Calcification of the ductus venosus: a cause of right upper quadrant calcification in the newborn

The authors report three cases of ductus venosus calcification as an additional cause of vascular liver calcification in the newborn. All three infants had umbilical venous catheters. The calcification may be caused by extravasated fluids given through the catheter or by local trauma due to catheter insertion. An obliquely oriented, paravertebral "tram-track" calcification in the right upper quadrant, particularly in a premature infant with a history of umbilical venous catheterization, should suggest the diagnosis of calcified ductus venosus.     

Binding characteristics of anti-Rh0(D) antibodies to Rh0(D)-positive and Du red cells

The relation of human erythrocyte Rh0(D) to Du sites is an important unresolved question in the field of immunohematology. To compare the immunological reactivity of Rh0(D)-positive and Du erythrocytes, the binding characteristics of two anti-Rh0(D) antisera to human Rh0(D)- positive and Du ("low-grade") erythrocytes were studied. 14C-Protein A and direct antibody-labeled techniques were used to generate binding curves and to derive double-reciprocal plots. The results show that the number of antigen sites differ by a factor of 10 to 15 between the Rh0(D)-positive and Du red cells, but that the dissociation constants between anti-Rh0(D) and the Rh0(D) and Du antigens are indistinguishable when studied by the two labeling methods and two different anti-Rh0(D) antibodies. The extent of binding to 112 different Du samples showed a normal distribution and was independent of apparent phenotype. These data suggest immunologic identity of Rh0(D) and Du ("low-grade") sites and that the difference between the antigens of Rh0(D) and Du cells is quantitative only. The data are incompatible with the "missing mosaic" and gene interaction theories of mechanism.     

含L-4-氧代赖氨酸寡肽的合成及其抗白念珠菌活性

本文运用“违法传送”概念,根据白念珠菌对寡肽的传送特点,设计并合成了十个含L-4-氧代赖氨酸(以下称I-677)的寡肽,以提高I-677的抗白念珠菌活性。体外抗白念珠菌试验表明:I-677-肽(I-677-X₁,I-677-X₁-X₂和I-677-X₁-X₂-Gly,其中X₁,X₂=Met,Leu,Ile,Ala,β-Ala,Gly)较I-677单体摩尔活性提高了2.1～28倍,其摩尔最低抑菌浓度为8.7×10^-8～9.3×10^-9mol/ml,传送肽和赖氨酸分别逆转I-677-肽抗菌活性的实验结果证实了I-677的“违法传送”途径。     

精胺对精子获能和受精的影响

精胺广泛存在于动物组织和体液中,它在生殖过程中的作用还存在着很大的争议,作者综述了这些研究成果,并对其今后的发展动态作了展望．     

Heterologous expression of rat P450 2E1 in a mammalian cell line: in situ metabolism and cytotoxicity of N-nitrosodimethylamine

GM0637, a human fibroblast cell line, was transfected with pCMV2E1, an expression vector containing the full length cDNA for rat cytochrome P450 2E1 (P450 2E1), and with pCMVneo, which contained vector alone, and the selected clones were designated GM2E1 and GMneo, respectively. Western blot analysis showed that GM2E1, but not GMneo, expressed a protein that reacted with anti-human P450 2E1 antibody. The 7- ethoxycoumarin O-deethylase,p-nitrophenol hydroxylase, and N- nitrosodimethylamine (NDMA) demethylase activities of the P450 in these cells were measured in monolayer cell cultures without preparing microsomes. Exposure of the GM2E1 cells to NDMA for 4 days caused severe decreases in cell viability, as determined by crystal violet uptake, and showed a sigmoidal dose-response curve with a median lethal dose of 17 microM. In contrast, the viability of GMneo cells was not altered by NDMA even at concentrations up to 10 mM. Time- and concentration-dependent methylation of DNA, RNA and protein by [14C]NDMA was only observed in cells expressing P450 2E1. Inhibitors of P450 2E1 activity such as ethanol, 4-methylpyrazole, and isoniazid caused a 90% decrease in the methylation of cellular macromolecules and also completely protected the cells against NDMA-mediated toxicity. The cytotoxicity due to exposure to NDMA was partially inhibited by antioxidants such as N-acetylcysteine, ascorbic acid, butylated hydroxyanisole and N-t-butyl-alpha-phenylnitrone but was not potentiated upon glutathione depletion. These results document the ability of rat P450 2E1 to metabolize NDMA to toxic reactive intermediates and demonstrate that this cell line provides a useful model for studying the mechanisms of metabolism-mediated toxicity and carcinogenesis.      

