Mouse Anti Chicken Collagen type III Hybridoma [4C3]

The stability constants and structures of the complexes of Co2+, Cu2+, Zn2+, Ni2+ and Cd2+ with 2-methyl-1-vinylimidazole in aqueous solution have been determined by potentiometric and spectrophotometric methods. The stability of the compounds depended much on the presence of the electron-attracting vinyl substituent contributing to the pi(M --> L) back bonding. Further, nitrato complexes of cobalt(II) and copper(II) with 2-methyl-1-vinylimidazole (L) of general formulae [CoL3(H2O)(NO3)]NO3 1, [CoL2(NO3)(2)] 2, [CuL4(NO3)(2)]. 2H(2)O 3 and [CuL2(NO3)(2)] 4 have been prepared in the solid state. Full single-crystal X-ray analyses have been accomplished for compounds 1 and 4 which enabled the determination of angles and bond lengths.The compounds were identified on the basis of elemental analyses, EPR spectroscopy, IR, FIR and VIS-NIR absorption spectra and magnetochemical data. The immediate environment of the central ions is described by a distorted tetragonal bipyramid.

A network of inflammation factors is related to pulmonary fibrosis induced by paraquat (PQ) poisoning. At high doses, the superantigen staphylococcal enterotoxin C1 (SEC1) can induce immunological unresponsiveness and inhibit release of inflammation factors. In this study, site-directed mutagenesis was performed at the H118 and H122 amino acid residues of SEC1 to reduce SEC1 toxicity. The SEC1 mutant showed significantly decreased pyrogenic toxicity, but retained clonal anergy at high dosages in vitro. Pretreatment with the SEC1 mutant prior to PQ poisoning in mice reduced symptom duration and severity, prolonged survival time, and decreased the splenocyte response to ConA induction. The SEC1 mutant also down-regulated several important cytokines related to fibrosis in the plasma after PQ poisoning. SEC1 decreased the expression of genes related to pulmonary fibrosis, including alpha-SMA, COL1a1, COL3 and TGF-beta 1, in PQ poisoned mice. Histomorphological observation indicated alleviation of pathological changes in the lungs after SEC1 pretreatment compared to mice in the PQ group. In conclusion, the SEC1 mutant reduced pulmonary interstitial fibrosis induced by PQ poisoning.