Heme and menaquinone induced electron transport in lactic acid bacteria

<p>Abstract</p> <p>Background</p> <p>For some lactic acid bacteria higher biomass production as a result of aerobic respiration has been reported upon supplementation with heme and menaquinone. In this report, we have studied a large number of species among lactic acid bacteria for the existence of this trait.</p> <p>Results</p> <p>Heme- (and menaquinone) stimulated aerobic growth was observed for several species and genera of lactic acid bacteria. These include <it>Lactobacillus plantarum, Lactobacillus rhamnosus, Lactobacilllus brevis, Lactobacillus paralimentarius, Streptococcus entericus </it>and <it>Lactococcus garviae</it>. The increased biomass production without further acidification, which are respiration associated traits, are suitable for high-throughput screening as demonstrated by the screening of 8000 <it>Lactococcus lactis </it>insertion mutants. Respiration-negative insertion-mutants were found with <it>noxA</it>, <it>bd</it>-type cytochrome and menaquinol biosynthesis gene-disruptions. Phenotypic screening and <it>in silico </it>genome analysis suggest that respiration can be considered characteristic for certain species.</p> <p>Conclusion</p> <p>We propose that the <it>cyd</it>-genes were present in the common ancestor of lactic acid bacteria, and that multiple gene-loss events best explains the observed distribution of these genes among the species.</p

How central obesity influences intra-abdominal pressure:a prospective, observational study in cardiothoracic surgical patients

Background: Intra-abdominal hypertension (IAH) is frequently present in critically ill patients and is an independent predictor for mortality. Better recognition of clinically important thresholds is necessary. Increased intra-abdominal pressure (IAP) is associated with renal dysfunction, and renal failure is one of the most consistently described organ dysfunctions associated with IAH. Obesity is also associated with kidney injury. The underlying mechanisms are not yet fully understood. Increased IAP may be a link in this association. The aim of this study was firstly to find the range in values of intra-abdominal pressure (IAP) in cardiothoracic surgery patients a secondly to investigate the relationship between central obesity, body mass index (BMI) and IAP and thirdly to investigate the relationship between IAP, inflammation and renal function in this population. Methods: Consecutive adult patients admitted to the cardiothoracic unit of the intensive care unit (ICU) after undergoing elective cardiothoracic surgery were included in this prospective, observational study. C-reactive protein (CRP) as a marker of inflammation and serum creatinine as a marker of renal function were measured pre- and postoperatively. Estimated glomerular filtration rates were calculated pre-and postoperatively. BMI was calculated. Waist circumference (WC), hip circumference (HC) and transvesical IAP were measured once directly after admission to the ICU postoperatively. Waist/ hip ratio (WHR) was calculated (WC divided by HC). Three definitions of central obesity were used. Central obesity was defined according to WC, WHR or median WHR. Results: In total, 186 patients undergoing cardiothoracic surgery were included. Mean IAP was 9.1 mmHg (SD 4.4). IAP = 12 mmHg was observed in 50 patients (26.9 %). IAP > 20 mmHg was measured in 4 patients (2.2 %). There was a positive correlation between IAP and BMI (r(2) = 0.05, p = 0.003). Correlations between IAP and WC (r(2) = 0.02, p = 0.054) and between IAP and WHR (r(2) = 0.01, p = 0.173) were not significant. There were no correlations between pre-or postoperative CRP and IAP (r(2) = 2.3 x 10(-4), p = 0.839 and r(2) = 0.013, p = 0.117, respectively). In obese patients postoperative CRP was significantly higher than in non-obese patients (p = 0.034). There were no correlations between pre-operative serum creatinine and IAP (r(2) = 3.3 x 10(-5), p = 0.938) or postoperative serum creatinine and IAP (r(2) = 0.003, p = 0.491). Conclusions: The range in IAP in patients undergoing cardiothoracic surgery was wide. There was a positive correlation between IAP and BMI. Correlations between IAP and indices for central obesity were not significant. In a multiple regression model BMI was a better predictor of IAP than WHR in this population. There were no correlations between pre- or postoperative CRP and IAP. Furthermore, this study did not find evidence for a relation between IAP and pre- and postoperative serum creatinine

Puddle formation, persistent gaps, and non-mean-field breakdown of superconductivity in overdoped (Pb,Bi)2Sr2CuO6+{\delta}

The cuprate high-temperature superconductors exhibit many unexplained electronic phases, but it was often thought that the superconductivity at sufficiently high doping is governed by conventional mean-field Bardeen-Cooper-Schrieffer (BCS) theory[1]. However, recent measurements show that the number of paired electrons (the superfluid density) vanishes when the transition temperature Tc goes to zero[2], in contradiction to expectation from BCS theory. The origin of this anomalous vanishing is unknown. Our scanning tunneling spectroscopy measurements in the overdoped regime of the (Pb,Bi)2Sr2CuO6+{\delta} high-temperature superconductor show that it is due to the emergence of puddled superconductivity, featuring nanoscale superconducting islands in a metallic matrix[3,4]. Our measurements further reveal that this puddling is driven by gap filling, while the gap itself persists beyond the breakdown of superconductivity. The important implication is that it is not a diminishing pairing interaction that causes the breakdown of superconductivity. Unexpectedly, the measured gap-to-filling correlation also reveals that pair-breaking by disorder does not play a dominant role and that the mechanism of superconductivity in overdoped cuprate superconductors is qualitatively different from conventional mean-field theory

Taking One Step Back in Familial Hypercholesterolemia:STAP1 Does Not Alter Plasma LDL (Low-Density Lipoprotein) Cholesterol in Mice and Humans

International audienceSTAP1, encoding for STAP1 (signal transducing adaptor family member 1), has been reported as a candidate gene associated with familial hypercholesterolemia. Unlike established familial hypercholesterolemia genes, expression of STAP1 is absent in liver but mainly observed in immune cells. In this study, we set out to validate STAP1 as a familial hypercholesterolemia gene. Approach and Results: A whole-body Stap1 knockout mouse model (Stap1 -/ - ) was generated and characterized, without showing changes in plasma lipid levels compared with controls. In follow-up studies, bone marrow from Stap1 -/ - mice was transplanted to Ldlr -/ - mice, which did not show significant changes in plasma lipid levels or atherosclerotic lesions. To functionally assess whether STAP1 expression in B cells can affect hepatic function, HepG2 cells were cocultured with peripheral blood mononuclear cells isolated from heterozygotes carriers of STAP1 variants and controls. The peripheral blood mononuclear cells from STAP1 variant carriers and controls showed similar LDLR mRNA and protein levels. Also, LDL (low-density lipoprotein) uptake by HepG2 cells did not differ upon coculturing with peripheral blood mononuclear cells isolated from either STAP1 variant carriers or controls. In addition, plasma lipid profiles of 39 carriers and 71 family controls showed no differences in plasma LDL cholesterol, HDL (high-density lipoprotein) cholesterol, triglycerides, and lipoprotein(a) levels. Similarly, B-cell populations did not differ in a group of 10 STAP1 variant carriers and 10 age- and sex-matched controls. Furthermore, recent data from UK Biobank do not show association between STAP1 rare gene variants and LDL cholesterol