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.     

血栓前体蛋白与心脏瓣膜置换术后的抗凝监测

目的：探讨血栓前体蛋白(TPP)在心脏机械瓣膜置换术后抗凝治疗监测中的意义，及制定术后抗凝治疗的合理方案。方法：比较抗凝组(60例)和对照组(20例)的国际标准化比率(INR)、TPP，并比较抗凝组中有、无房颤的病人华法林用量、INR和TPP，对抗凝组病人TPP和INR的关系作一元线性回归分析，比较各组的INR和血浆TPP浓度。结果：抗凝组与对照组相比，TPP低、INR高。抗凝组有房颤者的血浆TPP浓度高于窦性心律者。线性回归分析结果表明，TPP和INR无明显相关性。出血病人的血浆TPP浓度明显低于正常高限(6μg／ml)。结论：TPP是心脏机械瓣置换术后抗凝治疗理想的辅助监测指标。术后有房颤心律者的血栓栓塞危险性增加。抗凝治疗应同时检测INR和TPP。     

不同强度运动后大鼠心肌细胞热休克蛋白72mRNA的表达

目的 :探讨不同运动强度和持续时间运动对大鼠心肌细胞热休克蛋白 72mRNA表达的影响。方法 :分别使SD大鼠进行低强度 (6 0 %VO2 max)、中等强度 (75 %VO2 max)和高强度 (85 %VO2 max)跑台运动 1天、2天和 3天 ,在末次运动结束后 2 4小时以RT -PCR法检测大鼠心肌细胞热休克蛋白 72mRNA的表达。结果 :在安静情况下大鼠心肌细胞存在HSP72mRNA的基础结构性表达 ;低强度运动 1天后心肌细胞HSP72mRNA表达与对照组相比无显著性差异 ,但随着运动时间的延长 ,HSP72mRNA表达逐渐增加 ;中等强度运动后心肌细胞HSP72mRNA表达随运动持续时间的延长显著增加 ,但运动 2天和 3天组表达量无显著性差异 ;大强度运动后心肌细胞HSP72mRNA表达随运动持续时间的延长显著增加。结论 :运动可以造成心肌细胞HSP72mRNA的表达增加 ,不同强度运动诱导心肌细胞HSP 72mRNA表达程度不同 ,且与运动持续时间存在内在关系。     

重组人骨形成蛋白2骨诱导中神经生长因子及其受体的表达

目的 观察重组人骨形成蛋白2（recombined human bone morphogenetic protein2，rhBMP-2）异位诱导成骨过程中神经生长因子（nerve growth factor，NGF）及其高亲和力受体（tyrosine kinasere ceptor A，TrkA）的表达，探讨NGF在BMP骨诱导中的作用。方法ICR小鼠36只，随机分为实验组和对照组，每组18只，均制备右侧股后部肌袋异位成骨模型。实验组植入含rhBMP-2胶原复合物，对照组仅植入相同体积的胶原海绵。分别于术后7、14和21d取材，行大体、组织学、免疫组织化学观察及RT-PCR检测。结果大体观察实验组术后7d，右股后部可扪及较硬肿块；术后14、21d，肿块硬度增加。对照组各时间点未发现肿块。组织学观察实验组中rhBMP-2胶原复合物具有良好的诱导成骨能力，免疫组织化学结果显示骨诱导材料植入后7d，NGF于成纤维细胞、成软骨细胞、软骨细胞、肥大软骨细胞和成骨细胞中均有阳性表达；14d，NGF阳性表达局限于部分成骨细胞、幼稚骨细胞和成骨样细胞，同时在骨髓中单核巨噬细胞、多核巨噬细胞和破骨细胞中有明显表达；21d，只有少量成骨样细胞和破骨细胞以及骨髓中多核巨噬细胞有NGF表达；TrkA免疫组织化学染色与NGF的表达基本一致。对照组术后各时间点未见成骨现象。实验组NGFmRNA的RT-PCR检测显示，术后7dNGF的mRNA表达最高，14d表达下降，21d只有微量表达。结论rhBMP-2复合物是一种有效的诱导成骨材料。在外源性BMP诱导成骨过程中有明显的NGF及其高亲和力受体TrkA的表达，NGF可以通过直接和间接的方式参与BMP的诱导成骨过程。     

Designed polyanionic coiled-coil proteins: acceleration of heparin cofactor II inhibition of thrombin

Novel polyanionic proteins were designed to increase the rate of heparin cofactor II (HC) inhibition of α-thrombin, an essential protease in the coagulation cascade. Two α-helical coiled-coil proteins, a 62-residue dimer containing 8 Glu residues (E8C) and a 104-residue dimer containing 14 Glu residues (E14C), plus two 31-residue control peptides containing 8 Glu residues each (E8A and E8B), were chemically synthesized, structurally characterized and enzymatically assayed. Circular dichroic spectrophotometry indicated that both E8C and E14C formed stable two-chain α-helical coiled coils at pH 7 and 25 °C. The control peptides were only partially α-helical. E14C remained folded at 90 °C but E8C was half unfolded at 49 °C. Coiled-coil proteins E8C and E14C maximally accelerated by 35- and 33-fold, respectively, the rate of HC inhibition of α-thrombin. None of these compounds accelerated antithrombin inhibition of α-thrombin, and neither control peptide accelerated HC inhibition of α-thrombin. Acceleration of the HC inhibition of α-thrombin showed bimodal dependence on the concentration of the polyanionic protein, which is consistent with formation of a HC-coiled-coil-thrombin ternary complex. The results suggest that antithrombotic polyanionic α-helical coiled-coil proteins can be designed and synthesized and that the occurrence of secondary structure can be correlated with biologcal activity. © Munksgaard 1995.     

L158,809和西拉普利对体外培养系膜细胞TGF-β1表达和细胞外基质蛋白分泌的影响

目的：观察血管紧张素受体拮抗剂(ARBs)L158，809和血管紧张素转换酶(ACE)抑制剂西拉普利对体外培养人肾小球系膜细胞转化生成因子(TGF—β1)表达和纤维连接蛋白、层粘连蛋白和Ⅳ型胶原分泌的影响。方法：分别在不同葡萄糖浓度(5.6mmol／L和30mmol／L)和药物浓度(1、10、100和500μmol／L)下体外培养人肾小球系膜细胞，分别于24、48和72h后测定细胞增殖。然后将系膜细胞分为低糖(5．6mmol／L)对照组(LG)、高糖(30mmol／L)对照组(HG)、L158，809(10μmol／L)组和西拉普利(10μmmol／L)组，48h后，分别用RT-PCR法测定TGF-β1表达，ELISA和放射免疫法测定细胞上清液中TGF-β1、纤维连接蛋白、层粘连蛋白和Ⅳ胶原浓度。结果：与低糖对照组相比，高糖对照组系膜细胞过度增殖，细胞上清液中TGF-βl、纤维连接蛋白、层粘连蛋白和Ⅳ胶原浓度明显升高，TGF-βlmRNA表达也显升高；而L158，809组和西拉普利组TGF-β1和细胞外基质(ECM)蛋白水平明显低于高糖对照组，且TGF-β1mRNA水平亦表达明显降低。结论：高糖可刺激体外培养系膜细胞过度增殖，TGF-β1表达增高，ECM蛋白分泌明显增加，而L158，809和西拉普利均可抑制高糖环境下上述现象。     

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.