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灵芝孢子对非酒精性脂肪性肝病ApoB100和SREBP-1 c mRNA的影响
目的:研究灵芝孢子对非酒精性脂肪性肝病(non-alcoholic fatty liver disease, NAFLD)小鼠肝脏载脂蛋白B100(apolipopro-tein B100, ApoB100)和固醇调节元件结合蛋白1c (sterol-regulatory element binding protein-1c, SREBP-1c)表达的影响,从分子水平探讨灵芝孢子对于NAFLD的预防及治疗效果。方法:应用RT-PCR方法对比正常组、NAFLD模型组、灵芝孢子预防组、灵芝孢子治疗组中肝脏ApoB100及SREBP-1c的mRNA表达。结果:ApoB100及SREBP-1c mRNA在模型组表达增高,而在灵芝孢子预防组和灵芝孢子治疗组表达均降低,差异有统计学意义(P<0.05)。灵芝孢子预防组和灵芝孢子治疗组组间比较差异无统计学意义(P>0.05)。结论:NAFLD模型组肝脏中ApoB100及SREBP-1c 的表达明显增高;灵芝孢子预防及治疗小鼠NAFLD过程中对于其肝脏ApoB100及SREBP-1c表达的影响无明显差异。
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泌乳素诱导蛋白基因及其在肿瘤中作用的研究进展
泌乳素诱导蛋白(prolactin inducible protein,PIP)是存在于人精液中17 kD的多肽[1].因其在不同部位被发现而有多种名称,在受泌乳素和雌激素调控的人乳腺癌细胞系T47D中被发现,而被称作PIP[1- 2];在乳腺囊液、人乳和唾液中被发现而被称为gross cystic disease fluid protein 15(GCDFP-15)[3];作为17 kD类肌动蛋白结合蛋白在人精液中被发现,而被命名为分泌性肌动蛋白结合蛋白(secretory actin binding protein,SABP),也称作gp17[4];因其来源于下颌下腺和舌下腺的唾液而被称作腮腺外糖蛋白(extraparotid glycoprotein,EP-GP)[5].目前,GCDFP-15、PIP、SABP、gp17、EP-GP在基因术语中被统一称作PIP,人PIP基因位于7号染色体[6].PIP虽是一种小蛋白,但却在抗菌、受精、免疫调节、细胞凋亡及肿瘤进程中发挥着重要的生物学作用.本文着重对PIP基因及其在肿瘤中作用的相关研究进展进行综述.
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黄酮类化合物改善记忆的机制研究进展
黄酮类化合物是一类具有显著抗氧化和螯合性能的次生植物酚类物质。黄酮类化合物能够诱导提高记忆的获取、巩固、存储和重现。它们通过作用于记忆相关脑区的细胞和分子结构来有效地逆转与年龄相关的记忆力减退。它们可能涉及激活细胞外信号调节激酶(extracellular signal-regulated kinase 1/2, ERK1/2)和cAMP应答元件结合蛋白(cAMP-response element binding protein, CREB)信号通路,磷脂酰肌醇-3-羟激酶/丝氨酸/苏氨酸蛋白激酶(phosphatidyl inositol 3-kinase/serine/threonine protein kinase, PI3K/Akt)信号通路,诱导产生海马区血管效应,抑制神经炎症反应等。本文就黄酮类化合物改善记忆力的机制进行综述。
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系统性红斑狼疮患者24小时尿视黄醇结合蛋白水平及临床意义
肾脏病变是系统性红斑狼疮(SLE)的重要并发症之一,除肾小球病变外,肾间质、小管性损害在SLE中亦相当常见[1].本研究对62例SLE患者进行24h尿视黄醇结合蛋白(retinol binding protein, RBP)的检测,并探讨其临床意义.材料与方法临床资料男5例,女57例,年龄17~58岁,平均33.2±7.9岁,病程2周~12年,全部病例均符合美国风湿病协会1982年修订的SLE分类诊断标准.
