The single-cell as the basic unit of biological organs and tissues has recently been considered an important window to furthermore understand molecular mechanisms of organ function and biology. The current issue with a special focus on single cell biomedicine is the first effort to collect the evidence of diseaseassociated single cell research, define the significance of single cell biomedicine in the pathogenesis of diseases, value the correlation of single cell gene sequencing with diseasespecific biomarkers, and monitor the dynamics of RNA processes and responses to microenvironmental changes and drug resistances.

Diabetic retinopathy (DR) is one of the most common and challenging ocular complications of diabetes mellitus. As a chronic, progressive ocular disease that poses a serious threat to vision, DR has gradually become a leading cause of blindness worldwide. Emerging evidence points to an important role of endoplasmic reticulum (ER) stress in not only maintaining the steady-state equilibrium in the body, but also in intracellular synthesis, protein folding, and other essential functions. Recent studies have demonstrated clear associations between ER stress-related physiological functions and the pathogenesis of DR. When cells are stimulated by external stimuli, UPR pathway is activated firstly to protect it. However, long-term harmful factors can induce ER stress. which interferes with the physiological metabolism of retinal cells and participates in the occurrence of DR via the ATF6 pathway, PERK pathway and IRE1 pathway. At present, ER stress blocker is expected to become a new anti-DR therapy. Thus, understanding the relationship between ER stress and DR will help to develop new effective preventative treatments. In this review, we summarize the risk factors of DR pathogenesis induced by ER stress toward revealing potentially new therapeutic targets.

Objective To explore the association between esophageal cancer and serum vitamin E level and to provide evidences for researches and prevention of esophageal cancer.Methods Case-control studies on esophageal cancer and serum vitamin E level published from January 1980 to December 2015 were searched through China National Knowledge Infrastructure,Wanfang Database,PubMed,and Web of Science.Meta-analysis was performed with Stata 12.0.Results A total of 9 literatures (7 in Chinese and 2 in English),involving in 358 esophageal cancer cases and 538 controis,were included in the meta-analysis.The meta-analysis showed that the serum vitamin E level of esophageal cancer cases was lower than that of the controls (standardized mean difference [SMD] =-0.50,95 ％ confidence interval [95 ％ CI] =-0.65-0.36,P ＜ 0.001).Subgroup analysis found that the serum vitamin E levels of the esophageal cancer cases were lower than those of the controls for the studies conducted in China (SMD =-0.50,95％ CI =-0.67-0.33) and in United States (SMD =-0.51,95％ CI =-0.77-0.25),with the controls selected from communities (SMD =-0.54,95％ CI=-0.69-0.39),with the sample size of larger than 50 (SMD =-0.56,95％ CI=-0.71-0.41),with age-matched controls (SMD =-0.57,95％ CI =-0.72-0.42),and with serum vitamin E level detection using high performance liquid chromatography (HPLC) (SMD =-0.41,95％ CI =-0.59-0.24) and using method other than HPLC (SMD =-0.67,95％ CI =-0.91-0.43) (all P ＜ 0.001).Sensitivity analysis and publication bias test showed that the results of the study were stable and there was no publication bias for the literatures included in the study.Conclusion Serum vitamin E level is low in esophageal cancer patients.

We aimed to detect the role of HSP70 in endoplasmic reticulum (ER) stress-induced cell apoptosis, and to reveal the molecular mechanism underlying the HSP70 regulated ER stress induced-apoptosis, secretion and calcium signal transduction. The findings provide new intervention targets and theoretical basis of subcellular molecular application for myocardial protection. We used SD neonatal rat cardiomyocyte to establish a hypoxia cell model, and then we further detected the role of HSP70 in cell apoptosis, in production of ROS, in expression of casepase-12, CHOP, JNK pathway, CaSR and SERCA in ER caused by ER stress, as well as in the immunohistochemical staining of Bcl-xL, Bcl-2 and BAX, and Fas and FasL by overexpression or downexpression of HSP70. Results showed that hypoxia-induced cell apoptosis was inhibited by HSP70, but was promoted by HSP70 anti-sense oligonucleotide. Hypoxia-induced ROS production was also inhibited by HSP70, but was not inhibited by HSP70 anti-sense oligonucleotide. HSP70 significantly inhibited the expression of Caspase-12, CaSR and CHOP. HSP70 increased the expression of JNK, but did not influent the expression of SERCA. HSP70 anti-sense oligonucleotide significantly increased the expression of CHOP, but did not significantly influent other tested molecules. Bcl-xL and Bcl-2 were highly expressed in HSP70-treated cells, but were low expressed in HSP70 anti-sense oligonucleotide-treated cells. Bax, Fas, FasL were predominantly expressed in cell treated with HSP70 anti-sense oligonucleotide, but were not in HSP70-treated cells. Thus, HSP70 inhibited the cell apoptosis via inhibiting the expression of Caspase 12, CHOP, Bax, Fas and FasL, and inhibited the Ca2+ current via inhibiting the expression of CaSR, and that the JNK pathway might play important roles in cell apoptosis and ROS-induced Ca2+ current.

