Objective: We evaluated the effects of sheath injury and trimetazidine (TMZ) on endothelial dysfunction of the radial artery (RA) after transradial coronary artery angiography (TRCAG) or transradial percutaneous coronary intervention (TRPCI) with flow-mediated dilation (FMD). Methods: One hundred twenty patients who underwent TRCAG or TRPCI with either a long 5Fr or 6Fr sheath were randomly assigned to the TMZ group or the control group. Baseline, postsheath injury (<24 hours after sheath injury), and 10-week FMDs were performed. Results: In all cannulated RAs, the postsheath injury FMDs were significantly lower than the baseline FMDs (P < 0.01). In the control group, the 10-week FMD was significantly lower than the baseline FMD, but no difference was found in the TMZ group (10.4 ± 3.4% vs. 6.3 ± 2.9%, P < 0.01 and 10.1 ± 3.6% vs. 9.2 ± 3.6%, P = 0.09, respectively). Repeated measures ANOVA revealed significant differences in FMD between the TMZ group and the control group (F = 9.87, P < 0.01). Including coronary artery disease, heparin dose during procedure, sheath size, sheath-RA size ratio, sheath indwelling time in RA, RA spasm, repeated RA sheath injury (upsizing from 5Fr to 6Fr), and TMZ use, the multivariate analysis showed that repeated RA sheath injury and TMZ use (OR 7.40, 95% CI 1.42-38.53, P < 0.05, and OR 0.08, 95% CI 0.02-0.30, P < 0.01, respectively) were independent predictors of the decrement of FMD > 50%(ΔFMDbaseline - 10 week > 50%). Conclusion: Repeated sheath injury negatively influences endothelial recovery after long 6Fr sheath injury to the RA, and TMZ lessens endothelial dysfunction of the RA after radial catheterization.(J Interven Cardiol 2012;**:1-7).

The role of serine palmitoyltransferase (SPT) and de novo ceramide biosynthesis in cardiac ceramide and sphingomyelin metabolism is unclear. To determine whether the de novo synthetic pathways, rather than ceramide uptake from circulating lipoproteins, is important for heart ceramide levels, we created cardiomyocyte-specific deficiency of Sptlc2, a subunit of SPT. Heart-specific Sptlc2 deficient (hSptlc2 KO) mice had a >35% reduction in ceramide, which was limited to C18:0 and very long chain ceramides. Sphingomylinase expression, and levels of sphingomyelin and diacylglycerol were unchanged. But surprisingly phospholipids and acyl CoAs contained increased saturated long chain fatty acids. hSptlc2 KO mice had decreased fractional shortening and thinning of the cardiac wall. While the genes regulating glucose and fatty acid metabolism were not changed, expression of cardiac failure markers and the genes involved in the formation of extracellular matrices were upregulated in hSptlc2 KO hearts. In addition, ER-stress markers were upregulated leading to increased apoptosis. These results suggest that Sptlc2-mediated de novo ceramide synthesis is an essential source of C18:0 and very long chain, but not of shorter chain, ceramides in the heart. Changes in heart lipids other than ceramide levels lead to cardiac toxicity.

This study is aimed at evaluating 1-year clinical outcomes and their predictors in patients with unprotected left main coronary artery (ULMCA)-related acute myocardial infarction (AMI). In total 248 patients diagnosed with AMI involving the ULMCA as the culprit vessel and registered in the Korean Acute Myocardial Infarction database were enrolled in this study. Patients were divided according to the absence (shock-, n = 206) or presence (shock+, n = 42) of cardiogenic shock at initial presentation. Independent risk factors of in-hospital cardiac death associated with ULMCA-related AMI were elucidated by multivariate regression analysis. In-hospital mortality rates were 8.7% in the shock- group and 47.6% in the shock+ group (p = 0.001). During 1-year follow-up after discharge, major adverse cardiac events developed in 16.3% of patients in the shock- group and 18.2% of patients in the shock+ group (p = 0.828); cardiac death, MI, and ischemia-driven target vessel revascularization were similar between the 2 groups at 1 year. On multivariate analysis, initial shock presentation (odds ratio 8.9, confidence interval 4.1 to 19.2, p = 0.004) and left ventricular ejection fraction <30%(odds ratio 7.6, confidence interval 2.7 to 21.1, p = 0.001) were independent risk factors of in-hospital cardiac death associated with ULMCA-related AMI. In conclusion, almost 1/2 of patients with ULMCA-related AMI presenting with cardiogenic shock had a fatal in-hospital outcome compared to <10% of those without cardiogenic shock; however, clinical outcomes after survival of the in-hospital period were not different between these groups.

