益生菌在消化系肿瘤治疗中的潜在应用价值

应用细菌治疗肿瘤有着悠久的历史, 但毒性等不良反应限制了相关基础研究及临床应用. 益生菌的发现和相关技术的进步, 使其在治疗肿瘤的同时降低毒副作用. 近年来的研究进展使益生菌有望成为一种肿瘤基因治疗的载体. 作为益生菌寄居的主要场所, 消化系与益生菌关系密切, 为益生菌和消化系肿瘤的结合提供了新的切入点, 也为消化系肿瘤的治疗带来新的契机. 本文将对益生菌及其在消化系肿瘤治疗中的产生、发展及发展方向作一综述.     

人CXCR3基因转染细胞株的构建、鉴定及初步功能研究

目的:构建含有人CXCR3基因的重组逆转录病毒载体,获得稳定表达人CXCR3分子的基因转染细胞株L929-CXCR3,研究CXCR3与其配体Mig、IP-10及I-TAC相互作用引起的L929-CXCR3的迁移效应。方法:TRIzol一步法从经PHA和IL-2活化的人PBMC中抽提总RNA,RT-PCR扩增人CXCR3全长基因,装入逆转录病毒载体pEGZ-term,与两辅助病毒载体脂质体法共转染包装细胞293T,收集培养上清感染L929细胞,500μg/mlzeocin加压筛选获得稳定表达人CXCR3分子的基因转染细胞株L929-CXCR3。采用流式细胞术和RT-PCR分别从蛋白及基因水平对CXCR3的表达进行鉴定。Transwell分析L929-CXCR3细胞在Mig、IP-10及I-TAC作用下的迁移率。结果:构建了含人CXCR3基因的重组逆转录病毒载体,建立了人CXCR3基因转染细胞株L929-CXCR3,其膜表面CXCR3分子的阳性表达率为98.4%;趋化L929-CXCR3发生迁移的最小配体浓度分别为Mig10ng/ml、IP-105ng/ml及I-TAC1ng/ml,相应迁移率分别为2.46%、2.34%及2.24%。结论:L929-CXCR3细胞株的建立为研究CXCR3信号转导与生物学功能及制备相应的单克隆抗体奠定了基础。     

甲异靛对K562和HL-60细胞Wnt信号通路的影响

本研究探讨甲异靛对K562细胞和HL-60细胞Wnt信号通路的影响。采用RT-PCR和Western blot方法分别检测甲异靛处理的K562和HL-60细胞中GSK-3β及其下游相关基因及蛋白的表达水平。结果表明:甲异靛可使HL-60细胞中β-catenin和c-myc基因表达下降,但对K562细胞的这两种基因表达无明显影响;甲异靛略能增加HL-60细胞中GSK-3β蛋白表达,但明显降低K562细胞和HL-60细胞中p-GSK-3β和c-MYC蛋白表达水平;甲异靛对K562细胞中β-catenin表达没有明显影响,但能使HL-60细胞中β-catenin表达下降。结论甲异靛可抑制K562细胞和HL-60细胞中Wnt信号通路的传导,降低癌基因和相关蛋白的表达,从而发挥治疗白血病的作用。     

Combined effect of age and severity on the risk of dementia in Parkinson's disease

Age and severity of extrapyramidal signs have been consistently associated with incident dementia in Parkinson's disease. We evaluated the separate and combined effects of age and severity of extrapyramidal signs on the risk of incident dementia in Parkinson's disease in the setting of a population-based prospective cohort study. Age and the total Unified Parkinson's Disease Rating Scale motor score at baseline evaluation were dichotomized at the median. Four groups of Parkinson's disease patients were defined: younger age/low severity (reference), younger age/high severity, older age/low severity, and older age/high severity. Risk ratios for incident dementia were calculated with Cox proportional hazards models controlling for gender, education, ethnicity, and duration of Parkinson's disease. Of 180 patients, 52 (28.9%) became demented during a mean follow-up period of 3.6 +/- 2.2 years. The median age at baseline of the Parkinson's disease patients was 71.8 years (range, 38.5-95.9 years), and the median total Unified Parkinson's Disease Rating Scale motor score was 24 (range, 2-65). The group with older age/high severity had a significantly increased risk of incident dementia (relative risk, 9.7; 95% confidence interval, 3.9-24.4) compared with the group with younger age/low severity (reference), whereas the groups with older age/low severity (relative risk, 1.6; 95% confidence interval, 0.5-4.8) and younger age/high severity (relative risk, 1.2; 95% confidence interval, 0.5-3.2) did not. These findings suggest that the increased risk of incident dementia in Parkinson's disease associated with age and severity of extrapyramidal signs is related primarily to their combined effect rather than separate effects.     

