KChIP1 and frequenin modify shal-evoked potassium currents in pyloric neurons in the lobster stomatogastric ganglion

The transient potassium current (I(A)) plays an important role in shaping the firing properties of pyloric neurons in the stomatogastric ganglion (STG) of the spiny lobster, Panulirus interruptus. The shal gene encodes I(A) in pyloric neurons. However, when we over-expressed the lobster Shal protein by shal RNA injection into the pyloric dilator (PD) neuron, the increased I(A) had somewhat different properties from the endogenous I(A). The recently cloned K-channel interacting proteins (KChIPs) can modify vertebrate Kv4 channels in cloned cell lines. When we co-expressed hKChIP1 with lobster shal in Xenopus oocytes or lobster PD neurons, they produced A-currents resembling the endogenous I(A) in PD neurons; compared with currents evoked by shal alone, their voltage for half inactivation was depolarized, their kinetics of inactivation were slowed, and their recovery from inactivation was accelerated. We also co-expressed shal in PD neurons with lobster frequenin, which encodes a protein belonging to the same EF-hand family of Ca(2+) sensing proteins as hKChIP. Frequenin also restored most of properties of the shal-evoked currents to those of the endogenous A-currents, but the time course of recovery from inactivation was not corrected. These results suggest that lobster shal proteins normally interact with proteins in the KChIP/frequenin family to produce the transient potassium current in pyloric neurons.     

Changes of plasma volume and plasma composition in water-deprived rats

Summary Plasma volume, hematocrit, protein and electrolyte concentrations in plasma were measured in control and water-deprived rats every three days after starting the experiment until the 15th day. Plasma volume variations, as related to body weight, suggest that water loss from plasma was proportional to total body water at three days and after 9 days of water deprivation. Greater plasma water than body water loss was found during the period between 3 and 9 days. Plasma protein and electrolyte variations suggest that during water deprivation there is a loss of protein, sodium and potassium from plasma, which is proportionally less than that of plasma water. Potassium, calcium and inorganic phosphorus were lost proportionally to plasma water. The variations in plasma volume changes were partially explained as due to variations in plasma protein and electrolyte concentrations.     

利用CT扫描及CAD技术建立腰椎活动节段的有限元模型

目的 :探讨腰椎活动节段有限元模型的建立。方法 :选取一正常自愿者L4～L5节段为研究对象 ,通过CT扫描、图像数字化处理及计算机辅助设计建立了腰椎活动节段的有限元模型 ,通过Super SAP有限元分析软件包对模型进行了应力分析。结果 :建立了L4～L5活动节段的有限元模型 ,并分析了生理载荷下腰椎活动节段不同组成部分的应力分布。结论 :为腰椎活动节段有限元模型的建立提供了一种简便、准确的方法 ,为分析和研究该模型在各种情况下的生物力学表现创造了条件     

动态脑电图对缺血缺氧性昏迷病人的预后评估

目的：观察动态脑电图和临床检测指标对缺血缺氧性昏迷病人预后的评估价值。方法：在45例缺血缺氧性昏迷病人急性期进行动态脑电图检测和Glasgow评分、瞳孔对光反应、脑干反应检查，随访3个月时病人的预后，将动态脑电图检测和各项临床检查结果与病人的预后结果进行相关分析。结果：动态脑电图对昏迷病人预后的评估在敏感性(83．3％)、特异性(100％)和对预后评估的准确率(91．7％)方面均比临床检测结果高，临床指标Glasgow评分、瞳孔对光反射、脑干反射的敏感性、特异性及准确率分别为73．1％、84．2％及77．9％；76.9％、73．7％及75．6％；76．0％、68.4％及68．9％。结论：动态脑电图检测对急性缺血缺氧性昏迷病人预后的评估有确定的价值。     

An unusual expression of a squamous cell marker, small proline-rich protein gene, in tracheobronchial epithelium: differential regulation and gene mapping.

