绵羊fertilin β基因编码区的钓取与结构分析

Fertilin β与精卵的结合和融合有密切关系。为探讨fertilin β蛋白在绵羊受精过程中的作用机理, 采用RACE技术, 首次钓取了该基因的编码区。结果绵羊fertilin β基因的编码区cDNA全长为2,217 bp。同源性分析显示, 绵羊的fertilin β氨基酸序列与牛、猪和人的fertilin β具有79.4%、66.7%和58.1%的同源性。系统发育分析表明, 绵羊fertilin β与牛属于同一分支, 并且也显示了绵羊和牛分类地位最近, 这和传统的分类一致。Fertilin β蛋白结构域分析显示, 绵羊fertilin β去整合素识别序列为TDE, 与牛的序列相同。除了上述三肽序列外, 紧随X-D/E-E的ECD保守序列, 从而形成了X-D/E-ECD五肽保守序列, 在绵羊fertilin β中该五肽序列为TDECE。     

The JAK–STAT Pathway Is Critical in Ventilator-Induced Diaphragm Dysfunction

Mechanical ventilation (MV) is one of the lynchpins of modern intensive-care medicine and is life saving in many critically ill patients. Continuous ventilator support, however, results in ventilation-induced diaphragm dysfunction (VIDD) that likely prolongs patients’ need for MV and thereby leads to major associated complications and avoidable intensive care unit (ICU) deaths. Oxidative stress is a key pathogenic event in the development of VIDD, but its regulation remains largely undefined. We report here that the JAK–STAT pathway is activated in MV in the human diaphragm, as evidenced by significantly increased phosphorylation of JAK and STAT. Blockage of the JAK–STAT pathway by a JAK inhibitor in a rat MV model prevents diaphragm muscle contractile dysfunction (by ~85%, p < 0.01). We further demonstrate that activated STAT3 compromises mitochondrial function and induces oxidative stress in vivo, and, interestingly, that oxidative stress also activates JAK–STAT. Inhibition of JAK–STAT prevents oxidative stress-induced protein oxidation and polyubiquitination and recovers mitochondrial function in cultured muscle cells. Therefore, in ventilated diaphragm muscle, activation of JAK–STAT is critical in regulating oxidative stress and is thereby central to the downstream pathogenesis of clinical VIDD. These findings establish the molecular basis for the therapeutic promise of JAK–STAT inhibitors in ventilated ICU patients.     

高血压患者用药的依从性

高血压是人类健康面临的一个重要挑战,对患者及其家庭和社会造成了巨大的疾病负担。药物治疗是控制高血压的重要手段,合理应用抗高血压药能使90%的患者血压处于正常范围,但实际高血压的控制率仍很低,且发病率逐年上升,究其根本原因,是由于患者用药依从性不良。本文综述了高血压患者用药依从性的概念、现状及评估方法,并对其影响因素进行了详细的阐述,指出应积极干预及加强健康教育,以最大限度提高患者的用药依从性,降低高血压带来的靶器官损害,并进一步对寻求更准确、客观的用药依从性评估方法做出展望。     

Dietary long-chain omega-3 fatty acids of marine origin: a comparison of their protective effects on coronary heart disease and breast cancers

The relationship between high fish consumption and low mortality following coronary heart disease (CHD) and low incidence of breast cancer was first mentioned 3 decades ago. The fishes of interest are rich in omega-3 long-chain polyunsaturated fatty acids (ω-3 LC-PUFAs), especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which could be the active nutrients. The current consensus about cardioprotection is that ω-3 LC-PUFAs would mainly exert antiarrhythmic effects. One of the proposed mechanisms is that circulating non-esterified LC-PUFAs partition into cardiac cells membrane phospholipids and exert a direct effect on ionic channels and/or modify intracellular calcium homeostasis. In another hypothesis, changes in the metabolism of phosphoinositides would be involved and lead to the differential activation of PKC isoforms. As compared to the mechanisms proposed for the cardioprotective effects of omega-3 LC-PUFAs, less is known about the molecular mechanisms involved in breast cancers prevention. Some proposed mechanisms such as the modulation of phosphoinositides metabolism and/or modulation of intracellular calcium homeostasis, are common to both pathologies. Other hypotheses involve the alteration of the cellular redox status induced by highly peroxidizable polyunsaturated fatty acids (FA), or the modulation of gene expression, both phenomena being tightly linked to apoptosis. In this review, we report and compare some proposed mechanisms for the involvement of omega-3 LC-PUFAs in both cardiac and breast cancer protection. Deliberately, we chose to discuss only the mechanisms, which are less described in other reviews such as ionic channels in cancer, calcium homeostasis, PKC activation or matrix metalloproteinases in both cancer and cardiac models. The leitmotiv along this review is that cardio- and cancero-protective effects use common pathways. Comparison of the cellular effects might therefore help to highlight the “protective” pathways.     

