黄芪注射液对培养神经细胞损伤的保护作用

目的：研究黄芪对体外培养的胎鼠大脑皮层神经细胞损伤的保护作用。方法：在体外培养大鼠胎鼠的大脑皮层细胞，通过去除培养液中的小牛血清造成细胞损伤，实验组每毫升培养液中加入不同剂量的黄芪（0．05－0．5g)，观察黄芪对上术损伤的作用。结果：黄芪治疗组（0.2-0.5g/ml)的神经细胞线粒体活性较单纯去血清组明显增高（P＜0．05），在0．05－0．5g/ml范围内黄芪的抗损伤作用呈剂量相关性增加。结论：黄芪对体外培养的神经细胞去血清损伤有保护作用。     

欣生静片治疗广泛性焦虑症的随机、双盲、双模拟、多中心平行对照Ⅲ期临床试验研究

目的：评价欣生静片治疗广泛性焦虑症（心肝火旺证）的有效性和安全性。方法：采用随机、双盲双模拟、多中心平行对照试验设计,试验组和对照组分别给予欣生静片和丁螺环酮治疗4周。结果：试验组的总有效率和疗效指数均优于对照组（P＜0.05）。两组均能显著改善HAMA评分,组间差异具有统计学意义（P＜0.01）。两组患者的中医症状均能改善,但试验组的总有效率及中医证候的愈显率和评分均优于对照组（P＜0.01）。两组的HAMD17项评分均有显著改善（P＜0.01）,试验组优于对照组（P＜0.01）。试验组的不良反应发生率、严重程度显著低于对照组（P＜0.01）。结论：欣生静片治疗广泛性焦虑症安全、有效,显著优于丁螺环酮,临床应用价值高。     

内镜超声检查在胃癌诊断和分期中的临床应用

目的评价内镜超声检查(EUS)对胃癌患者术前诊断和分期的准确性,以指导临床治疗方案的选择。方法22例经胃镜加活检病理检查确诊(17例)和疑诊为胃癌但常规活检阴性的患者(5例),同时行EUS、腹部螺旋CT检查,疑诊者在EUS检查的同时行EUS引导下细针穿刺活检(FNAB)以明确诊断。确定肿瘤侵犯深度(T)、局部淋巴结转移(N)、周围及远处器官转移(M)等分期情况,并与手术及病理对照,以评价EUS对胃癌诊断及TNM临床分期的准确性。结果5例疑诊者行EUS引导下FNAB全部成功取得肿瘤组织,病理诊断腺癌4例,印戒细胞癌1例。1例术前EUS诊断为T1N0M0期的患者行内镜下黏膜切除术,其余患者全部行外科胃癌根治术。与手术和病理结果比较,EUS对于TNM分期诊断总的敏感性和特异性分别为T:84.9%,74.2%;N:92.1%,77.1%;M:63.4%,87.5%。螺旋CT对于胃壁是否增厚及N、M分期的敏感性和特异性分别为T:27.3%,75%;N:31.5%,100%;M:50%,100%。其中EUS对于T和N分期的敏感性较CT高(P<0.05)。结论EUS术前评价胃癌临床分期具有显著的优越性,尤其是对于肿瘤侵犯深度和局部淋巴结转移的诊断,对指导临床治疗方案的选择及术后随访具有重要的参考价值。     

变异催乳素受体Delta S2促使p53基因组蛋白甲基化

Background Prolactin （PRL） is a pituitary polypeptide hormone characterized by multiple biological actions includingstimulation of growth in the prostate and formation of secretory alveoli and stimulation of milk protein gene expression inthe mammary gland. PRL exerts its effect by dimerizing its receptor （PRLR） on the plasma membrane and regulating geneexpression through the JAK-Stat signal pathway. We have previously described a natural variant of the PRLR in which the$2 subdomain of the extracellular domain is missing （Delta S2）. Delta S2 PRLRs are dimerized in the absence of PRL andhave constitutive activity in the promotion of breast cancer cell growth. Enhancer of zeste homolog 2 （EZH2）, as one of thehistone-modifying enzymes, is a key factor regulating gene expression by epigenetic modification. We hypothesized thatthese constitutive activated Delta S2 PRLRs played a pathogenic role in breast cancer in part through alterations in theexpression of EZH2 and the trimethylation of histone 3 on lysine 27 （H3K27Me3）.     

