Objective To observe the treatment effects of trimetazidine on myocardial bridge. Methods A total of 76 patients with clinical symptoms, such as different degrees of chest tightness, palpitation, breath shortness, chest pain, were diagnosed as coronary myocardial bridge by coronary angiography, and were divided into two groups randomly. While control group (n=40) was given beta-blocker or (and) calcium antagonist as routine treatment. The treatment group (n=36) was given routine treatment and trimetazidine, 20 mg, three times daily. The mean follow-up period was 12 weeks. The episodes of chest pain per week, exercise tolerance, anxiety and depression scores, total ischemic burden in 24 h and walking distance in 6 min were observed in two groups of patients. Results The parameters of chest pain times per week, exercise tolerance, anxiety and depression scores, total ischemic burden in 24 h and walking distance in 6min were improved in treatment group compared with control group, and the symptoms were effectively relieved, the life quality of patients were improved. Conclusion The conventional treatment combined with trimetazidine is safe and effective, which can further improve myocardial energy metabolism and exercise tolerance, and enhance the clinical effect and the life quality of patients.

Objective To investigate the expression change of renal NLR family pyrin domain containing-3 protein(NALP3) in-flammasome in the nephrotic syndrome(NS) patients with focal segmental glomerulosclerosis(FSGS) and its relation with the tubu-lointerstitial pathogenic injury degree ,expression of inflammatory factors and clinical biochemical indexes .Methods Immunohisto-chemistry was used to detect the expressions of NALP3/ASC/caspase-1 and their downstream effector molecule IL-1β,IL-18 in re-nal tubular epithelial cells .The tubulointerstitial injury score and the activated macrophages F4/80 in renal interstitium of the FSGS patients and NS patiens were evaluated .The serum creatinine ,urea ,total protein ,albumin ,24 h urine protein and estimated glomer-ular filtration rate(eGFR) were observed .The correlation of tubulointerstitial injury with NALP3/ASC/caspase-1 ,IL-1β,IL-18 were respectively analyzed .Results The expression of NALP3/ASC/caspase-1 ,IL-1β,IL-18 in the renal tissue of the FSGS pa-tients was significantly increased compared with that in the control group (P<0 .01) .NALP3/ASC/capspase-1 expression was pos-itively correlated with the expression of IL-1β,IL-18(P< 0 .01) .NALP3/ASC/caspase-1 ,IL-1β,IL-18 expression was positively correlated with renal tubulointerstitial injury and the F4/80 expression intensity(P<0 .01) .NALP3/ASC/caspase-1 ,IL-1β,IL-18 was significantly positively correlated with 24 h urine protein and Scr ,and negatively correlated with the eGFR (P<0 .05) ,but had no obvious correlation with plasma urea ,plasma total protein and albumin concentrations .Conclusion The NALP3 inflammasome might participate in the pathogenic mechanism of FSGS through the activation of its downstream inflammatory factor of IL-1β,IL-18 ,the more higher its expression degree ,the more severe the renal tissue injury ,whether which could be served as the warning in-dex needs the further clinical verification .

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.

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.

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.

In order to explore tick proteins as potential targets for further developing vaccine against ticks, the total proteins of unfed female Dermacentor silvarum were screened with anti-D. silvarum serum produced from rabbits. The results of western blot showed that 3 antigenic proteins of about 100, 68, and 52 kDa were detected by polyclonal antibodies, which means that they probably have immunogenicity. Then, unfed female tick proteins were separated by 12% SDS-PAGE, and target proteins (100, 68, and 52 kDa) were cut and analyzed by LC-MS/MS, respectively. The comparative results of peptide sequences showed that they might be vitellogenin (Vg), heat shock protein 60 (Hsp60), and fructose-1, 6-bisphosphate aldolase (FBA), respectively. These data will lay the foundation for the further validation of antigenic proteins to prevent infestation and diseases transmitted by D. silvarum.
Animals ; Antigens/*chemistry/immunology ; Arthropod Proteins/*chemistry/immunology ; Electrophoresis, Polyacrylamide Gel ; Female ; Ixodidae/*chemistry/immunology ; Molecular Weight ; Rabbits ; Tandem Mass Spectrometry

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.