Effect of systemic zinc administration on delayed neuronal death in the gerbil hippocampus

The divalent cation zinc has been reported to possess several physiological properties such as blocking apoptotic cell death through an inhibitory effect on Ca²⁺-Mg²⁺ endonuclease activity, or modulating the neurotoxicity via glutamate receptor subtypes. In the present study, we investigated the effect of peripherally injected zinc on delayed neuronal death seen in the hippocampus after transient global ischemia, in order to elucidate a possible beneficial role on zinc in ischemic neuronal cell death. Forty-five adult Mongolian gerbils of both sexes underwent transient bilateral clipping of the common carotid arteries for 3 min. In the pretreated animals, ZnCl₂ (20 mg/kg) was injected subcutaneously once, 1 h before ischemia (superacute group; n=6) or twice at 24 and 48 h before ischemia (subacute group; n=14). Histological survey was carried out 3 days later by in situ DNA fragmentation method and 4 days later by hematoxylin-eosin staining by semiquantatively counting dead neurons in the CA1 sector. Subacute zinc pre-administration significantly reduced the nuclear damage and subsequent neuronal death; however, superacutely pre-administered zinc did not protect hippocampal neurons against ischemia but it did not aggravate the effect of ischemia, either. The present study suggested that transfer of exogenous zinc into the intracellular space is required for neuroprotection, presumably via the anti-endonuclease activity.     

前列腺素E1对尸体肾移植术后肾功能延迟恢复的影响

目的探讨前列腺素E1(PGE1)应用于尸体肾移植术后肾功能延迟恢复(DGF)患者对移植肾功能恢复的影响.方法回顾性分析因急性排斥(AR)和急性肾小管坏死(ANT)导致DGF的127例临床资料,其中应用PGE1治疗56例(PGE1组),未用PGE1者71例(对照组).比较两组在出现DGF后的透析治疗时间、肾功能恢复情况、彩超的移植肾血流阻力指数(RI)及6个月内AR发生率.结果与对照组比较,PGE1组透析治疗时间明显缩短(P＜0.05),移植肾的血肌酐下降速度快(P＜0.05),RI及6个月内AR发生率低(P＜0.05).结论PGE1有利于尸体肾移植术后DGF患者移植肾功能的早期恢复,并能降低AR的发生率.     

不同海拔高度严重烧伤延迟复苏大鼠脑组织中能量负荷的变化及其意义

目的：探讨不同海拔高度严重烧伤延迟复苏大鼠脑组织能量负荷变化及其意义。方法：以120只雄性Wistar大鼠建立高原（海拔3800m）实验模型（TBSA30％，Ⅲ度），随机分为延迟、即时复苏组和正常对照组，分别于伤后1、6、12、24、72h及7d取材。兰州地区取相等数量动物重复实验。应用高效液相色谱法检测脑组织中AMP、ADP、ATP的含量，并计算能量负荷。结果：能量负荷在高原正常对照组与兰州地区正常对照组差异显著（P〈0．01）。高原烧伤后脑组织能量负荷与对照组相比均降低，即时复苏组伤后早期即出现显著变化（P〈0．01），伤后72h开始恢复，伤后7d差异无显著，延迟复苏组伤后7d仍星显著差异（P〈0．01）。与即时复苏组比较伤后6～24h无显著差异，伤后72h～7d呈显著性差异（P〈0．01）。高原地区各时相点与兰州地区比较，EC值均降低，除即时复苏组6h外，具有统计学意义。结论：不同海拔高度严重烧伤延迟复苏大鼠脑组织能量负荷的改变一定程度上反映了脑损伤的严重程度。     

一氧化碳中毒迟发性脑病的临床预防

目的　探讨临床治疗措施对一氧化碳中毒迟发性脑病的预防。方法　将 130例一氧化碳中毒患者随机分为A、B、C 3组 ,A组采用纳络酮、低分子肝素、高压氧治疗 ;B组采用胞二磷胆碱、醒脑注射液、高压氧治疗 ;C组采用胞二磷胆碱、醒脑注射液治疗。结果　A组昏迷时间与B、C组对比 ,B组与C组对比 ,明显缩短 ,有显著性差异 (P <0 .0 5或P <0 .0 1) ;本组 130例患者中 ,共发生迟发性脑病15例 ,发生率为 11.5 % ,迟发性脑病发生率A组与B、C组对比 ,B组与C组对比 ,明显降低 ,有显著性差异 (P <0 .0 5或P <0 .0 1)。结论　选择有效的药物 ,及早应用高压氧和充足的疗程是迟发性脑病临床预防的关键。     