Participation of immune complexes in adenovirus infection

To determine the participation of immune complexes during adenovirus infection, we evaluated serum and necropsy specimens of patients with confirmed adenovirus infection of the lower respiratory tract. In lung and kidney from seven dead patients, immunofluorescence revealed the presence of hexon, immunoglobulins and complement. These patients had clinical manifestations of kidney dysfunction. In dead patients (3/3 in whom serum was available) neither anti-adenovirus antibodies nor adenovirus-specific immune complexes could be found in the final stage of the infection. However, two of these patients had anti-adenovirus antibodies and immune complexes in samples obtained early in the infection. Most patients (16/19) who survived the infection had circulating anti-adenovirus antibodies. Half also had immune complexes specific for adenovirus in some moment of the illness. This suggests that immune complexes arise during respiratory infection by adenovirus, probably contributing to its clinical picture.     

The fetal alcohol syndrome in adolescence

At present, alcohol is recognized as the leading teratogenic agent in long-lasting CNS dysfunction. Little is known about the long-term development and outcome of children with fetal alcohol syndrome (FAS). Forty-four FAS patients who were diagnosed in early childhood were followed up for 10–14 years. This study documents the developmental changes of the manifestations of FAS from childhood to adolescence and describes a characteristic "juvenile" pattern of FAS, which may help to identify this syndrome even in adolescence. This is especially relevant for patients who were not diagnosed earlier.     

肝脏缺血预处理过程中蛋白激酶C活性的变化

目的:观察在肝脏缺血预处理过程中蛋白激酶C的活性改变及细胞内信号转导机制。方法:实验于2004-03/2005-03在南方医科大学珠江医院中心实验室完成。实验分组:36只大鼠随机分成6组,每组6只。①假手术组。②缺血再灌注组。③缺血预处理组。④缺血再灌注 豆蔻酸佛波酰乙脂组。⑤缺血预处理 白屈菜季铵碱组。⑥缺血预处理 PD98059组。实验干预:①假手术组仅分离肝十二指肠韧带,不阻断肝门,不进行其他干预处理。②缺血再灌注组在第一肝门用小血管夹阻断尾状叶及左肝叶血流40min松开血管夹肝脏再灌注3h,再灌注开始后关腹。③缺血预处理组先行3个循环的缺血预处理,阻断第一肝门10min,开放再灌注10min为1个循环,随后操作同缺血再灌注组。④缺血再灌注 豆蔻酸佛波酰乙脂组:按4μg/kg共0.5mL蛋白激酶C激动剂豆蔻酸佛波酰乙脂溶液,经静脉通道缓慢推注,推注10min,推注后等待10min,余处理同缺血再灌注组。⑤缺血预处理 白屈菜季铵碱组:按5mg/kg共0.5mL蛋白激酶C抑制剂白屈菜季铵碱溶液,同样用10min经静脉通道缓慢推注,推注后等待10min,其余处理同缺血预处理组。⑥缺血预处理 PD98059组:按5mg/kg共0.5mL丝裂原激活的蛋白激酶抑制剂PD98058溶液,同上速度缓慢静脉推注,推注后等待10min,余处理同缺血预处理组。实验评估:①在ECHNICONRA-1000全自动生化分析仪上采用速率法检测血清谷草转氨酶和血清谷丙转氨酶活性。②按蛋白激酶C活性测定试剂盒操作步骤检测肝组织蛋白激酶C活力。③Westernblot免疫印迹法检测肝组织磷酸P44/42MAPKs活性。结果:36只大鼠均进入结果分析,中途无脱落和死亡。①血清谷草转氨酶和血清谷丙转氨酶活性:缺血预处理组低于缺血再灌注组(P<0.01)。缺血预处理 白屈菜季铵碱组、缺血预处理 PD98059组显著高于缺血预处理组(P<0.01)。缺血再灌注 豆蔻酸佛波酰乙脂组显著低于缺血再灌注组(P<0.01)。②蛋白激酶C活力:缺血预处理组高于缺血再灌注组[(1877.2±81.0),(713.1±37.0)pkat/g,P<0.01];缺血再灌注 豆蔻酸佛波酰乙脂组亦显著高于缺血再灌注组[(2758.4±454.3),(713.1±37.0)pkat/g,P<0.01];缺血预处理 白屈菜季铵碱组明显低于缺血预处理组[(567.9±46.2),(1877.2±81.0)pkat/g,P<0.01]。③磷酸P44/42MAPKs活性:与假手术组比较,其在缺血再灌注组的表达量轻度升高;缺血预处理组较缺血再灌注组升高显著;缺血预处理 白屈菜季铵碱组较缺血预处理组明显降低,缺血预处理 PD98059组表达量下降更为显著;缺血再灌注 豆蔻酸佛波酰乙脂组表达量较缺血再灌注组明显升高。结论:缺血预处理保护效应中,蛋白激酶C对P44/42MAPKs信号通路的激活是细胞保护效应的一个重要环节。