Effects of Ligustrum robustum on gut microbes and obesity in rats

AIM: To investigate the anti-obesity and antibacterial effects of Ligustrum robustum(L. robustum) in vivoand in vitro and its possible mechanisms. METHODS: The effects of L. robustum aqueous extract(LR) on various gut bacteria in vitro were evaluated. The effects of LR on high-fat diet-fed(HFD) rats in vivo were also assessed. Culture methods,quantitative polymerase chain reaction,and terminalrestriction fragment length polymorphism were used to analyze the effects of LR on gut bacteria. Biochemical tests were also performed to detect the changes in obesity-related indicators after LR treatment. RESULTS: LR treatment lowered adipose weight and decreased Lee's index,blood glucose,total cholesterol,and lipid in the tested groups relative to control(P 0.05). To determine the reasons for these changes,we assessed the potential bacteriostatic and bactericidal effects of LR on specific bacterial species in vitro. LR affected the richness,diversity,and evenness of gut bacteria,increased fecal Lactobacillus,and decreased Enterococci in HFD rats(P 0.05). CONCLUSION: L. robustum may be a safe and effective food for weight loss and obesity control,and the effects of L. robustum might be mediated by the regulation of gut bacteria.     

核工业某厂放射工作人员与非放射工作人员的MDM2基因表达调查与分析

目的 探讨核工业某厂放射工作人员与非放射工作人员辐射敏感基因表达的差异。 方法 采集了3名健康人外周血进行60Co γ射线照射,建立辐照后鼠双微体基因2（MDM2）表达的剂量-效应关系,抽取核工业某厂96名工作人员（49名放射工作人员、47名非放射工作人员）外周血,利用实时荧光定量PCR技术检测放射工作人员外周血中MDM2基因的表达情况。 结果 在0~2 Gy剂量范围内,MDM2的表达水平随照射剂量增加而上升。某厂96名工作人员外周血MDM2基因表达水平的检测分析结果表明,非放射工作人员年龄因素对外周血MDM2基因表达无影响（F=2.11,P＞0.05）;放射工作人员外周血MDM2基因表达与非放射工作人员相比,差异具有统计学意义（t=7.78,P＜0.05）。 结论 电离辐射可以诱导人离体外周血MDM2基因表达改变,且基因表达与照射剂量存在一定的剂量相关性,MDM2有望成为核工业放射工作人员健康调查的敏感指标。     

100例血清HBsAg阴性乙型肝炎恢复期病人血清中HBV-DNA检测分析

目的探讨血清 HBsAg 呈阴性的乙肝恢复期病人血中 HBV-DNA 存在情况。方法选取血清 HBsAg 阴性的处于乙肝恢复期病例100例,分析这部分人血液 HBV-DNA 的检测结果,其中两对半检测用单克隆抗体免疫放射分析法。HBV-DNA 用ELISA-PCR 法。结果 HBsAg 为阴性的100例乙肝恢复期血样中,HBV-DNA 全部呈阴性。结论单克隆抗体免疫放射分析法检测血清 HBsAg 能真实反映受检者是否携带乙肝病毒。     

