隐动脉筋膜蒂的交腿皮瓣修复小腿严重软组织缺损

目的探讨一种小腿严重软组织缺损的修复方法。方法以健侧隐动脉为蒂的顺行或逆行交腿皮瓣修复患侧小腿软组织缺损。结果本组8例均有效地覆盖受区创面,随访三个月,皮瓣全部成活。结论该皮瓣不牺牲小腿的重要血管,质地与受区相似,方法简单易行,血运可靠,血管蒂长,是修复小腿严重软组织缺损的较好方法。     

贯众提取液对革兰氏阳性球菌的抑菌作用

目的：了解贯众(Dryopteris crossirhizomz)不同提取液对革兰氏阳性球菌的抑菌作用。方法：分别用水以及3种不同pH值的70％乙醇为溶媒提取贯众干品以制备贯众提取液，利用打孔法和试管稀释法测定提取液对13种微生物的抑制效果。结果：每1ml含生药1g的贯众醇提液、水提液对革兰氏阳性菌有较强的抑制作用，尤其是革兰氏阳性球菌如金黄色葡萄球菌和甲型溶血性链球菌等。对革兰氏阴性菌和真菌的抑制作用较弱，但对普通变形杆菌则有较强的抑制作用。不同pH值的抽提溶剂对药物的有效抑菌成份的提出效果不同，抽提溶剂pH越小，有效成份的提出效果越好。结论：贯众醇提液、水提液对革兰氏阳性菌有较强的抑制作用，尤其是对革兰氏阳性球菌，而对革兰氏阴性菌和真菌的抑制作用则较弱。贯众的抗菌成份易溶于水，抽提效果随pH减小而增加。     

广州家禽、家畜批发市场六种动物隐孢子虫感染情况的调查

目的调查广州家禽、家畜批发市场兔、鸭(含雏鸭)、羊、鸡、狗、鸽6种动物的隐孢子虫感染情况。方法取上述动物的粪便292份，用金胺-酚-改良抗酸复染法染色，镜检卵囊。结果检查的6种动物均发现有隐孢子虫感染，自然感染率分别为：64．1％，54．3％(45．0％)，21．7％，20．6％，20．0％，14．6％。结论广州家禽、家畜批发市场6种动物存在隐孢子虫感染。     

人外周血单核细胞和脐血CD34+细胞来源的树突细胞比较

目的比较从人外周血单核细胞及脐血CD34+细胞诱导树突细胞(DC)的方法及其特性.方法用淋巴细胞分离液分离外周血单个核细胞,贴壁法获得单核细胞;经GM-CSF及IL-4诱导获得DC.磁性活化细胞分选系统(MACS)分选脐血CD34+细胞,以GM-CSF、IL-4、TNF-α、SCF、FL、TPO等细胞因子诱导获得DC.用电镜、普通显微镜观察DC形态;流式细胞仪分析DC表型;同种混合淋巴细胞反应(allo-MLR)观察DC刺激T淋巴细胞增殖的能力.结果外周血单核细胞在因子GM-CSF、IL-4、TNF-α,脐血CD34+细胞在GM-CSF、IL-4、TNF-α、SCF、FL、TPO等因子作用下,可生成DC,并表达相应的DC分化抗原CD14、CD80、CD83、CD86、HLA-DR.脐血CD34+细胞具有较强的扩增能力,经2周诱导,体系细胞数可增加173.8士26.7倍,两种来源的DC均能刺激同种异体淋巴细胞的增殖反应.结论外周血单核细胞与脐血CD34+细胞,在体外均可诱导成DC,并具有相应的DC分化抗原和功能.     

癌基因c-fos、c-jun蛋白在鳞状细胞癌皮损中的表达及意义

目的　探讨癌基因c fos、c jun的表达与皮肤鳞癌发生和发展的关系。　方法　采用免疫组化法对 6 0例皮肤鳞癌的c fos、c jun的表达情况进行检测 ,并与正常皮肤组织进行对照。　结果　c fos、c jun在正常皮肤组织不表达 ,在皮肤鳞癌中的表达阳性率分别为 6 1.7%和 4 8.3% ,其表达水平与癌组织的分化程度有关 (P <0 .0 5 ) ,肿瘤的分化程度越高其表达水平越高。　结论　c fos、c jun的表达水平可作为判定皮肤鳞癌分化的指标。     

