登革病毒感染后小鼠细胞免疫功能的动态变化

从登革Ⅱ型病毒感染成年ＢＡＬＢ／ｃ小鼠为模型，观察感染后不同时间机体细胞免疫反应的变化。结果表明：感染后７－１４ｄ免疫功能处于激活状态，表现为腹腔巨噬细胞的吞噬功能和脾淋巴细胞对ＣｏｎＡ的反应及ＩＬ－２产生水平都明显高于对照组，感染２１ｄ后免疫功能则转为抑制状态，上棕免疫反应明显低于对照组，脾中的Ｌ３Ｔ４＾＋细胞亚群的百分比逐渐下降；相反，ＬＹＴ２＾＋细胞亚群的百分比逐渐升高，这种抑制现象可维持到     

Transfer of clonidine and dexmedetomidine across the isolated perfused human placenta

Background: The placental transfer of the a₂ receptor agonist clonidine, earlier used as an adjuvant in obstetric epidural analgesia, was compared with the transfer of the newer and more %-selective agonist dexmedetomidine.
Methods: Term placentas were obtained immediately after delivery with maternal consent and a 2-hour recycling perfusion of a single placental cotyledon was performed. Disappearance from the maternal circulation, accumulation in placental tissue and appearance in the fetal circulation of clonidine or dexmedetomidine with the reference compound antipyrine were followed in 4 experiments for both drugs.
Results: At 2 hours the percent dexmedetomidine found in the fetal circulation was 12.5 (SD 5.1)%, while 48.1 (SD 20.3)% was found in the perfused placental cotyledon. A higher mean clonidine than dexmedetomidine concentration was achieved in the fetal circulation (1.90 vs. 0.56 nmol/l, P <0.05). At 2 hours the percent clonidine found in the fetal circulation was 22.1 (SD 2.4)% ( P <0.05), while 11.3 (SD 3.3)% ( P <0.05) was re tained in the perfused placental cotyledon. The transfer indexes, describing maternal-to-fetal transfer of dexmedetomidine and clonidine normalized with the transfer of antipyrine, were 0.88 (SD 0.07) and 1.04 (SD 0.08) respectively ( P <0.05).
Conclusions: Dexmedetomidine disappeared faster than clonidine from the maternal circulation, while even less dexmedetomidine was transported into the fetal circulation. This was due to its greater placental tissue retention, the basis for which probably is the higher lipophilicity of dexmedetomidine.     

脂肪乳剂对健康人外周血单个核细胞磷脂脂肪酸组成的影响

目的探讨脂肪乳剂对健康人免疫细胞脂肪酸组成的影响。方法采用毛细管气相色谱法检测8名健康志愿者连续7天外周静脉输注脂肪乳剂(20%intralipid)后,外周血单个核细胞磷脂脂肪酸谱的变化。结果静脉输注脂肪乳剂对健康人外周血单个核细胞数量、肝功能和血脂无影响,软脂酸(C16∶0)、油酸(C18∶1N9)比例在单个核细胞磷脂酰乙醇胺(PE)中明显增加(P<0.05,P<0.01);硬脂酸(C18∶0)减少(P<0.05);亚麻酸(C18∶3N3)、软油酸(C16∶1N7)在磷脂酰胆碱(PC)中明显增加(P<0.05),而其余脂肪酸均未发生明显改变。饱和脂肪酸与不饱和脂肪酸的比值(S/U)和脂肪酸的不饱和指数(UI)在单个核细胞PE、PC中均保持不变。结论脂肪乳剂不可能通过影响免疫细胞磷脂脂肪酸组成的途径对免疫功能产生影响。     

三七多糖对创伤大鼠CD+4/CD+8和IL-2水平的影响(摘要)

观察三七多糖对创伤大鼠免疫功能的影响.方法:40只SD大鼠,随机分为正常对照组(A)、创伤对照组(B)、创伤后三七多糖28.5 mg·kg-1.     

Mucopolysaccharidosis VII as cause of fetal hydrops in early pregnancy

We report on fetal hydrops presenting at 18 weeks of gestation and diagnosed as β-glucuronidase deficiency. The parents were first cousins and there were 2 previous similar fetal deaths. β-Glucuronidase was absent in cultured fetal fibroblasts and lymphoblasts but was normal in the tested relatives. The activities of other lysosomal enzymes were normal. © 1992 Wiley-Liss, Inc.     

