Bisphenol A exposure at an environmentally relevant dose induces meiotic abnormalities in adult male rats

Whether environmental exposure to bisphenol A (BPA) may induce reproductive disorders is still controversial but certain studies have reported that BPA may cause meiotic abnormalities in C. elegans and female mice. However, little is known about the effect of BPA on meiosis in adult males. To determine whether BPA exposure at an environmentally relevant dose could induce meiotic abnormalities in adult male rats, we exposed 9-week-old male Wistar rats to BPA by gavage at 20 μg/kg body weight (bw)/day for 60 consecutive days. We found that BPA significantly increased the proportion of stage VII seminiferous epithelium and decreased the proportion of stage VIII. Consequently, spermiation was inhibited and spermatogenesis was disrupted. Further investigation revealed that BPA exposure delayed meiosis initiation in the early meiotic stage and induced the accumulation of chromosomal abnormalities and meiotic DNA double-strand breaks (DSBs) in the late meiotic stage. The latter event subsequently activated the phosphatidylinositol 3-kinase-related protein kinase (ATM). Our results suggest that long-term exposure to BPA may lead to continuous meiotic abnormalities and ultimately put mammalian reproductive health at risk.     

颍上八里河自然保护区鹭卵p3种重金属残留分析

2005年5月,采集了淮河地区颍上八里河集群繁殖的夜鹭（Nycticorax nycticorax）和小白鹭（Egretta garzetta）鸟卵共18枚,用原子吸收法测定了卵壳、内容物中重金属Cd、Pb、Cr的残留量。结果表明,所有卵壳样品中均检出一定水平的Cd、Pb和Cr残留量,夜鹭卵壳中重金属残留量为Pb〉Cr〉Cd,小白鹭卵壳中重金属残留量为Cr〉Pb〉Cd,卵壳中Pb和Cr残留量的种间差异都不显著,但Cd的种间差异显著;在2种鹭卵内容物中,Cr都被检出,在夜鹭卵内容物样品中,Pb只被部分检出,Cd在2种鹭卵内容物样品中都没有被检出,3种重金属在内容物中残留量的种间差异都不显著。2种鹭卵壳中Pb和Cd残留量极其显著地高于卵内容物,但Cr的这种残留分布上的差异不显著。本研究进一步证明卵壳可用作重金属污染物的指示物,监测和评价湿地生态系统中重金属的污染状况。     

一种基于主成分分析的混杂人群祖代信息遗传标记选择算法

鉴定群体的结构可以帮助追溯群体的发展史,定位疾病的易感基因．结构相关是一种常用的群体结构鉴定和关联作图方法．结构相关应用中的一个主要问题是它的统计效力高度依赖于所使用的祖代信息遗传标记．目前主要的祖代信息遗传标记选择方法大多要求已知研究样本的祖代信息,但是实际研究中个体的祖代信息大多未知或者难以确定．为了解决这个问题,本研究开发了一种新的基于主成分分析的祖代信息遗传标记选择算法．该方法不需要事先已知研究样本的祖代信息．模拟研究和真实的遗传数据分析提示,与传统的随机挑选祖代信息遗传标记的方法相比,新方法可以显著提高群体结构推断的准确性．本方法可以容易地应用于全基因组数据,挑选出富含群体结构信息的遗传标记．这些遗传标记可被广泛用于鉴定群体的结构和校正关联作图中群体混杂引起的统计偏差．     

Characterization of the most abundant Lactobacillus species in chicken gastrointestinal tract and potential use as probiotics for genetic engineering

The count and diffusion of Lactobacilli species in the differ ent gastrointestinal tract （GI） regions of broilers were investigated by quantitative realtime polymerase chain reaction, and the probiotic characteristics of six L. reuteri species isolated from broilers＇ GI tract were also investi gated to obtain the potential target for genetic engineering. Lactobacilli had the highest diversity in the crop and the lowest one in the cecum. Compared with the lower GI tract, more LactobaciUi were found in the upper GI tract. Lactobacillus reuteri, johnsonii, L. acidophilus, L. crispatus, L. salivarius, and L. aviarius were the predominant Lactobacillus species and present throughout the GI tract of chickens. Lactobacillus reuteri was the most abundant Lactobacillus species. Lactobacillus reuteri XC1 had good probiotic characteristics that would be a potential and desirable target for genetic engineering.     

Cloning, expression, and characterization of the human mitochondrial beta-ketoacyl synthase. Complementation of the yeast CEM1 knock-out strain

A human beta-ketoacyl synthase implicated in a mitochondrial pathway for fatty acid synthesis has been identified, cloned, expressed, and characterized. Sequence analysis indicates that the protein is more closely related to freestanding counterparts found in prokaryotes and chloroplasts than it is to the beta-ketoacyl synthase domain of the human cytosolic fatty acid synthase. The full-length nuclear-encoded 459-residue protein includes an N-terminal sequence element of approximately 38 residues that functions as a mitochondrial targeting sequence. The enzyme can elongate acyl-chains containing 2-14 carbon atoms with malonyl moieties attached in thioester linkage to the human mitochondrial acyl carrier protein and is able to restore growth to the respiratory-deficient yeast mutant cem1 that lacks the endogenous mitochondrial beta-ketoacyl synthase and exhibits lowered lipoic acid levels. To date, four components of a putative type II mitochondrial fatty acid synthase pathway have been identified in humans: acyl carrier protein, malonyl transferase, beta-ketoacyl synthase, and enoyl reductase. The substrate specificity and complementation data for the beta-ketoacyl synthase suggest that, as in plants and fungi, in humans this pathway may play an important role in the generation of octanoyl-acyl carrier protein, the lipoic acid precursor, as well as longer chain fatty acids that are required for optimal mitochondrial function.     

