硝酸铋与丙磺舒合用对顺铂肾毒性的防护作用

毒性剂量的顺铂（ＣＰ３０μｍｏｌ·ｋｇ－１ｉｐ）可引起血尿素氮（ＢＵＮ）升高。硝酸铋（ＢＮ）５μｍｏｌ·ｋｇ－１于ＣＰ前４８和２４ｈｓｅ，丙磺舒（Ｐｒｏ）７００μｍｏｌ·ｋｇ－１于ＣＰ前１５，１ｈ及ＣＰ后５ｈｉｇ，或ＢＮ与Ｐｒｏ二者半量合用，按上述给药，均能抑制ＣＰ引起的ＢＵＮ升高，尤以ＢＮ＋Ｐｒｏ组抑制作用显著。肾脏光镜和电镜标本显示，ＣＰ使肾小管受损严重；ＢＮ组，Ｐｒｏ组和ＢＮ＋Ｐｒｏ组均使ＣＰ引起的肾小管受损减轻，尤以ＢＮ＋Ｐｒｏ组减轻明显。ＢＮ２．５－２０μｍｏｌ·ｋｇ－１剂量依赖性地诱导小鼠肾脏金属硫蛋白合成。Ｐｒｏ可使ＣＰ后２４ｂ肾铂含量明显降低；Ｐｒｏ或Ｐｒｏ＋ＢＮ使尿铂累积排出量增加，血浆铂浓度降低。提示ＰＦＯ防护ＣＰ肾毒性与其减少肾铂分布，增加尿铂排出有关。     

骨髓增生异常综合症几项实验指标研究进展

本文对MDS染色体、骨髓祖细胞体外培养及免疫功能几项实验指标的研究进展予以介绍。     

Long-term effects of physiologic concentrations of dexamethasone on human bone-derived cells

Bone cells derived from human trabecular explants display osteoblastic features. We examined the modulation of alkaline phosphatase activity and cAMP production as the result of exposing trabecular explants to physiologic concentrations of dexamethasone for 4 weeks during cellular outgrowth and subculture. Cells treated with dexamethasone were observed to grow generally more slowly than control cells. Cells appeared larger and more polygonal, and staining for alkaline phosphatase was more intense in the dexamethasone-exposed cultures. There was a progressive increase in cellular PTH responsiveness with increasing duration of exposure of cells to dexamethasone. Cells grown for 6 weeks in 3 x 10(-8) M dexamethasone had a 10-fold increase in PTH-stimulated cyclic AMP accumulation. Dexamethasone-treated cells also had a significantly increased alkaline phosphatase activity. 1,25-(OH)2D3-stimulated alkaline phosphatase activity was increased approximately 20-fold. cAMP responses were significantly increased to PTH (21.7-fold), PGE1 (2.67-fold), and forskolin (4.81-fold), but not to cholera toxin. Dexamethasone-treated cells also had a mean decrease in 1,25-(OH)2D3-stimulated osteocalcin production to 26.2% of control values (p less than 0.001). Hydrocortisone treatment gave rise to similar effects but of smaller magnitude than those of dexamethasone. Testosterone did not have a significant effect on alkaline phosphatase activity or cAMP production. Skin fibroblasts showed a significant enhancement of alkaline phosphatase activity in response to dexamethasone, but of a much smaller magnitude than in bone cells. The phenotypic changes induced by long-term culture in dexamethasone are consistent with the promotion of a more differentiated osteoblastic phenotype.     

DNA限制性内切酶分析应用于伴放线放线杆菌的鉴定和分型

本文用限制性内切酶分析(REA)作伴放线放线杆菌(Aa)的鉴定和分型研究,提取Aa染色体DNA,井分别用BamHI、HindⅢ,Sal Ⅰ和Xho Ⅰ消化,作琼脂糖凝胶电泳。结果显示,Aa和嗜沫嗜血杆菌的DNA片段图谱明显不同;分属于两种不同血清型的两株Aa菌株,其DNA片段图谱也明显不同。这表明,REA可用于Aa菌的鉴定和分型,在所用的4种酶中,以Sal Ⅰ和Xho Ⅰ消化的DNA片段图谱差异最明显。     

海岛纤恙螨经卵传递恙虫病立克次体的研究

1985年8月～1986年11月,作者以我国发现的恙螨新种海岛纤恙螨子代幼虫656只,分为21组,叮咬健康小鼠,从子1代到子4代幼虫叮咬过的小鼠中,连续分离出7株恙虫病立克次体,证明海岛纤恙螨能够经卵传递恙虫病立克次体至少4代.同时在该螨的卵、幼虫、若虫、成虫组织细胞内发现有恙虫病立克次体寄生,并发现有分裂增殖形态的立克次体,证明海岛纤恙螨各变态期内均保有恙虫病立克次体,这些立克次体能在恙螨体内大量增殖,连续传代.此项研究结果,对于确认海岛纤恙螨为浙江沿海地区恙虫病的传染媒介和宿主,提供了重要的科学依据.     

