核黄素缺乏大鼠红细胞维生素E水平的变化及脂质过氧化关系的研究

对两组大鼠分别喂饲核黄素缺乏（ＲＤ）膳和核黄素添加（Ｒ８，２２ｍｇ／ｋｇ饲料）膳８周后，测定了两组大鼠的红细胞维生素Ｅ（ＲＢＬＶｅ）、红细胞超氧化物歧化酶（ＳＯＤ）和红细胞丙二醛（ＭＤＡ）的水平。结果发现：ＲＤ组ＲＢＣＶｅ水平（４．７１７３±０．７７１０ｍｇ／ｇ蛋白质）显著低于ＲＳ组（５。３８６８±１．１５３７ｍｇ／ｇ蛋白质，Ｐ＜０．０５）。而ＲＤ组的ＲＢＣＳＯＤ（７７４５．２±６１０．１ｕ／ｇ蛋白质）和ＭＤＡ（０．６８６８±０．１３７２μｇ／ｇ蛋白质）则分别显著低于和高于ＲＳ组（８２６８．５±３０１．０ｎｕ／ｇ蛋白质，０．５５４８±０．０９８０，Ｐ＜０．０５）。研究提示，核黄素缺乏引起细胞膜脂质过氧化加重可能ＲＢＣＶｅ消耗增加。     

Dietary Vitamin E Modulation of Cytokine Production by Splenocytes and Thymocytes from Alcohol-Fed Mice

As vitamin E enhances immune responses, it may reduce dietary ethanol (EtOH)-induced immune suppression, thereby favorably afffecting host disease resistance. The effects of dietary vitamin E at higher level in alcohol-fed female C57BL/6 mice was determined via in vitro cytokine production by splenocytes and thymocytes, and some other immune functions. A 15-fold increase of vitamin E (160IU/liter) in a liquid diet (National Council Research), with or without EtOH (4.5%, v/v), was fed to mice for 10 weeks. Vitamin E supplementation restored production of interleukin-2, -5, -6, -10, and inter-feron-γ by concanavalin A (Con A)-stimulated splenocytes and in terleukin-6 and tumor necrosis factor-a by lipopolysaccharide-stimulated splenocytes, which were suppressed by dietary EtOH. However, it had no effect on interleukin-4 secretion, which was also reduced by splenocytes from EtOH-fed mice. Vitamin E supplementation also restored EtOH-suppressed, mitogen-induced splenocyte proliferation, but not thymocyte proliferation, although it slightly increased production of immunoglobulin A and G by lipopolysaccha-ride-stimulated splenocytes, which were suppressed by dietary EtOH. Dietary vitamin E, furthermore, significantly increased interleu-kin-2 and -6 secretion by Con A-stimulated thymocytes, which were suppressed by dietary EtOH, although it had no effect on interleukin- 4 and interferon-γ production by Con A-stimulated thymocytes from EtOH-fed mice. These data suggest that dietary vitamin E supple-mentation can modulate dysregulation of cytokines initiated by dietary EtOH and restore immune dysfunctions induced by EtOH ingestion.     

前列腺液中尿酸引起ⅢB前列腺炎84例报告

目的 :探讨前列腺液 (EPS)中尿酸 (UA)与前列腺素E2 (PGE2 )浓度与慢性盆痛症状之间的相互关系 ,以及UA引发ⅢB前列腺炎的可能机制。方法 :按国际慢性前列腺炎分类诊断标准诊断 ,将 84例慢性前列腺炎患者分为两组 ,即ⅢA组 39例 ;ⅢB组 4 5例 ;正常对照 (对照组 ) 13例。分别进行国际前列腺炎症状评分 (CP SI)和检测EPS中白细胞数、pH值、UA和PGE2 浓度。结果 :①ⅢB组患者慢性盆痛症状评分 (CPSI P)高于ⅢA组 ,EPS中UA浓度高于ⅢA组和正常对照组 ,pH值低于ⅢA和正常对照组 ,均差异有显著性意义 (均 P <0 .0 5 )。②ⅢB组和ⅢA组的PGE2 平均浓度高于正常对照组 ,差异有显著性意义 (P <0 .0 5 ) ,但是ⅢA组和ⅢB组间差异无显著性意义 (P >0 .0 5 )。CPSI P与EPS中的UA ,PGE2 之间存在正相关 (P <0 .0 1)。结论 :ⅢB组患者EPS中高浓度的UA激活环氧化酶 ,使局部的PGE2 升高 ,从而引起慢性盆痛症状 ,其严重程度与EPS中的UA、PGE2 浓度呈正比。同时PGE2 又使UA更容易渗入EPS ,形成UA和PGE2 之间的恶性循环 ,使ⅢB前列腺炎迁延不愈。     

