Immunological blockade of endogenous thyrotropin-releasing hormone impairs recovery from hyperglycemia in mice

Administration of antiserum to thyrotropin-releasing hormone (TRH) into the lateral cerebral ventricle of mice significantly attenuated recovery from hyperglycemia induced by treatment with 2-deoxyglucose but had no effect on the plasma glucose of saline-treated mice. TRH, injected centrally together with the anti-TRH antibody, reversed the effect of the antiserum and blocked the development of hyperglycemia. These findings suggest that activation of TRH neurons in the central nervous system may be a physiological event influencing recovery from hyperglycemia.     

教室空气中微生物和CO_2的形成、分布及其相互关系的研究

对初中学生鼻咽部溶血性链球菌（ＨＳ）和教室空气中微生物和ＣＯ２调查得出：学生鼻咽部携带ＨＳ除坐前右位外，其他各处皆有检出（４／５０）；空气中ＨＳ从早读开始后迅速上升２８．７倍（Ｐ＜０．０１），至第二节课下课前达全日最高峰（６５．５倍），细菌总数（ＢＴ）和ＣＯ２的时间分布亦呈现与ＨＳ相似的特征（ｒ＝０．７４３和０．８２０Ｐ＜０．０１），但其峰度不及ＨＳ突出；ＨＳ及ＢＴ的最低值在教室前右方，最高值在后右及中央（Ｐ＜０．０１）。而ＣＯ２最高浓度在教室垂直高度的２．０ｍ处。表明：室内空气中微生物和ＣＯ２的形成和分布主要受到学生鼻咽部携带ＨＳ能力及呼吸与学习活动的影响，当然与空气自身的紊流和层流、冷空气从门缝侵入及污染物的性状也有关。     

The 21-aminosteroid antioxidant, U74389F, prevents estradiol-induced depletion of hypothalamic β-endorphin in adult female rats

A single intramuscular injection of 2 mg estradiol valerate (EV) results in neuronal degeneration and β-endorphin depletion in the hypothalamic arcuate nucleus of adult female rats. We have hypothesized that peroxidase-positive astrocytes in this brain region oxidize estrogens and catecholestrogens to semiquinone radicals which mediate oxidative neuronal injury. In the present study, dietary administration of the potent antioxidant 21-aminosteroid, U-74389F, completely blocked EV-induced β-endorphin depletion in the hypothalami of adult female rats. Neither EV nor 21-aminosteroid treatment had any effect on hypothalamic concentrations of neuropeptide Y and Met-enkephalin, confirming that the estradiol lesion is fairly selective for the β-endorphin cell population. The present findings support the hypothesis that the toxic effect of estradiol on hypothalamic β-endorphin neurons is mediated by free radicals.     

A case report of deficiency in an inhibitor of calcium-dependent association of protein S with C4B-binding protein suggested by a modified crossed immunoelectrophoresis

We have experienced a coagulation factor VIII-deficient patient whose plasma has normal protein S (PS) activity and masses of free PS and its bound form in complex with C4b-binding protein (C4BP). Although the patient's plasma showed a normal ratio of free PS to PS-C4BP complex in the presence of 5 mM EDTA, the plasma gave an abnormally retarding major C4BP peak together with a major PS peak in the crossed immunoelectrophoresis (CIE) in the presence of 2 mM CaCl₂. It was revealed that the major peak was formed by a mixture of PS-C4BP complex and free form. The addition of normal human plasma (NHP) to the patient's plasma inhibited the retardation of the major PS-C4BP complex. These suggest that the patient's plasma lacks some component(s) to inhibit Ca²⁺-dependent association of PS with C4BP.     

川芎嗪治疗急性脑梗塞的临床研究

研究发现,血管生物活性物质中前列腺素代谢产物TxB_2、6-K-PGF_(1α)在缺血性脑血管病的病理过程中发挥着重要作用,为了寻找有效的防治手段,笔者观察了川芎嗪对急性脑梗塞患者的血浆TxB_2、6-K-PGF_(1a)含量的影响,为应用川芎嗪治疗急性脑梗塞提供依据,并探讨其作用机制。1 资料与方法1.1 临床资料 选取2000年2月～2003年2月的急性脑梗塞住院患者62例,均经头颅CT确诊为非出血性脑梗塞,以     

高频喷射通气时麻醉犬动脉血二氧化碳分压的估计

作用测定５－８次常频呼吸后呼气末二氧化碳分压的方法，探讨了高频喷射通气时麻醉犬动脉脉血二氧化碳分压与Ｐｅｔｃｏ２的关系，结果表明，在通气频率分别为６０，１００及２００次／ｍｉｎ时，Ｐｅｔｃｏ２和Ｐａｃｏ２均无显性差异，Ｐｅｔｃｏ２呈显相关（ｒ＝０．８３，Ｐ＜０．０１）。结果提示，测定５－８次常频呼吸后的Ｐｅｔｃｏ２可较准确地评估ＨＦＪＶ时麻醉犬的Ｐａｃｏ２。     