PC-3细胞中雄激素受体突变体的表达和转录激活功能的研究

目的:探讨不同时间点移植骨髓单个核细胞(bone marrow mononuclear cells,BMMCs)对心肌梗死后的心功能的影响.方法:取成年雄性近交系Wistar大鼠股骨和胫骨,常规抽取骨髓,分离制备BMMCs悬液.将成年雄性近交系Wistar大鼠64只随机分为空白对照组(组Ⅰ,n=10)、梗死对照组(组Ⅱ,n=18)、即刻移植组(组Ⅲ,n=18)和两周移植组(组Ⅳ,n=18).用结扎冠状动脉左前降支的方法建立大鼠心肌梗死模型,在建模后即刻和2周分别将10μl BMMCs液(6×106个细胞)植入组Ⅲ和组Ⅳ的梗死周边区,组Ⅱ于建模后14 d植入等量的磷酸盐缓冲液(PBS).用心脏超声和血流动力学检查观察细胞移植后4周的心脏功能改变.结果:骨髓单个核细胞移植4周后,与组Ⅱ、组Ⅲ相比,组Ⅳ左室功能重建指标[左室射血分数(EF)、左室短轴缩短率(FS)、左室前壁厚度(LVAWT)]和血流动力学检查指标[左室收缩压(LVSP)、左室舒张末压(LVEDP)和左室舒张压力时间变化最大速率±dp/dtmax]均明显改善(P＜0.05);而组Ⅱ、Ⅲ间上述指标相比无显著差异.结论:心肌梗死后2周骨髓单个核细胞移植治疗效果优于即刻移植,可能是由于在心肌梗死后1周时炎症反应最重,而2周时逐渐减弱.     

Screening and evaluation of the role of immune genes of brain metastasis in lung adenocarcinoma progression based on the TCGA and GEO databases

BackgroundBrain metastasis was one of the factors leading to the poor long-term prognosis of patients with lung adenocarcinoma (LUAD).MethodsThe expression levels of immune genes in LUAD and LUAD brain metastases tissues were analyzed in {"type":"entrez-geo","attrs":{"text":"GSE161116","term_id":"161116"}}GSE161116 dataset using the GEO2R, and the levels of differential immune genes in normal lung and LUAD tissues were verified. The biological functions and signaling mechanisms of the differential immune genes were explored via Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis. Cox regression analysis was used to screen the prognostic factors of LUAD patients, and a risk model was constructed. The role of the model was checked in the development of LUAD via receiver operating characteristic analysis, gene set enrichment analysis, and Cox regression analysis.ResultsDifferentially expressed genes (DEGs) in brain metastasis were involved in the adaptive immune response, B cell differentiation, leukocyte migration, NF-kB signaling pathway, among others. The expression levels of TNFRSF11A, MS4A2, IL11, CAMP, MS4A1, and F2RL1 were independent factors affecting the poor prognosis of LUAD patients via Cox regression analysis and Akaike information criterion. In the constructed risk model, the overall survival of LUAD patients in the high-risk group was poor. The risk model was significantly related to the gender, clinical stage, T stage, lymph node metastasis, and survival status of LUAD patients. In addition, the risk model score was an independent risk factor that affected the poor prognosis of LUAD patients. TNFRSF11A, CAMP, F2RL1, IL11, MS4A1, and MS4A2 of the risk factors had diagnostic significance in LUAD brain metastasis and LUAD. The risk model participated in cytokinetic process, cell cycle, citrate cycle TCA cycle, etc. The risk model score was correlated with the levels of B cells memory, mast cells resting, macrophages M0, mast cells activated, neutrophils, eosinophils, T cells gamma delta, and immune cell markers.ConclusionsThe risk model based on the LUAD brain metastasis immune factors TNFRSF11A, MS4A2, IL11, CAMP, MS4A1, and F2RL1 was related to the diagnosis, poor prognosis, and immune infiltrating cells of LUAD patients, and is expected to provide a reference for the development of treatment strategies for LUAD patients.     

三氧化二砷对人肺腺癌细胞的细胞毒作用及其机制

背景与目的:三氧化二砷(arsenictrioxide,As2O3)应用于急性早幼粒细胞性白血病(acutepromyelocyticleukemia,APL)的临床化疗已显示较好疗效。目前,已开展了将As2O3用于治疗胃癌、头颈部癌和食管癌等实体瘤的实验研究。本研究旨在探讨As2O3对人肺腺癌SPCA1细胞的毒性及其作用机制。方法:MTT法检测As2O3对SPCA1细胞的生长抑制作用;流式细胞术测定经不同浓度As2O3处理后的SPCA1细胞的细胞周期改变、凋亡相关蛋白Fas和Bcl-2阳性细胞百分率及细胞内钙离子(IECa2+)含量变化。结果:As2O3可显著抑制SPCA1细胞生长增殖,且呈剂量-效应关系(r=0.973,P<0.05),其IC50为8.56μmol/L;As2O3能显著增加Fas蛋白表达和IECa2+含量(P<0.05),并使细胞周期阻滞在G2/M期,但对Bcl-2表达无影响(P>0.05)。结论:As2O3对SPCA1细胞有显著的毒性作用,其机制可能与上调Fas表达和增加IECa2+含量及阻滞细胞周期有关。     