An unusual expression of a putative squamous cell marker, small proline-rich protein (spr1), in mucociliary epithelial cells of conducting airways was demonstrated in a serum-free culture system. A cDNA clone was isolated from the cDNA library of monkey tracheobronchial epithelial (TBE) cells by differential hybridization. This cDNA clone, MT5, exhibited 98% homology to a DNA sequence obtained from human keratinocytes treated with either UV light or phorbol esters (T. Kartasova et al., 1988, Mol. Cell. Biol. 8:2195-2230). The predicted peptide of MT5 is unusual for its high content of proline (29%), glutamine (18%), and cysteine (9%) and its repeated PKVPEPC units. The level of spr1 mRNA in cultured cells was inhibited more than 90% by vitamin A. In contrast, phorbol 12-myristate 13-acetate (PMA) stimulated the level of spr1 mRNA by 3- to 8-fold. This differential regulation coincided with the effects of these chemicals on the cornification of cultured TBE cells. Using MT5 as a probe, we have localized the tracheal spr1 gene on the human chromosome 1 by a Southern blot analysis using a panel of human-rodent somatic cell hybrid DNAs. The gene was further sublocalized to bands q22-23 by in situ hybridization.     

测定血清LSA与TSA对恶性血液病诊断的价值比较

本组应用研究结果表明:恶性血液病患者血清LSA与TSA含量(175±61mg/L与1025±388mg/L,n=72)均显著高于良性血液病组(110±46mg/L与733±295mg/L,n=80)和对照组(93±19mg/L与639±178mg/L,n=205)(P<0.001)。测定血清LSA与TSA诊断恶性血液病的敏感度分别为87.5％与72.2％(P<0.05),特异度分别为72.5％与67.5％(P>0.1),准确度为81.6％与71.7％(P<0.05),诊断效率为63.4％与48.7％(P<0.01),证明LSA对恶性血液病诊断的价值优于TSA。该二法诊断恶性病的假阳性主要来自感染性疾病。血清LSA含量监测对患者疗效与病情监视、预后分析等具有显著意义。     

人嗜铬细胞瘤细胞的原代培养及鉴定

本研究拟建立人嗜铬细胞瘤细胞的原代培养方法。采用连续分次胶原酶消化法分离培养人嗜铬细胞瘤细胞，采用细胞培养液中儿茶酚胺水平检测、多聚甲醛诱发荧光及细胞嗜铬粒蛋白A(CgA)和神经元特异性烯醇化酶(NSE)的免疫组化染色等方法进行细胞性质和功能鉴定，并用噻唑兰(MTT)法观察原代培养的人嗜铬细胞瘤细胞的生长状况。结果表明，人嗜铬细胞瘤细胞在培养3～7天时生长较快，7天后细胞开始分化。经检测细胞培养液中的儿茶酚胺浓度、多聚甲醛诱发荧光等，证明该细胞有合成和分泌儿茶酚胺的功能。并且培养的细胞CgA和NSE免疫组化染色阳性。因此，本研究成功建立了人嗜铬细胞瘤细胞的原代培养方法，并鉴定其具有嗜铬细胞瘤的分泌和表达功能，国内尚未见报告。     

大鼠眶皮质的间脑和脑干的传入投射

目的：研究间脑和脑干对眶皮质的传入投射。方法：ＨＲＰ逆行示踪法。结果：将ＨＲＰ分别导入１８只大鼠的内侧及腹侧眶区、腹外侧内和外侧区后，在同侧丘脑背内侧核中可见密集的标记细胞，并有一定的局部定位，其次在内丘脑的胶状核、前内侧核、菱形核、腹我侧和腹内侧核中可见大量标记细胞。在同侧下丘脑餐侧区、背侧区、未定带和背内侧核中可见少量标记细胞。在脑干的黑质致密部、腹侧被盖区、中缝背核、导水管周灰质中也可见标记     

The dysregulated glomerular cell growth in Denys–Drash syndrome

While diffuse mesangial sclerosis is traditionally described as being the glomerulopathy of Denys–Drash syndrome (DDS), the podocyte proliferative lesions may be overlooked in these DDS cases. In the present study, an evolving process is extrapolated from a selected case of DDS that demonstrated glomerulopathy with conspicuous podocyte proliferation. The observation that podocytes express proliferation markers (Ki67, proliferating-cell nuclear antigen and topoisomerase II) in non-proliferative, mature-looking glomeruli suggests an initial pathogenic act to activate or to keep podocytes from quiescence. The subsequent proliferation of podocytes is in keeping with downregulation of WT1 and cyclin kinase inhibitors of p16 and p21. The emergence of cytokeratin-positive cells in glomeruli that show typical mesangial sclerosis implies elimination of podocytes and replacement with tubular and/or parietal epithelial cells. The final scene of evolving glomerulopathy displays apoptosis and expression of Fas-L and Bax in sclerotic mesangial lesions, which eventually end up with global sclerosis. This novel concept of DDS glomerulopathy implies complex molecular mechanisms involved in glomerular injury.