白簕叶挥发油的化学成分

用GCMS联用技术首次研究了云南西双版纳白簕叶挥发油的化学成分,并应用色谱峰面积归一化法计算各成分的相对含量。一共分离出108个峰,确认了其中的81种成分,所鉴定的组分占挥发油总量的96.50%,主要是萜烯类及其含氧衍生物等。     

垂体瘤转化基因1(PTTG1)的表达变化对人前列腺癌细胞LNCaP生长增殖的影响

垂体肿瘤转化基因1(PTTG1)具有促进肿瘤生长和转移的作用.通过上调或下调基因表达的策略,观察PTTG1基因对人前列腺癌细胞株LNCaP细胞生长增殖的影响.利用PCR技术分离出PTTG1全长cDNA,分别正向和反向插入真核表达载体pIRES2-EGFP,重组载体分别命名为正义PTTG1-S/pIRES2-EGFP(即pI-P-S)和反义PTTG1-AS/pIRES2-EGFP(即pI-P-AS),将这两种重组载体稳定转染LNCaP细胞,通过流式细胞仪和MTT法分别检测了细胞周期和细胞增殖的情况.转染正义PTTG1后处于S期和G2期的细胞明显增加,细胞生长增殖能力增强;相反,转染反义PTTG1后处于S期和G2期细胞明显减少,细胞生长增殖能力减弱(P<0.05).结果表明,PTTG1能明显改变人前列腺癌细胞株LNCaP的细胞周期和细胞生长增殖能力,它的异常表达可能参与前列腺癌细胞生长增殖过程.     

4种桦树幼苗耐盐性分析与评价

耐盐植物引种和培育是开发利用盐碱地的主要方式,具有重要的研究价值。本试验以哈萨克斯坦引进的吉尔吉斯白桦（Betula kirghisorum）、欧洲白桦（B.pendula）、毛枝桦（B.pubescens）和本地的白桦（B.platyphylla Suk.）1年生幼苗为试验材料,于2014年7月在东北林业大学进行中性盐（NaCl）和碱性盐（NaHCO₃）的胁迫试验,测定生长量、光合参数和叶绿素含量,并通过因子分析法,对比评价4种桦树幼苗的耐盐碱能力,筛选出综合性状优良的桦树树种,为耐盐植物引种和培育提供有价值的数据。结果表明：随着盐浓度的升高,桦树幼苗的高生长和光合效率受到显著抑制,而当浓度≥0.5%时,大部分幼苗枯死。株高增长量、基径增长量、净光合速率（P_n）、光能利用效率（SUE）、羧化效率（CUE）、表观量子效率（AQY）及叶绿素含量之间的相关性多数达到了显著水平;最后利用因子分析法分别构建了0.1% NaCl、0.3% NaCl、0.1% NaHCO3和0.3% NaHCO₃胁迫处理的综合评价公式,并分别筛选出了综合性状相对优良的单株,其中NaCl胁迫下较优单株为32、33、34、35;NaHCO₃胁迫下较优单株为262、263、264、35。综合比较认为,吉尔吉斯白桦对低中浓度的中性盐的抗性最强,本地对照白桦对低中浓度碱性盐的抗性最强,而吉尔吉斯白桦和毛枝桦对高浓度碱性盐抗性较强。     

Identification of over-expressed genes in human renal cell carcinoma by combining suppression subtractive hybridization and cDNA library array

Renal cell carcinoma (RCC) is a common uro- genital malignancy and often shows odd biological features. RCC accounts for approximately 2% of ma- lignancies worldwide. The incidence of and mortality from RCC have continuously increased during the last 50 years. One third of the patients already have me- tastases when first consulting the doctors. Another 30%—40% of patients develop metastasis after surgi- Identification of over-expressed genes in human RCC 149 cal excision of the pri…