Anti-Collagen II polyclonal antibody

The thermal dissociation of three cobalt(II) azido complexes of the type CoL4(N-3)(2) where L = 4-benzoyl-, 4-ethyl-, and 5-hydroxypyridine, have been studied by thermogravimetry (TGA and DTA) and IR spectroscopy, The three complexes form an intermediate 1 : 2 complex which explodes in the case of the 4-benzoylpyridine complex. Hydrogen bonding plays a significant role in the stability and decomposition of the 1.4 and 1 : 2 complexes in the case of 3-hydroxypyridine ligand. (C) 1999 Elsevier Science B.V. All rights reserved.

The important clinical problems of diabetic nephropathy are both proteinuria and decrease of renal function. Pathological analysis showed decrease of GFR was correlated to degree of mesangial expansion but not thickening of GBM nor the other findings in human type 1 diabetic nephropathy. From the perspective in renal dysfunction, mesangial, matrix expansion was crucial for diabetic nephropathy. However, there was no difference of mesangial expansion between normal and microalbuminuria stage in type 1 and 2 diabetes mellitus (DM). On the other hand, microalbuminuria definitely shows a key related factor for cardiovascular events, but it does not indicate a clear interaction for glomerulosclerosis. We need to search a new clinical marker for renal injury. We have first shown that Smad1 is a transcription factor for alpha 1 and 2 of type 4 Collagen (Col4), which is a major component of glomerulosclerosis. We have also identified Smad1 is a critical responsible molecule for developing glomerulosclerosis in rat diabetic nephropathy. We have found the good correlation between glomerulosclerosis and urinary Smad1 but not between glomerulosclerosis and urine albumin. These data suggests that urine Smad1 is a promising clinical marker for underlying glomerular damages in early stage diabetic nephropathy. The study also implicates that angiotensin II (AngII)-Src-Smad1 signaling pathway has played a key role for development of diabetic nephropathy. These suggest that it is necessary to clarify the whole mechanism related to Smad1 to identify the pathogenesis of diabetic nephropathy. (C) 2008 Elsevier Ireland Ltd. All rights reserved.