Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II

Cerebral cell volume regulatory mechanisms are activated by sustained disturbances in plasma osmolality. Acute hypernatremia causes a predictable shrinkage of brain cells due to the sudden imposition of a plasma-to-cell osmolal gradient. However, during chronic hypernatremia cerebral cell volume is maintained close to the normal range as a result of the accumulation of electrolytes and organic osmolytes including myo-inositol, taurine, glutamine, glycerophosphorylcholine, and betaine. The increased cytosolic level of these molecules is generally accomplished via increased activity of sodium (Na⁺)-dependent cotransport systems. The slow dissipation of these additional osmotically active solutes from the cell during treatment of hypernatremia necessitates gradual correction of this electrolyte abnormality. Acute hyponatremia leads to cerebral cell swelling and severe neurological dysfunction. However, prolonged hyponatremia is associated with significant reductions in brain cell electrolyte and organic osmolyte content so that cerebral cell volume is restored to normal. While acute hyponatremia can be treated with the administration of moderate doses of hypertonic saline in order to control seizure activity, chronic hyponatremia should be corrected slowly in order to prevent subsequent neurological deterioration. If the rate of correction exceeds 0.5 mmol/l per hour, or if the total increment in serum [Na⁺] exceeds 25 mmol/l in the first 48 h of therapy, then there is an increased risk of the development of cerebral demyelinating lesions. Chronic hyperglycemia activates the brain cell volume regulatory adaptations in the same manner as hypernatremia. Therefore, during the treatment of diabetic ketoacidosis, it is imperative to restore normoglycemia gradually in order to prevent the occurrence of cerebral edema. It is possible that excessive administration of electrolyte-free solutions and high doses of insulin may increase the risk of this complication. While there are some data to suggest that brain cell size is disturbed during acute uremia, additional work is necessary to clarify the role of cerebral cell volume regulation during acute and chronic uremia.     

建立新型医患关系是医院工作的当务之急

《医疗事故处理条例》《最高人民法院关于民事诉讼证据的若干规定》这两个法规的出台，给医院提出了新的课题，结合目前实际，提出了医院全面贯彻执行这两个法规，必须从围绕改善医患关系这个中心问题入手。建立新型和医患关系，并根据多年的观察与实践，着重论述了如下见解：医务人员在为患者的攻关服务过程中，要真正认识自己是医患矛盾中的主要方面；医务人员要转变传统的服务思维定势，尊重和理解患者，医务人员要确立既为患者生命和利益负责，又重视患者权利的观念，医务人员要增强法制观念，做到依法行医，医院要设置监控部门或配备专兼职人员，对全院的医疗服务进行检查监督。     

Evidence for a human IgG1 class switch program

In activated murine B lymphocytes, immunoglobulin class switch recombination occurs as a highly regulated process which is targeted to distinct switch regions. Here we present first evidence that in human B lymphocytes, switch recombination is targeted to distinct switch regions as well. In a panel of clonally unrelated IgG1-expressing human B cells, immortalized by Epstein-Barr virus (EBV) transformation, seven out of nine cells show switch recombination between Sμ and Sγ1 on both alleles, the active and inactive one. The remaining cells show no switch recombination on the inactive IgH locus. The very strong correlation of switch recombination on both alleles of IgG1-expressing cells proves that class switch recombination to IgG1 is not random but directed in human B lymphocytes.     

参芪扶正注射液对淋巴细胞的作用

目的:观察参芪扶正注射液对淋巴细胞的作用.方法:用参芪扶正注射液处理Jurkat淋巴细胞,通过台盘兰染色计数和流式细胞计观察其对淋巴细胞的作用,用参芪处理过的淋巴细胞分别加入化疗药和肝癌细胞,观察两种细胞的反应.结果:参芪扶正注射液处理过的淋巴细胞,细胞增殖快,有较强的抵抗化疗药诱导凋亡的能力,杀伤肝癌细胞的能力增强.结论:参芪扶正注射液具有多方面的免疫调节作用.     

Expression of Na+/HCO3− co‐transporter proteins (NBCs) in rat and human skeletal muscle

Aim: Sodium/bicarbonate co‐transport (NBC) has been suggested to have a role in muscle pH regulation. We investigated the presence of NBC proteins in rat and human muscle samples and the fibre type distribution of the identified NBCs. Methods and results: Western blotting of muscle homogenates and sarcolemmal membranes (sarcolemmal giant vesicles) were used to screen for the presence of NBCs. Immunohistochemistry was used for the subcellular localization. The functional test revealed that approximately half of the pH recovery in sarcolemmal vesicles produced from rat muscle is mediated by bicarbonate‐dependent transport. This indicates that the NBCs are preserved in the vesicles. The western blotting experiments demonstrated the existence of at least two NBC proteins in skeletal muscle. One NBC protein (approximately 150 kDa) seems to be related to the kidney/pancreas/heart isoform NBC1, whereas the other protein (approximately 200 kDa) is related to the NBC4 isoform. The two NBC proteins represent the electrogenic isoforms named NBCe1 and NBCe2. Membrane fractionation and immunofluorescence techniques confirmed that the two NBCs are located in the sarcolemmal membrane as well as in some internal membranes, probably the T‐tubules. The two NBCs localized in muscle have distinct fibre type distributions. Conclusions: Skeletal muscle possesses two variants of the sodium/bicarbonate co‐transporter (NBC) isoforms, which have been called NBCe1 and NBCe2.     

PCBP1:一种在多水平上参与基因表达调控的蛋白因子

多聚胞嘧啶结合蛋白1 (poly C binding protein-1,PCBP1),属于RNA结合蛋白亚家族,因其具有同RNA的多聚胞嘧啶(poly C)区域特异的结合活性而得名.目前该亚家族共有5个成员:hnRNP K(heterogeneous nuclear ribonucleoprotein K)、PCBP1、PCBP2、PCBP3和PCBP4.PCBP1蛋白在多个水平参与基因的表达调控,如转录、mRNA加工、mRNA的转运、mRNA稳定以及翻译水平调控等.本文对PCBP1基因的结构和生物学功能进行了综述.     

细胞凋亡相关新基因TFAR19(PDCD5)研究进展

细胞凋亡是在一定的生理或病理条件下。由基因控制的细胞自我毁灭过程。凋亡异常与许多疾病(尤其是肿瘤)的形成及发展进程密切相关。细胞凋亡调控机制研究证明。多种基因(如P53、C-myc、Bcl-2、Bax等)参与了细胞凋亡的调控过程。TFAR19基因是由我国科研人员最近新发现的另一重要的凋亡相关基因，笔者主要就其结构特点、性质功能、临床意义作一概述。     

兔骨髓基质细胞诱导分化为胰岛素分泌细胞的方法

目的 探讨将骨髓基质细胞（MSCs）诱导成为胰岛素分泌细胞（IPCs）的方法。方法 体外培养新西兰兔骨髓及胰腺基质细胞和SD大鼠胰腺基质细胞，利用含有胰腺基质细胞培养基的混合培养基诱导培养MSCs。结果 以兔及SD大鼠胰腺基质细胞培养基均可诱导兔MSCs生成IPCs。结论 兔及SD大鼠的胰腺基质细胞培养基均可将兔MSCs诱导分化为IPCs。