Under local anesthesia and external fixator in the treatment of intertrochanteric fracture of femur in the elderly, relationresultNeutralization and inhibition of endogenous abnormality of IL 18 activity in the results, on the other hand is IL. 18Ab can adjust the imbalance of Th1 type immune response. Key words interleukin 18 interleukin 18; antibodies; primary nephrotic syndrome; interferon V; tumor necrosis factor o CLC number: R692 document code: A article number 1671-8194 (2010): 01 - 0040 - 03 primary nephrotic syndrome (primarynephroticsyndrome, PNS) in the pathogenesis of not yet clear and no special effective treatment method. Immune inflammatory reaction may play a central part in recent years, ugg online, a large number of studies have found a variety of cytokines are involved in the disease occurrence and development. Interleukin 18 (interleukin 18, IL 18) is a newly identified primarily by activation of monocytes macrophages secrete a multifunctional cytokine, in PNS at the physiological and pathological process may serve as an important member of. We now with respect to its relationship with PNS and IL.18Ab related to treatment review. Overview of 1IL-18 IL in 1995 18 is the first by the Japanese scholar Okamura from infected sores blister Corynebacterium (P. acnes) in the liver of mice in the separation and cloning, because it can induce Thl cells to produce interferon Y (interferon-V, IFN-V), originally named IFN-V inducing factor (IGIF). .. . Ushio 1996 cloned human IGIF cDNA, and in Escherichia coli (E.Coli) expression, in view of the amino acid sequence of IGIF and database in any known proteins are not the same, and because of its and IL.1p have similar structures, and shared part of the receptor via, canada goose tilbud, and IL-L2 has the similar function, belonging to the IL family, so named for the IL-l8. IL 18 receptor by 0 and P chains form, where C chain (IL 1 receptor associated protein 1) as receptor affinity subunit, ralph lauren polo, whereas P chain (IL 1 receptor accessory protein analogues) for information transmission subunits, IL 1Ro IL-18RD chain chain, belong to IL 1 family, in the families of IL-1 IL.1 receptor accessory protein analogues (IL-18p chain) in IL& # 183;L8 is highly specific, for IL.18 binding is required, it and IL.18Ro chain expression in Thl cells common. Corresponding author: E-mail: [email protected] precursor IL a 18 conversion to active IL 18 expression in mononuclear a macrophage, T cells, B cells, requiring secondary to cell apoptosis protease (caspase-1) effect. Patients with PNS promoter -656 -607 -137 gene were GT, AC and GG, UGG Online, IL 18mRNA expression was significantly increased, probably because these sites of nucleotide changes in the tranｓｃｒｉｐｔional activity of IL-18 enhancement. PNS in peripheral blood of patients with IL a 18 elevated gene levels as protein levels, so that the translation level rise is also involved in the reaction process. The mechanism of action of 2. 1PNS 2IL-18EPNS in patients with glomerular endothelial cells, parietal epithelial cells and mesangial cell (mesangial cells and infiltrating inflammatory cells), renal tubular epithelial cells and renal interstitial cells were relatively strong and extensive IL 18 protein expression, indicating that PNS patients with glomerular local excessive secretion of IL.18 possible involvement of glomerular filtration membrane damage and urinary protein formation 0 based on different pathological types of PNS glomerular pathological features and degree each are not identical, glomerular expression of IL-18 in different, mesangial proliferative glomerulonephritis (MPGN) the highest expression level, mesangial proliferative glomerulonephritis (MsPGN) is the second, and minimal change disease nephrotic (MCD) expression quantity minimum and a number of studies indicate that IL.18 is not involved in PNS early inflammatory process 6-8, 17,. 2.2 reinforced Thl immune response function of mononuclear macrophage 2.2.1IL.18 is a an autocrine regulatory factor, positive feedback pathway stimulation of Thl cells to produce IFN,V, tumor necrosis factor 0 (tumornecrosisfactor-a,TNF.0) and granulocyte colony-stimulating factor (G.CSF), causing cellular immune mediated inflammation injury, and the IL.18R up-regulation, resulting in immune inflammatory processes may More articles related to topics： canada goose outlet ehm gftl xeuj abercrombie and fitch pui jvht wmoh nike free herren tfv drxc hggl