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胰岛素治疗脊髓损伤的研究进展
胰岛素样生长因子(insulin-like growth factor system,IGFS)包括胰岛素、胰岛素样生长因子-Ⅰ(IGF-Ⅰ)、胰岛素样生长因子-Ⅱ(IGF-Ⅱ)及3个相应的受体即胰岛素受体(insulin receptor, IR)、胰岛素样生长因子-Ⅰ受体(IGF-Ⅰ receptor, IGF- IR)、胰岛素样生长因子-Ⅱ受体( IGF- ⅡR),同时还有6个结合蛋白(IGF binding protein, IGFBP).
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视黄醇结合蛋白4与胰岛素抵抗的研究进展
长期以来,脂肪组织一直被认为仅是机体供能的器官.但随着研究的不断深入,开始认识到脂肪组织还是一种内分泌器官,能分泌瘦素、脂联素、脂肪源性肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)等多种脂肪因子来调节胰岛素在各组织器官的作用,参与胰岛素抵抗(insulin resistance,IR)的发生与发展.目前,脂肪因子已成为肥胖与2型糖尿病(T2DM)、IR研究领域的热点.视黄醇结合蛋白4(retinol binding protein 4,RBP4)是新近发现的一种脂肪因子,主要来源于脂肪细胞和肝细胞,与IR、肥胖及多种心血管危险因子密切相关.已有多项研究证实肥胖可导致RBP4分泌增多,RBP4能引起和加重机体胰岛素抵抗[1-2].
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Lipopolysaccharide (LPS), or endotoxin, is the major component of the outer surface of gram-negative bacteria. LPS is a potent activator of the cells of the immune and inflammation systems, including macrophages, monocytes and endothelial cells, and contributes to systemic changes seen in septic shock.1,2 It has long been believed that LPS is responsible for several fatal consequences of gram-negative infection. Cell activation by LPS constitutes the first step in the cascade of events believed to lead to the manifestation of gram-negative sepsis, which results in approximately 20 000 annual deaths in the United States3 and 30% mortality rate of known cases in China.Therefore, the action mechanism of LPS is one of the most important problems in the research field of immunity, inflammation and surgery. Researchers have investigated the mechanism of cell activity and injury of LPS for a long time. In 1990, CD14,the glycosyl-phosphatidylinositol (GPI)-linked plasma membrane protein, was identified as a proximal LPS receptor on the cell surface of macrophages, and it was suggested that CD14 and LBP (lipopolysaccharide binding protein) played an important role in the effect mechanism of LPS. CD14 seemed to receive LPS via transfer from the plasma protein LBP. Then, two action patterns were recognized. CD14 positive cells, such as macrophages and leukocytes, were activated after LPS combined with LBP and interacted with CD14. But, CD14 negative cells (for example, endothelial cells), were activated through other receptors that we did not know of in the cell surface after LPS, LBP and soluble CD14 (sCD14) combined with the compounds. However, there are some questions to be answered. Firstly, because CD14 lacks cytoplasmic doman, it is unlikely to act as the transducer. Secondly, the action pattern of LPS through CD14 and LBP may be in dose-dependent mode, but, in conditions of high dosage and long exposure to LPS action, CD14 and LBP do not play an important role in LPS activation effect. Finally, for CD14 negative cells, the receptor combined LPS-LBP-sCD14 compound has not yet been identified. Some details indicated that a “co-receptor” for LPS signal transduction must exist. Although standard biochemical approaches, transfection assay, and immunologic tacties were all employed to search for this co-receptor, it has not yet been found. The find of Toll-like receptor 4 (TLR4) provides a new opportunity to study the mechanism of LPS action.