Terminal deletion of chromosome 4p (4p16.3) shows a breakpoint between loci linked to Huntington disease

A 15-year-old boy with a terminal deletion of the short arm of chromosome 4 is described. The patient has a mild clinical phenotype that is incompatible with Wolf-Hirschhorn syndrome. Careful neurological examination including CT scan did not show any signs of Huntington disease. The chromosomal breakpoint was analyzed by means of polymorphic DNA probes localized close to the tentative Huntington (HD) locus. The breakage has occurred between D4S43 and D4S90 loci and thus deletes part of the chromosomal candidate regions for the HD locus. © 1992 Wiley-Liss, Inc.     

Hyperglycaemia compensates for the defects in insulin-mediated glucose metabolism and in the activation of glycogen synthase in the skeletal muscle of patients with Type 2 (non-insulin-dependent) diabetes mellitus

Summary Insulin resistance and a defective insulin activation of the enzyme glycogen synthase in skeletal muscle during euglycaemia may have important pathophysiological implications in Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia may serve to compensate for these defects in Type 2 diabetes by increasing glucose disposal through a mass action effect. In the present study, rates of whole-body glucose oxidation and glucose storage were measured during fasting hyperglycaemia and isoglycaemic insulin infusion (40 mU·m^–2min^–1, 3 h) in 12 patients with Type 2 diabetes. Eleven control subjects were studied during euglycaemia. Biopsies were taken from the vastus lateralis muscle. Fasting and insulin-stimulated glucose oxidation, glucose storage and muscle glycogen synthase activation were all fully compensated (normalized) during hyperglycaemia in the diabetic patients. The insulin-stimulated increase in muscle glycogen content was the same in the diabetic patients and in the control subjects. Besides hyperglycaemia, the diabetic patients had elevated muscle free glucose and glucose 6-phosphate concentrations. A positive correlation was demonstrated between intracellular free glucose concentration and muscle glycogen synthase fractional velocity insulin activation (0.1 mmol/l glucose 6-phosphate: r=0.65, p<0.02 and 0.0 mmol/l glucose 6-phosphate: r= 0.91, p<0.0001). In conclusion, this study indicates an important role for hyperglycaemia and elevated muscle free glucose and glucose 6-phosphate concentrations in compensating (normalizing) intracellular glucose metabolism and skeletal muscle glycogen synthase activation in Type 2 diabetes.     

654─2在小儿急性脑水肿及中枢性呼吸衰竭中的应用探讨

感染性脑水肿病儿在感染得到有效控制，应用654—2（山莨菪碱）后未再用脱水剂，笔者认为．654—2具有解除脑血管痉挛及微循环障碍的作用。急性脑水肿在脱水剂应用后，用654—2有利于脑水肿液的吸收和回流。目前，治疗小儿捂热综合征（IMS）之细胞内水肿仍没有有效的方法，研究结果表明654—2能改善脑细胞供氧．其还能通过解除呼吸中枢血管痉挛而治疗中枢性呼吸衰竭。     

失血性休克状态下肢体缺血再灌注影响休克发展的研究

目的：研究失血性休克状态下骨骼肌缺血再灌注对休克发展的影响。方法：雌性家兔１２只，随机等分为休克对照组（Ⅰ组）和休克伴双后肢缺血再灌注组（Ⅱ组）。戊巴比妥钠麻醉，气管切开，自主呼吸，并全身肝素化。经左颈外静脉，按１ｍｌ·ｋｇ－１·ｍｉｎ－１的速度放血５分钟，停５分钟，以左颈总动脉ＭＡＰ达４．０±０．２ｋＰａ为休克开始，此时Ⅱ组阻断腹主动脉末端，９０分钟后松开。结果：休克后１２０分钟，血中ＴＸＢ２、ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α、乳酸、酸性磷酸酶及Ｍｇ２＋，Ⅱ组均显著高于Ⅰ组，而休克９０分钟时，各值两组间无显著性差异。结论：失血性休克状态下肢体骨骼肌缺血再灌注可能对休克的发展产生不利影响。     

Breast Cancer Genes

Abstract: The identification of familial breast cancer genes heralds an era of directed breast cancer treatment. Currently, two hereditary breast cancer genes have been identified, BRCA-1 and BRCA-2 . Although accounting for only approximately 5% of all breast cancers, they are being used to identify women with germ-line alterations that are at high risk of developing breast or ovarian cancer. With the identification of such genes comes a need for consideration of the ethical issues associated with testing. These genes are also being examined from a biochemical standpoint encompassing both their biological roles and biochemical pathways in which they reside. Such studies are likely to lead to novel breast cancer therapies.