PROGRAM AND NONPROGRAM WHEAT ACREAGE RESPONSES TO PRICES AND RISK

Wheat acreage responses to expected wheat price and price risk are reversed for program and nonprogram-planted acreage in the northern plains, central plains, southern plains, and U.S. Expected wheat price has a strong negative effect on program-complying wheat acreage. Government support prices have a positive effect on program-complying and program-planted acreage. Price risk has a positive effect on program-complying wheat acreage and a negative effect on nonprogram-planted acreage. Estimated price elasticities are higher than in studies where risk was ignored.Demand and Price Analysis, Risk and Uncertainty,

High-efficiency Bidirectional Buck-Boost Converter for Residential Energy Storage System

This paper proposes a bidirectional dc-dc converter for residential micro-grid applications. The proposed converter can operate over an input voltage range that overlaps the output voltage range. This converter uses two snubber capacitors to reduce the switch turn-off losses, a dc-blocking capacitor to reduce the input/output filter size, and a 1:1 transformer to reduce core loss. The windings of the transformer are connected in parallel and in reverse-coupled configuration to suppress magnetic flux swing in the core. Zero-voltage turn-on of the switch is achieved by operating the converter in discontinuous conduction mode. The experimental converter was designed to operate at a switching frequency of 40-210 kHz, an input voltage of 48 V, an output voltage of 36-60 V, and an output power of 50-500 W. The power conversion efficiency for boost conversion to 60 V was >= 98.3% in the entire power range. The efficiency for buck conversion to 36 V was >= 98.4% in the entire power range. The output voltage ripple at full load was <3.59 V-p.p for boost conversion (60 V) and 1.35 V-p.p for buck conversion (36 V) with the reduced input/output filter. The experimental results indicate that the proposed converter is well-suited to smart-grid energy storage systems that require high efficiency, small size, and overlapping input and output voltage ranges.11Ysciescopu

Activation of spleen tyrosine kinase is required for TNF-α-induced endothelin-1 upregulation in human aortic endothelial cells

AbstractEndothelin-1 (ET-1) promotes atherosclerosis. We tested whether spleen tyrosine kinase (Syk) mediates tumor necrosis factor-α (TNF-α)-induced ET-1 upregulation in human aortic endothelial cells (HAECs) and sought to identify the signal pathways involved. TNF-α-induced reactive oxygen species (ROS) activated Syk and phosphatidylinositol 3-kinase (PI3K), which was required for the activation of AP-1 and subsequent ET-1 gene transcription. ROS mediated c-Jun NH2-terminal kinase (JNK) is also required for AP-1 activation, but Syk and PI3K regulated AP-1 activation independently of JNK. Through regulation of ET-1 production, Syk could be implicated in atherosclerosis

Repeated Gene Transfection Impairs the Engraftment of Transplanted Porcine Neonatal Pancreatic Cells

BackgroundPreviously, we reported that neonatal porcine pancreatic cells transfected with hepatocyte growth factor (HGF) gene in an Epstein-Barr virus (EBV)-based plasmid (pEBVHGF) showed improved proliferation and differentiation compared to those of the control. In this study, we examined if pancreatic cells transfected repeatedly with pEBVHGF can be successfully grafted to control blood glucose in a diabetes mouse model.MethodsNeonatal porcine pancreatic cells were cultured as a monolayer and were transfected with pEBVHGF every other day for a total of three transfections. The transfected pancreatic cells were re-aggregated and transplanted into kidney capsules of diabetic nude mice or normal nude mice. Blood glucose level and body weight were measured every other day after transplantation. The engraftment of the transplanted cells and differentiation into beta cells were assessed using immunohistochemistry.ResultsRe-aggregation of the pancreatic cells before transplantation improved engraftment of the cells and facilitated neovascularization of the graft. Right before transplantation, pancreatic cells that were transfected with pEBVHGF and then re-aggregated showed ductal cell marker expression. However, ductal cells disappeared and the cells underwent fibrosis in a diabetes mouse model two to five weeks after transplantation; these mice also did not show controlled blood glucose levels. Furthermore, pancreatic cells transplanted into nude mice with normal blood glucose showed poor graft survival regardless of the type of transfected plasmid (pCEP4, pHGF, or pEBVHGF).ConclusionFor clinical application of transfected neonatal porcine pancreatic cells, further studies are required to develop methods of overcoming the damage for the cells caused by repeated transfection and to re-aggregate them into islet-like structures