Literacy and memory decline among ethnically diverse elders

Literacy may be a more powerful indicator of brain reserve than years of education. Literacy level may be a proxy for native intellectual capacity or life experience that can compensate for brain damage or provide brain reserve. Alternately, the experience of acquiring literacy skills may in itself change the organization of the brain and increase protection against cognitive decline. However, because people with low levels of literacy obtain poor scores on most cognitive measures, only longitudinal studies can elucidate the role of reading ability in reserve. We determined whether literacy skills could predict cognitive change in a sample of 136 English-speaking African American, Caucasian, and Hispanic elders selected from a longitudinal aging study in New York City. According to a physician's independent examination, all participants were nondemented throughout the four longitudinal assessments. Literacy level was assessed using the WRAT-3 reading subtest. After accounting for age at baseline and years of education, GEE analyses showed that elders with low levels of literacy had a steeper decline in both immediate and delayed recall of a word list over time as compared to high literacy elders. Our findings suggest that literacy skills are protective against memory decline among nondemented elders.     

基于“痰瘀互结”辨治糖尿病前期

糖尿病前期可归属中医的"脾瘅",是一种血糖异常的高代谢综合征。糖尿病前期人群是糖尿病高危人群。中医认为"脾瘅"的病位在脾,脾虚为其起病之根源,而痰瘀互结贯穿病机之始终。治疗采用祛痰化浊、活血化瘀之法,以二陈汤合桃红四物汤加减治疗为主,直除病根;以健脾祛湿食疗方为辅,配合饮食控制和适当运动,可获良效。     

蜕皮甾酮对氧化损伤的人晶状体上皮细胞凋亡的防护作用

目的:探讨蜕皮甾酮(ECR)对氧化损伤的人晶状体上皮细胞(HLEC-B3)凋亡有无抑制作用。方法:本研究在终浓度300μmol/LH2O2培养液中复制HLEC凋亡模型,并以雌二醇(E2)作为阳性对照,在透射电子显微镜下观察HLEC-B3超微结构的改变,采用FCM法检测HLEC-B3凋亡率及线粒体膜电位的变化。结果:超微结构研究显示,H2O2组绝大多数HLEC-B3发生凋亡,并呈凋亡各期改变的全过程;E2、ECR组仅少数HLEC-B3发生凋亡,并多为早期或中期的轻微改变。FCM结果显示:H2O2组HLEC凋亡率显著高于空白对照组;E2和ECR组凋亡率均低于H2O2组(P0.01)。H2O2组线粒体跨膜电位比对照组显著下降;E2组和ECR组的线粒体跨膜电位均比H2O2组升高(P0.01)。结论:ECR可减轻实验性氧化损伤的HLEC凋亡程度,为寻求防治老年性白内障的药物提供实验依据。     

紫外分光光度测定特麻滴鼻剂的含量

本文采用双波长分光光度法消除组分间干扰进行含量测定,特非那定含量测定波长为261．5,253nm,对应平均回收率99．8％（RSD＝0．9％,n=9),盐酸麻黄碱含量测定波长为254．8nm,对应平均回收率99．5％（RSD＝1．5％,n=9),本方法简便,快速,准确。     

Protein kinase C-dependent activation of P44／42 mitogen-activated protein kinase and heat shock protein 70 in signal transduction during hepatocyte ischemic preconditioning

AIM: To investigate the significance of protein kinase C (PKC), P44/42 mitogen-activated protein kinase (MAPKs) and heat shock protein (HSP)70 signal transduction during hepatocyte ischemic preconditioning. METHODS: In this study we used an in vitro ischemic preconditioning (IP) model for hepatocytes and an in vivo model for rat liver to investigate the significance of protein kinase C (PKC), P44/42 mitogen-activated protein kinase (P44/42 MAPKs) and heat shock protein 70 (HSP70) signal transduction in IP. Through a normal liver cell hypoxic preconditioning (HP) model in which cultured normal liver cells were subjected to 3 cycles of 5 rain of incubation under hypoxic conditions followed by 5 rain of reoxygenation and subsequently exposed to hypoxia and reoxygenation for 6 h and 9 h respectively. PKC inhibitor, activator and MEK inhibitor were utilized to analyze the phosphorylation of PKC, the expression of P44/42 MAPKs and HSP70. Viability and cellular ultrastructure were also observed. By using rat liver as an in vivo model of liver preconditioning (3 cycles of 10-min occlusion and 10-min reperfusion), in vivo phosphorylation of PKC and P44/42MAPKs, HSP70 expression were further analyzed. AST/ALT concentration, cellular structure and ultrastruture were also observed. All the data were statistically analyzed. RESULTS: Similar results were obtained in both in vivo and in vitro IP models. Compared with the control withouts IP (or HP), the phosphorylation of PKC and P44/42 MAPKs and the expression of HSP70 were obviously increased in IP (or HP) treated model in which cytoprotection could be found. The effects of preconditioning were mimicked by stimulating PKC with 4β phorobol-12-myristate 13-acetate (PMA). Conversely, inhibiting PKC with chelerythrine abolished the protection given by preconditioning. PD98059, inhibitor of MEK (the upstream kinase of P44/42MAPKs), also reverted the cytoprotection exerted by preconditioning. CONCLUSION: The results demonstrate that preconditioning induces a rapid activation of P44/421VlAPKs and PKC activation plays a pivotal role in the activation of P44/42 MAPKs pathway that participates in the preservation of liver cells. HSP expression is regulated by signals in PKC dependent P44/42 MAPKs pathway.