妊娠高血压综合征尿蛋白的丢失对新生儿出生体重的影响

目的: 几乎没有研究报道妊娠高血压综合征 (妊高征 ) 患者尿蛋白对新生儿出生体重的影响, 该研究欲探讨妊高征患者不同水平尿蛋白对新生儿出生体重的影响关系。方法: 1997年 1月 ~2004年 6月期间, 住院分娩患中、重度妊高征产妇 136例, 对新生儿出生体重与各种因素进行回归分析及t检验分析。结果: 单变量回归分析尿蛋白、孕龄分别与新生儿出生体重有高度显著性关系 (P<0. 01); 尿蛋白和孕龄一起进入多元回归分析, 校正影响因素, 尿蛋白和孕龄仍然是影响新生儿出生体重显著性因素 (P<0 .01); 与妊高征尿蛋白 ( +) 比较, 尿蛋白 无显著性影响新生儿出生体重 (P>0. 05), 尿蛋白 有显著性影响新生儿出生体重 (P<0. 01)。结论: 新生儿出生体重与妊高征患者尿蛋白丢失有关, 尿蛋白 丢失将严重影响新生儿出生体重。     

Observations on pathological and histochemical changes in piglet livers infected with Taenia saginata asiatica

To study the pathological and histochemical characteristics of lesions in piglet livers infected with Taenia saginata asiatica (T. saginata asiatica) throughout the different stages, piglets were fed with eggs of T. saginata asiatica and raised in isolation in an animal center to establish the T. saginata asiatica infection model with normal piglets as control. The pathological changes in the piglet livers were observed after the infection using liver sections stained with hematoxylin and eosin. Histochemical methods were used to check the changes in lipid, glycogen and protein content in the liver. The data collected by image analysis were analyzed statistically with Statistical Package for the Social Science. The results show that T. saginata asiatica-exposed piglets were indeed infected. Inflammatory reactions began on the fourth day and progressed rapidly. Kupffer cell hyperplasia, hepatic hydropic degeneration and ballooning degeneration were found in the 10th–20th days after infection. Hepatic central veins and hepatic sinusoids were dilated and congested. Spotty necrosis occurred in some local liver tissues. In the 40th–60th days, granulomatous reactions and mild hepatocirrhosis were the main lesions. In the 70th–80th days, hepatocirrhosis and bile duct proliferation were observed in the liver. In the different stages, lipid drops were increased while glycogen and protein levels were decreased to some degree. There was a significant difference in metabolism between the infected group and the control group (P < 0.01). It is concluded that pigs are the favorable intermediate host of T. saginata asiatica and its infection can result in serious pathological and histochemical lesions in host organs. Translated from Journal of Guiyang Medical College, 2006, 31(4): 296–300 [译自: 贵阳医学院学报]     

发作性睡病与HLA—DQB1＊0602基因的相关性研究

目的 探讨发作性睡病与HLA—DQB1基因的相关性。方法 对30例发作性睡病患者的临床资料进行分析。用序列特异性引物-聚合酶链反应（PCR-SSP）分型技术测定HLA—DQB1等位基因，并与44例健康人检测的数据进行比较。结果 发作性睡病患者组DQB1＊0602基因频率为40％，与正常对照组9．09％相比较明显增高；未检出DQB1＊0401—0402基因，与正常对照组9．09％相比较，经统计学分析，差异有显著性（P〈0．05）。结论 HLA—DQB1＊0602基因为中国发作性睡病人群的易感基因；HLA-DQB1＊0401—0402基因为中国发作性睡病人群的保护基因。     

牙本质黏结剂增强根管倒充填材料密闭性能的实验研究

目的观察在使用MTA进行根尖倒封闭术时,牙本质粘结剂对其密闭抗微渗漏的影响.方法取40颗离体单根恒牙,分别用MTA、MTA 牙本质粘结剂进行根尖倒封闭术,用染料渗透法检测根尖微渗漏的情况.结果MTA 牙本质粘结剂组的根尖密闭效果明显优于单纯使用MTA组,其差别具有统计意义(P<0.05).结论在使用MTA进行根尖倒封闭术时,使用牙本质粘结剂可提高充填体的密闭效果.     

