https://cancerbiologyprogram.med.wayne.edu/pdfs/hallmarks_cancer_article.pdf

Hallmarks of cancer: the next generation.

抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Background Hyperglycemia and insulin resistance are common in critically ill patients, even if they have not previously had diabetes. Whether the normalization of blood glucose levels with insulin therapy improves the prognosis for such patients is not known. Methods We performed a prospective, randomized, controlled study involving adults admitted to our surgical intensive care unit who were receiving mechanical ventilation. On admission, patients were randomly assigned to receive intensive insulin therapy (maintenance of blood glucose at a level between 80 and 110 mg per deciliter) or conventional treatment (infusion of insulin only if the blood glucose level exceeded 215 mg per deciliter and maintenance of glucose at a level between 180 and 200 mg per deciliter). Results At 12 months, with a total of 1548 patients enrolled, intensive insulin therapy reduced mortality during intensive care from 8.0 percent with conventional treatment to 4.6 percent (P<0.04, with adjustment for sequential analyses). The ...

https://www.nejm.org/doi/pdf/10.1056/NEJMoa011300

Intensive Insulin Therapy in Critically Ill Patients

https://www.um.es/biomybiotec/web/Seminarios/2010/papers/Cano_2.pdf

Epithelial-Mesenchymal Transitions in Development and Disease

The origins of the mesenchymal cells participating in tissue repair and pathological processes, notably tissue fibrosis, tumor invasiveness, and metastasis, are poorly understood. However, emerging evidence suggests that epithelial-mesenchymal transitions (EMTs) represent one important source of these cells. As we discuss here, processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias. The identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions.

/pdf/the-basics-of-epithelial-mesenchymal-transition-xe9crzoewf.pdf

The basics of epithelial-mesenchymal transition

The use of purified self-antigens can facilitate the further analysis of pathogenic mechanisms in autoimmunity (1, 2). This report describes the isolation of the nephritogenic antigen of anti-tubular basement membrane (a-TBM)l-induced interstitial nephritis. First described by Steblay and Rudofsky (3) over a decade ago, this experimental lesion is now induced in a variety of inbred strains of mice, rats, and guinea pigs after an injection of rabbit renal tubular basement membrane (renal tubular antigen; RTA) in complete Freund's adjuvant (CFA). Disease-susceptible rodents develop a-TBM antibodies after 9-10 d, and an intense interstitial infiltrate by 2-7 wk, depending on the species (3-5). Phenotypic characterization of the predominantly mononuclear cell infiltrate reveals the presence of an admixture of T cells, B cells, macrophages, and natural killer cells (6, 7). Additional studies have provided insights into the immunoregulation

Nephritogenic antigen producing anti-tubular basement membrane disease

With this issue of JASN , we introduce a new feature for original manuscripts, the Brief Communication. These articles are short, about 1500 words, and written in letter format followed by concise methods and no more than four figures; some of the dataset may be submitted supplemental to the

Eric G. Neilson

Papers

Nephritogenic antigen producing anti-tubular basement membrane disease

The appearance of brief communications in JASN