单纯脑白质疏松症与皮质下动脉硬化性脑病的临床对比研究

目的探讨单纯脑白质疏松症(LA)和皮质下动脉硬化性脑病(BD)的临床表现、影像学及脑诱发电位的改变特征。方法(1)调查114例单纯脑白质疏松症患(LA组)和41例皮质下动脉硬化性脑病患(BD组)的发病危险因素和临床表现。(2)两组患均行CT检查，并按照脑白质异常程度分为3型。(3)LA组74例患，BD组35例患行MRI检查，根据T2WI显示的脑室周围高信号分为5型。(4)两组分别选择部分伴有高血压的患进行躯体感觉诱发电位(SEP)、脑干听觉诱发电位(BAEP)和视觉诱发电位(VEP)检查。结果(1)LA组患的危险因素呈多样化，无神经局灶体征，临床表现仅为轻度记忆力减退、步态不稳。CT显示脑白质异常以1型为主，占70．2％(80／114)；MRI脑白质异常也同样以1型为主，占71．6％(53／74)，均无脑室扩大。电生理学检查显示，SEP异常率为83．7％(36／43)，其中轻度60．5％，中度23．2％；BAEP异常率为62．8％(27／43)，潜伏期和峰间期延长；VEP异常率为53．5％(23／43)，各波潜伏期延长，均无波形消失。(2)BD组患危险因素以高血压为主(95．1％)，临床表现以神经局灶体征、明显认知功能障碍和卒中样发作为主。CT分型以3型多见，为73．2％(30／41)；MRI检查显示3型为54．3％(19／35)，4型45．7％(16／35)，41例患均有双侧脑室对称性扩大。电生理学检查显示，SEP异常率为96．7％(29／30)，其中轻度6．7％，中度46．7％，重度43．3％；BAEP异常率86．7％(26／30)，潜伏期和峰间期进一步延长，部分伴有Ⅲ、Ⅴ波缺失；VEP异常率为83．3％(25／30)，各波潜伏期进一步延长，部分P2单侧波形消失。结论单纯脑白质疏松症无特征性临床表现，诊断主要以影像学1型脑白质异常为依据；诱发电位表现为各波潜伏期延长，无波形完全缺失。皮质下动脉硬化性脑病的危险因素为高血压，临床有较明显的认知功能障碍，常见卒中样发作等特征，影像学检查CT显示3型脑白质异常，MRI显示3型或4型为诊断依据；诱发电位呈现各波潜伏期进一步延长并伴有部分波形完全缺失。     

The predictive value of specific immunoglobulin E levels for the first diagnosis of cow''s milk allergy. A critical analysis of pediatric literature

Investigators have tried to identify a level of seric specific immunoglobulin E (IgE) that had a sufficient predictive value to diagnose a food allergy without having will resort to the food challenge. To search in literature, all the studies that have estimated the possibility to identify a level of seric specific cow milk IgE with a positive predictive value (PPV) of 95% for the first diagnosis of cow's milk allergy (CMA) in pediatric age. We have identified six studies, nearly all studies suffer from relevant methodological bias. Proposed cut-off are all different. The studied pediatric populations were highly selected. Also neglecting the methodological bias of the studies and the great difference of value between the proposed cut-off, it always remains to consider that the pre-test probability of having a CMA between the children enrolled in the six studies included in this review is particularly high. The likelihood ratio helps to transfer the results of a study on a diagnostic test just to our population, and it is more realistic rather than to entrust itself to the PPV or the negative predictive value, that are much influenced from the prevalence of the disease in the studied population.     

钙调素拮抗剂E6对大鼠脑一氧化氮合酶活性和突触体谷氨酸释放的影响

目的 探讨钙调素拮抗剂E6的抗脑缺血作用机制。方法 用[3H]-L-Glu（glutamic　acid,Glu）标记大鼠脑突触体,测定突触体的Gln释放量和用一氧化氮合酶（nitric oxide synthase,NOS）试剂盒测定成年大鼠脑匀浆上清中NOS活性。结果　E6促进Glu释放（与对照组比,10-5mol·L-1组增加81.0％）,但对KCl（50 mmol·L-1）引起的Glu释放有抑制作用,10-5mol·L-1E6的抑制率为23.2％。E6浓度依赖性地抑制NOS活性。钙调素（calmodulin,CaM）（30μg·ml-1）可逆转E6的抑制作用（10-6mol·L-1E6的抑制率为13.7％）,N-硝基-精氨酸（（N-nitro-arginine,L-NNA）（10μmol·L-1）可加强E6的抑命作用（10-6mol·L-1的抑制率为76.5％）。结论 E6是与CaM结合后发挥抑制 NOS活性效应的,E6对Glu 释放的影响可能与其对NOS活性及其对神经细胞内Ca2+影响有关。     

维生素E对高脂血症的影响

本文报道用高脂饲料造成家兔高脂血症的研究。经6周后,测定血脂、脂蛋白及血浆假胆硷脂酶等项指标,高脂组各项指标均明显高于对照组,但高脂加维生素E组的各项指标均低于高脂组,结果说明维生素E能降低兔的高脂血症。     

Type II pneumocytes modulate surfactant production in response to cigarette smoke constituents: Restoration by vitamins A and E

This study was to evaluate the effects of cigarette smoke constituents upon type II pneumocyte surfactant production in vitro, and how vitamins A and E may alter the response. Freshly isolated type II pneumocytes from Sprague–Dawley rats were incubated 20 h in medium with fetal bovine serum that was or was not treated with cigarette smoke. The number of adherent cells was inversely related to the dose of smoke or benzo(a)pyrene. Despite the decreased number of treated cells, the total amount of surfactant per culture well was unchanged, whereas surfactant production per cell was significantly increased (P < 0.05). Vitamin A concentration was significantly (P < 0.05) lower in the smoke-treated serum compared with untreated serum. When vitamin A or E was added to the cigarette smoke-treated serum, cell adherence and surfactant production returned to control values. In conclusion, cigarette smoke constituents or benzo(a)pyrene alone decreased the number of adherent type II pneumocytes, but did not alter surfactant amounts because of an increased production of surfactant per cell. Type II pneumocytes seem to adjust surfactant production dependent upon the number of type II pneumocytes to produce it and vitamin A or E enhance cell attachment in the presence of the smoke toxins.