significantly increased expressions of Daxx protein ( < 0.05). AngⅡ treatment of the cells infected with the pCDH-Daxx-EGFP, as compared with the cells infected with the empty vector, significantly lowered the cell viability, S phase cell ratio and cell migration ability ( < 0.05), and significantly decreased the expression level of p-Akt protein ( < 0.05). CONCLUSIONS We successfully constructed the recombinant lentiviral vector pCDH-Daxx-EGFP and overexpressed Daxx in primary cultured VSMCs using this vector. Daxx overexpression can inhibit AngⅡ-induced proliferation and migration in VSMCs probably by regulating p-Akt protein.

This article, based on the current quality management of medical institutions in China, put forward the concept of implementing the core medical quality system by way of path-based management. This effort aims at achieving the homogenization of the medical quality core systems among different medical institutions,thus ultimately homogenizing the management and service homogeneity in different regions, levels and categories of medical institutions. The present experiment proves satisfactory within a small scale.

Objective:To explore the effects of caffeine on the prevention of Alzheimer's disease (AD).Methods:Use Ethanol as a solvent to extract the caffeine in tea and then injecting 5％ D-galactose saline solution 1ml/d/kg to establish aging model mice.Divide mice randomly into experimental group (high-dose/low-dosecaffeine),positive control group,negative control group,and normal con-trol group (NS) and injecting appropriate drugs for consecutive four weeks.Test superoxyde dismutase (SOD) and malondialdehvde (MDA) periodically.Take mice's hippocampus and use Western blotting to detect the expression of brain derived neurotrophic factor (BDNF) and extracellular signal-regulated kinasesl/2 (p-ERK1/2).Results:The expression of BDNF and p-ERK1/2,negative control group is less than low-dose experimental group and positive control group (P＜0.01);The p-ERK1/2 expression of injecting D-galactose mice was significantly lower than normal group,negative control group compared weth the normal group,the differencd was significant (P＜0.05).The level of SOD in model group was significantly lower than that in normal control group,high,low dose caffeine group and positive control group (P＜0.01),but the level of MDA is opposite.Conclusions:Caffeine can delay aging process by increasing the level of SOD in aging mice,and enhancing the expression of BDNF and P-ERK1/2.Caffeine does a lot to prevent AD.