0195 +/- 0.0056 d(-1), which was about 2.6-fold higher than that of the control batch (0.0075 d(-1)). Conversely, in Case II, the rate constants for treatments with amendments and those for the control batch were found to be comparable, 0.0172 +/- 0.0015 d(-1) and 0.0158 d(-1), respectively. Microarray results indicated a less diverse indigenous bacterial community in Case I and an abundant indigenous community in Case II both from the control batches on Day 0. The dynamics of the two microbial communities,

revealed by NMS plots, emphasized the similarity among the different treatments during the first degradation stage.

CONCLUSIONS: Prior to a remediation project, the usefulness of a bioaugmentation approach see more can be investigated selleck using an ITS oligonucliotide microarray. Results from the microarray answered why the bioaugmentation approach was useful in Case I, but not in Case II. The abundance of the diesel-degrading community determined the usefulness of bioaugmentation. Relatively quantified TRFLP results analyzed via the NMS plots demonstrated comparable microbial communities during the first degradation stage,

regardless of differences between the two batches. The bacterial community structure might shift with the availability of hydrocarbons. (C) 2009 Society of Chemical Industry”
“Background: The incidence of human chronic kidney failure with associated cardiovascular disease is increasing. Kidney damage can be induced in rats by chronic dietary adenine intake. We have used this intervention to investigate the development of concurrent kidney and cardiovascular injury. Methods: Dose-ranging studies were undertaken on male Wistar rats by feeding with adenine (0.075%, 0.25%, 0.5% or 0.75%) for up to 16 weeks. 0.075% adenine produced minimal changes while 0.5% or 0.75% adenine produced marked kidney damage; 0.25% adenine was chosen for further studies

since it produced moderate kidney and cardiovascular damage. In rats fed 0.25% adenine, renal function (blood urea nitrogen (BUN), plasma creatinine, and their clearances; plasma uric acid; proteinuria); renal SC79 chemical structure structure (collagen, apoptosis, inflammation, glomerulopathy); and protein expression of markers for oxidative stress (HO-1), fibrosis (TGF-beta, alpha-SMA) and inflammation (TNF-alpha, NF-kappa B p52, NF-kappa B p50, PLA(2) and ED1) were measured, along with cardiovascular parameters (blood pressure, left ventricular stiffness, vascular responses). Allopurinol (25 mg/kg/day, final 8 weeks only) was administered to determine the role of uric acid. Results: 0.25% adenine diet induced characteristics of human chronic kidney disease at 16 weeks including increased BUN (0.25% adenine 56.5 +/- 5.4*; control 6.2 +/- 0.6 mmol/L; * = p < 0.05) and plasma creatinine (0.25% adenine 268 +/- 23*; control 41.9 +/- 2.