Effects of histamine on inositol phosphates and intracellular Ca2+ in human glomerular epithelial cells

The effect of histamine on the phosphoinositide turnover andintracellular free calcium activity [Ca²⁺]_i was examined inhuman glomerular epithelial cells in culture. Addition of histamineto glomerular epithelial cells resulted in formation of inositolphosphates in a time- and dose-dependent manner. A transientmaximum of inositol trisphosphate (InsP₃) was observed within10 s. Stimulation of protein kinase C by short-term pretreatment(15 mm) of glom erular epithelial cells with phorbol 12-mynstate13-acetate caused a dose-dependent inhibition of the histamine-inducedinositol phosphate accumulation. The baseline of [Ca²⁺]_i inthe cells was 115 ±2.7 nmol/l (n=103). Histamine (ED₅₀:approx. 2x10^–7mol/l) caused a rapid and transient increasein [Ca²⁺]_i, as detected by fura-2 microfluorimetry studies.In a calcium-free extracellular solution the rapid increaseof [Ca²⁺]_i was still present. The H₁ receptor antagonist mepyramine(IC₅₀: approx. 8 x 10^–9 mol/l) inhibited the histamine(10^–6 mol/l) response on [Ca²⁺]_i Cimetidine, a potentH₂ receptor antagonist, showed no effect. This data indicates that H₁ receptor activation causes hydrolysisof phosphatidylinositol 4, 5-bisphosphate by phospholipase Cactivation, and consecutive mobil ization of intracellular calcium.Since histamine is a mediator of inflammation, antigen responseand cellular injury, these findings could be of importance forthe understanding of glomerular epithelial cell pathology.     

黑木耳抗动脉粥样硬化的实验研究

本文观察黑木耳对实验性动脉粥样硬化(AS)家兔AS病变及有关生化指标的影响。实验结果,黑木耳有降低血浆胆固醇(TC)、过氧化脂质(LPO)、血栓素A_2(TXA_2)的含量,提高前列环素/血栓素A_2(PGI_2/TXA_2)比值,减轻AS病变的作用。表明黑木耳具有抗AS作用。其机理可能是通过降血TC,保护动脉内膜,抑制血小板聚集,并由此抑制TXA_2合成;血TC降低亦可减少脂质过氧化,从而使环氧化酶、TXA_2合成酶活性降低,TXA_2合成减少。黑木耳通过以上途径维系PGI_2/TXA_2平衡,保护血管完整性的内环境相对稳定,对抗动脉粥样硬化的发生。     

人PD-L2基因克隆及其在大肠杆菌中的表达

目的 克隆人PD-L2基因并构建PD-L2胞外区的原核表达载体，在大肠杆菌中进行表达。方法 以RT-PCR方法从活化的人外周血单个核细胞总RNA中克隆PD-L2基因的cDNA，构建PD-L2胞外区的原核表达载体，在大肠杆菌BL21(ED3)中进行表达并鉴定。结果 克隆到PD-L2基因cDNA编码区全长序列，经DNA测序证明其与已报道的序列一致。进而构建了PD-L2胞外区的原核表达载体，并在大肠杆菌表达，免疫印迹分析表明在IPTG诱导后表达PD-L2胞外区蛋白，相对分子质量Mr为22000，与理论值大小相符。结论 成功克隆PD-L2基因，其胞外区蛋白在大肠杆菌中获得表达，为进一步研究PD-L2功能提供了条件。     

CD4+CD25+ regulatory T cells: I. Phenotype and physiology

The immune system protects us against foreign pathogens. However, if fine discrimination between self and non-self is not carried out properly, immunological attacks against self may be launched leading to autoimmune diseases, estimated to afflict up to 5% of the population. During the last decade it has become increasingly clear that regulatory CD4⁺CD25⁺ T cells (T_reg cells) play an important role in the maintenance of immunological self-tolerance, and that this cell subset exerts its function by suppressing the proliferation or function of autoreactive T cells. Based on human and murine observations, this review presents a characterization of the phenotype and functions of the Treg cells in vitro and in vivo . An overview of the surface molecules associated with and the cytokines produced by the Treg cells is given and the origin, activation requirements and mode of action of the Treg cells are discussed. Finally, we address the possibility that Treg cells may play a central role in immune homeostasis, regulating not only autoimmune responses, but also immune responses toward foreign antigens.