艾滋病患者抗病毒督导治疗疗效分析

目的:探讨提高抗病毒疗效和服药依从性,延缓病毒耐药发生的方法。方法:377名来源于同一乡村的HIV感染者,分为督导治疗组(n=134)和未督导治疗组(n=243),均给予HAART治疗,仅督导治疗组患者给予严格督导治疗。分别于治疗后第1、2、3、6、9和12个月,抽取外周血,应用PCR检测HIV-RNA载量,流式细胞仪检测CD4+、CD8+T淋巴细胞数量,血常规检测白细胞数量变化。结果:随着治疗时间的延长,2组患者外周血CD4+、CD8+T淋巴细胞及白细胞数量均逐渐上升;2组间比较,差异无统计学意义。2组患者外周血HIV-RNA载量差异有统计学意义(F组间=3.781,F时间=2.561,F交互=352.79,P﹤0.05);治疗后6、9和12个月督导治疗组高于未督导治疗组。结论:督导治疗有利于持续抗病毒疗效,延缓耐药毒株的发生。     

e抗原阴性的慢性乙型肝炎患者的临床与病理特点

目的探讨HBeAg阴性组的慢性乙型肝炎（慢乙肝）患者的临床和病理学特点。方法对我院收治的235例慢性乙型肝炎患者进行研究,比较HBeAg阴性组的慢乙肝患者与HBeAg阳性组的慢乙肝患者的临床资料和病理学分级分期特点。结果HBeAg阴性组的慢乙肝患者年龄偏大、病程较长,ALT、AST水平,HBVDNA载量低于HBeAg阳性组的慢乙肝患者,但病理学GS分级较HBeAg阳性组的慢乙肝患者高。结论应对HBeAg阴性的慢乙肝患者进行随访和必要的治疗。     

甲胎蛋白升高可怕吗?

正甲胎蛋白(AFP)是一种糖蛋白,正常情况下体内含量较少,不同检测厂家,参考值差异较大。这种蛋白主要来自正在发育肝细胞或肿瘤原始细胞。也可见于孕妇,胎儿出生约两周后AFP从血液中消失。AFP主要在胎儿肝中合成,在胎儿13周后逐渐升高,也是孕妇胎儿肝脏逐渐发育重要标记。在妊娠30周以后维持高峰,出生时血浆中浓度为高峰期的1%左右,在周岁时接近成人水平(低于30μg/L)。AFP在产妇羊水或母体血浆中     

头孢地嗪对正常小鼠外周血中CD3+,CD4+,CD8+及CD4+/CD8+的影响

目的 探讨头孢地嗪(CDZM)对正常小鼠外周血中CD3 ,CD4 ,CD8 及CD4 /CD8 的影响.方法 采用完全随机实验设计,分设6组,对小鼠分别连续7 d注射胸腺肽(Thy)10 mg/kg、头孢地嗪(500,200,50 mg/kg)、头孢曲松500 mg/kg及生理盐水后,在第7,14,21天分别采集外周血,经流式细胞仪对小鼠外周血中CD3 ,CD4 ,CD8 ,CD4 /CD8 进行检测,观察头孢地嗪对机体免疫功能的影响.结果 CDZM具有较好的免疫调节作用,可明显地提高外周血CD4 /CD8 的比值,与Thy相比,CDZM对机体免疫系统的影响更为持久.结论 头孢地嗪可通过调整CD4 和CD8 之间的平衡,有效地提高机体的免疫功能.     

实验性高血氨对肝细胞钠－氢交换蛋白1型转运活性和细胞内 pH 值的影响

目的：研究高血氨对肝细胞钠－氢交换蛋白1型转运活性和细胞内pH值的影响。方法采用5 mmol／L NH4 Cl处理HL－7702细胞24 h,构建高血氨肝细胞模型,采用细胞计数法、流式细胞法、BCECF－AM法和Western blot法测定细胞数量、凋亡率、细胞内pH值以及NHE1蛋白的转运活性和表达水平。结果高血氨肝细胞模型肝细胞内pH值下降,NHE1蛋白的转运活性和表达水平升高,肝细胞数量降低和凋亡率升高。结论高血氨导致的肝细胞损伤可能与降低肝细胞内pH值,激活NHE1蛋白有关。     

