毫米波辐射对植入前小鼠胚胎及早期胚胎的影响

本文报道小鼠受精卵体外及在体受毫米波辐照后一些改变。毫米波源为36.11GHz固态微波连续发生器,波长8mm,功率密度为10mW/cm~2、8mW/cm~2、4mW/cm~2及2mW/cm~2。结果发现2-4mW/cm~2毫米波辐照即可使体外培养之受精卵细胞表面微绒毛减少、脱落,细胞表面形成许多囊泡。透射电镜下可见细胞间隙扩大、胞浆中线粒体膨胀、空化,用FITC-ConA试验可见细胞表面结合荧光减少。酶试验证明辐照后卵胚细胞表面AKP,ATPase,5′-Nase均有降低。在体受精卵细胞经辐射后证明,辐射可使胎儿体重增长减慢,囊胚形成数量下降,植入率降低,而表面酶下降不明显。     

Expression and characterization of the human YWK-II gene, encoding a sperm membrane protein related to the alzheimer betaA4-amyloid precursorprotein

The YWK-II cDNA, RSD-2, encoding a sperm membrane protein was isolated from a rat testis cDNA expression library. Using the RSD-2 insert in combination with rapid amplification of cDNA ends (RACE), the corresponding human gene was isolated from a human testis cDNA expression library. The human testis cDNA, HSD-2, is 3654 bp in length and contains an open reading frame of 763 codons. Hydropathicity analysis showed that the deduced polypeptide is a single strand transmembrane protein. The deduced polypeptide has partial homology with the amyloid precursor protein (APP) and high homology with the amyloid precursor homologue, APLP2/APPH. The YWK-II gene was mapped and assigned to human chromosome locus: 11q24-25. Northern blotting of various human tissue RNAs using the HSD-2 cDNA as a probe showed that the gene is transcribed ubiquitously. The cytoplasmic domain of HSD-2 was expressed in Escherichia coli. In-vitro studies showed that the recombinant polypeptide bound to a GTP-binding protein (G(o)) and was phosphorylated by protein kinase C and cdc2 kinase. In mammalian F11 cells, the recombinant polypeptide was found to be coupled to G(o). Thus, the YWK-II component has the characteristics of a G(o)-coupled receptor and may be involved in G(o)-mediated signal transduction pathway. Protein kinase C and cdc2 kinase may regulate this pathway in spermatozoa by phosphorylating the cytoplasmic domain of the YWK-II component.     

经单侧穿刺椎体后凸成形术治疗侧方椎体压缩性骨折

目的研究经单侧椎弓根穿刺椎体后凸成形术治疗侧方骨质疏松性椎体压缩骨折(osteoporotic vertebral compression fractures,OVCF)的疗效。方法选择我院2009年10月~2011年10月收治的30例侧方OVCF患者,随机行凹侧或双侧球囊撑开椎体后凸成形术治疗,分别在术后1、6、12个月进行随访,对椎体高度恢复、脊柱后凸、侧凸Cobb角及并发症进行评价。结果术后1、6、12个月的随访结果比较发现,凹侧撑开及双侧撑开组患者椎体高度均较术前明显恢复(P0.05),脊柱后凸、侧凸Cobb角均较术前明显纠正(P0.05)。术后定期随访无丢失。凹侧撑开组与双侧撑开组之间比较,上述指标差异无统计学意义(P0.05)。结论经凹侧球囊撑开椎体成形治疗侧方OVCF,与双侧撑开相比疗效相当,可简化手术、缩短手术时间、减小创伤、减少费用,是治疗侧方OVCF的有效方式。     

Differential immune response to B:9-23 insulin 1 and insulin 2 peptides in animal models of type 1 diabetes

Mice have two insulin genes that differ in the insulin sequence by two amino acids, including the B9 position. Given prior studies of the B:9-23 insulin peptide in NOD mice, a fundamental question is whether the immune response to the B:9-23 peptide of the two insulins is identical. We investigate responses to the immunization with B:9-23 insulin 1 and 2 peptides in NOD and RIP-B7.1 Balb/c mice. NOD and F1 (Balb/c x C57/Bl6) B7.1 transgenic mice were given either B:9-23 insulin 1, B:9-23 insulin 2 or tetanus toxoid (TT) control peptide. Insulin autoantibodies (IAA), and anti-B:9-23 antibodies (IgG1 and IgG2c) were measured. Subcutaneous injection of the insulin 2 but not the insulin 1 peptide significantly protected NOD mice from diabetes. Conceptually similar, insulin 1 peptide immunization accelerated diabetes in the B7.1 mice compared with insulin 2 peptide. Insulin 1 and 2 peptides induced similar levels of IAA in the NOD mice except at week 26, where insulin 2 induced higher levels of IAA. Anti-IgG1 B:9-23 peptide antibodies were higher in the insulin 2 immunized group of NOD mice, while IgG2c anti-B:9-23 peptide antibodies were higher in the insulin 1 group. Adoptive transfer of splenocytes from insulin 1 immunized mice to NOD.scid mice demonstrated accelerated diabetogenicity. The protection afforded by insulin 2 peptide but not insulin 1 peptide in the NOD mouse is reflected by its predominant Th2 humoral response. This may relate to the protection conferred by the insulin 1 knockout when bred onto NOD mice in contrast to acceleration of disease with an insulin 2 knockout.     

Functional polymorphisms in cell death pathway genes FAS and FASL contribute to risk of lung cancer

Background: The FAS and FASL system plays a key role in regulating apoptotic cell death and corruption of this signalling pathway has been shown to participate in immune escape and tumorigenesis. There is reduced expression of FAS but elevated expression of FASL in many types of human cancers including lung cancer. We recently reported an association between functional polymorphisms in FAS (–1377G→A) and FASL (–844T→C) and risk of oesophageal cancer.     

