多囊卵巢综合征妊娠患者与非多囊卵巢综合征孕妇妊娠结局比较

目的比较多囊卵巢综合征(PCOS)妊娠患者与非PCOS孕妇的妊娠结局。方法选取200例PCOS妊娠患者作为研究组,并选取同期200例非PCOS孕妇作为对照组,比较两组孕妇的妊娠结局、新生儿情况及妊娠期并发症情况。结果研究组的先兆流产、早产、足月剖宫产发生率显著高于对照组(P <0.05);两组的先兆早产发生率比较无统计学差异(P>0.05)。两组的新生儿情况比较无统计学差异(P>0.05)。研究组的妊娠期高血压综合征、妊娠期糖尿病、羊水异常、胎儿窘迫发生率显著高于对照组(P <0.05)。结论与非PCOS孕妇相比,PCOS妊娠患者的早产风险增加,且妊娠期高血压综合征、妊娠期糖尿病、羊水异常、胎儿窘迫发生率显著升高。     

祛风抑肝通督方治疗神经根型颈椎病110例

目的:观察祛风抑肝通督方对神经根型颈椎病的治疗效果.方法:选择符合入选标准的神经根型颈椎病患者220例,随机分为治疗组与对照组各110例,治疗组用自拟祛风抑肝通督方,对照组用颈复康颗粒,两组均连续用药4周.观察两组临床症状的改善,症状积分的改善等.结果:治疗组总有效率为90%,对照组总有效率为70%,两组比较差异有显著性(P<0.05).结论:祛风抑肝通督方对神经根型颈椎病具有较好的治疗效果.     

外周炎症时大鼠背根神经节细胞μ-和κ-阿片受体mRNA的表达

目的观察外周炎症时大鼠背根神经节(dorsalrootganglion,DRG)细胞μ-和κ-阿片受体mRNA表达的变化。方法用角叉菜胶(carrageenan,CAR)在大鼠右后足皮下注射产生外周炎症,分别于正常和炎症后6、12、24和72h取右L4~5DRG。用原位杂交的方法观察正常及炎症期间DRG细胞μ-和κ-阿片受体mRNA表达的变化。结果正常大鼠的部分DRG细胞内可见μ-和κ-阿片受体mRNA表达。外周炎症后6h,表达μ-和κ-阿片受体mRNA的DRG细胞的数和μ-和κ-阿片受体mRNA表达量增加,24h表达量最高,72h下降至正常。结论外周炎症能使大鼠DRG细胞μ-和κ-阿片受体mRNA表达增加。提示外周炎症时大鼠DRG细胞μ-和κ-阿片受体合成增加。为阿片类物质应用于外周镇痛提供理论依据。     

不同婴儿食品铝含量的测定

本文应用原子吸收光谱法测定母乳、牛奶、奶粉及不同喂养方式婴儿血清中锌、铜、铁及铝含量。母乳中锌、铜、铁含量均较牛奶丰富，铝含量低于牛奶；奶粉中锌、铜、铁含量高于牛奶，与母乳无显著差异，铝含量高于牛奶。母乳、牛奶及奶粉喂养的贫血患儿血清铝含量无显著差异，均明显低于铝中毒的血清铝水平。     

复配杀虫母液灭蚊效果评价

目的 :评价复配杀虫母液灭蚊虫效果。方法 :设试验区和对照区 ,试验区用有效成分含量 2 0 %的复配杀虫母液按 5 m l/ m3超低容量喷雾 ;对照区用 2 0 % DDVP同浓度超低容量喷雾。结果 :复配杀虫母液超低容量喷雾 2 h后 ,蚊密度下降率为 93.3% ,RPI为 2 6 .7;4h后下降率为 98.3% ,RPI为 12 .4。结论 :复配杀虫母液用超低容量喷雾能迅速杀灭成蚊 ,是特殊情况下短时间内降低室内成蚊密度较为理想的杀虫药剂。     

高效液相色谱/质谱法检测人尿中的糖皮质激素及其它兴奋剂

采用液相色谱/质谱(LC/MS)方法检测糖皮质激素、甾体和β2激动剂。本文采用Zorbax 30 mm×2.1mm,1.8μm短柱,对12种糖皮质激素、3种甾体和2种β2激动剂的液相色谱/质谱的测定方法进行了研究,建立了6分钟内快速检测人尿中多种糖皮质激素、甾体和β2激动剂的测定方法。检测限低于5ng/ml。该方法适用于兴奋剂的筛选及确证。     