Adenosine induces ATP release via an inositol 1,4,5-trisphosphate signaling pathway in MDCK cells

ATP is released into extracellular space as an autocrine/paracrine molecule by mechanical stress and pharmacological-receptor activation. Released ATP is partly metabolized by ectoenzymes to adenosine. In the present study, we found that adenosine causes ATP release in Madin-Darby canine kidney cells. This release was completely inhibited by CPT (an A1 receptor antagonist), U-73122 (a phospholipase C inhibitor), 2-APB (an inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) receptor blocker), thapsigargin (a Ca2+-ATPase inhibitor), and BAPTA/AM (an intracellular Ca2+ chelator), but not by DMPX (an A2 receptor antagonist). However, forskolin, epinephrine, and isoproterenol, inducers of cAMP accumulation, failed to release ATP. Adenosine increased intracellular Ca2+ concentrations that were strongly blocked by CPT, U-73122, 2-APB, and thapsigargin. Moreover, adenosine enhanced accumulations of Ins(1,4,5)P3 that were significantly reduced by U-73122 and CPT. These data suggest that adenosine induces the release of ATP by activating an Ins(1,4,5)P3 sensitive-Ca2+ pathway through the stimulation of A1 receptors.     

Inflammatory Stress Increases Hepatic CD36 Translational Efficiency via Activation of the mTOR Signalling Pathway

Inflammatory stress is an independent risk factor for the development of non-alcoholic fatty liver disease (NAFLD). Although CD36 is known to facilitate long-chain fatty acid uptake and contributes to NAFLD progression, the mechanisms that link inflammatory stress to hepatic CD36 expression and steatosis remain unclear. As the mammalian target of rapamycin (mTOR) signalling pathway is involved in CD36 translational activation, this study was undertaken to investigate whether inflammatory stress enhances hepatic CD36 expression via mTOR signalling pathway and the underlying mechanisms. To induce inflammatory stress, we used tumour necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) stimulation of the human hepatoblastoma HepG2 cells in vitro and casein injection in C57BL/6J mice in vivo. The data showed that inflammatory stress increased hepatic CD36 protein levels but had no effect on mRNA expression. A protein degradation assay revealed that CD36 protein stability was not different between HepG2 cells treated with or without TNF-α or IL-6. A polysomal analysis indicated that CD36 translational efficiency was significantly increased by inflammatory stress. Additionally, inflammatory stress enhanced the phosphorylation of mTOR and its downstream translational regulators including p70S6K, 4E-BP1 and eIF4E. Rapamycin, an mTOR-specific inhibitor, reduced the phosphorylation of mTOR signalling pathway and decreased the CD36 translational efficiency and protein level even under inflammatory stress resulting in the alleviation of inflammatory stress-induced hepatic lipid accumulation. This study demonstrates that the activation of the mTOR signalling pathway increases hepatic CD36 translational efficiency, resulting in increased CD36 protein expression under inflammatory stress.     

Endoscopic Biopsy in Gastrointestinal Neuroendocrine Neoplasms: A Retrospective Study

Background

Gastrointestinal neuroendocrine neoplasms (GI-NENs) are often located in the deep mucosa or submucosa, and the efficacy of endoscopic biopsy for diagnosis and treatment of GI-NENs is not fully understood.

Objective

The current study analyzed GI-NENs, especially those diagnosed pathologically and resected endoscopically, and focused on the biopsy and cold biopsy forceps polypectomy (CBP) to analyze their roles in diagnosing and treating GI-NENs.

Methods

Clinical data of all GI-NENs were reviewed from January 2006 to March 2012. Histopathology was used to diagnose GI-NENs, which were confirmed by immunohistochemistry.

Results

67.96% GI-NENs were diagnosed pathologically by endoscopy. Only 26.21% were diagnosed pathologically by biopsies before treatment. The diagnostic rate was significantly higher in polypoid (76.47%) and submucosal lesions (68.75%), than in ulcerative lesions (12.00%). However, biopsies were only taken in 56.31% patients, including 51.52% of polypoid lesions, 35.56% of submucosal lesions and 100.00% of ulcerative lesions. Endoscopic resection removed 61.76% of GI-NENs, including six by CBP, 14 by snare polypectomy with electrocauterization, 28 by endoscopic mucosal resection (EMR) and 15 by endoscopic submucosal dissection (ESD). 51.52% polypoid GI-NENs had infiltrated the submucosa under microscopic examination. CBP had a significantly higher rate of remnant (33.33%) than snare polypectomy with electrocauterization, EMR and ESD (all 0.00%).

Conclusions

Biopsies for all polypoid and submucosal lesions will improve pre-operative diagnosis. The high rate of submucosal infiltration of polypoid GI-NENs determined that CBP was inadequate in the treatment of GI-NENs. Diminutive polypoid GI-NENs that disappeared after CBP had a high risk of remnant and should be closely followed up over the long term.     

黄芩苷对家兔离体子宫平滑肌的作用

目的:观察黄芩苷对家兔离体子宫平滑肌收缩的作用及其与Ca2+的关系.方法:制作常规离体家兔子宫平滑肌肌条,考察黄芩苷对子宫肌条反应的影响.结果:(1)黄芩苷(5-10mmol-L-1)剂量依赖抑制子宫平滑肌收缩;(2)黄芩苷对催产素及高K去极化液中Ca2+所致的离体子宫平滑肌收缩均呈剂量依赖性抑制;使CaC12累积量-效曲线非平行性右移,最大效应下降,呈非竞争性抑制;(3)且对子宫平滑肌依细胞内、外Ca2+两种收缩成分均呈抑制作用.结论:黄芩苷对家兔离体子宫平滑肌条的抑制作用,可能与其拮抗Ca2+有关.