Single unit responses in the cervical sympathetic trunk upon somatic nerve stimulation

Pflügers Archiv - European Journal of Physiology -     

Der Nachweis tubulärer Funktionsstörungen der Niere durch Bestimmung der Aminopeptidase-Aktivität im Harn

Zusammenfassung Aminopeptidase findet sich im lumennahen Cytoplasma der Zellen des proximalen Tubulus der Niere in hoher Konzentration. Bei Schädigungen der Tubuluszellen, die mit einer Änderung der Permeabilität der Zellmembranen einhergehen, kann sie in den Harn übertreten. Dementsprechend ist bei akuten Läsionen des proximalen Tubulus eine erhöhte Aminopeptidase-Aktivität im Harn zu erwarten.An einer Reihe von Beispielen sollte gezeigt werden, daß die Bestimmung der Aminopeptidase-Aktivität im Harn zum Nachweis akuter Funktionsstörungen des proximalen Tubulus geeignet ist.

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Summary Aminopeptidase occurs in high concentration in the luminal portion of the cytoplasma of cells of the proximal convoluted tubules. In case of damage of the tubular cells this enzyme can pass into the urine. Thus, in acute lesions of the proximale tubule an elevated aminopeptidase activity in the urin is to be expected.The task was to demonstrate in a series of cases, that the determination of the aminopeptidase activity in the urine serves for the evaluation of acute disturbances of the proximal tubule.

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Als Aminopeptidase (sog. Leucin-Aminopeptidase, LAP), bezeichnen wir in der vorliegenden Arbeit dasjenige Enzym oder diejenigen Enzyme, die in der Lage sind,l-Leucyl--Naphthylamid zu spalten.     

Ti gamma A + delta TCS1+ T cells in human thymus. Analysis of the T cell receptor.

TcR1+ T cells in peripheral blood have been shown to express in an exclusive fashion either the Ti gamma A or the delta TCS1 epitope. Here, we characterize a subset of TcR1+ T cells in fresh thymus co-expressing the Ti gamma A and delta TCS1 epitopes. TcR1dim and TcR1bright clones can be distinguished. Biochemical and molecular studies on both types of clones generated from these thymocytes reveal a unique T cell receptor structure characterized by the use of a V gamma 9/C gamma 2-encoded 55-kDa gamma chain nondisulfide linked to a V delta 1-encoded delta chain.     

一株抗人BLys单克隆抗体的制备及其生物学功能研究

研究以稳定高表达BLys的基因转染细胞L-BLys为免疫原,常规免疫BALB/c小鼠,采用B淋巴细胞杂交瘤技术进行细胞融合,L-BLys细胞和天然表达BLys的HL60细胞为抗体筛选阳性细胞株,经免疫荧光标记分析反复筛选和以有限稀释法反复克隆化培养。将获得的克隆4F7培养细胞注射入经致敏的小鼠体内,-抽取的腹水经Protein G亲和层析柱纯化。将纯化所得的抗体作用于经BLys分子刺激的扁桃体B细胞,3H-TdR检测细胞的增殖效率。结果获得1株持续、稳定分泌鼠抗人BLys单克隆抗体的杂交瘤细胞株。该细胞株所分泌的抗体能阻断膜型和可溶性BLys分子对扁桃体B细胞的促增殖作用。对这株单克隆抗体生物学功能的研究表明,这株单抗能特异性识别人BLys分子及阻断膜型和可溶性BLys发挥生物学活性。     

藤黄微球菌Rpf及其结构域蛋白对结核分枝杆菌生长的影响

目的 表达纯化藤黄微球菌(Micrococcus luteus)复活促进因子(Rpf)及结构域(domain)蛋白,研究其对结核分枝杆菌牛长的影响.方法 诱导表达含有藤黄微球菌Rpf及其结构域基因的融合表达载体pPro-EXHT-Rpf和pPro-EXHT-Rpf domain,在变性条件下对目的 蛋白进行纯化.用不同浓度的纯化蛋白刺激不可培养状态结核分枝杆菌的生长.结果 获得藤黄微球菌Rpf及其结构域融合蛋白的纯度分别为95%和93%,相对分子质量(Mr)大小分别为30×103和12×103,蛋白质含量分别为471 mg/L和337 mg/L.Western blot证实,获得的蛋白为我们所需要的目的 蛋白.所获得的藤黄微球菌Rpf及其结构域融合蛋白能够促进不可培养状态的结核分枝杆菌的生长,而抗藤黄微球菌Rpf结构域的单克隆抗体可以明显抑制结核分枝杆菌的生长.结论 表达的藤黄微球菌Rpf及其结构域融合蛋白可以促进结核分枝杆菌的生长,而且藤黄微球菌Rpf蛋白与Rpf结构域蛋白具有一致的生物活性.     