Triterpenes and triterpenoid saponins from the leaves of Ilex kudincha

One new triterpene, kudinchalactone A (1), and four new triterpenoid saponins, ilekudinchosides A-D (2- 5), were isolated from the leaves of Ilex kudincha C.?J. Tseng along with eight known triterpenoids. These new compounds were elucidated by spectroscopic methods including 1D and 2D NMR, HR-TOF-MS, and CD spectra. Compounds 2, 3, 12, and 13 showed antibacterial activities against Staphylococcus aureus (SA) and methicillin-resistant Staphylococcus aureus (MRSA).     

Isoflurane preconditioning increases endothelial cell tolerance to in-vitro simulated ischaemia

Objectives Isoflurane preconditioning has been shown to protect endothelial cells against lipopolysaccharide and cytokine induced injury. This study was designed to determine whether isoflurane preconditioning increased endothelial cell tolerance to ischaemia. Methods Bovine pulmonary arterial endothelial cells were exposed or not exposed to various concentrations of isoflurane for 1 h. After a 30‐min isoflurane‐free period, cells were subjected to oxygen‐glucose deprivation (OGD) for 3 h and reoxygenation for 1 h. Lactate dehydrogenase release from cells was used to measure cell injury. In some experiments, various protein kinase C (PKC) inhibitors and ATP‐sensitive potassium channel (K_ATP channel) inhibitors were present from 30 min before isoflurane treatment to the end of isoflurane treatment. Key findings Isoflurane preconditioning dose‐dependently decreased the OGD induced lactate dehydrogenase release. This protection was inhibited by 2 µM chelerythrine, a general PKC inhibitor, or 10 µM Gö6976, an inhibitor for the conventional PKCs. This protection was also inhibited by 0.3 µM glybenclamide, a general K_ATP channel inhibitor, and 500 µM 5‐hydroxydecanoate, a mitochondrial K_ATP channel blocker. In addition, pretreatment with 100 µM diazoxide, a K_ATP channel activator, for 1 h also reduced OGD induced endothelial cell injury. This diazoxide induced protection was inhibited by chelerythrine. Conclusions The results suggest that isoflurane preconditioning induces endothelial protection against in‐vitro simulated ischemia. This protection may be mediated at least in part by conventional PKCs and mitochondrial K_ATP channels. The results also indicate that PKCs may be downstream of K_ATP channels in causing endothelial protection.     

Miltefosine induces apoptosis-like cell death in yeast via Cox9p in cytochrome c oxidase

Miltefosine has antifungal properties and potential for development as a therapeutic for invasive fungal infections. However, its mode of action in fungi is poorly understood. We demonstrate that miltefosine is rapidly incorporated into yeast, where it penetrates the mitochondrial inner membrane, disrupting mitochondrial membrane potential and leading to an apoptosis-like cell death. COX9, which encodes subunit VIIa of the cytochrome c oxidase (COX) complex in the electron transport chain of the mitochondrial membrane, was identified as a potential target of miltefosine from a genomic library screen of the model yeast Saccharomyces cerevisiae. When overexpressed in S. cerevisiae, COX9, but not COX7 or COX8, led to a miltefosine-resistant phenotype. The effect of miltefosine on COX activity was assessed in cells expressing different levels of COX9. Miltefosine inhibited COX activity in a dose-dependent manner in Cox9p-positive cells. This inhibition most likely contributed to the miltefosine-induced apoptosis-like cell death.