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。     

我国登革2型病毒43株包膜E蛋白基因的特征

对我国1987年流行的登革2型病毒43株包膜E蛋白基因的核苷酸序列进行了分析。结果表明登革2型病毒43株包膜E蛋白基因核苷酸序列含1485个核苷酸，编码495个氨基酸，并就其核苷酸序列及其相应的氨基酸序列与其它的登革2型病毒株进行了比较，发现核苷酸序列与我国1985年分离的登革2型病毒04株，新几内亚C株（NGC），牙买加株1409（JAM）和马来西亚当地流行株M1（登革出血热）、血2（登革休克综合征）、M3（登革热）同源性分别是95.8%、94.6%、97.5%、925%、92.7%和939%，氨基酸序列的同源性分别是94.3%、94.3%、96.0%、93.7%、93.7%和91.5%，推断出的氨基酸序列显示出12个保守的半胱氨酸残基和两个潜在的糖基化位点，分别位于Asn-67和Asn-153位。     

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.     

细脚拟青霉对大鼠血液蛋白质水平及其生长的影响

用１０％细脚拟青霉水煎剂１．０ｍｌ·ｄ（－１）给大鼠灌胃，连续２１ｄ，对ｉｐ环磷酰胺（２０ｍｇ·ｋｇ（－１）×７ｄ）所致免疫抑制大鼠血液中血红蛋白、血清总蛋白、球蛋白水平下降及体重减轻等均有显著的保护和逆转作用；对正常大鼠血液中血红蛋白水平也有显著提高。提示：细脚拟青霉可改善机体的营养状况，促进生长，逆转免疫抑制作用。     

Effects of phorbol ester on carbachol-induced contraction in bovine ciliary muscle: possible involvement of protein kinase C

The aim of the research was to characterize muscarinic receptors of bovine ciliary muscle and to investigate the desensitization process. The role of protein kinase C was analyzed. The results show that muscarinic receptors of bovine ciliary muscle have the pharmacological characteristics of the M₃ subtype. Acute exposure to phorbol esters (1 μM phorbol 12,13-dibutyrate, PDB, or 0.1 μM phorbol 12-myristate 13-acetate, PMA, for 15 and 5 min, respectively) resulted in antagonism of muscarinic receptor-mediated contraction. Long-term pretreatment (18 h) with PMA to down-regulate protein kinase C resulted in potentiation of carbachol-induced contraction, reduction of agonist-induced desensitization and loss of phorbol ester-induced desensitization. Staurosporine (3 μM) and H₇ [1-(5-isoquinolinesulfonyl)-2-methyl-piperazine] (1 μM), protein kinase C inhibitors, produced a significant potentiation of the contractile effect of carbachol, reduced the desensitization produced by repeated addition of carbachol and suppressed that induced by phorbol esters. In vitro incubation with carbachol, PDB or PMA did not cause any modification of the binding of labeled [³H]quinuclidinyl benzilate. In vitro incubation with PDB and PMA produced, as expected, a significant translocation of protein kinase C from the cytosol to the membrane. The incubation of the ciliary muscle with carbachol, using the protocol of exposure that induced maximal desensitization of contractile responses, produced a significant redistribution of the enzyme from the cytosol to the membrane. These findings suggest that agonist-induced modulation of functional cholinergic sensitivity in ciliary muscle is correlated, at least partially, to the translocation of protein kinase C from the cytosol to the membrane. The desensitization by phorbol esters is completely due to protein kinase C activation; during the desensitization process, direct modification of the density and affinity of muscarinic receptors is not involved.     

他汀类药物早期干预对急性冠脉综合征患者血脂、高敏C反应蛋白和纤维蛋白原的影响

目的 比较他汀类药物和阿司匹林联合用药与单用阿司匹林对急性冠脉综合征患者血脂、高敏C反应蛋白及纤维蛋白原的影响。方法 所有患者均在急性冠脉综合征发病后72h内开始接受药物治疗，他汀组(40例)应用他汀类药物加阿司匹林治疗8周，对照组(16例)单用阿司匹林治疗，观察两组总胆固醇、低密度脂蛋白胆固醇、高敏C反应蛋白和纤维蛋白原水平的变化。结果 治疗8周后，他汀组各指标显著降低，面对照组仅高敏C反应蛋白水平显著下降。他汀类药物降低高敏C反应蛋白、纤维蛋白原的程度与其降脂作用无关。结论 他汀类药物与阿司匹林联合用药降低高敏C反应蛋白和纤维蛋白原的作用可能优于单用阿司匹林，并与其抗炎作用有关。     

尿核基蛋白22检测在膀胱癌诊断中的价值

目的:探讨尿核基蛋白22(NMP22)在膀胱移行细胞癌诊断中的临床价值。方法:采用ELISA法定量分析16例膀胱移行上皮癌(TCC)、14例TCC术后随访患者和12例泌尿系良性疾病患者的尿NMP22含量,并同时行尿脱落细胞学检查。设定NMP22的临界值为10U/ml。结果:16例膀胱移行癌患者、14例膀胱癌术后随访患者和12例泌尿系良性疾病患者的尿NMP22中位值分别为31.65、5.41和6.74U/ml,前者与后两者均有统计学差异(P<0.001)。以10U/ml为界值,尿NMP22诊断膀胱癌的敏感性为93.7%,特异性为69.2%,阴性预测值为94.7%,准确性为78.6%。同期尿细胞学的敏感性为31.3%,特异性100%,阴性预测值为70.2%。结论:与脱落细胞学比较,尿NMP22测定有更高的敏感性,是一种较理想的早期膀胱移行细胞癌诊断指标,对预后判断亦有价值。     

高压氧对家兔面神经撞击伤后面神经核内生长相关蛋白变化的影响(论著)

目的：研究面神经撞击伤后面神经核内生长相关蛋白（ＧＡＰ－４３）的变化及高压氧（ＨＢＯ）治疗的影响。方法：利用ＢＩＭ－Ⅱ型生物撞击机致家兔右侧面神经干损伤，应用ＳＰ免疫组化染色法观察损伤后１、３、７、１４和２１天（分别用ＨＢＯ治疗及不用ＨＢＯ为对照）面神经核内ＧＡＰ－４３的变化，并用电镜观察面神经干超微结构变化。结果：面神经损伤第１天，伤侧面神经核区ＧＡＰ－４３样免疫反应性神经元（ＧＬＩＮ）开始增多，第１４天其增多达到高峰，第２１天逐渐下降。ＨＢＯ治疗组伤后不同时期ＧＬＩＮ的增多明显高于对照组。伤后第２１天，与对照组相比ＨＢＯ组面神经干电镜观察可见较多的新生髓鞘。结论：ＨＢＯ治疗可使伤后面神经核内ＧＬＩＮ增多，因而有助于面神经损伤后的修复与再生。