Venous ischemia as a cause of ureteral necrosis in transplanted ureters

BACKGROUND: Urologic complications after pediatric renal transplantation can adversely effect the outcome and may result in decreased graft survival. Efforts to prevent these complications are worthwhile. This study investigates the incidence of these complications in a clinical transplant program and reports on an animal model used to investigate one possible cause. METHODS: In the clinical study, the results of a pediatric renal transplant program at a large children's hospital for a 5(1/2)-year period were reviewed with special attention paid to patients suffering ureteral necrosis. In the experimental study, 9 swine underwent laparotomy, bilateral complete infrahilar ureteric dissection, and extravesical ureteroneocystostomy. On the left side only, the renal and adrenal veins were ligated. The arterial supply remained intact. The right side did not undergo vessel ligation and served as the control. Three pigs each were killed at 3, 8, and 15 days. Kidneys, ureters and a cuff of bladder were examined histologically. RESULTS: In the clinical study 75 renal transplants were performed with a total of 5 cases of early ureteral necrosis. Two of these 5 displayed venous congestion and ischemia, and 2 were associated with kidneys displaying primary nonfunction of the graft. Seventy-one of 75 grafts are continuing to function. One of the 4 early graft losses also had an ischemic ureter. In the experimental study all right kidneys and ureters were normal. All left kidneys had complete hemorrhagic necrosis. Necrosis also was found in 5 of 9 proximal left ureters and in 7 of 9 distal left ureters. Viable left ureters displayed moderate to severe submucosal and periureteric hemorrhage. Four of 9 ureters displayed more damage distally than proximally. The extent of necrosis was similar at 3, 8, and 15 days. CONCLUSION: In both clinical and experimental studies, venous congestion and subsequent ischemia have been shown to be important causes of ureteral necrosis after renal transplantation.     

Effects of cerebrospinal fluid from patients with Parkinson disease on dopaminergic cells

BACKGROUND: The pathogenesis of substantia nigra pars compacta neuronal injury in Parkinson disease (PD) remains unknown. Cerebrospinal fluid (CSF) has been reported to contain factors toxic to dopaminergic neurons. OBJECTIVES: To determine whether the cytotoxic effects of CSF of PD patients are specific for dopaminergic neurons, dependent on prior levodopa therapy, and mediated by the cytokine tumor necrosis factor alpha (TNF-alpha). DESIGN: Specimens of CSF were evaluated in dopaminergic (MES 23.5) and nondopaminergic (N18TG2) cell lines for cytotoxicity by viability assay and by the inhibition of tyrosine hydroxylase. After specificity and time and dose response were established, CSF specimens were assayed in a blinded manner. The TNF-alpha levels in CSF were determined by enzyme-linked immunosorbent assay. The toxicity of TNF-alpha in MES 23.5 cells was determined. SETTING: A university-based research facility. SUBJECTS: There were 4 groups of subjects: normal control subjects (n = 10), control subjects with neurologic disease (n = 8), PD patients treated with levodopa (n = 10), and untreated subjects with PD (n= 20). RESULTS: Specimens of CSF from 15 (50%) of 30 PD patients and 2 (11%) of 18 control subjects were cytotoxic to dopaminergic MES 23.5 cells and were nontoxic to the parental cell line N18TG2. There was no correlation between the degree of PD CSF cytotoxicity, levodopa therapy, or the severity and duration of PD. Terminal deoxynucleotidyl transferase-mediated biotin-deoxyuridine triphosphate nick-end labeling (TUNEL) for DNA fragmentation suggested the involvement of apoptotic mechanisms. The inhibition of tyrosine hydroxylase was an early effect of cell injury by PD CSF and correlated with the viability assay. The mean TNF-alpha level was 2.6-fold higher in CSF specimens from PD patients than in those of controls. The addition of recombinant human TNF-alpha equivalent to the highest level determined in PD CSF was not cytotoxic to MES 23.5 cultures. CONCLUSIONS: Blinded CSF specimens from PD patients, regardless of therapy, contain factors that cause specific dopaminergic neuronal cell injury. These factors are present in a substantial proportion of CSF specimens from patients with early PD, before the institution of medical therapy. Levels of TNF-alpha are elevated in the CSF of PD patients, but TNF-alpha is not responsible for the cytotoxicity.     

Protection against amyloid beta peptide toxicity by zinc

Zinc (Zn) is an essential element in normal development and biology, although it is toxic at high concentrations. Recent studies show that Zn at high concentrations accelerates aggregation of amyloid beta peptide (Abeta), the major component of senile plaques in Alzheimer's disease (AD). This study reports the effect of varying Zn concentrations on Abeta toxicity and the mechanism by which low concentrations function in a protective role. At Abeta/Zn molar ratios of 1:0.1 and 1:0.01, Zn produces significant protection against Abeta toxicity in cultured primary hippocampal neurons. At higher concentrations (1:1 molar ratio), Zn offers no protection or enhances Abeta toxicity. The protective effect of Zn against Abeta toxicity is due in part to the enhancement of Na+/K+ ATPase activity which prevents the disruption of calcium homeostasis and cell death associated with Abeta toxicity. Analysis of Na+/K+ ATPase activity in cultured rat cortical cells indicated that Zn exposure alone afforded a 20% increase in enzyme activity, although the differences were statistically insignificant. However, in cortical cultures exposed to a toxic dose of Abeta (50 microM), Zn at concentrations of 5 and 0.5 microM led to significant increases in Na+/K+ ATPase activity compared with levels in cells treated with Abeta alone. Zn at a 1:1 molar ratio (50 microM) led to a significant decrease in enzyme activity. Together, these data suggest that Zn functions as a double-edged sword, affording protection against Abeta at low concentrations and enhancing toxicity at high concentrations.     

