组织扩张术皮肤胶原的代谢改变

目的：研究常规扩张（ＩＴＥ）和持续快速扩张（ＣＴＥ）对皮肤胶原代谢的影响。方法用白色小家猪制作组织扩张术动物模型，用Ｇｏｒｄｅｌａｄｚｅ法测定血清和扩张组织的羟脯氨酸（ＨＰ）含量，藻酸盐印模材膜片法测量标记区面积；光镜测量真皮厚度。结果：ＩＴＥ组血清ＨＰ含量升高，０．８倍，ＣＴＥ组升高１．２倍，ＩＴＥ和ＣＴＥ组皮肤含量与正常皮肤相同，组织中ＨＰ总量均明显升高，持续扩张皮瓣组（ＣＴＥＦ）术后４ｗｋ皮     

Evidence for a NO synthase in porcine platelets which is stimulated during activation/aggregation

Abstract: We tried to characterize the porcine platelet nitric oxide (NO) synthase and its L-arginine (L-arg)/NO metabolism. Using RT-PCR we could show a constitutive endothelial NOS (ecNOS) and an inducible NOS (iNOS) similar mRNA in platelets. The NOS protein could be evidenced by an ecNOS specific antibody which also bound in platelets. This finding could be confirmed by Western blot showing an ecNOS in the membrane but not the cytosolic fraction; iNOS protein could not be detected. Using NADPH-diaphorase staining we could show NO synthase in preactivated platelets but not in resting platelets, indicating that the platelet NOS may be activated during platelet activation/aggregation. Porcine L-arg plasma levels (9.31 × 10^–5 mol/l ± 10%) could be shown to be in the same range as human plasma levels. Moreover, we could show that the NO precursor L-arg and hydroxy-L-arginine (OHarg) concentration dependently inhibited collagen induced platelet aggregation. Summarizing these results confirm the existence of and further characterize porcine platelet NO synthases.     

茶多酚对老化相关酶GSH－Px、SOD及代谢产物过氧化脂质的影响

本实验研究了连续服用茶多酚２０天，对１４月龄小鼠血及肝中ＳＯＤ、ＧＳＨ－Ｐｘ和ＬＰＯ的影响。结果表明茶多酚能提高血及肝中ＳＯＤ及ＧＳＨ－Ｐｘ活性，与正常对照组比较Ｐ＜０．０１，同时能降低血及肝中ＬＰＯ含量，与正常对照组比较Ｐ＜０．０１。提示茶多酚可通过降低机体自由基水平，起到抗衰老作用。     

Glucose attenuation of atropine-induced deficits in paradoxical sleep and memory

When administered systemically, glucose attenuates deficits in memory produced by several classes of drugs, including cholinergic antagonists and opiate agonists. Glucose also enhances memory in aged rats, mice, and humans. In addition, glucose ameliorates age-related reductions in paradoxical sleep. Because deficits in paradoxical sleep are most marked in those individual aged rats that also have deficits in memory, treatments which improve one of these functions may similarly improve the other. The present experiments show that glucose attenuates deficits in paradoxical sleep and memory after atropine administration, with similar dose-response curves for both actions. In the first experiment, rats received saline, atropine (1 mg/kg), glucose (100 mg/kg) or combinations of atropine + glucose (10, 100, 250, and 500 mg/kg) 30 min before assessment on a spontaneous alternation task. In the second experiment, 3-h EEGs were assessed for spontaneous daytime sleep in rats administered saline, atropine (1 mg/kg), glucose (100 mg/kg) or combinations of atropine + glucose (10, 100 and 250 mg/kg). In both experiments, glucose significantly attenuated deficits at an optimal dose of 100 mg/kg. A third experiment assessed blood glucose levels after injections of atropine + glucose (100 mg/kg) and determined that blood glucose levels were similar to those produced by other treatments which enhance memory. These results are consistent with the view that paradoxical sleep and at least one test of memory are similarly influenced by atropine and glucose.     

Evidence of an abnormal intramuscular component of fatigue in multiple sclerosis

The goals of this study were to investigate muscle fatigue in patients with multiple sclerosis (MS), and to determine the relationships between muscle fatigue, clinical status, and perceived fatigue. The fatigability of the anterior tibial muscle was quantitated in patients and controls during 9 min of intermittent stimulation (used to eliminate central sources of muscle fatigue). During exercise, the decline in tetanic force, phosphocreatine, and intracellular pH was greater in patients than in controls. The compound muscle action potential amplitude did not decrease during exercise, indicating that there was no failure of neuromuscular transmission during fatigue. Thus, the excessive fatigue in MS developed from sources beyond the muscle membrane. Following exercise, the recovery of tetanic force was delayed in patients (a pattern that suggests abnormal excitation–contraction coupling), whereas the recovery of metabolites was complete in both groups. Muscular fatigue was correlated with clinical disability but not with perceived fatigue. These results suggests that fatigue in MS has both central (perception, upper motor neuron dysfunction) and peripheral (impaired metabolism and excitation–contraction coupling) components.© 1995 John Wiley &Sons, Inc.     

