带有时变时滞的中立型随机系统的鲁棒镇定和H_∞控制

研究了带有时变时滞的中立型随机系统的鲁棒镇定和H∞控制问题.利用Lyapunov泛函方法和It o^公式,基于状态反馈控制器,以线性矩阵不等式(LMI)形式给出了闭环系统鲁棒镇定及H∞控制的新方法.最后,数值算例说明了该方法的有效性.     

甘青青兰挥发性成分GC/MS分析

目的：分离鉴定出甘青青兰（Dracocephalum tanguticum Maxim.）挥发油的化学成分.方法：用气相色谱-质谱（GC/MS）联用技术及峰面积归一化法测定各组分的相对含量.结果：共鉴定出23种化合物,占总色谱峰总面积的87.46%.结论：甘青青兰挥发油中的化学成分主要为[-]-反-松香芹乙酯和桉油精,两者分别占总挥发油中化学成分的60.30%和9.31%.     

Anti-type 2 transglutaminase antibodies as modulators of type 2 transglutaminase functions: a possible pathological role in celiac disease

Auto-antibodies to the ubiquitous enzyme type-2 transglutaminase (TG2) are a specific hallmark of celiac disease (CD), a widely diffused, multi-factorial disease, affecting genetically predisposed subjects. In CD an inflammatory response, at the intestinal level, is triggered by diet consumption of gluten-containing cereals. Intestinal mucosa displays various degrees of atrophy and hyperplasia, with consequent global intestinal dysfunction and other relevant extra-intestinal symptoms. Through deamidation of specific glutamines of gluten-derived gliadin peptides, TG2 strongly enhances gliadin immunogenicity. In addition, TG2 cross-linking activity may generate complexes between TG2 itself and gliadin peptides, and these complexes seem to cause the auto-immune response by means of an apten-carrier-like mechanism of antigen presentation. Anti-TG2 antibodies can be early detected in the intestinal mucosa of celiac patients and are also abundantly present into the serum, thus potentially reaching other organs and tissues by blood circulation. Recently, the possible pathogenetic role of auto-antibodies to TG2 in CD has been investigated. Here, we report an overview about the genesis of these antibodies, their specificity, their modulating ability toward TG2 enzymatic or non-enzymatic activities and their biological effects exerted by interacting with extracellular TG2 or with cell-surface TG2. We also discuss the auto-immune response occurring in CD against other TG members (i.e. type 3 and type 6) and analyze the occurrence of anti-TG2 antibodies in other auto-immune CD-related diseases. Data now available let us to suppose that, even if antibodies to TG2 do not represent the triggering molecules in CD, they could be important players in disease progression and manifestations.     

Ultrastrukturänderung leukämischer retikulärer Zellen nach Zusatz von RNS aus normaler Milz zum Kulturmedium

Riassunto Vengono descritte le modificazioni morfologiche, rilevate al microscopio elettronico, delle cellule reticolari leucemiche coltivate in presenza di ARN estratto dalla milza di embrioni di vitello.     

Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease

Genes and mechanisms involved in common complex diseases, such as the autoimmune disorders that affect approximately 5% of the population, remain obscure. Here we identify polymorphisms of the cytotoxic T lymphocyte antigen 4 gene (CTLA4)--which encodes a vital negative regulatory molecule of the immune system--as candidates for primary determinants of risk of the common autoimmune disorders Graves' disease, autoimmune hypothyroidism and type 1 diabetes. In humans, disease susceptibility was mapped to a non-coding 6.1 kb 3' region of CTLA4, the common allelic variation of which was correlated with lower messenger RNA levels of the soluble alternative splice form of CTLA4. In the mouse model of type 1 diabetes, susceptibility was also associated with variation in CTLA-4 gene splicing with reduced production of a splice form encoding a molecule lacking the CD80/CD86 ligand-binding domain. Genetic mapping of variants conferring a small disease risk can identify pathways in complex disorders, as exemplified by our discovery of inherited, quantitative alterations of CTLA4 contributing to autoimmune tissue destruction.