The yield of charged particles associated with high-p_{t} trigger particles (8<p_{t}<15  GeV/c) is measured with the ALICE detector in Pb-Pb collisions at sqrt[s_{NN}]=2.76  TeV relative to proton-proton collisions at the same energy. The conditional per-trigger yields are extracted from the narrow jetlike correlation peaks in azimuthal dihadron correlations. In the 5% most central collisions, we observe that the yield of associated charged particles with transverse momenta p_{t}>3  GeV/c on the away side drops to about 60% of that observed in pp collisions, while on the near side a moderate enhancement of 20%-30% is found.

The ALICE Collaboration has studied J/ψ production in pp collisions at sqrt[s]=7  TeV at the LHC through its muon pair decay. The polar and azimuthal angle distributions of the decay muons were measured, and results on the J/ψ polarization parameters λ_{θ} and λ_{ϕ} were obtained. The study was performed in the kinematic region 2.5<y<4, 2<p_{t}<8  GeV/c, in the helicity and Collins-Soper reference frames. In both frames, the polarization parameters are compatible with zero, within uncertainties.

ABSTRACT: BACKGROUND: The rice roots are highly salt-sensitive organ and primary root growth is rapidly suppressed by salt stress. Sucrose nonfermenting 1-related protein kinase2 (SnRK2) family is one of the key regulator of hyper-osmotic stress signalling in various plant cells. To understand early salt response of rice roots and identify SnRK2 signaling components, proteome changes of transgenic rice roots over-expressing OSRK1, a rice SnRK2 kinase were investigated. RESULTS: Proteomes were analyzed by two-dimensional electrophoresis and protein spots were identified by LC-MS/MS from wild type and OSRK1 transgenic rice roots exposed to 150 mM NaCl for either 3 h or 7 h. Fifty two early salt -responsive protein spots were identified from wild type rice roots. The major up-regulated proteins were enzymes related to energy regulation, amino acid metabolism, methylglyoxal detoxification, redox regulation and protein turnover. It is noted that enzymes known to be involved in GA-induced root growth such as fructose bisphosphate aldolase and methylmalonate semialdehyde dehydrogenase were clearly down-regulated. In contrast to wild type rice roots, only a few proteins were changed by salt stress in OSRK1 transgenic rice roots. A comparative quantitative analysis of the proteome level indicated that forty three early salt-responsive proteins were magnified in transgenic rice roots at unstressed condition. These proteins contain single or multiple potential SnRK2 recognition motives. In vitro kinase assay revealed that one of the identified proteome, calreticulin is a good substrate of OSRK1. CONCLUSIONS: Our present data implicate that rice roots rapidly changed broad spectrum of energy metabolism upon challenging salt stress, and suppression of GA signaling by salt stress may be responsible for the rapid arrest of root growth and development. The broad spectrum of functional categories of proteins affected by over-expression of OSRK1 indicates that OSRK1 is an upstream regulator of stress signaling in rice roots. Enzymes involved in glycolysis, branched amino acid catabolism, dnaK-type molecular chaperone, calcium binding protein, Sal T and glyoxalase are potential targets of OSRK1 in rice roots under salt stress that need to be further investigated.

Protein kinase C (PKC)-interacting cousin of thioredoxin (PICOT) has distinct anti-hypertrophic and inotropic functions. We have previously shown that PICOT exerts its anti-hypertrophic effect by inhibiting calcineurin-NFAT signaling through its C-terminal glutaredoxin domain. However, the mechanism underlying the inotropic effect of PICOT is unknown. The results of protein pull-down experiments showed that PICOT directly binds to the catalytic domain of PKCζ through its N-terminal thioredoxin-like domain. Purified PICOT protein inhibited the kinase activity of PKCζ in vitro, which indicated that PICOT is an endogenous inhibitor of PKCζ. The inhibition of PKCζ activity with a PKCζ-specific pseudosubstrate peptide inhibitor was sufficient to increase the cardiac contractility in vitro and ex vivo. Overexpression of PICOT or inhibition of PKCζ activity down-regulated PKCα activity, which led to the elevation of sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) 2a activity, concomitant with the increased phosphorylation of phospholamban (PLB). Overexpression of PICOT or inhibition of PKCζ activity also down-regulated protein phosphatase (PP) 2A activity, which subsequently resulted in the increased phosphorylation of troponin (Tn) I and T, key myofilament proteins associated with the regulation of contractility. PICOT appeared to inhibit PP2A activity through the disruption of the functional PKCζ/PP2A complex. In contrast to the overexpression of PICOT or inhibition of PKCζ, reduced PICOT expression resulted in up-regulation of PKCα and PP2A activities, followed by decreased phosphorylation of PLB, and TnI and T, respectively, supporting the physiological relevance of these events. Transgene- or adeno-associated virus (AAV)-mediated overexpression of PICOT restored the impaired contractility and prevented further morphological and functional deterioration of the failing hearts. Taken together, the results of the present study suggest that PICOT exerts its inotropic effect by negatively regulating PKCα and PP2A activities through the inhibition of PKCζ activity. This finding provides a novel insight into the regulation of cardiac contractility.