Identification of a putative Salmonella enterica serotype typhimurium host range factor with homology to IpaH and YopM by signature-tagged mutagenesis

The genetic basis for the host adaptation of Salmonella serotypes is currently unknown. We have explored a new strategy to identify Salmonella enterica serotype Typhimurium (S. typhimurium) genes involved in host adaptation, by comparing the virulence of 260 randomly generated signature-tagged mutants during the oral infection of mice and calves. This screen identified four mutants, which were defective for colonization of only one of the two host species tested. One mutant, which only displayed a colonization defect during the infection of mice, was further characterized. During competitive infection experiments performed with the S. typhimurium wild type, the mutant was defective for colonization of murine Peyer's patches but colonized bovine Peyer's patches at the wild-type level. No difference in virulence between wild type and mutant was observed when calves were infected orally with 10(10) CFU/animal. In contrast, the mutant possessed a sixfold increase in 50% lethal morbidity dose when mice were infected orally. The transposon in this mutant was inserted in a 2.9-kb pathogenicity islet, which is located between uvrB and yphK on the S. typhimurium chromosome. This pathogenicity islet contained a single gene, termed slrP, with homology to ipaH of Shigella flexneri and yopM of Yersinia pestis. These data show that comparative screening of signature-tagged mutants in two animal species can be used for scanning the S. typhimurium genome for genes involved in host adaptation.     

锌对培养的乳鼠心肌细胞自发性搏动和电活动的影响

本文研究了不同浓度的Zn对培养的乳鼠心肌细胞自发性搏动及心肌细胞动作电位的影响。实验结果表明,加Zn在0.125—2ppm范围内,自发性搏动群落的出现率增高,与对照组比较,P<0.001。但Zn的浓度超过一定范围(4 ppm),自发搏动率则呈降低趋势;8 ppm组明显低于对照组,P<0.01.Zn对心肌细胞动作电位的影响表现为动作电位的发放频率减慢,波幅降低,波宽变窄和最大除极速度减慢。     

北京地区汉族人群DNA修复基因XPD单核苷酸多态性与肺癌及食管癌风险的研究

目的：研究核苷酸切除修复基因XPD单核苷酸多态性与北京地区汉族人群肺癌及食管癌风险的关系。方法：采用以医院患者为基础的病例－对照研究方法，包括正常对照383人，肺癌患者351例，食管癌患者325例。以聚合酶链反应－限制性片段长度多态性方法分析了XPD基因Asp312 Asn和Lys751Gln多态性，比较不同基因型与肺癌及食管癌风险的关系，并探讨吸烟与基因多态交互作用对患癌风险的影响。结果：与携带312 Asp/Asp基因型者比较，携带至少1个312Asn等位基因者（即Asp/Asn和Asn/Asn基因型）罹患肺鳞癌的风险增加1．8倍（95％CI1．10－2．93），而与肺腺癌无关（校正的比值比为1．07，95％CI0．55－2．08）。分层分析显示，风险型等位基因312Asn和751Gln与吸烟有明显的交互作用。吸烟剂量≥29包／年且携带312Asn或751Gln者罹患肺鳞癌的风险最高，校正的比值比分别为12．44（95％CI4．97－31．17）和10．74（95％CI4．51－25．57）。XPD基因Asp312Asn和Lys751Gln多态与食管鳞癌风险无关。结论：XPD基因Asp312Asn和Lys751Gln多态是地区汉族人群肺鳞癌遗传易感因素，而与肺腺癌以及食管鳞癌风险无关，可能反映了不同组织学类型肺癌以及肺癌和食管癌之间的病因学差异。     

流行性脑脊髓膜炎的流行趋势变化与其疫苗接种

在过去几十年,随着疫苗的广泛使用,不同国家和区域引起流行性脑脊髓膜炎(简称流脑)病原体的血清群也发生了变迁。本文将脑膜炎球菌疫苗免疫接种、感染人群、不同区域和国家流脑的流行趋势及其内在机制研究进展进行综述,为进一步了解流脑流行趋势变化与其疫苗接种和后续制定免疫策略提供参考。     

丹参多酚酸盐通过AMPK/Sirt1/PGC-1α信号通路诱导膜性肾病大鼠足细胞自噬的机制

目的：通过观察丹参多酚酸盐对膜性肾病(MN)大鼠肾组织中腺苷酸活化蛋白激酶(AMPK)、沉默信息调节因子(Sirt1)、过氧化物酶体增殖物激活受体γ辅激活因子-1α(PGC-1α)蛋白的表达及细胞自噬和凋亡的情况,探讨其治疗MN的可能的分子机制。方法：80只雄性SD大鼠随机分为正常组,模型组,盐酸贝那普利组(10 mg·kg^-1),丹参多酚酸盐低、中、高剂量组(16.7、33.3、66.7 mg·kg^-1),通过尾静脉注射阳离子化牛血清白蛋白(C-BSA)的方法造模。造模成功后,各组按照相应比例剂量连续给药4周后留取24 h尿、血清和肾组织,尿液用于检测24 h尿蛋白定量(24 h UTP)、血清用于检测血尿素氮(BUN)、血肌酐(SCr)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、C反应蛋白(CRP)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、丙二醛(MDA)的含量。采用光镜、电镜、免疫荧光法观察肾脏病理学变化,蛋白免疫印迹法(Western blot)检测大鼠肾组织磷酸化(p)-AMPK、AMPK、p...