消炎利胆片与经胆道镜取石术治疗老年肝胆结石对患者血清Ins、C－P、HA水平的影响比较

目的：比较消炎利胆片与经胆道镜取石术治疗老年肝胆结石对患者血清胰岛素（ Ins）、C－肽（ C－P）、透明质酸（ HA）水平的影响。方法将老年胆结石患者212例随机分为试验组和对照组各106例。试验组采用经胆道镜取石术,对照组给予包括消炎利胆片口服在内的药物治疗。于治疗前后检测2组患者血清Ins、C－P及HA水平,并比较2组临床疗效。结果治疗后2组患者Ins和HA水平均显著低于治疗前,且试验组降低幅度大于对照组,差异均有统计学意义（P＜0．05）。但2组患者治疗后C－P水平差异无统计学意义（P＞0．05）。试验组的总有效率96．23％高于对照组的82．08％,差异有统计学意义（P＜0．05）。结论经胆道镜取石术治疗老年肝胆结石患者可显著降低血清Ins和HA水平,对C－P水平无影响,较药物治疗具有更好的治疗效果。     

心力衰竭患者心肌细胞外信号调节激酶及磷脂酰肌醇3激酶通路的信号蛋白表达

目的观察充血性心力衰竭(CHF)患者心肌组织细胞外信号调节激酶(ERK)和磷脂酰肌醇3激酶(PI3K)通路的信号蛋白表达.方法通过手术取材,选择因瓣膜性心脏病接受二尖瓣置换术的CHF患者40例,对照组38例(其中8例为意外伤亡的器官损献者).免疫沉淀法检测心肌组织ERK、PI3K蛋白表达及磷酸化, α-骨骼肌蛋白表达.结果CHF患者心肌组织呈典型的重构心肌的病理改变,心肌组织ERK蛋白表达光密度值(A)比值(ERK1/β-actin)、(ERK2/β-actin)、PI3K磷酸化比值(p-PI3K/β-actin)、α-骨骼肌蛋白表达A比值(α-skeletal-actin/β-actin)逐渐增强,且随心功能恶化逐渐增强, CHF组中不同心功能级别者与对照组相比差异均有统计学意义(P＜0.05 或P＜0.01).结论ERK及PI3K通路共同参与调节CHF患者心肌重构的病理生理过程.     

微量元素对超氧化物歧化酶活性的影响

用ＮＢＴ－Ｐ法、火焰原子吸收法，测定了不同浓度Ｓｅ、Ｍｇ、Ｆ－条件下ＳＯＤ标准品的活性和反应体积中Ｓｅ、Ｍｇ、Ｆ－含量。结果显示：（１）Ｓｅ浓度为７．５μｇ／Ｌ，ＳＯＤ活性达５９．００ｍｇ／Ｌ；Ｓｅ浓度由０．００μｇ／Ｌ增加至７．５μｇ／Ｌ时，ＳＯＤ活性由４２．５ｍｇ／Ｌ升至５９．００ｍｇ／Ｌ；Ｓｅ浓度继续增加到１０．００μｇ／Ｌ、２０．００μｇ／Ｌ时，ＳＯＤ活性均降为４２．５ｍｇ／Ｌ。（２）Ｍｇ浓度为３０．００ｍｇ／Ｌ时，ＳＯＤ活性由９６．５ｍｇ／Ｌ，Ｍｇ浓度由０．００ｍｇ／Ｌ增至３０．００ｍｇ／Ｌ，ＳＯＤ活性达４２．５ｍｇ／Ｌ，升至９６．５ｍｇ／Ｌ；继续增加Ｍｇ浓度到５０．００ｍｇ／Ｌ，ＳＯＤ活性降为７５．５ｍｇ／Ｌ。（３）Ｆ－由０．００ｍｇ／Ｌ增加到５．００ｍｇ／Ｌ时，ＳＯＤ活性由４２．５ｍｇ／Ｌ升到４９．５ｍｇ／Ｌ；继续增加Ｆ浓度到１０．００ｍｇ／Ｌ，ＳＯＤ活性降为４４．５ｍｇ／Ｌ；再增加Ｆ浓度至２０．００ｍｇ／Ｌ、４５．００ｍｇ／Ｌ后，ＳＯＤ活性维持在４９．５～５１．０ｍｇ／Ｌ之间。提示：ＳＯＤ活性受微量元素Ｓｅ、Ｍｇ、Ｆ－浓度的影响较大，只有在最适微量元素浓度条件下，ＳＯＤ活性方可达最高。     

Serotonin transporter gene polymorphisms and treatment-resistant depression

Major Depression Disorder (MDD) is a serious mental illness that is one of the most disabling diseases worldwide. In addition, approximately 15% of depression patients are defined treatment-resistant (TRD). Preclinical and genetic studies show that serotonin modulation dysfunction exists in patients with TRD. Some polymorphisms in the promoter region of the serotonin transporter gene (SLC6A4) are likely to be involved in the pathogenesis/treatment of MDD; however, no data are available concerning TRD.     

