A neosynthesis of sodium channels is involved in the evolution of the sodium current in isolated adult DUM neurons

Short-term culture of isolated adult dorsal unpaired median (DUM) neurons of the cockroach Periplaneta americana has been used to study the evolution of the sodium current during the time in culture after axotomy and deafferentation treatment. An increase in the maximum peak amplitude of the sodium current recorded under voltage-clamp conditions with the patch-clamp technique in the whole-cell recording configuration, was only observed between 24h and 72h (75%) without any modification of the kinetics and the voltage-dependence of the current. A decrease in the level of foetal calf serum in the culture medium reduces the amplitude of the sodium current on all days but does not affect its time-course of development which was on the contrary completely abolished by both protein synthesis inhibitors, actinomycin D and cycloheximide. The results obtained in these neurons strongly suggest that a neosynthesis of sodium channel proteins is involved in the evolution of the sodium current induced by axotomy and deafferentation.     

急性胰腺炎血清免疫抑制酸性蛋白检测的临床意义

目的 :了解急性胰腺炎患者血清免疫抑制酸性蛋白 (IAP)的临床意义。方法 :应用免疫扩散法检测 32例患者和 2 0例健康人中的IAP水平。结果 :正常组 (2 0例 )、轻症组 (2 0例 )和重症组 (12例 )的血清IAP在入院时分别为(32 5± 10 5 )mg/L、(40 4± 15 1)mg/L和 (5 75± 14 5 )mg/L ,重症组血清IAP水平高于正常组 (P <0 .0 1) ,也高于轻症组 (P <0 .0 5 )。其次重症组IAP值在入院后第 3、5、7天与轻症组比较仍明显升高 ,两组有统计上的差异性。结论 :检测IAP可以作为了解急性胰腺炎炎症程度的指标     

重组人生长激素对老年人骨盆骨折蛋白质代谢及免疫功能的影响

目的 探讨应用重组人生长激素(recombinant human growth hormone,rhGH)对接受常规肠内营养支持的老年骨盆骨折患者蛋白质代谢及免疫功能的调理作用.方法 选择多发性骨盆骨折(骨折3处以上),年龄＞70岁患者30例,随机分为2组: 治疗组15例,采用标准肠内营养 rhGH[rhGH 0.2U/(kg·d)皮下注射,共计8天];另外15例作为对照组,治疗前和治疗后的第8天,分别测定血清白蛋白、血清转铁蛋白、血清前白蛋白浓度、免疫球蛋白(IgA、IgG、IgM)、T淋巴细胞亚群(CD3、CD4、CD8),并统计医院获得性肺炎的发生情况.结果 治疗组患者在治疗后第8天的血清白蛋白、血清转铁蛋白和血清前白蛋白水平比对照组显著升高(P＜0.05), IgA、IgG、IgM、CD3、CD4、CD4/CD8与对照组相比有明显增高(P＜0.05);治疗组患者医院获得性肺炎的发生率也较对照组显著降低(P＜0.05).结论 在肠内营养支持下加用rhGH可以明显促进老年骨盆骨折患者的蛋白质合成代谢,并改善免疫功能,增加肌肉的收缩力,增强排痰力度,减少医院获得性肺炎的发生率.     

葡萄糖酸内酯为凝固剂时大豆蛋白的胶凝特性

测定了以葡萄糖酸内酯(GDL)作为凝固剂时不同热处理条件下大豆蛋白主要组分———7S和11S单独胶凝时的流变学曲线,证实了蛋白质的充分变性是GDL引发大豆蛋白胶凝的前提,且已充分热变性的7S和11S组分在单独胶凝时具有大致相当的凝胶强度.通过测定7S和11S组分的物理化学性质,解释了在以GDL作为凝固剂时两组分表现出基本相似的胶凝能力,与7S组分较高的疏水性和11S组分较高的巯基含量有关.     

Absence of a differential induction of cytochrome P450 2E1 by different alcoholic beverages in rats: implications for the aetiology of human oesophageal cancer

Alcohol is an important risk factor for human oesophageal cancer. There is evidence from epidemiological studies that some specific alcoholic drinks, e.g. Calvados apple brandy, are associated with a greater risk than others. Alcohol induces cytochrome P450 2E1 (CYP2E1) and the hypothesis was tested that different alcoholic beverages, containing a variety of alcoholic compounds, could differentially induce expression of cytochrome P450 enzymes. Twelve groups of five rats each were treated for 3 days with different alcoholic beverages (ethanol alone, whisky, farm-produced or commercial Calvados brandy, beer, cider, wine) adjusted to 4, 10 or 20% of ethanol in drinking water. Immunoblotting using a monoclonal antibody specific for rat CYP2E1 revealed a single protein band in liver microsomes. Densitometric quantitation of microsomal proteins demonstrated a significant two-, three- and sixfold increase in band intensity after treatment with ethanol concentrations of 4, 10 and 20% respectively, compared to control rats drinking water alone. There was a dose-dependent increase in liver microsomal metabolism of CYP2E1 substrates (para-nitrophenol and dimethylnitrosamine) in ethanol-treated rats. However, there were no significant differences in the level of CYP2E1 protein or enzymatic activity between the different alcoholic beverages at the same ethanol concentration. There was a slight increase in hepatic CYP1A-related enzymatic activities in the alcohol-treated rats compared to the controls, but no difference between the treated groups either with dose of ethanol or type of beverage. These data show that induction of CYP2E1 with acute alcohol treatment is predominantly determined by the ethanol content of the beverage. Received: 10 February 1997 / Accepted: 26 May 1997     

