2 to -2.7; P<0.0001), lower low-density lipoprotein cholesterol (-5.2 mg/dL; 95% CI, -4.5 to -5.8; P<0.0001), higher high-density lipoprotein cholesterol (4.8 mg/dL;
95% CI, 4.5-5.0; P<0.0001), and lower triglycerides (-7.5 mg/dL; 95% CI, -6.2 to -8.7; P<0.0001). For the retrospective cohort analysis, raising vitamin D levels from <20 to >= 30 ng/mL (n=6260), compared with remaining at <20 ng/mL (n=2332), was associated with a mean increase in total cholesterol (0.77 mg/dL; 95% CI, 0.18-1.36; P=0.01) and high-density lipoprotein cholesterol (0.42 mg/dL; 95% CI, 0.08-0.76; GM6001 ic50 P=0.02) but nonsignificant changes in low-density lipoprotein cholesterol (0.32 mg/dL; 95% CI, -0.01 to 0.66; P=0.06) and triglycerides (0.04 mg/dL; 95% CI, -2.16 to 2.23 mg/dL; P=0.97).\n\nConclusions-Although vitamin D deficiency is associated with an unfavorable lipid profile in cross-sectional analyses, correcting for a deficiency might not translate into clinically meaningful changes in lipid concentrations; however, data from intervention trials are required to confirm these findings. (Circulation. 2012; 126: 270-277.)”
“The purpose of this study was to investigate the prevalence of beta-lactamase and the genomic clonality of a large collection of Kingella kingae isolates from Israeli
patients with a variety of invasive infections and asymptomatic pharyngeal carriers. Selleckchem EVP4593 beta-lactamase production was studied by the nitrocefin method and the minimum inhibitory concentrations (MICs) Apoptosis Compound Library mw of penicillin and amoxicillin-clavulanate were determined by the epsilon (Etest) method. The genotypic clonality of isolates was investigated
by pulsed-field electrophoresis (PFGE). beta-lactamase was found in 2 of 190 (1.1 %) invasive isolates and in 66 of 429 (15.4 %) randomly chosen carriage organisms (p < 0.001). Overall, 73 distinct PFGE clones were identified (33 among invasive organisms and 56 among carriage isolates). beta-lactamase production was found to be limited to four distinct PFGE clones, which were common among carriage strains but rare among invasive strains, and all organisms in the collection belonging to these four clones expressed beta-lactamase. The penicillin MIC of beta-lactamase-producing isolates ranged between 0.094 and 2 mcg/mL (MIC50: 0.25 mcg/mL; MIC90: 1.5 mcg/mL) and that of amoxicillin-clavulanate between 0.064 and 0.47 mcg/mL (MIC50: 0.125 mcg/mL; MIC90: 0.125 mcg/mL). The penicillin MIC of beta-lactamase non-producing isolates ranged between < 0.002 and 0.064 mcg/mL (MIC50: 0.023 mcg/mL; MIC90: 0.047 mcg/mL). Although beta-lactamase production is prevalent among K. kingae organisms carried by healthy carriers, the low invasive potential of most colonizing clones results in infrequent detection of the enzyme in isolates from patients with clinical infections. The exceptional presence of beta-lactamase among invasive organisms correlates with the favorable response of K.