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06 Jan 2013 
Familial Mediterranean fever (FMF) is an autoinflammatory disease in MEFV gene mutations and is characterized by recurrent episodes of self-limited fever and local serositis. The complement system is a key regulator of the inflammatory process. The purpose of this study is to investigate the genetic change and C5aR and C5L2 gene attacks FMF patients neutrophil gene expression patterns. Observed in the two receptor gene mutations, while observed in C5aR1 genetic change is determined as N279ķ polymorphic variants. In addition, the C5L2 gene mRNA expression were observed in the neutrophils FMF patients compared with the control group. Binding capacity rhC5a and the ability to generate reactive oxygen species is of similar neutrophils from healthy subjects and FMF patients and independent existence N279ķ polymorphism C5L2 mRNA expression.

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06 Jan 2013 
Regulatory approval of intravenous infusion-related adverse reactions nanomedicines intrinsic mechanism is still elusive. There are great inter-individual differences observed adverse reactions, which may include cardiovascular disease, bronchial lung, skin, mucous membranes, physically and mentally, and autonomic nervous symptoms. Although the nano-mediated complement activation trigger has suggested that these adverse events is an important factor in the activation of the complement can still be non-responders. These reactions are similar immunological mechanisms and supporting drug allergies, genetic factors remains to be further studied. Genetic correlation study, the anatomy of the pathogenic factors, and reveal a variety of molecular pathways, induction of infusion-related adverse reactions may be a powerful tool. It is envisaged that this study may lead to the design of a reliable risk assessment and treatment decisions impact analysis test, which completely changed the practice of medicine nanopharmaceuticals. This program may further improve the regulatory approval process currently underway nanomedicines and reduce the overall cost of health care. Here, we discuss some important innate immune gene polymorphism of the symptomatic transfusion reactions related to nano-mediated.

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06 Jan 2013 
C5a receptor C5ar the (coded C5ar) and C5L2 (Gpr77 coding), especially C5L2, was originally known as the "default receptor function, is still a controversial topic here, the role of each receptorusing antibody-induced blockade of C5a receptor knockout mice by cecal ligation and puncture-induced sepsis set in the "mid-range" C5ar or C5L2 blockade or absence of sepsis (30-40% survival), greatly improving the survival andattenuation of the accumulation of inflammatory mediators in the plasma. appearance in the body or in the in vitro release of high mobility group protein -1 (HMGB1) C5L2, but not C5ar. "high-grade" sepsis (100% lethality), onlythe joint blockade of C5L2 and C5ar the protected conditions. these data suggest that the harmful consequences of sepsis C5ar and C5L2 collaborative, C5L2 release of HMGB1 earlier speculation, C5L2 is a functional receptor, rather than just a defaultthe receptor.

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30 Dec 2012 
MUC1 cytoplasmic tail of the β-catenin interaction. A SXXXXXSSL theme MUC1 is a conservative combination of β-catenin and other partners. This interaction has been shown to be dependent on cell adhesion. Expression of MUC1 phosphorylation on a YEKV the theme. LYN this website through phosphorylation has been shown to mediate interleukin 7, the source epidermal growth factor receptor through mediation PRKCD. This interaction is antagonizing the degradation of β-catenin GSK3B. The the MUC1 block phosphorylation-dependent degradation of β-catenin by final results of GSK3B.The is stable expression of β-catenin, MUC1 increased cancer increase. This promotes the expression vimentin and CDH2. These proteins with the mesenchymal phenotype, characterized by increased motility and invasiveness. Promote tumor cell invasion through β-catenin, increased expression of MUC1 in tumor cells, leading to epithelial - mesenchymal transition, began to promote the formation of metastases.

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30 Dec 2012 

MUC1 cytoplasmic tail of the binding of p53 has been shown. This interaction is genotoxic stress increase. MUC1 and p53 protein expression and p21 gene promoter p53 response element. This will lead to the activation of the p21 gene, leading to cell cycle arrest. MUC1 with p53 in p53-mediated tumor suppressor p53-mediated apoptosis and promote cell cycle arrest.

MUC1 fibroblasts over-expression increases the phosphorylation of Akt. Phosphorylated Akt phosphorylation of Bcl-2-related deaths start. This will lead to the separation of the Bcl-2-related deaths to promote expression of Bcl-2 and Bcl-xL. Activates the proof is dependent on the upstream activation of PI3K. Moreover, MUC1 results show that the increase of the expression of Bcl-xL. MUC1 overexpression in tumors. Free expression of Bcl-2 and Bcl-xL exist to prevent the release of cytochrome c from mitochondria, thereby preventing apoptosis. MUC1 cytoplasmic tail through interaction with HSP90 mitochondrial shuttle. The cause of this interaction is through phosphorylation MUC1 SRC (genes) of the cytoplasmic tail. SRC the ligand Neuregulin activation of the epidermal growth factor receptor family. Cytoplasmic tail, and then inserted into the outer mitochondrial membrane. Mitochondrial localization of MUC1 prevent activation of the apoptosis mechanism

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