吡那地尔对高血压心脏结构和功能重构的影响

在等降压剂量下吡那地尔和赖诺普利可使４月龄自发性高血压大鼠的血压下降６．０￣８．０ｋＰａ，并接近同种属正常血压大刀瓣血压水平。     

明胶-聚乳酸载药纳米微球的制备及其体外释药研究

采用复合乳液—溶剂挥发法制得明胶—聚乳酸载五氟脲嘧啶(5—Fu)微球，以混合型乳化剂Tween—80：Span—80＝5：1—作为初乳乳化剂，O—羧甲基壳聚糖作为复乳乳化剂，考察了明胶—聚乳酸载药微球的制备条件对微球的成球性、药物包封率及体外释药的影响。结果表明乳化剂的选择、内部水相药物浓度和PLA分子量等均对载药微球的结构与性能产生影响，经优化条件得到了成球性和体外释放都比较好的载药微球。     

Studies on mutants deficient in the photosystem I reaction centers in Chlamydomonas reinhardtii

Summary Genetic analysis of 25 nuclear mutants defective in the chlorophyll-protein complex CP1 was undertaken. The mutants belong to 13 complementation groups scattered throughout the nuclear genome. All these mutants lack the apoprotein of CP1 and, in addition, a specific set of six low molecular weight thylakoid polypeptides. System I particles obtained by treating WT thylakoid membranes with detergent specifically contain those polypeptides which the mutants lack. These observations suggest that a particular sub-structure of the thylakoid membrane associated with the photosystem I activity is missing from all 25 mutants studied, and that this general phenotype can result from mutation at any one of several unlinked Mendelian loci.     

Role of Periductal and Ductular Epithelial Cells of the Adult Rat Pancreas in Pancreatic Hepatocyte Lineage: A Change in the Differentiation Commitment

Development of pancreatic hepatocytes in adult rats maintained on copper deficient diet containing 0.6% trien (CuDT) has been reported recently. To elucidate the histogenesis of hepatocytes a sequential study was undertaken using morphologic, histochemical, immunochemical, in situ hybridization, and Northern blot analysis. Male F-344 rats weighing 80 to 90 g were fed CuDT for 8 weeks and returned to normal rat chow. Beginning from 4 weeks of copper depletion, there was a progressive loss of acinar cells and by 8 weeks more than 90% of the acinar tissue was lost. During this period, there was an increase in the number of adipocytes in the interstitium, and in the number of interstitial and ductular cells. Morphologic observations were confirmed by immunoblot and Northern blot analysis, in which the amount of pancreatic proteins and their mRNAs decreased between 5 and 8 weeks. During this period, a progressive increase in the level of albumin mRNA was observed. In situ hybridization, performed at 7 weeks of copper deficiency, showed localization of albumin mRNA over interstitial and ductular cells. Pancreatic hepatocytes were identified immediately after the rats were returned to a normal diet and gradually increased in number. The hepatocytes occupied almost 60% of the pancreatic volume by 8 weeks. During the early recovery phase, hepatocytes were identified in ductules as well as in the interstitium. Based on these studies, it is concluded that both the ductular cells and interstitial cells, which resemble oval cells of liver, are capable of transforming into pancreatic hepatocytes and these cells may be considered stem-cell equivalent.     

CD1d deficiency exacerbates inflammatory dermatitis in MRL-lpr/lpr mice

Mechanisms responsible for the development of autoimmune skin disease in humans and animal models with lupus remain poorly understood. In this study, we have investigated the role of CD1d, an antigen-presenting molecule known to activate natural killer T cells, in the development of inflammatory dermatitis in lupus-susceptible MRL-lpr/lpr mice. In particular, we have established MRL-lpr/lpr mice carrying a germ-line deletion of the CD1d genes. We demonstrate that CD1d-deficient MRL-lpr/lpr mice, as compared with wild-type littermates, have more frequent and more severe skin disease, with increased local infiltration with mast cells, lymphocytes and dendritic cells, including Langerhans cells. CD1d-deficient MRL-lpr/lpr mice had increased prevalence of CD4(+) T cells in the spleen and liver and of TCR alpha beta (+)B220(+) cells in lymph nodes. Furthermore, CD1d deficiency was associated with decreased T cell production of type 2 cytokines and increased or unchanged type 1 cytokines. These findings indicate a regulatory role of CD1d in inflammatory dermatitis. Understanding the mechanisms by which CD1d deficiency results in splenic T cell expansion and cytokine alterations, with increased dermal infiltration of dendritic cells and lymphocytes in MRL-lpr/lpr mice, will have implications for the pathogenesis of inflammatory skin diseases.