Stat5b/Survivin信号转导通路调控结肠癌细胞凋亡的机制

目的: 探讨Stat5b/Survivin信号转导通路调控结肠癌细胞凋亡的作用机制。方法: 用阳离子脂质体介导Stat5反义寡核苷酸转染人结肠癌HT29细胞，MTT法检测细胞增殖状态；流式细胞术检测细胞周期与凋亡；EMSA检测Stat5活性；Western blotting检测Stat5、p-Stat5、cyclin D1、Survivin与Bcl-2凋亡家族成员Bcl-2和Bcl-x_L的表达。结果: 转染Stat5反义寡核苷酸后HT29细胞增殖受抑制，凋亡细胞增多，Stat5、p-Stat5与Survivin表达下降，Bcl-2与Bcl-x_L变化不明显。结论: 阻断Stat5通路可以抑制靶基因Survivin表达并诱导结肠癌细胞凋亡。     

人缺血脑组织中IP-10和IFN-γ的表达

目的：探讨趋化因子IP-10和细胞因子IFN-γ是否参与人缺血脑损伤过程。方法：将21例脑梗死死亡病例按发病持续时间分为〈7天、7～14天和15～21天3组，以非缺血侧半球做对照，用HE染色法观察炎性细胞浸润情况；通过免疫组织化学方法检测缺血半球脑组织与非缺血半球脑组织中趋化因子IP-10和细胞因子IFN-γ的表达。结果：在〈7天组和7～14天组中，缺血脑组织可见大量炎性细胞浸润。在〈7天组、7～14天组和15～2l天组中，趋化因子IP-10在缺血半球脑组织中的表达高于非缺血半球（分别是1．74倍增高，P〈0．01；1．41倍增高，P〈0．05和1．52倍增高，P〈0．01）。在对细胞因子IFN-γ的检测中发现〈7天和7～14天组中，IFN-γ在缺血半球脑组织中的表达高于非缺血半球（分别是1．65倍增高，P〈0．05和1．32倍增高，P〈0．05）；在15～21天组中，IFN-γ在缺血半球与非缺血半球中的表达没有显著差异（P〉0．05）。结论：在人缺血脑组织中观察到IP-10和IFN-γ的表达，提示IP-10和IFN-γ参与了炎症反应对脑组织的损伤过程。同时也提示IP-10可能参与后期对损伤脑组织的修复。     

Association analysis between a Cys23Ser substitution polymorphism of the human 5-HT2c receptor gene and neuronal hyperexcitability

Transgenic mice lacking a functional 5-HT2c receptor gene are extremely susceptible to audiogenic seizures, suggesting that 5-HT2c receptors mediate inhibition of neuronal network excitability. The present association study tested the hypothesis that a Cys23Ser substitution polymorphism within the human 5-HT2c receptor gene modulates neuronal excitability. Genotypes of the Cys23Ser polymorphism were assessed in 454 subjects of German descent, comprising: 1) 93 severely affected alcohol-dependent males with a history of alcohol withdrawal seizure or delirium, 2) 119 patients affected by an idiopathic generalized epilepsy, and 3) 242 controls. Both sexes were analyzed separately because of the X-chromosomal location of the 5-HT2c receptor gene. The allele frequencies of the Cys23Ser variants did not differ significantly between the controls and either the severely affected alcohol-dependent males (P = 0.34), or patients with idiopathic generalized epilepsy (P > 0.57). Our results suggest that the common Cys23Ser substitution polymorphism of the human 5-HT2c receptor gene does not confer susceptibility to neuronal hyperexcitability in either idiopathic generalized epilepsy or alcohol withdrawal seizure or delirium.     

Mapping of linear B-cell epitopes of the S2 subunit of pertussis toxin.

The linear immunogenic and antigenic structure of the S2 subunit of pertussis toxin was investigated with synthetic peptides corresponding to regions of the protein sequence predicted to contain surface-exposed hydrophilic beta turns. Five peptides as peptide-bovine serum albumin conjugates were recognized by anti-pertussis toxin antiserum and were thus designated "immunogenic epitopes." Two prominent immunogenic epitopes were specified by peptides corresponding to sequences spanning R107-120 and R186-199, whereas peptides corresponding to residues R35-50 and R91-106 were only bound in low titer. Three peptides as thyroglobulin conjugates elicited antisera in rabbits that bound intact pertussis toxin by enzyme-linked immunosorbent assay and immunoblot. These peptides were designated "antigenic epitopes." The most prominent antigenic determinant was localized to the N-terminal end of the S2 sequence encompassing residue R1-7. Peptides R35-50 and R91-106 represented two minor antigenic epitopes. Antisera to two additional peptides corresponding to residues R134-149 and R186-199 recognized the S2 subunit only by Western blotting (immunoblotting). Only antiserum raised against peptide R91-106 also recognized the S3 subunit by Western blotting, indicating a marked antigenic and probably also structural difference between the two highly homologous subunits.