腹茧症16例诊治体会

目的 探讨腹茧症的诊断及治疗方法。方法 回顾性分析l6例腹茧症的临床资料及随访结果。结果 16例腹茧症均经手术治疗并确诊。术前11例误诊为机械性肠梗阻2～l0年，4例为误诊慢性阑尾炎，l例误诊为腹部肿块。术后并发症2例，全部患者均临床治愈。并获随访1～l0年，2例分别因反复发作肠梗阻于1年和5年死亡，2例反复发作不完全性肠梗阻合并营养不良，12例情况良好。结论 腹茧症术前诊断困难，上消化道造影和B超及CT对诊断可能有帮助；包膜切除，肠粘连松解是治疗本病的有效方法。     

间置空肠贲门再造术在抗返流性食管炎上的应用

作者对１５例贲门癌患者行根治术同时，采用食管残胃间插入带蒂空肠并附加贲门再造术，通过ＳＰＥＣＴ胃食管返流指数测定、食管下端ｐＨ检测及返流症状评定方法，并与单纯食管胃套叠吻合术进行随机对比分析，证明该术式具有单向住屏障作用，能有效地预防返流性食管炎的发生。     

Stimulation of inositol phosphate formation in cultured human retinal pigment epithelium.

Several hormones, neurotransmitters, and neuropeptides were screened for the ability to stimulate inositol phosphate formation in cultured human retinal epithelial (RPE) cells. Carbachol, vasopressin and thrombin were found to be effective. Treatment of RPE cells with all three agents produced increases in inositol monophosphate, inositol bisphosphate and inositol trisphosphate in the presence of 10 mM LiCl. Carbachol stimulated a 4-fold increase in the total of inositol phosphates at 1 mM. Studies with cholinergic antagonists showed a rank order of 4 DAMP greater than QNX greater than pirenzepine greater than methoctramine, suggesting the presence of M3 muscarinic receptors. Vasopressin gave a 2.5-fold stimulation at 10 microM. Agonists of vasopressin were also tested and gave differential responses. Studies using a V1 agonist (PIOVP) and a V2 agonist (DAVP) showed DAVP matching the level of stimulation elicited by vasopressin whereas treatment with PIOVP only reached 50% of the vasopressin response. These data suggested the presence of V2 receptors in the RPE cells. Several proteases were tested for their ability to stimulate RPE inositol phosphates. Thrombin caused a 7-fold increase in inositol phosphate formation at 1 U/ml, whereas trypsin and plasmin elicited smaller responses (approximately 2-fold). The thrombin effect was blocked by the thrombin-specific inhibitor, hirudin, but not by other protease inhibitors. Several mediators of inflammation such as bradykinin, histamine and serotonin were also tested, and they were ineffective in stimulating inositol phosphate turnover in the RPE cells.     

Ⅴ-Ti催化剂低氧催化氧化邻二甲苯制苯酐——Ⅱ.TiO_2晶体结构及助剂作用的影响

研究了V-Ti体系中TiO_2晶体结构与催化活性的联系,本系统中,当焙烧温度超过650℃,由于TiO_2由锐钛矿型转变为金红石型,使催化活性降低。助剂作用的ESCA、XRD、LRS研究表明,与通常V-Ti系催化剂不同,本催化剂由于助剂的作用,使V=O键减弱而利于活化;且随K助剂含量增加,V_2O_(4.33)晶胞的001面取向优化加强,更宜于催化活性的充分显示。     

烧伤后淋巴细胞膜流动性变化

报告以ＤＰＨ作为膜标记探剂，用荧光偏振法测定烧伤后淋巴细胞膜流动性变化。将小鼠背部造成１１％～１２％体表面积Ⅲ度烧伤，于伤后第６天取脾淋巴细胞，测其膜流动性。结果表明：烧伤后淋巴细胞膜流动性明显下降（Ｐ＜０．００１），同时淋巴细胞增殖反应及ＣｏｎＡ刺激的ＩＬ－２生成亦下降；淋巴细胞功能受抑制的程度与淋巴细胞膜流动性呈负相关；脾淋巴细胞膜流动性与脾组织过氧化脂质水平呈负相关。结果提示烧伤后淋巴细胞膜流动性下降可能是烧伤后淋巴细胞功能抑制的原因之一，膜流动性降低与脂质过氧化亢进有关