Chronic parasite infection in mice induces brain granulomas and differentially alters brain nerve growth factor levels and thermal responses in paws

Schistosoma mansoni infection, both in humans and in animal models, is known to induce granulomas in the liver and intestine. It has also been reported that in humans the eggs of this parasite can reach the brain, causing psychiatric and neuropathological disorders. Whether this also occurs in rodents is unknown. To answer this question, mice were infected with this parasite and the central nervous system (CNS) examined at various time intervals. The results show that schistosomiasis induced granulomas in several regions of the CNS and increased nerve growth factor (NGF) levels in the cortex, hypothalamus and brain stem, but not in the hippocampus. The infection also caused paw hyperalgesia, as determined by the hot-plate test, and a local increase in NGF, but not in substance P. These findings indicate that the murine model of infection can be used for studying mechanisms leading to human neuroschistosomiasis and suggest that the neuropathological disorders and the sensory deficits observed in human schistosomiasis are associated with impaired levels of NGF in the peripheral and central nervous system. Received: 18 January 1996 / Revised, accepted: 16 April 1996     

衰老红细胞与带3蛋白

循环系统里的成熟红细胞在其生命过程里经历着氧化性衰老，相应细胞组份出现血红蛋白变性、膜蛋白交联、带3蛋白聚集以及带3蛋白降解等多种修饰。这些修饰作为红细胞膜上的衰老信号参与构成衰老细胞抗原，由此启动与IgG自身抗体(主要为带3蛋白抗体)的结合以及补体的沉淀，最终是免疫吞噬系统对异常细胞的识别清除．现就衰老红细胞与带3蛋白的关系作一综述。     

Association of a 70-kDa tyrosine phosphoprotein with the CD16:ζ:γ complex expressed in human natural killer cells

The CD16: ζ: γ receptor complex allows natural killer (NK) cells to recognize and eliminate antibody-coated target cells. Whereas the ectodomain of CD16 is the receptor for Fcγ domains of immunoglobulins, disulfide-linked homo- and heterodimers composed of ζ and γ are required for the cell surface expression, and signal transduction properties of the complex. Engagement of CD16 activates the tyrosine kinase pathway, which induces the tyrosine phosphorylation of several substrates, including the ζ subunit and the phospholipase C γ-1 and γ-2 isoforms. Here we show that CD 16 stimulation of either peripheral blood NK cells, leukemic NK cells, or Jurkat transformants expressing a CD16:ζ:γ receptor complex, results in the tyrosine phosphorylation of a 70 kDa ζ-associated protein (pp70). Similarly, a 70-kDa ζ-associated phosphoprotein in T cells has been shown to be a tyrosine kinase (ZAP-70). Peptide mapping analysis indicates that the 70-kDa ζ-associated phosphoproteins from T cells and NK cells are structurally indistinguishable. We conclude that the CD16:ζ:γ complex may use a ZAP-70-related non-receptor tyrosine kinase, in the CD16 signaling cascade leading to NK cell activation.     

Protein kinase C in focal ischemic rat brain: dual autoradiographic analysis of [C]iodoantipyrine (IAP) and [H]phorbol-12,13-dibutyrate (PDBu)

Protein kinase C (PKC) activity was measured in rat brain with 2 h of middle cerebral artery (MCA) and common carotid artery (CCA) occlusion, using dual autoradiography of [¹⁴C]iodoantipyrine (IAP) and [³H]phorbol-12,13-dibutyrate (PDBu). In the ischemic brain, it required more than 120 min of incubation to obtain a plateau in PDBu binding. In contrast, the binding of PDBu in non-ischemic brain reached a plateau with incubation for 60 min. This delay of PDBu binding in the ischemic brain suggests that the affinity of this ligand is reduced due to a change in structure of the cell membrane caused by ischemia. PDBu binding in the ischemic brain increased significantly compared to the non-ischemic brain. This finding provides further evidence that excessive activation of PKC in the ischemic brain may play an important role in ischemic neuronal damage. ©1997 Elsevier Science B.V. All rights reserved.     

Protein kinase C agonist and antagonist effects in normal human epidermal keratinocytes

Abstract Several lines of evidence implicate protein kinase C (PKC) in the development of basal cell and squamous cell carcinomas, tumors which originate from epidermal keratinocytes. To examine PKC in a model relevant to human skin, we exposed normal human epidermal keratinocytes (NHEK) in serum-free media to a variety of PKC agonists and antagonists. NHEK PKC activity increased up to 10-fold within the 1st hour of exposure to tetradecanoyl phorbol acetate (TPA), and gradually returned to control values within 72 h. TPA-induced PKC activity was enhanced by pretreatment of cultures with protein and RNA synthesis inhibitors. TPA-induced growth arrest and differentiation was antagonized by staurosporine. Down-regulation by bryostatin pretreatment blocked TPA-stimulated differentiation. Our overall conclusion is that activation of PKC in cultured human keratinocytes is required for differentiation. These results are crucial to the analysis of compounds suspected of promoting or inhibiting epidermal tumors.