The effect of fluconazole and ketoconazole on the metabolism of sulphamethoxazole

1 Cytochrome P450-mediated bioactivation of sulphamethoxazole to a hydroxylamine has been implicated in the hypersensitivity reactions associated with co-trimoxazole administration. Inhibiting the formation of the hydroxylamine may be one method of preventing the high frequency of toxicity which is observed in HIV-infected patients. Therefore, in this study, we have investigated the ability of fluconazole and ketoconazole, known cytochrome P450 inhibitors, to inhibit the formation of sulphamethoxazole hydroxylamine.
2 Ten healthy male volunteers were given co-trimoxazole (800  mg sulphamethoxazole and 160  mg trimethoprim) alone or 1  h after either fluconazole (150  mg) or ketoconazole (200  mg) in a randomized fashion with a washout period of at least 1 week between each phase. Urine was collected for 24  h, and sulphamethoxazole and its metabolites were quantified by electrospray LC-MS.
3 Ketoconazole had no effect on the urinary recovery of sulphamethoxazole or any of its metabolites. In contrast, fluconazole significantly ( P <0.001) inhibited the formation of sulphamethoxazole hydroxylamine by 50.0±15.1%. Fluconazole also inhibited the oxidation of sulphamethoxazole to the 5-methylhydroxy and 5-methylhydroxy acetate metabolites by 69.9±15.8% and 64.0±12.0%, respectively, but had no effect on the amount of sulphamethoxazole, N₄-acetyl sulphamethoxazole, or sulphamethoxazole N₁-glucuronide excreted in urine.
4 The potential clinical benefit of using fluconazole to prevent hypersensitivity to co-trimoxazole in patients with AIDS needs to be assessed in a prospective study using both metabolite formation and the clinical occurrence of adverse reactions as end-points.     

两种不同抗体双弹头标记物导向治疗肝癌的比较

在动物实验的基础上，比较了抗ＡＦＰ单克隆抗体（ｍＡｂ）和抗ＡＦＰ多克隆抗体（ｐＡｂ）两种不同抗体双弹头标记物在肝癌患者体内的生物代谢情况。结果显示，两种抗体标记物的血浆清除半衰期均在２４ｈ左右，ｍＡｂ标记物的清除较ｐＡｂ标记物略慢。尿清除的半衰期，ｍＡｂ标记物约为１２０ｈ，而ｐＡｂ标记物则约为１８ｈ，表明二者的体内生物代谢不同，疗效可能不一。     

Changes in Neutrophil Oxidative Potential in Patients Undergoing Cardiopulmonary Bypass with Polypropylene Hollow Fiber Oxygenators

Neutrophil oxidative metabolism, C3d and beta 2 microglobulin levels, were assessed in nine consecutive patients undergoing cardiopulmonary bypass surgery with polypropylene hollow fiber oxygenators for open cardiac operations. Generation of oxygen free radicals by neutrophils was measured as luminol-enhanced chemiluminescence after stimulation with opsonized Zymosan and phorbol myristate acetate. A significant increase in light emission was detected by using both of the chemiluminescence stimulators. Moreover, a remarkable and significant increase in C3d levels was found already at 10 min. Conversely minimal changes in levels of beta 2 microglobulin were detected during cardiopulmonary bypass surgery. These data suggest that the impact of the patient blood with the foreign surface of cardiopulmonary bypass results in activation of phagocyte cells with increased potential in oxygen consumption. These effects could be partially complement-mediated.     

家兔缺血与再灌流肾内脂质过氧化物含量的变化

本研究发现:家兔缺血60min(未再灌流)肾皮质和髓质内,脂质过氧化物含量均显著降低;缺血60min再灌流15min的肾皮质和髓质内,脂质过氧化物含量均显著增加。实验提示:缺血再灌流贤内氧自由基“爆发性”生成所引发的脂质过氧化可能是肾缺血性损伤的重要机制之一。     

实验性糖尿病大鼠肝,肾,心,脑脂肪酸代谢的动态变化

报道对链脲佐菌素（STZ）诱导的实验性糖尿病大鼠几种重要脏器（肝、肾、心、脑）卵磷脂、脑磷脂中脂肪酸构成的变化。不饱和脂肪酸变化的模式（C18：2n-6，C20：3n-6，C22：5n-3，C22：6n-3增加，C20：4n-6降低）基本相同，改变的先后顺序是肝→心、肾→脑。