目的 建立使用通用荧光引物分步PCR法筛选裸鼹鼠微卫星位点的方法.方法 在特异性引物F链的5'端连接通用引物,先以特异引物R链和加长引物F链进行PCR,再加入通用荧光引物进行第二步PCR,最后使用琼脂糖电泳和毛细管电泳检测扩增产物,同时以传统的荧光引物PCR为对照.结果 琼脂糖电泳结果显示,通用荧光引物PCR产生的目的片段清晰,引物特异性强,目的片段多态性与传统PCR产生的多态性一致,且片段大小均比传统PCR产生的目的片段大15 bp左右,与预期一致.毛细管电泳结果也显示,通用引物PCR结果检测的等位基因数与传统荧光引物PCR方法产生的数量完全一致,无杂带,扩增效率高,具有较强的可操作性.结论 使用通用荧光引物分步PCR法结果可应用于裸鼹鼠基因组大量微卫星位点的筛选.

Objective: Growing evidence indicates that microRNAs (miR) have been shown to regulate cardiac hypertrophy in animal models of myocardial infarction (MI). This study aimed to evaluate the role of the miR-10a in cardiac hypertrophy after myocardial infraction. Methods: The expression of miR-10a was compared in sham-operation and MI surgery. Then, the cell surface area and the cardiac hypertrophy gene expression were analyzed under miR-10a overexpression in primary cardiomyocytes. In addition, the luciferase assay and western blot were used for determine the target gene regulated by miR-10a. Lastly, the effect of miR-10a in cardiac hypertrophy was determined by in vivo overexpression of miR-10a in MI surgery group. Results: We found that miR-10a was down-regulated in cardiac hypertrophy both in vitro and in vivo. In vitro overexpressing of miR-10a inhibits cardiomyocytes hypertrophy. Then we identified a novel target gene of miR-10a, HDAC4. In contrast to miR-10a, HDAC4 was up-regulated during cardiac hypertrophy. Moreover, in vivo overexpressing miR-10a effectively attenuated myocardial infarction-induced cardiac hypertrophy through decreased the expression of HDAC4. Conclusion: Our results show that miR-10a is a key regulator or cardiac hypertrophy, thus offering a new therapeutic strategy of myocardial infarction-induced cardiac hypertrophy.

目的 建立一种裸鼹鼠骨髓巨噬细胞分离培养的方法,并通过与小鼠骨髓巨噬细胞进行比较研究其吞噬功能.方法 分离裸鼹鼠骨髓细胞,在含60 ng/mL巨噬细胞集落刺激因子(M-CSF)完全培养基的诱导下,体外贴壁培养6～7 d,采用倒置显微镜观察细胞的生长状态.裸鼹鼠骨髓细胞诱导结束后,采用流式细胞术检测贴壁细胞表面抗原CD11b和F4/80的阳性率,鉴定骨髓巨噬细胞的纯度;采用异硫氰酸荧光素(FITC)-dextran根据荧光强度比较裸鼹鼠和ICR小鼠骨髓巨噬细胞的吞噬功能.结果 通过本方法获得的贴壁细胞具有典型的巨噬细胞的形态特征,且细胞表面抗原CD1 1b和F4/80的阳性率均高于80％;裸鼹鼠与ICR小鼠骨髓巨噬细胞的吞噬率分别为99.87％士0.13％和88.79％±0.90％.结论 本文建立的方法是一种简单实用的体外分离培养裸鼹鼠骨髓巨噬细胞的方法,且能够获得高纯度、高活性的巨噬细胞.裸鼹鼠骨髓巨噬细胞的吞噬功能高于小鼠骨髓巨噬细胞.