Modulation of calcium oxalate monohydrate crystallization kinetics in vitro

Modulation of calcium oxalate monohydrate crystallization kinetics in vitro. The effects of several low and high molecular weight (mol wt) compounds on the kinetics of calcium oxalate crystallization were examined using a seeded crystal growth method in which the solubility, the growth and the agglomeration of calcium oxalate crystals were measured as three separate and system-independent parameters. Git-rate, magnesium, phosphate, pyrophosphate, chondroitinsulphate, pen-tosanpolysulphate and heparin were tested in a wide range of concentrations. The solubility of calcium oxalate crystals Was increased only by citrate and magnesium. The crystal growth was inhibited by all compounds tested, but those with the high mol wt had the greatest effect at low concentrations. In contrast, inhibition of crystal agglomeration was achieved only by the low mol wt compounds; citrate was found to be the most potent inhibitor at concentrations likely to be present in normal urine. The high mol wt substances, despite their potent crystal growth inhibitory activity, had no effect on agglomeration. The results show that growth and agglomeration of calcium oxalate crystals are separate processes which are differently modulated by various compounds. They further provide a possible explanation for the pathogenetic role of citrate in hypocitraturic renal stone disease

OXA-carbapenemases present in clinical acinetobacter baumannii-calcoaceticus complex isolates from patients in kurdistan region, Iraq

In addition to intrinsic resistance in Acinetobacter baumannii, many different types of acquired resistance mechanisms have been reported, including the presence of VIM and IMP metallo β-lactamases and also of blaOXA-23-like and blaOXA-58-like enzymes. In the Kurdistan region of Iraq, the multiresistant A. baumannii-calcoaceticus complex is prevalent. We characterized the different mechanisms of resistance present in clinical isolates collected from different wards and different hospitals from the Kurdistan region. One hundred twenty clinical nonduplicate A. baumannii-calcoaceticus complex isolates were collected from four hospitals between January 2012 and October 2013. The identification of the isolates was confirmed by MALDI-TOF. The sus

Ongelijke discontering van zorgkosten en -effecten: verwarrend

Discounting is a widely accepted practice in cost-effectiveness analysis to weigh future costs and effects for their timing. In 2006, the Dutch Health Care Insurance Board revised its recommended rates for discounting. They recommended differential discounting of costs and effects, whereby effects are discounted at a lower rate relative to the costs. The question is whether this guideline is to be generally used for decision-making in the Netherlands. We show how the use of unequal discount rates leads to confusing cost-effectiveness results and why further implementation guidelines are essential

Pathological and Therapeutic Significance of Cellular Invasion by Proteus mirabilis in an Enterocystoplasty Infection Stone Model

Proteus mirabilis infection often leads to stone formation. We evaluated how bacterium-mucin adhesion, invasion, and intracellular crystal formation are related to antibiotic sensitivity and may cause frequent stone formation in enterocystoplasties. Five intestinal (Caco-2, HT29, HT29-18N2, HT29-FU, and HT29-MTX) and one ureter cell line (SV-HUC-1) were incubated in artificial urine with five Proteus mirabilis strains. Fluorescence-activated cell sorting (FACS), laser scanning microscopy, and electron microscopy evaluated cellular adhesion and/or invasion, pathologic changes to mitochondria, and P. mirabilis-mucin colocalization (MUC2 and MUC5AC). An MTT (thiazolyl blue tetrazolium bromide) assay and FACS analysis of caspase-3 evaluated the cellular response. Infected cells were incubated with antibiotics at dosages representing the expected urinary concentrations in a 10-year-old, 30-kg child to evaluate bacterial invasion and survival. All cell lines showed colocalization of P. mirabilis with human colonic mucin (i.e., MUC2) and human gastric mucin (i.e., MUC5AC). The correlation between membrane mucin expression and invasion was significant and opposite for SV-HUC-1 and HT29-MTX. Microscopically, invasion by P. mirabilis with intracellular crystal formation and mitochondrial damage was found. Double membranes surrounded bacteria in intestinal cells. Relative resistance to cotrimoxazole and augmentin was found in the presence of epithelial cells. Ciprofloxacin and gentamicin remained effective. Membrane mucin expression was correlated with relative antibiotic resistance. Cell invasion by P. mirabilis and mucin- and cell type-related distribution and response differences indicate bacterial tropism that affects crystal formation and mucosal presence. Bacterial invasion seems to have cell type-dependent mechanisms and prolong bacterial survival in antibiotic therapy, giving a new target for therapeutic optimalization of antibiotic treatment

Modulation of calcium oxalate monohydrate crystallization kinetics in vitro

Modulation of calcium oxalate monohydrate crystallization kinetics in vitro. The effects of several low and high molecular weight (mol wt) compounds on the kinetics of calcium oxalate crystallization were examined using a seeded crystal growth method in which the solubility, the growth and the agglomeration of calcium oxalate crystals were measured as three separate and system-independent parameters. Git-rate, magnesium, phosphate, pyrophosphate, chondroitinsulphate, pen-tosanpolysulphate and heparin were tested in a wide range of concentrations. The solubility of calcium oxalate crystals Was increased only by citrate and magnesium. The crystal growth was inhibited by all compounds tested, but those with the high mol wt had the greatest effect at low concentrations. In contrast, inhibition of crystal agglomeration was achieved only by the low mol wt compounds; citrate was found to be the most potent inhibitor at concentrations likely to be present in normal urine. The high mol wt substances, despite their potent crystal growth inhibitory activity, had no effect on agglomeration. The results show that growth and agglomeration of calcium oxalate crystals are separate processes which are differently modulated by various compounds. They further provide a possible explanation for the pathogenetic role of citrate in hypocitraturic renal stone disease