白细胞介素1α mRNA在神经胶质瘤中的表达及意义

目的定量检测白细胞介素1α（IL-1α）mRNA在神经胶质瘤组织和正常脑组织中的表达,并探讨其与临床特征的关系。方法运用实时荧光定量PCR检测31例神经胶质瘤组织和22例正常脑组织中IL-1α mRNA的表达,分析其与临床特征的相关性。结果IL-1α mRNA在神经胶质瘤组织中的相对表达量为0．10,在正常组脑组织中为0．01,两者差异具有统计学意义（U=207．0,P=0．016）。IL-1α mRNA在WHO Ⅲ-Ⅳ级神经胶质瘤中的相对表达量为0．72,在Ⅰ-Ⅱ级中为0．02,两者差异具有统计学意义（U=36．0,P=0．001）;而IL-1α RNA相对表达量在性别和年龄之间差异无统计学意义（P〉0．05）。结论IL-1α mRNA在神经胶质瘤组织中呈显著高表达,其可能在神经胶质瘤的恶变过程中发挥重要作用。     

绵羊在四季中生精规律的研究(Ⅰ.精子发生的季节变化)

利用发育的精子细胞顶体形态变化的分类法对绵羊在四季中睾丸曲细精管横切面上的精原细胞、精母细胞和精细胞进行了观察和统计,并对生殖细胞的比率和精子发生的效率进行了研究。结果表明,繁殖季节和非繁殖季节在精子发生水平等方面均存在着显著的季节变化。     

比较密骨胶囊与维生素D3对糖皮质激素性骨质疏松模型骨量、骨强度影响的研究

目的：比较性地研究密骨胶囊与维生素Ｄ３对糖皮质激素性骨质疏松模型骨量、骨强度的影响。方法；采用１２月龄ＳＤ雄性大鼠４６只，随机分为空白对照组１４只、地塞米松组１６只、密骨胶囊组８只、维生素Ｄ３组８只。地塞米松的剂量是０．２５ｍｇ／１００ｇ体重／次（每周两次）；密骨胶囊浸膏的剂量是０．１６６ｇ／１００ｇ体重／次（每天一次）；维生素Ｄ３的剂量是０．２５Ｕ／１００ｇ体重／次（第一周每天一次，一周以后每周三次）。各组施行相应处理，１８周以后分别测定各组大鼠全身骨密度、股骨抗弯强度。结果：密骨胶囊既能部分地恢复模型大鼠已经丢失的骨量（高于地塞米松组ｐ＜０．０５，低于空白对照组ｐ＜０．０５），又能部分地回升模型大鼠已经降低的骨强度（高于地塞米松组ｐ＜０．０５，低于空白对照组ｐ＜０．０５）；维生素Ｄ３也能部分地恢复模型大鼠已经丢失的骨量（高于地塞米松组ｐ＜０．０５，低于空白对照组ｐ＜０．０５），亦能部分地回升模型大鼠已经降低的骨强度（高于地塞米松组ｐ＜０．０５，低于空白对照组ｐ＜０．０５），但回升能力比较密骨胶囊有下降趋势。结论：密骨胶囊是一种具有开发潜力的抗糖皮质激素性骨质疏松的中药复方．其中密骨胶囊能够明显地回升模鼠     