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肝硬化急性肾损伤患者的肾脏生物学标志物与鉴别诊断
急性肾损伤(acute kidney injury,AKI)在肝硬化患者中较为常见,并伴有较高的死亡率。肝硬化背景下,AKI常见的病因包括肾前性氮质血症(pre-renal azotemia,PRA)、急性肾小管坏死(acute tubular necrosis ,ATN)和肝肾综合征(hepatorenal syndrome,HRS)。不同病因AKI的治疗方法具有明显差异,因此准确鉴别病因尤为重要且极具挑战性。肾损伤的尿液生物学标志物可以区分AKI属于结构性还是功能性,有助于迅速准确地做出诊断。本研究在肝硬化AKI患者中开展了一项多中心前瞻性队列研究,评价多个生物学标志物对临床确诊AKI的鉴别诊断价值。36例患者肌酐在48小时内降至基线的25%以内,诊断为PRA。盲法回顾性确诊74例患者为进展性AKI,其中39例(51.3%)诊断为ATN,19例(25.0%)为PRA,16例(21.0%)为HRS。不同病因组患者的中性粒细胞明胶酶相关脂质运载蛋白(neutrophil gelatinase-associated lipocalin,NGAL)、白细胞介素-18(IL-18)、肾损伤分子-1(kidney injury molecule-1,KIM-1)、肝型脂肪酸结合蛋白(liver-type fatty acid binding protein,L-FABP)和白蛋白平均值不同,在确诊为ATN的患者中显著升高。HRS组患者钠排泄分数(fractional excretion of sodium, FENa)低,为0.10%,而PRA组患者FENa(0.27%)与ATN组患者(0.31%)间差异无统计学意义(P=0.54)。超过优诊断临界值的生物学标志物越多,则该患者被诊断为ATN的可能性越大。结论:ATN所致AKI的肝硬化患者尿液中的肾损伤生物学标志物升高;将生物学标志物应用于临床能更准确地区分AKI患者是否具有结构性损伤并指导治疗;HRS特异性生物学标志物仍需进一步研究。
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新型脂类分子--支链脂肪酸酯的生物学作用(详见光盘)
支链脂肪酸酯发现背景:促进脂肪细胞从头合成脂类[碳水化合物反应元件结合蛋白(carbohydrate response element binding protein,CHREBP)、酶和葡萄糖转运载体4(glucose transporter 4,GLUT 4)]与增加胰岛素敏感性密切相关;小鼠脂肪细胞过表达GLUT 4(AG4OX)增加循环脂肪酸、增加储脂、降低空腹血糖和增强葡萄糖耐量;循环脂肪酸成分和比例与胰岛素敏感性和葡萄糖耐量密切相关。
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快速 H-FABP 检测在缩短急性心肌梗死患者急诊 PCI准备时间中的应用
急性心肌梗死(acute myocardial infarction,AMI)是临床常见的一种严重威胁患者生命的急危重症。从胸痛患者中早期诊断从而进入快速的再灌注治疗,是降低死亡率和改善预后的关键[1]。美国心脏病学会/美国心脏协会(ACC/AHA)在2004年修订的 AMI 治疗指南中指出,门一首次球囊扩张(door-to-balloon, DTB)时间即患者从入院到急诊接受经皮冠状动脉介入术(percutaneous coronary intervention, PCI)的时间应在90 min 以内[2],但国内外文献报道很多院内 PCI 并未达到这一标准[3,4,5],院内 PCI 延迟的现象普遍存在。在实际临床工作中,常规心肌损伤标记物如心肌肌钙蛋白 I(cardiac troponin I,cTnI)、肌酸激酶同工酶(creatine kinase isoenzymes,CK-MB)等,需在发病4h 后才能检测到,在 AMI 早期均不够敏感[6],因此许多 AMI 患者在等待化验结果的同时丧失了佳的治疗时机。然而,心脏型脂肪酸结合蛋白(heart-typefatty acid binding protein,H-FABP)是目前 AMI 超早期诊断的敏感指标,即使 AMI症状发生后1-3小时内(早20分钟)就已释放入血[7],采血静置15min 后即可判断,具有简单、迅速、高效等特点。本文旨在探讨 H-FABP 检测对 AMI 患者早期诊断和及时急诊 PCI 的应用效果。