Low levels of essential fatty acids are related to impaired delayed skin hypersensitivity in malnourished chronically ill elderly people

Abstract Essential fatty acid (FA) deficiency, which may accompany protein-energy malnutrition (PEM), has been associated with impaired inflammatory reactions. We evaluated this relationship by analysing FA profiles and delayed cutaneous hypersensitivity in 20 malnourished elderly non-cancer patients and in 20 age-matched control patients. As indicated by serum cholesterol and serum triglycerides, the lipid levels were decreased by about one-third in the subjects with PEM. In comparison with the controls, there was a reduction in the ω 3 FA (e.g. eicosapentanoate) in total serum lipids (mgl^-1) and serum phospholipids (%) of 40% and 47%, respectively. Reductions in serum ω 6 FA (e.g. linoleate and arachidonate) levels corresponded to the drop in total FA concentrations (30%). The cutaneous hypersensitivity was impaired in 14 of the malnourished patients. The magnitude of the skin reaction was positively correlated ( P < 0·05) to the concentrations of eicosapentanoate in serum lipids and serum phospholipids, as well as to the linoleate concentration in total serum lipids. Six of the malnourished patients took part in a nutritional intervention programme for 3 months. In parallel with an improvement in the nutritional status there was a 35% increase ( P < 0·05) in the total ω 3 FA serum concentration. Negative skin tests became positive and the median skin induration enlarged threefold ( P < 0·05). Thus, deficiency of ω 3 FA might be one factor contributing to cutaneous anergy in elderly malnourished patients.     

Delayed pain response after lumbar discography

Summary The delayed onset of symptomatic pain following lumbar discography (with no immediate pain response) is described in six patients, five with a minimum 2-year follow-up. It is usually seen in patients with nearly normal disc morphology who have incomplete or discrete annular tears that are not filled at the time of injection. Later (2–12 h in this study), dye leakage occurs through these lesions, thereby precipitating the discogenic pain This phenomenon may be missed and is probably more common than previously believed due to early discharge from the hospital, the patient expecting discomfort after the invasive study (hence no complaint is made), and the clinician being unaware of this delayed symptom, thereby not asking about it in follow-up. Close patient questioning regarding a delayed onset of symptomatic pain after discography is, therefore, an essential element in diagnostic information following this study.     

γ射线诱发人正常肝细胞基因组不稳定性研究

目的探讨电离辐射诱发的基因组不稳定性效应。方法采用^60Co γ射线照射人正常肝细胞，检测克隆形成率和微核发生率，利用单细胞凝胶电泳（SCGE）技术检测DNA损伤情况。照射2、4、6、8和10Gy后传代培养，在40代后各剂量组再次统一照射2Gy，进行辐射损伤的检测。结果首次照射后，克隆形成率随受照剂量的增大而降低。存活细胞经二次照射后，SCGE结果和微核发生率结果表明，首次照射剂量与子代二次照射后的损伤程度存在剂量效应关系。结论γ射线不仅在肝细胞中产生直接的生物效应，而且还可以诱发产生可遗传的基因组不稳定性，使子代细胞中的突变频率增加，表现出滞后的遗传改变。二次事件的放大作用是研究基因组不稳定性的一种较好方法。     

An immunohistochemical study of MAP2 and clathrin in gerbil hippocampus after cerebral ischemia

Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia. MAP2 immuno-reactivity decreased significantly by 1 h in the subiculum-CA1 and CA2 areas which correspond to reactive change, while no decrease was observed in CA1 until day 4. Before the initiation of delayed neuronal death, MAP2 immunoreactivity was not changed in CA1. On the other hand clathrin immunoreactivity increased in the pyramidal cell layer of CA1 by 3 h after ischemia and remained high for 2 days. Clathrin immunoreactivity in the pyramidal cell layer of CA1 diminished after delayed neuronal death. The transient change of clathrin was noted especially in CA1 in the period prior to delayed neuronal death. These results imply an abnormal change in clathrin turnover after ischemia, which may participate in the pathogenesis of delayed neuronal death.