Leucine-rich glioma inactivated 3 (LGI3) is a secreted protein and a member of LGI/epitempin family. We previously showed that LGI3 was highly expressed in brain and played regulatory roles in neuronal exocytosis and differentiation. Beside the nervous system, LGI3 was shown to be expressed in diverse tissues. In this study, we found that LGI3 and its receptor candidate ADAM23 were expressed in adipose tissues and 3T3-L1 cells. 3T3-L1 preadipocytes secreted a 60-kDa protein, a major secreted form of LGI3, which declined with adipocyte differentiation. LGI3 was also expressed in adipose tissue macrophages in the ob/ob mice and in macrophage cell line. The 60-kDa LGI3 protein was selectively increased in the ob/ob adipose tissues comparing with the lean mice. Pull-down experiments, coimmunoprecipitation and immunocytochemistry indicated that LGI3 associated with ADAM23 in adipose tissues and 3T3-L1 cells. Knockdown of LGI3 or ADAM23 by siRNA increased adipogenesis in 3T3-L1 cells. Treatment with LGI3 protein did not affect preadipocyte proliferation but attenuated adipogenesis and this effect was reversed by siRNA-mediated knockdown of ADAM23. Taken together, we propose that LGI3 may be a candidate adipokine that is perturbed in obesity and suppresses adipogenesis through its receptor, ADAM23.

BACKGROUND AND PURPOSE: While performing respiratory training, an elastic chest band has great benefits for clinical use due to its safety and easy application. However, to our knowledge, there is no published data on the clinical use of an elastic chest band into inspiratory training for people with limited rib mobility. This study aimed to investigate the effects of an elastic chest band integrated into inspiratory exercise for people with decreased chest function. METHOD: Sixteen subjects with limited rib mobility were randomly assigned to either experimental group (EG) or control group (CG), with eight subjects in each group. All subjects received an inspiratory exercise using incentive spirometer for 30 minutes. For the subjects of the EG, an elastic chest band was incorporated into the inspiratory exercises to provide compressive resistance to the chest. The chest function was measured using an electronic spirometer to determine the vital capacity (VC), tidal volume (TV), inspiratory reserve volume (IRV), expiratory reserve volume, forced vital capacity (FVC), forced expiratory volume (FEV), FEV in 1-second (FEV(1)) and the ratio of FEV(1) to FVC (FEV(1)%). RESULTS: Significant differences were found for the VC, TV, IRV, FVC and FEV(1) between pre-test and post-test in the two groups (p < 0.05). Further, the changes in the values of VC (0.47 L vs. 0.22 L), FVC (0.55 L vs. 0.25 L) and FEV(1)(0.65% vs. 0.21%) in the EG subjects were significantly greater than those in the CG subjects (p < 0.05). CONCLUSIONS: These findings suggest that an elastic chest band combined with inspiratory exercise produces additional positive effect on improving chest function in people with limited rib mobility. Copyright © 2012 John Wiley & Sons, Ltd.

The objective of this study was to find optimum microwave pretreatment conditions for methane production and methane yield in anaerobic sludge digestion. The sludge was pretreated using a laboratory-scale industrial microwave unit (2450 MHz frequency). Microwave temperature increase rate (TIR)(2.9-17.1 degrees C/min) and final temperature (FT)(52-108 degrees C) significantly affected solubilization, methane production, and methane yield. Solubilization degree (soluble chemical oxygen demand (COD)/total COD) in the pretreated sludge (3.3-14.7%) was clearly higher than that in the raw sludge (2.6%). Within the design boundaries, the optimum conditions for maximum methane production (2.02 L/L) were TIR = 9.1 degrees C/min and FT = 90 degrees C, and the optimum conditions for maximum methane yield (809 mL/g VS(removed)) were TIR 7.1 degrees C/min and FT = 92 degrees C.