胶质瘤组织中GRK5和Ki-67的表达情况及临床意义

目的:探讨GRK5和Ki-67在胶质瘤组织中的表达情况,与胶质瘤临床病理特征之间的关系及GRK5和Ki-67在胶质瘤中的预后价值。方法:本研究收集2014年1月至2017年1月我院手术切除的104例脑胶质瘤患者的组织标本及同期因颅内损伤行颅内减压术手术切除的正常脑组织20例,采用免疫组化SP法检测胶质瘤组织及其正常脑组织中GRK5和Ki-67的表达水平。相关分析采用Spearman等级相关分析法。采用卡方检验分析GRK5和Ki-67在胶质瘤组织中的表达与临床病理特征的相关性。生存分析采用Kaplan-Meier和Log-rank 检验,预后分析采用Cox比例风险模型。结果:通过免疫组化检测结果显示,GRK5在104例胶质瘤组织中阳性表达66例,阳性率为63.5%;在20例正常脑组织中阳性表达2例,阳性率为10.0%。Ki-67在104例胶质瘤组织中阳性表达69例,阳性率为66.3%;在20例正常脑组织中阳性表达率为0.0%。通过Spearman等级相关分析得出,胶质瘤组织中GRK5和Ki-67表达呈正相关（r=0.558,P=0.000）。分析GRK5和Ki-67的表达与胶质瘤患者临床病理特征之间的关系,结果显示GRK5和Ki-67的表达与WHO分级有关（P＜0.05）,与患者性别、年龄、肿瘤直径、肿瘤类型无关（P＞0.05）。对104例患者进行生存分析,结果显示GRK5阳性表达患者生存率显著低于阴性表达患者（P=0.033）;Ki-67阳性表达患者生存率显著低于阴性表达患者（P=0.033）。Cox回归模型分析结果显示,GRK5阳性表达和Ki-67阳性表达均是影响胶质瘤患者预后的独立危险因素（P＜0.05）。结论:GRK5和Ki-67与胶质瘤的发生发展及细胞增殖有关,GRK5和Ki-67有可能作为胶质瘤患者的预后标志物及临床检测或联合检测的指标,提高临床诊断率。     

NLRP3 Deletion Inhibits the Non-alcoholic Steatohepatitis Development and Inflammation in Kupffer Cells Induced by Palmitic Acid

The cleavage and secretion of pro-inflammatory cytokines IL-1β and IL-18 is regulated by NLRP3 (NACHT, LRR, and PYD domain-containing protein 3) inflammasome activation. Kupffer cells (KCs) are implicated in the pathogenesis of various liver diseases, such as non-alcoholic fatty liver disease (NAFLD), alcoholic liver disease, and liver fibrosis. However, the role of NLRP3 played in the non-alcoholic steatohepatitis (NASH) has yet to be evaluated. In the present study, methionine–choline-deficient (MCD) diet was used to establish the mice NASH model. The expression levels of F4/80 and NLRP3 in liver tissues were evaluated, and the IL-1β and IL-18 in serum were also evaluated. KCs were isolated from wild-type (WT) mice and NLRP3 knockout (NLRP3^?/?) mice and then randomly divided into two groups: the control and palmitic acid (PA) groups. The expression levels of NLRP3, ASC, and caspase-1 in KCs were determined by RT-PCR, western blotting, and immunofluorescence. The levels of IL-1β and IL-18 in the supernatant (SN) of KCs were evaluated by enzyme-linked immunosorbent assay (ELISA). We found that KCs and NLRP3 play pro-inflammatory roles in the progression of NASH, probably through secretions of IL-1β and IL-18 by KCs induced by PA. PA could act as a kind of damage-associated molecular patterns to elevate the messenger RNA and protein expression levels of NLRP3, ASC, and caspase-1 in KCs from WT mice. In the contrast, NLRP3 deletion could inhibit the NLRP3 inflammasome upregulation and activation in KCs induced by PA. Furthermore, the levels of pro-inflammatory cytokines IL-1β and IL-18 in the SN of KCs from WT mice were all elevated with the stimulation of PA, and the increase of these cytokines in the SN was blocked by NLRP3 deletion. In conclusion, our novel findings demonstrate that NLRP3 plays a pivotal role in NASH development and pro-inflammatory cytokines IL-1β and IL-18 secretion induced by PA stimulation, and NLRP3 might be an effective potential target for the treatment of liver inflammatory diseases associated with NLRP3 inflammasome activation.