Karlsenbernard4283

Overall survival was 8.1 y (SIM), 4.8 y (PV), and 5.9 y (A, n.s.)). None of the SIM-recipients underwent re-transplantation, while the rate was 32% in the PV-group. The 8.1 y graft survival in SIM-recipients was significantly longer than in the other 2 groups, which were 3.3 y (PV) and 5.5 y (A, P=0.013). CONCLUSIONS Although SIM-reperfused recipients were the oldest and received grafts of inferior quality, these recipients showed superior results in terms of overall patient and graft survival. Multicentric randomized controlled trials with larger study populations are required to confirm this finding.BACKGROUND The multiple rapid swallows (MRS) test is used to assess esophageal contraction reserve. In this study, we characterized the expression of the MRS test in patients with reflux burden and other symptomatic phenotypes with refractory gastroesophageal reflux disease (rGERD). MATERIAL AND METHODS Patients with rGERD who underwent high-resolution manometry (HRM) and esophageal pH-impedance monitoring (EIM) between September 2018 and January 2020 were retrospectively studied. RESULTS We enrolled 151 patients and divided them into 4 phenotypes according to the results of EIM. In phenotype 1, the MRS distal contractile integral (DCI) was significantly positively correlated with acid-liquid reflux episodes. find more In phenotype 2, lower esophageal sphincter pressure (LES) length was significantly positively correlated with MRS DCI, and MRS/single-swallow (SS) DCI ratio. In phenotype 3, MRS DCI was negatively correlated with the DeMeester score, acid exposure time (AET), upright AET, long-term acid reflux episodes, acid-mixed reflux episodes, recumbent acid reflux episodes, and total acid reflux episodes. There was a significant negative correlation between MRS/SS DCI and recumbent acid reflux episodes. In phenotype 4, nonacid-liquid episodes and recumbent nonacid reflux episodes were significantly higher in the abnormal MRS group. However, acid-gas episodes, weakly acid-gas episodes, and upright gas reflux episodes were higher in the normal MRS group than in the abnormal MRS group. CONCLUSIONS Esophageal contraction reserve is heterogeneous within the reflux burden and symptomatic phenotypes of patients with rGERD.We study a systematic evolution of the topological properties of a Chern insulator upon smooth variation of a hopping parameter (t1) of the electrons among a pair of nearest neighbour sites on a honeycomb lattice, while keeping the other two hopping terms (t) fixed. In the absence of a Haldane flux, the tuning oft1results in gradual shifting of the Dirac cones which eventually merge into one at theMpoint in the Brillouin zone (BZ) att1= 2twith a gapless semi-Dirac dispersion at low energies. In the presence of a Haldane flux, the system becomes a Chern insulator fort1 2t. The Chern number phase diagram obtained via integrating the Berry curvature over the BZ shows a gradual shrinking of the 'topological' lobes, and vanishes just beyondt1= 2t, where a small but a finite Berry curvature still exists. Thus, there is a phase transition from a topological phase to a trivial phase across the semi-Dirac point (t1= 2t). The vanishing of the anomalous Hall conductivity plateau and the merger of the chiral edge states with the bulk bands near theMpoint provide robust support of the observed phase transition.Far-infrared rays (FIR) are known to have various effects on atoms and molecular structures within cells owing to their radiation and vibration frequencies. The present study examined the effects of FIR on gene expression related to glucose transport through microarray analysis in rat skeletal muscle cells, as well as on mitochondrial biogenesis, at high and low glucose conditions. FIR were emitted from a bio-active material coated fabric (BMCF). L6 cells were treated with 30% BMCF for 24 h in medium containing 25 or 5.5 mM glucose, and changes in the expression of glucose transporter genes were determined. The expression of GLUT3 (Slc2a3) increased 2.0-fold (p less then 0.05) under 5.5 mM glucose and 30% BMCF. In addition, mitochondrial oxygen consumption and membrane potential (ΔΨm) increased 1.5- and 3.4-fold (p less then 0.05 and p less then 0.001), respectively, but no significant change in expression of Pgc-1a, a regulator of mitochondrial biogenesis, was observed in 24 h. To analyze the relationship between GLUT3 expression and mitochondrial biogenesis under FIR, GLUT3 was down-modulated by siRNA for 72 h. As a result, the ΔΨm of the GLUT3 siRNA-treated cells increased 3.0-fold (p less then 0.001), whereas that of the control group increased 4.6-fold (p less then 0.001). Moreover, Pgc-1a expression increased upon 30% BMCF treatment for 72 h; an effect that was more pronounced in the presence of GLUT3. These results suggest that FIR may hold therapeutic potential for improving glucose metabolism and mitochondrial function in metabolic diseases associated with insufficient glucose supply, such as type 2 diabetes.Nicotinamide adenine dinucleotide phosphate oxidases (NOXs) are the major enzymatic source of reactive oxygen species (ROS). NOX2 and NOX4 are expressed in the heart but its role in hypoxia-induced atrial natriuretic peptide (ANP) secretion is unclear. This study investigated the effect of NOX on ANP secretion induced by hypoxia in isolated beating rat atria. The results showed that hypoxia significantly upregulated NOX4 but not NOX2 expression, which was completely abolished by endothelin-1 (ET-1) type A and B receptor antagonists BQ123 (0.3 µM) and BQ788 (0.3 µM). ET-1-upregulated NOX4 expression was also blocked by antagonists of secreted phospholipase A2 (sPLA2; varespladib, 5.0 µM) and cytosolic PLA2 (cPLA2; CAY10650, 120.0 nM), and ET-1-induced cPLA2 expression was inhibited by varespladib under normoxia. Moreover, hypoxia-increased ANP secretion was evidently attenuated by the NOX4 antagonist GLX351322 (35.0 µM) and inhibitor of ROS N-Acetyl-D-cysteine (NAC, 15.0 mM), and hypoxia-increased production of ROS was blocked by GLX351322. In addition, hypoxia markedly upregulated Src expression, which was blocked by ET receptors, NOX4, and ROS antagonists. ET-1-increased Src expression was also inhibited by NAC under normoxia. Furthermore, hypoxiaactivated extracellular signal-regulated kinase 1/2 (ERK1/2) and protein kinase B (Akt) were completely abolished by Src inhibitor 1 (1.0 µM), and hypoxia-increased GATA4 was inhibited by the ERK1/2 and Akt antagonists PD98059 (10.0 µM) and LY294002 (10.0 µM), respectively. However, hypoxia-induced ANP secretion was substantially inhibited by Src inhibitor. These results indicate that NOX4/Src modulated by ET-1 regulates ANP secretion by activating ERK1/2 and Akt/GATA4 signaling in isolated beating rat hypoxic atria.