脑动脉硬化对视神经血供影响的形态学研究及其临床意义

①目的 探讨视神经动脉起源、数目、分布及相关动脉的病理变化，为视神经因缺血所致视野缺损提供形态学依据。②方法 在体视显微镜扣手术显微镜下对100侧成人脑标本观察视神经动脉来源、数目和分布，对其中年龄50-70岁60侧脑标本的视神经和相关动脉进行病理切片观察。③结果 视神经动脉主要来源于颈内动脉、大脑前动脉争前交通动脉。其中单来源3侧(3％)，双来源68侧(68％)，3来源29侧(29％)。病理切片观察动脉管壁有粥样硬化改变53侧(88．3％)，其中被硬化斑块阻塞眼动脉的3侧(5、7％)。阻塞垂体上动脉的4侧(7．5％)，小动脉管腔狭窄11侧(20．8％)。与小动脉阻塞相对应的视神经切片。可见有神经纤维萎缩、变性等病理改变。硬化的颈内动脉壁压迫视神经可以形成明显的压迹。④结论 50岁以上出现不明原因的周边或中央视野缺损。脑动脉硬化导致视神经供血障碍病因不能除外。     

玄胡索散通过下调粒细胞集落刺激因子抑制脾脏髓源抑制细胞分化发挥抗乳腺癌作用

目的:探讨玄胡索散抑制乳腺癌小鼠脾脏髓源抑制细胞(MDSC)分化的作用机制。方法:4～5周龄BALB/c雌性小鼠48只,其中6只为正常对照组,其他42只采用小鼠左侧第二对乳腺皮下脂肪垫接种4T1细胞构建乳腺癌荷瘤小鼠模型,分为粒细胞集落刺激因子(G-CSF)对照组、G-CSF敲减组、模型对照组、玄胡索散小剂量组、玄胡索散中剂量组、玄胡索散大剂量组和环磷酰胺组,每组6只。其中G-CSF对照组和G-CSF敲减组分别采用shRNA慢病毒转染联合嘌呤霉素构建相应4T1稳转细胞模型。各组造模48 h后,玄胡索散小剂量组、玄胡索散中剂量组、玄胡索散大剂量组分别按2、4、8 g·kg^-1·d^-1玄胡索散灌胃,每天一次;环磷酰胺组按30 mg/kg腹腔注射环磷酰胺,隔天一次;其他组给予等体积0.5%羟甲基纤维素纳。各组连续给药25 d。苏木精-伊红染色观察脾脏组织病理学改变,流式细胞术测定脾脏MDSC亚群比例,免疫荧光法检测脾脏CD11b、Ly6G共表达,酶联免疫吸附测定外周血G-CSF浓度。在体外,建立荷瘤小鼠脾脏与4T1稳转株共培养体系,玄胡索散(30μ...     

Genotypic and phenotypic variability of 22q11.2 microduplications: An institutional experience

Duplications in the 22q11.2 region can cause 22q11.2 duplication syndrome and encompass a variety of phenotypes including developmental delays, facial abnormalities, cardiovascular defects, central nervous system delays, and other congenital abnormalities. However, the contribution of these contiguous duplicated regions to the clinical phenotypes has not been fully elucidated. In this study, we identified nine patients carrying different 22q11.2 microduplications detected by chromosomal microarray. Of these patients, seven pediatric patients presented with various clinical features including two neonate cases died shortly after birth, and two healthy adults. We examined region specific genotype–phenotype associations and found unpredictability associated with 22q11.2 duplications in these nine patients.     

Adenovirus-mediated intratumoral lymphotactin gene transfer potentiates the antibody-targeted superantigen therapy of cancer

Bacterial superantigens are extremely potent activators of murine and human T lymphocytes. To engineer superantigens for cancer immunotherapy, staphylococcal enterotoxin A (SEA) was genetically fused to the Fab region of the human colon carcinoma-reactive monoclonal antibody (mAb) C215. Fusion protein C215Fab-SEA can trigger cytotoxic T cells against C215 antigen positive tumor cells and induce tumor-suppressive cytokines. However, the antitumor effect of C215Fab-SEA is often not satisfactory because of T cell deletion after activation and failure to induce potent CTL activity after repeated administration. Lymphotactin (Lptn) is a potent chemoattractant for T cells and NK cells. To improve the therapeutic efficacy of fusion protein C215Fab-SEA we investigated in this study the antitumor responses elicited by combination of C215Fab-SEA and adenovirus-mediated intratumoral Lptn gene transfer in the preestablished C215 antigen expressing B16 melanoma murine model. More significant inhibition of tumor growth and prolonged survival time were observed in tumor-bearing mice that received combined therapy of C215Fab-SEA and Ad-Lptn than those of mice treated with C215Fab-SEA or Ad-Lptn alone. The highest CTL activity of tumor-bearing mice was induced after combined therapy. Intratumoral coadministration of C215Fab-SEA and Ad-Lptn augmented splenic NK activity of tumor-bearing mice most markedly. Our data demonstrate that the in vivo antitumor effect of C215Fab-SEA immunotherapy is potentiated significantly by combination with intratumoral Lptn gene transfer through more efficient induction of specific and nonspecific antitumor immune responses.