PKCε-mediated ERK1/2 activation involved in radiation-induced cell death in NIH3T3 cells

AbstractProtein kinase C (PKC) isoforms play distinct roles in cellular functions. We have previously shown that ionizing radiation activates PKC isoforms (α, δ, ε, and ζ), however, isoform-specific sensitivities to radiation and its exact mechanisms in radiation mediated signal transduction are not fully understood. In this study, we showed that overexpression of PKC isoforms (α, δ, ε, and ζ) increased radiation-induced cell death in NIH3T3 cells and PKCε overexpression was predominantly responsible. In addition, PKCε overexpression increased ERK1/2 activation without altering other MAP-kinases such as p38 MAPK or JNK. Co-transfection of dominant negative PKCε (PKCε-KR) blocked both PKCε-mediated ERK1/2 activation and radiation-induced cell death, while catalytically active PKCε construction augmented these phenomena. When the PKCε overexpressed cells were pretreated with PD98059, MEK inhibitor, radiation-induced cell death was inhibited. Co-transfection of the cells with a mutant of ERK1 or -2 (ERK1-KR or ERK2-KR) also blocked these phenomena, and co-transfection with dominant negative Ras or Raf cDNA revealed that PKCε-mediated ERK1/2 activation was Ras–Raf-dependent. In conclusion, PKCε-mediated ERK1/2 activation was responsible for the radiation-induced cell death

Usefulness of fecal immunochemical test and fecal calprotectin for detection of active ulcerative colitis

Background/Aims Ulcerative colitis undergoes periods of exacerbation and remission. Fecal calprotectin levels increase with gut inflammation and correlate with endoscopic disease activity in ulcerative colitis. Intestinal blood loss and fecal immunochemical test levels also correlate with endoscopic disease activity. This study statistically evaluated the usefulness of fecal calprotectin, fecal immunochemical test, and C-reactive protein (CRP) as markers of disease activity. Methods A total 106 ulcerative colitis patients who underwent endoscopy and fecal calprotectin, fecal immunochemical test, and CRP testing, from March 2015 to August 2016, were retrospectively reviewed. Disease activity was assessed using a partial Mayo score and Mayo endoscopic score. The ability of fecal and serologic tests to reflect endoscopic disease severity was statistically evaluated. Results Among 106 patients, 68 underwent endoscopy and stool study within 2 weeks. In patients with mild to severe activity, fecal immunochemical test and fecal calprotectin were superior to CRP at Mayo endoscopic score detection rate. The area under the curves of fecal immunochemical test and fecal calprotectin for the detection of Mayo endoscopic score ≥1 were 0.956 and 0.942, respectively, and were superior to that of CRP (0.756). At Mayo endoscopic score, the effects of combination of fecal immunochemical test and CRP or fecal calprotectin and CRP were found to be higher than those of the independent fecal immunochemical test or fecal calprotectin. Conclusions Fecal immunochemical test and fecal calprotectin can effectively detect active ulcerative colitis better than remission. As these markers reflect the status of mucosal inflammation, they may reduce the requirement for invasive endoscopic examination

Antilipogenic and Anti-Inflammatory Activities of Codonopsis lanceolata in Mice Hepatic Tissues after Chronic Ethanol Feeding

This study evaluated the antilipogenic and anti-inflammatory effects of Codonopsis lanceolata (C. lanceolata) root extract in mice with alcohol-induced fatty liver and elucidated its underlying molecular mechanisms. Ethanol was introduced into the liquid diet by mixing it with distilled water at 5% (wt/v), providing 36% of the energy, for nine weeks. Among the three different fractions prepared from the C. lanceolata root, the C. lanceolata methanol extract (CME) exhibited the most remarkable attenuation of alcohol-induced fatty liver with respect to various parameters such as hepatic free fatty acid concentration, body weight loss, and hepatic accumulations of triglyceride and cholesterol. The hepatic gene and protein expression levels were analysed via RT-PCR and Western blotting, respectively. CME feeding significantly restored the ethanol-induced downregulation of the adiponectin receptor (adipoR) 1 and of adipoR2, along with their downstream molecules. Furthermore, the study data showed that CME feeding dramatically reversed ethanol-induced hepatic upregulation of toll-like receptor- (TLR-) mediated signaling cascade molecules. These results indicate that the beneficial effects of CME against alcoholic fatty livers of mice appear to be with adenosine- and adiponectin-mediated regulation of hepatic steatosis and TLR-mediated modulation of hepatic proinflammatory responses