头孢地嗪对小鼠T细胞亚群的影响

目的研究头孢地嗪对小鼠的免疫调节作用。方法对小鼠分别连续7d注射胸腺肽10mg/kg、头孢地嗪(500mg/kg、200mg/kg、50mg/kg)、头孢曲松500mg/kg及生理盐水后,经流式细胞仪对小鼠T细胞亚群进行检测。结果胸腺肽组、头孢地嗪(500mg/kg、200mg/kg、50mg/kg)组CD4 /CD8 均明显高于头孢曲松组和生理盐水组(P<0.05),而头孢曲松组与生理盐水组无差异(P>0.05)。结论头孢地嗪可通过调整CD4 和CD8 之间的平衡,有效地提高机体的免疫功能。     

右肝区不适或疼痛是肝癌表现的前兆吗

长期在门诊坐诊,经常有很多患者叙述右肝区不适,尤其是那些有乙肝或者丙肝的患者,以为是肝癌的表现,经常紧张得受不了,严重影响生活和工作。而真实情况又如何呢,怎么样正确看待右肝区不适和相关的疾病呢?下面从几个方面来阐述一下肝区疼痛和相关疾病。为什么会形成肝区疼痛肝区疼痛是肝区有炎症等刺激神经系统的一种预警机制。众所周知,肝脏内并没有神经系统,因此肝内血管瘤、囊肿、钙化灶、肝内结节等都不会诱发疼痛的表     

Expression profile of altered long non-coding RNAs in patients with HBV-associated hepatocellular carcinoma

In China, hepatitis B virus (HBV) infection is the major cause of hepatocellular carcinoma (HCC), which is called HBV-related HCC (HBV-HCC), but the pathogenesis has not been clearly elucidated. Long non-coding RNAs (lncRNAs) have been paid increasing attention to, as an important regulatory molecule involved in many biological processes, as well as a variety of diseases. This study examined lncRNA that might play an important role in HBV-HCC pathogenesis by conducting lncRNA and mRNA profile comparison between HBV-HCC and normal liver tissues. The differentially expressed lncRNA and mRNA profiles between HBV-HCC and normal liver tissues were analyzed by microarrays. The potential protein-encoding gene regulated by lncRNA, and the biological function (gene ontology, pathway analysis) of the target gene were investigated. The results showed that the expression levels of lncRNA and mRNA in HBV-HCC tissues were different from those in normal liver tissues. As compared with normal liver tissue, 837 (4.30%) lncRNAs exhibited more than two-fold change (P<0.05); 325 were up-regulated, and 512 were down-regulated; 991 (5.70%) mRNAs exhibited more than 2-fold change (P<0.05); 733 were up-regulated and 258 were down-regulated in HBV-HCC tissue. Besides, there were 7 lncRNAs with above 10-fold elevation, 6 lncRNAs with above 10-fold decrease, 18 mRNAs with above 10-fold elevation and 11 mRNAs with above 10-fold decrease. 444 (53.05%) lncRNAs had their corresponding mRNAs, some of which were adjacent to lncRNAs. The biological analysis showed that the target gene of differentially expressed lncRNAs took part in the important bio- logical regulatory function. Target gene-related pathway analysis revealed the pathways in carcinoma and mitogen-activated protein kinase (MAPK) signaling pathways significantly changed in the HBV-HCC tissues as compared with normal liver tissues (P<0.05). It was suggested that as compared with normal liver tissues, the expression of lncRNAs in HBV-HCC tissues changed significantly, and lncRNAs played a key role in the pathogenesis of HBV-HCC probably by mainly regulating the carcinoma-related signaling pathway and MAPK signaling pathways.     

丙型肝炎患者外周血丙型肝炎病毒载量自然衰减数学模式的初步分析

目的为研究HCV RNA载量在体外的衰减动力学变化规律，判断可能符合的数学函数关系，建立体外HCV RNA载量衰减的数学模型，模拟体内可能存在的HCV复制能力。方法抽取丙型肝炎患者外周全血4份，抗凝处理后，置于6孔无菌培养板中，在5％ CO2条件下，轻微震荡培养，间隔15min取血做HCV RNA定量分析（Real—time PCR）。HCVRNA定量检测结果通过计算机软件分析，建立HCV RNA载量体外衰减数学函数关系。结果HCV RNA定量结果显示类阻尼振荡下降趋势，计算机分析HCV定量值下降符合指数函数关系：Y=3E＋0．8e^-0.5467x（r=0．9547；其中Y为外周血HCV RNA拷贝变量，X为体外病毒载量衰减的时间变量，E为10的幂指数，e为自然常数；r为相关系数），半衰期约为45min。结论HCV体外病毒载量衰减呈幂指数而非线性下降，半衰期为45min，逐渐下降到很长时间。