术前精氨酸强化PN对结直肠癌病人免疫功能的影响

目的：探讨术前精氨酸强化肠外营养（ＰＮ）对结直肠癌病人免疫功能的影响。 方法：选择经病理证实的结直肠癌病人作为研究对象,术前随机分为三组,即对照组给常规术前准备,常规ＰＮ组和精氨酸强化ＰＮ组除常规准备外,分别给予常规ＰＮ和精氨酸强化ＰＮ７天,术前７天和手术当天早晨７：００采集外周静脉血,测定ＣＤ３、ＣＤ４、ＣＤ８、ＩＬ－２、ＮＫ细胞和ＮＫ细胞活性;取同期进行腹股沟疝手术的病人作为正常对照。 结果：     

蛇毒精氨酸酯酶Agkihpin对人鼻咽癌CNE-2细胞系MRP1表达的影响

目的探讨蛇毒精氨酸酯酶Agkihpin对人鼻咽癌CNE-2细胞系中多药耐药相关蛋白MRP1表达的影响,并试图阐明Agkihpin抑制CNE-2细胞的机制。方法用不同浓度的Agkihpin处理细胞72 h后,应用免疫细胞化学、Western blot、RT-PCR法检测MRP1在CNE-2细胞中的表达。结果不同浓度Agkihpin作用CNE-2细胞72 h后MRP1表达均降低,并呈现出一定的浓度依赖效应,显示Agkihpin可显著下调CNE-2细胞中MRP1表达。各加药组与不加Agkihpin组比较,差异具有统计学意义（P<0.05）。结论在人低分化鼻咽癌CNE-2细胞系中,Agkihpin能抑制MRP1的表达,并且随浓度的增大抑制作用增加,这可能是Agkihpin能降低鼻咽癌细胞活力的原因之一;Agkihpin抑制MRP1的表达提示在一定程度上可提高肿瘤细胞对化疗药物的敏感度。     

精氨酸血管加压素 mRNA在不同免疫应答期大鼠下丘脑室旁核的表达变化

目的研究大鼠下丘脑室旁核(PVN)内精氨酸血管加压素(AVP)mRNA的表达与免疫应答反应间的动态关系.方法建立免疫增强及免疫抑制大鼠模型,应用原位杂交组织化学及图像分析技术检测免疫反应不同时期大鼠PVN内AVP mRNA的动态变化.结果①免疫抑制组大鼠PVN单个细胞内AVP mRNA阳性杂交信号的平均面积明显低于免疫增强组及对照组(P＜0.05).②PVN单个细胞内AVP mRNA阳性杂交信号的平均灰度值在免疫反应高峰时显著低于免疫反应开始增强时(P＜0.05),在免疫抑制最低时却明显高于免疫反应开始受抑制时(P＜0.05).③AVP mRNA阳性杂交信号在PVN内所占的总面积在免疫反应高峰时显著大于免疫反应开始增强时和对照组(P＜0.05),在免疫抑制最低时则明显小于免疫反应开始受抑制时(P＜0.05).④AVP mRNA阳性杂交信号在整个PVN内的平均灰度值在免疫反应高峰时明显低于免疫反应开始增强时(P＜0.05),在免疫抑制最低时却明显高于免疫反应开始受抑制时(P＜0.05).结论 PVN内AVP mRNA的含量与免疫应答反应的强度成正比,AVP基因的转录随免疫应答反应的变化而变化.     

Streptococcal arginine deiminase regulates endothelial inflammation,mTOR pathway and autophagy

Endothelial cells (EC) are active participants in the inflammation process. During the infection, the change in endothelium properties provides the leukocyte infiltrate formation and restrains pathogen dissemination due to coagulation control. Pathogenic microbes are able to change the endothelium properties and functions in order to invade the bloodstream and disseminate in the host organism. Arginine deiminase (ADI), a bacterial arginine-hydrolyzing enzyme, which causes the amino acid deficiency, important for endothelium biology. Previous research implicates altered metabolism of arginine in the development of endothelial dysfunction and inflammation. It was shown that arginine deficiency, as well as overabundance affects the balance of mechanical target of rapamycin (mTOR)/S6 kinase (S6K) pathway, arginase and endothelial nitric oxide synthase (eNOS) resulted in reactive oxygen species (ROS) production and EC activation. ADI creating a deficiency of arginine can interfere cellular arginine-dependent processes. Thus, this study was aimed at investigation of the influence of streptococcal ADI on the metabolism and inflammations of human umbilical vein endothelial cells (HUVEC). The action of ADI was studied by comparing the effect Streptococcus pyogenes M49-16 paternal strain expressing ADI and its isogenic mutant M49-16delArcA with the inactivated gene ArcA. Based on comparison of the parental and mutant strain effects, it can be concluded, that ADI suppressed mTOR signaling pathway and enhanced autophagy. The processes failed to return to the basic level with arginine supplement. Our study also demonstrates that ADI suppressed endothelial proliferation, disrupted actin cytoskeleton structure, increased phospho-NF-κB p65, CD62P, CD106, CD54, CD142 inflammatory molecules expression, IL-6 production and lymphocytes-endothelial adhesion. In spite of the ADI-mediated decrease in arginine concentration in the cell-conditioned medium, the enzyme enhanced the production of nitric oxide in endothelial cells. Arginine supplementation rescued proliferation, actin cytoskeleton structure, brought NO production to baseline and prevented EC activation. Additional evidence for the important role of arginine bioavailability in the EC biology was obtained. The results allow us to consider bacterial ADI as a pathogenicity factor that can potentially affect the functions of endothelium.     

Systemic infection caused by the methicillin-resistant Staphylococcus aureus USA300-LV lineage in a Brazilian child previously colonized

The methicillin-resistant Staphylococcus aureus (MRSA) USA300-Latin American variant (USA300-LV) lineage is well documented in northern Latin American countries. It has replaced established clones in hospital environments. We herein report a systemic infection caused by a USA300-LV isolate in a 15-year-old boy, from a low-income area of Rio de Janeiro, previously colonized by the same strain. During hospital stay, seven pvl-positive MRSA USA300-LV isolates were recovered by nasal swab, blood and abscess secretion. The patient underwent intravenous vancomycin, daptomycin, and oral sulfamethoxazole/trimethoprim, and was discharged after 45 days after full recovery. This is the first documented case of a community-acquired MRSA infection caused by the USA300-LV variant in Brazil in a previously colonized adolescent with no history of recent travel outside of Rio de Janeiro. The need for improved surveillance programs to detect MRSA colonization in order to control the spread of hypervirulent lineages among community and hospital settings is highlighted.