The -141C Ins/Del and Taq1A polymorphism in the dopamine D2 receptor gene may confer susceptibility to schizophrenia in Asian populations

It has been reported that two single nucleotide polymorphisms (SNP) Taq1A and -141C Ins/Del in the DRD2 gene may be associated with susceptibility to schizophrenia. Due to inconclusive and mixed results, a meta-analysis was conducted to further clarify the relationship between the two SNP and schizophrenia susceptibility. A systematic literature search for the association of these two SNP with schizophrenia susceptibility was conducted using PubMed, ScienceDirect, Chinese Biomedical Literature Database, and Chinese National Knowledge Infrastructure. Odds ratios (OR) with 95% confidence intervals (CI) were used to assess the strength of the associations reported. A total of 5558 schizophrenic patients and 6792 healthy controls from 31 articles were included in this study. Evidence regarding the association between -141C Ins/Del polymorphism and schizophrenia was found in the allele frequency comparison (Ins versus Del: OR 1.29, 95% CI 1.06–1.57; p = 0.01, P_raw = 0.1, P_{False Discovery Rate} = 0.023). In ethnic subgroup analysis, the result revealed that the 141C Ins/Del polymorphism was associated with schizophrenia in all genetic models in Asians, but not in Caucasians. For Taq1A polymorphism, a significant association was found in the allele frequency (A1 versus A2: OR 0.71, 95% CI 0.52–0.98, p = 0.03). Stratification by ethnicity indicated an association between the Taq1A polymorphism and schizophrenia in Asians, but not Caucasians. The present study suggests that the -141C Ins/Del polymorphism carries a significantly increased risk of schizophrenia, while the Taq1A polymorphism carries a significantly decreased risk of schizophrenia susceptibility in Asians.     

Parathyroid hormone stimulates phosphoinositide metabolism and intracellular calcium mobilization in osteoblast-like clone MC3T3-E1 cells

The effects of parathyroid hormone (rat 1–34 fragment, rPTH) on phosphoinositide metabolism and intracellular Ca²⁺ mobilization were studied in a osteoblast-like clone MC3T3-E1 cells. rPTH caused a transient rise in intracellular Ca²⁺ in a dose-dependent manner. Significant Ca²⁺ increase was still observed under the extracellular Ca²⁺-free condition. In addition, 100nM rPTH stimulated rapid formation of both 1,2-diacylglycerol (1,2-DAG) and inositol 1,4,5-trisphosphate (Ins(1,4,5)P₃), indicating agonist-triggered hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP₂). The current observations suggested that the rPTH-induced increase of intracellular Ca²⁺ was in part due to internal Ca²⁺ release mediated by Ins(1,4,5)P₃. These results indicate possible involvement of phosphoiniositide metabolism in signal transduction of PTH-stimulated osteoblastic cells.     

Lithium: bipolar disorder and neurodegenerative diseases Possible cellular mechanisms of the therapeutic effects of lithium

Bipolar illness is a major psychiatric disorder that affects 1-3% of the worldwide population. Epidemiological studies have demonstrated that this illness is substantially heritable. However, the genetic characteristics remain unknown and a clear personality has not been identified for these patients. The clinical history of lithium began in mid-19th century when it was used to treat gout. In 1940, it was used as a substitute for sodium chloride in hypertensive patients. However, it was then banned, as it had major side effects. In 1949, Cade reported that lithium could be used as an effective treatment for bipolar disorder and subsequent studies confirmed this effect. Over the years, different authors have proposed many biochemical and biological effects of lithium in the brain. In this review, the main mechanisms of lithium action are summarised, including ion dysregulation; effects on neurotransmitter signalling; the interaction of lithium with the adenylyl cyclase system; inositol phosphate and protein kinase C signalling; and possible effects on arachidonic acid metabolism. However, none of the above mechanisms are definitive, and sometimes results have been contradictory. Recent advances in cellular and molecular biology have reported that lithium may represent an effective therapeutic strategy for treating neurodegenerative disorders like Alzheimer's disease, due to its effects on neuroprotective proteins like Bcl-2 and its actions on regulators of apoptosis and cellular resilience, such as GSK-3. However, results are contradictory and more specific studies into the use of lithium in therapeutic approaches for neurodegenerative diseases are required.     

216例糖尿病患者血清微量元素的含量及与胰岛素和血糖的关系

目的 :探讨非胰岛素依赖性糖尿病 (NIDDM )患者血清锌、铬、铜、铁的变化及与胰岛素和血糖的关系。方法 :对 2 16例NIDDM患者血清微量元素、胰岛素、血糖水平进行了观察 ,并与正常对照组做比较 ,各指标间做相关分析。结果 :糖尿病组血清Zn、Cr显著下降 ,Cu显著升高 ,Fe无明显改变。结论 :血清微量元素含量变化与糖尿病关系密切 ,动态检测Zn、Cr、Cu、Fe对防治糖尿病并发症的发生及判断预后有着特殊的诊断价值。     

大鼠Ins1基因启动子区域DNA甲基化状态的研究

目的:研究大鼠Ins1(Insulin 1)基因启动子在各种组织中DNA甲基化的状态及在转化分化过程中甲基化的变化情况,为从表观遗传学方面研究Ins1基因表达调控的机制奠定基础。方法:通过RT-PCR检测大鼠胰岛、大鼠胰岛素瘤细胞(INS-1)及大鼠肝干细胞(WB)中Ins1基因的表达情况。采用重亚硫酸盐测序法分析这三种细胞位于转录起始位点上游400 bp的Ins1基因启动子区域DNA甲基化的状态,并用焦磷酸测序法分析大鼠肺、脾、皮肤、小肠、脂肪和肝脏组织的甲基化状态及WB细胞转入PDX1慢病毒后甲基化的变化情况。结果:大鼠胰岛和INS-1细胞中Ins1基因高表达,启动子区域的甲基化程度非常低,而在大鼠肺、脾、皮肤、小肠、脂肪、肝脏组织和WB细胞中Ins1基因不表达,启动子区域的甲基化程度很高,当WB细胞转入PDX1慢病毒后可使Ins1基因启动子区域的甲基化程度降低。结论:Ins1基因的表达受甲基化调控,PDX1单个转录因子虽可降低Ins1基因甲基化程度但并不能使其完全去甲基化并表达Ins1基因。