DNA限制性内切酶分析应用于伴放线放线杆菌的鉴定和分型

本文用限制性内切酶分析(REA)作伴放线放线杆菌(Aa)的鉴定和分型研究,提取Aa染色体DNA,井分别用BamHI、HindⅢ,Sal Ⅰ和Xho Ⅰ消化,作琼脂糖凝胶电泳。结果显示,Aa和嗜沫嗜血杆菌的DNA片段图谱明显不同;分属于两种不同血清型的两株Aa菌株,其DNA片段图谱也明显不同。这表明,REA可用于Aa菌的鉴定和分型,在所用的4种酶中,以Sal Ⅰ和Xho Ⅰ消化的DNA片段图谱差异最明显。     

抗蝮蛇毒磷酸二酯酶单克隆抗体的制备及鉴定

从蝮蛇毒中提取磷酸二酯酶,用此酶免疫BALB/c小鼠,取其脾细胞与小鼠骨髓瘤细胞Fo融合,以间接ELISA检测杂交瘤细胞培养上清液和小鼠腹水中的特异性抗体,其效价分别为1∶128和1∶51 200.抗原阻断试验结果表明,此抗体对蛇毒磷酸二酯酶具有特异性.该杂交瘤细胞株定为G_8,该株单抗属鼠IgG_(2a)亚型,经体外持续培养6个月,其分泌抗体性能稳定.     

涎腺恶性肿瘤的回顾性研究

本文对52例涎腺恶性肿瘤进行了回顾性研究。52例中发生于腮腺者27例(51.9％);病理类型以腺样囊性癌和粘液表皮样癌最多见;随访2～8年,死亡19例,病死率最高者为腺癌(5/8)和鳞癌(3/5)。作者对腺样囊性癌的病理分型提出了不同看法。     

Antidepressant-like effects of trazodone on a behavioral screen are mediated by trazodone, not the metabolite m-chlorophenylpiperazine

Trazodone is an atypical antidepressant drug (i.e. blocks neither monoamine uptake nor monoamine oxidase) which tests as an antidepressant drug on the differential-reinforcement-of-low-rate 72-s (DRL 72-s) schedule of reinforcement by increasing the reinforcement rate and decreasing the response rate. m-Chlorophenylpiperazine (m-CPP) is a 5-HT1B and 5-HT1C agonist, weak 5-HT2 antagonist, and trazodone metabolite. It has been suggested that formation of m-CPP is responsible for the antidepressant action of trazodone. Administration of m-CPP (1-10 mg/kg i.p.) 60, 30 or 10 min before the behavioral session did not mimic the reinforcement rate-increasing effects of trazodone (10-20 mg/kg i.p.) on rats performing under the DRL 72-s schedule of water reinforcement. Pretreatment with proadifen (50 mg/kg i.p.), an inhibitor of trazodone metabolism, caused a greater than 30-fold leftward shift in the dose-response curve for both the reinforcement rate and the response rate. These results suggest that the parent compound and not the trazodone metabolite m-CPP, mediates the antidepressant-like effects of trazodone on DRL 72-s behavior.     

大鼠实验性脾虚证胰岛A、B和D细胞的免疫组织化学研究

用免疫组织化学ＰＡＰ法显示实验性脾虚组和正常对照组大鼠胰岛Ｂ细胞（胰岛素细胞）、Ａ细胞（胰高血糖素细胞）和Ｄ细胞（生长抑素细胞）．结果显示，实验组胰岛素分泌升高（Ｐ＜０．０１），胰高血糖素和生长抑素分泌下降（Ｐ＜０．０５）。实验结果提示大鼠胰岛Ａ、Ｂ和Ｄ细胞分泌活动的变化与脾虚证的症候可能有密切关系。     

Kinetic immunodominance: functionally competing antibodies against exposed and cryptic epitopes of Escherichia coli beta-galactosidase are produced in time sequence.

The murine antibody response to Escherichia coli beta-galactosidase (GZ) was analyzed in vivo and in vitro by focusing on two families of antibodies that exert distinct conformational/functional activity on the antigen. Activating antibodies--defined by their capacity to increase the enzymatic activity of defective GZ produced by mutant strains of E. coli--are detected early after secondary challenge. Inhibiting antibodies, which interfere with antibody-mediated enzyme activation, appear later and cause the abrupt fall of activating titer, a scenario suggesting either idiotype/anti-idiotype interaction or opposite pulsions exerted on the antigen molecule. Supporting the latter mechanism, the confrontation of mAbs of the two families produced classical competitive inhibition curves when the readout was enzyme activation, although they recognize two different epitopes of the same molecule: the activating mAb a quaternary conformation-dependent site of wild-type GZ, the inhibiting mAb a sequential determinant exposed only in denatured or in defective enzyme. The different timing of generation of these antibodies during the response may depend on a processing step necessary for unfolding of native antigen and consequent display of certain cryptic epitopes before they can trigger specific B cells. A picture emerges where the response to the various epitopes of a complex antigen is sequentially connected and where the uptake by antigen-presenting cells of antigen complexed with antibodies specific for the exposed epitopes may favor revelation of the cryptic ones.     

用结合^131碘和化疗药物的明胶微球作肝动脉...

Nine patients with inoperable hepatoma were treated by using hepatic arterial embolization 131I and chemotherapeutic agent gelatin microsphere (131I-CA-GM). The emission CT after operation detected that the microspheres were concentrated on tumor area. The ratio between the radioactivity in tumor and that in liver was 4.1:1. A case died of ictopic embolization; the others survived 3, 4, 5, 19, 24, 7, 8, and 12 months respectively. Three of them were still alive. 131I-CA-GM has triple anticarcinogenic actions, including the arterial occlusion, targeting chemotherapy and internal radiation. The microspheres can selectively accumulate in the tumor artery and can be easily traced by gamma-camera or emission CT. 131I-CA-GM is a hopeful embolic agent for the treatment of liver cancer, but some problems about ectopic arterial embolization should be further studied.     

Reversal of dexfenfluramine-induced anorexia and c-Fos/c-Jun expression by lesion in the lateral parabrachial nucleus

The external subdivision of the lateral parabrachial nucleus (LPBE) shows strong Fos-like immunoreactivity (FLI) following anorectic doses of the indirect serotonin agonist dexfenfluramine (DFEN). In an effort to determine the contribution of the LPBE to DFEN-induced anorexia, bilateral ibotenate lesions were made in the LPBE, and the effects of the lesion on DFEN-induced anorexia and FLI as well as c-June-like immunoreactivity (JLI) were examined. It was found that LPBE lesion significantly attenuated DFEN anorexia: in a 1-h food intake test following 24-h food deprivation, DFEN (2 mg/kg) suppressed food intake by 60% in intact rats but only 34% in rats with LPBE lesions. In addition to this behavioral change, LPBE lesion completely abolished DFEN-induced FLI and JLI in the lateral subdivision of the central nucleus of the amygdala (CeL) and laterodorsal subdivision of the bed nucleus of stria terminalis (BSTLD), both of which showed strong FLI and JLI in intact rats. DFEN-induced FLI and JLI in other brain regions were not affected by LPBE lesion, including the ventromedial and lateral hypothalamus, caudate-putamen, and the nucleus of the solitary tract (NST). The parallel loss of DFEN-induced anorexia and FLI/JLI following LPBE lesion raises the novel possibility that LPBE-CeL/BSTLD pathway may be involved in DFEN anorexia.