重组人神经营养因子-4/5蛋白抗三氧化二砷神经毒作用

目的初步观察重组人神经营养因子-4／5（hNT－4／5）蛋白对三氧化二砷毒性的抑制作用。方法利用hNT－4／5蛋白具有抗神经毒性的特点,采用本实验室克隆表达及部分纯化的具有天然hNT－4／5蛋白生物学活性的重组hNT-4／5蛋白,以不同水平的重组hNT4／5蛋白（0－100μl）与不同浓度的As2O3（0－160μmol／L）同时加入各组鸡胚前脑神经细胞和PC12细胞培养液中共同孵育24－48小时,观察其对染毒鸡胚前脑神经细胞存活和PC12细胞突起生长的影响作用。结果在鸡胚前脑神经细胞和PC12细胞中与As2O3共同培养48小时后,对照组与实验组的细胞存活率差异有显著性,而且细胞存活率和突起数目随hNT－4／5浓度增高而提高和增加。结论初步观察到重组hNT4／5蛋白具有抑制As2O3的毒性作用,为从基因工程途径寻找抗环境毒物因子提供了依据。     

神经元烟碱乙酰胆碱受体受阻滞所致早老型痴呆动物模型的建立

海马区内注射Ｋ－银环蛇毒素（Ｋ－ＢＧＴ）可造成小鼠学习记忆明显障碍,以建立早老性痴呆（ＡＤ）患者学习记忆缺损模型。对小鼠的损害作用随Ｋ－ＢＧＴ剂量增加而明显增加。水迷宫多项指标测试结果表明,Ｋ－ＢＧＴ损害组小鼠与对照组小鼠相比,空间学习和记忆能力显著下降。明暗回避反应实验结果也表明,Ｋ－ＢＧＴ损害小鼠潜伏期明显缩短,错误次数增多;两种检测方法均表明Ｋ－ＢＧＴ可导致小鼠学习记忆明显障碍,而且这种损害具有持久的作用。     

食品中分离的李斯特氏菌的致病基因分析

１９９６—１９９７年作者对全国１２个省市的７类食品共３７４６份进行了李斯特氏菌的污染调查,共分离出李斯特氏菌１６５株。用ＰＣＲ技术对分离菌株中李斯特氏菌的２种主要致病因子李氏溶血素Ｏ和内化素的基因进行了检测,其中５７株仅有内化素基因,２７株同时具有内化素基因和李氏溶血素Ｏ基因。两种致病基因均未检出的共有８１株。本研究说明判断单增李氏菌的主要指标是小鼠毒力试验阳性而不是其溶血反应,同时检测溶血素Ｏ和内化素２种基因对单增李氏菌有鉴别意义。     

烹调油烟对大鼠睾丸毒性的影响

作者探讨了烹调油烟（ Ｃ Ｏ Ｆ）对雄性大鼠生殖性损伤的毒作用机制。按时相（２０、４０、６０天）给雄性 Ｓ Ｄ 大鼠吸入同一浓度（３６～５３ ｍ ｇ／ｍ ３ ）的 Ｃ Ｏ Ｆ,观察 Ｃ Ｏ Ｆ对睾丸及其微量元素的影响。结果表明,吸入 Ｃ Ｏ Ｆ４０、６０天时大鼠体重均有降低趋势;睾丸、附睾脏器及其与体重的比值均分别低于对照组（ Ｐ＜ ００５）,且呈时 效关系;染毒４０、６０天时精子含量和存活率显著降低,而畸形率明显增高,且死精子多;染毒４０、６０天时睾丸中 Ｚｎ、 Ｍｎ 代谢紊乱,出现 Ｚｎ 低, Ｍｎ 高,均呈时 效关系。提示, Ｃ Ｏ Ｆ对性腺具有明显毒性,同时微量元素代谢紊乱可能对性腺的损害起了重要作用。     

学习障碍儿筛检测试的应用研究

目的：为在我国开展学习障碍的研究提供筛查工具,对日本PRS在江苏省进行标准化研究。方法：采用PRS测试江苏省12市城乡5～15岁普通学校中小学生和幼儿园儿童6676名,进行标准化研究。结果：PRS项目测试具有较高的可靠性,言语性以及非言语性领域Cronbach’sa系数均大于093,全项目则达到096;因子分析则间接提示本次测试的有效性;各项目得分比日本样本更接近正态分布,各项目以及各领域得分均略高于日本。作为筛查学习障碍界值是合适的。结论：PRS在江苏省可用于筛俭学习能力障碍,需进一步加强应用研究。     

重庆市1997年中小学生身体形态与机能发育研究

目的：了解重庆市中小学生生长发育现状和变化特点。方法：对1997年重庆市7－17岁中小学生的生长发育调查资料进行分析,并与本市1990年和全国1995年资料进行对比分析。结果：男生11－15岁,女生9－14岁为生长发育快速增长期;城市学生的生长发育好于乡村学生;男女生的形态发育出现两次交叉,机能发育无交叉。7年间,形态指标的发育在大多数年龄纷呈上升趋势,但均低于全国水平（P＜0．01）。机能发育指标,无论城乡男女,绝大多数年龄组均低于1990年本市水平和1995年全国水平（P＜0．01）。结论：重庆市中小学生形态发育存在长期增长趋势,而机能发育较差。     

藏药七十味珍珠丸对动物出血和凝血时间的影响

藏药七十味珍珠丸（RNSP）灌胃给药（ig）给药0．5g／kg和1g／kg对大、小鼠的出血时间和凝血时间无影响;对“血瘀”模型大鼠的凝血时间和血小板数也无统计学差异。而ig给药2g／kg对延长小鼠出血时间的作用非常明显。