TNF-α和低氧对胰腺癌细胞表达VEGF-A、C的调节

目的:探讨细胞活素肿瘤坏死因子-α(TNF-α)、SNAP(S-Nitroso-Nacetyl-penicillamine)对胰腺癌细胞产生血管内皮生长因子A、C(VEGF-A、C)的调节.方法:用Northern杂交和Western杂交法分析6种人胰腺癌细胞株中VEGF-A、C基因和蛋白的表达;以TNF-α或SNAP刺激其中两个细胞株后用逆转录-聚合酶链式反应技术(RT-PCR)分析其VEGF-A、C基因的表达.结果:Northern杂交法显示这6种胰腺癌细胞株均有4.1kb VEGF-A基因和2.4kb VEGF-C基因的表达;Western杂交法显示它们均有分子量为43kD的VEGF-A蛋白质和分子量为55kD的VEGF-C蛋白质的表达.RT-PCR分析法显示:TNF-α使细胞株COLO-357产生VEGF-A、VEGF-C mRNA分别减少约1～2.5倍、1～2倍,使细胞株CAPAN-1产生VEGF-A、VEGF-C mRNA分别减少约1倍、1.6～2.5倍;而SNAP刺激细胞株COLO-357产生VEGF-A mRNA增加约5倍,刺激细胞株CAPAN-1产生VEGF-A mRNA增加约4倍,但对这两种细胞株产生VEGF-C mRNA均无明显刺激作用.结论:细胞活素TNF-α和低氧通过调节血管内皮生长因子A、C的表达而影响胰腺癌细胞的生物学特性,抑制癌细胞的增殖,促进其凋亡、死亡或进展、恶化.     

间接免疫荧光法检测婴幼儿急性下呼吸道合胞病毒感染的特异性IgM

本文对1984年1～3月和1985年3～8月共107例急性下呼吸道感染的住院患儿,采用间接免疫荧光法检测其急性期血清抗RSV特异性IgM抗体,并与病毒分离和/或中和试验比较,敏感性为82.1％,特异性为71.8％。RSV感染患儿发病后3天内大多数病例即可从血清中检测出RSV-IgM,因此该法具有早期诊断价值。     

ULTRASTRUCTURAL INVESTIGATION OF EXPERIMENTAL FRACTURE HEALING ROLE OF OSTEOGENESIS PLAYED BY FIBROBLASTS

Transmission electron microscopic investigation of standardized fractures of radii in 50 rabbits re vealed that fibroblasts took part in the formation of bony callus. The osteogenetic role played by the fibroblasts can be categorized into the following 5 aspects: a. Fibroblasts synthesize and secrete Type collagen fibrils and induce deposition of calcium salt crystals in the collagen fibrils. b. Fibroblasts produce matrix vesicles in their surroundings. These matrix vesicles become calcified and turn into floccu- lent calcospherules which coalesce and fuse into bone tissues. c. Fibroblasts harbor calcium granules in their mitochondria, thus providing calcium for calci- fication of the intercellular matrix and bone forma tion between the cells. d. Fibroblasts can transform directly into osteocytes; there is bone formation around the fibroblasts, the bone tissues surround the fibroblast in the form of bony lacuna, then the fibro- blast in the lacuna transforms into osteocyte. e. Fibroblasts can undergo degenerative changes leading to decease and replacement by bone tissues.     

Role of basal insulin in the regulation of protein kinetics and energy metabolism in septic patients.

We have investigated the role of basal insulin concentration on leucine kinetics (determined by means of 1-[13C]leucine) and energy metabolism (determined by indirect calorimetry) in eight septic patients by reducing insulin (and glucagon) secretion by somatostatin infusion. Basal glucagon concentration was elevated (744 +/- 381 pg/mL), and insulin concentration was normal (10 +/- 4 microU/mL). Basal resting energy expenditure (REE) was 151 +/- 8% that of predicted basal energy expenditure, and leucine appearance (Ra), oxidation, and nonoxidative disposal rates were all elevated above the normal ranges. Somatostatin infusion reduced insulin concentration by 52% and glucagon concentration by 64%. This resulted in a significant increase in the rate of leucine oxidation from 0.96 +/- 0.08 to 1.18 +/- 0.14 mumol/kg/min (p less than 0.01), and nonoxidative leucine disposal decreased from 2.95 +/- 0.18 to 2.67 +/- 0.17 mumol/kg/min (p less than 0.01). Somatostatin infusion also caused significant increases in REE and fat oxidation from 1310 +/- 100 to 1505 +/- 128 kcal/m2/day (p less than 0.05) and from 1.72 +/- 0.24 to 2.41 +/- 0.41 mg/kg/min, respectively, and a slight decrease of carbohydrate oxidation from 1.51 +/- 0.49 to 1.31 +/- 0.49 mg/kg/min. These metabolic responses can be attributed to the reduction in insulin concentration, because they are in the opposite direction of changes that would occur as a consequence of a reduction in glucagon concentration. We conclude that the basal insulin plays an important role in attenuating net protein loss and energy expenditure.