Energy losses of solar neutrinos and the oscillation hypothesis

A formula for the stopping power of neutrinos interacting via the standard weak-interaction model, but incorporating the possibility of neutrino oscillations among the three flavors, is derived. The results are applied to study the solar-neutrino anomaly and it is found that the anomaly cannot be accounted for by many orders of magnitude from consideration of the energy losses of the neutrinos interacting with the solar matter, even if the oscillation hypothesis is found to be valid

Array-based high-throughput DNA markers for crop improvement

The last two decades have witnessed a remarkable activity in the development and use of molecular markers both in animal and plant systems. This activity started with low-throughput restriction fragment length polymorphisms and culminated in recent years with single nucleotide polymorphisms (SNPs), which are abundant and uniformly distributed. Although the latter became the markers of choice for many, their discovery needed previous sequence information. However, with the availability of microarrays, SNP platforms have been developed, which allow genotyping of thousands of markers in parallel. Besides SNPs, some other novel marker systems, including single feature polymorphisms, diversity array technology and restriction site-associated DNA markers, have also been developed, where array-based assays have been utilized to provide for the desired ultra-high throughput and low cost. These microarray-based markers are the markers of choice for the future and are already being used for construction of high-density maps, quantitative trait loci (QTL) mapping (including expression QTLs) and genetic diversity analysis with a limited expense in terms of time and money. In this study, we briefly describe the characteristics of these array-based marker systems and review the work that has already been done involving development and use of these markers, not only in simple eukaryotes like yeast, but also in a variety of seed plants with simple or complex genomes

Shell correction for the stopping power of K electrons

In view of the inapplicability of the asymptotic expressions for the stopping number available in the literature at high energies, an alternative approach is taken to compute the shell correction to the stopping number of K electrons. Anholt\u27s formula (1979) for the K-shell ionization has been used to calculate the excitation function for longitudinal interaction and numerical integration over energy has been carried out to evaluate the shell correction. Comparison with other theoretical calculations is made. It is proposed that, with the inclusion of relativistic effects, an asymptotic expansion of the stopping number with a leading-term logarithmic in the energy of the incident particle would be more meaningful and might enable one to extract the relativistic contribution to the shell correction from it

Parity-violating asymmetry in γd→n⃗p\gamma d \to \vec{n}p with a pionless effective theory

Nuclear parity violation is studied with polarized neutrons in the photodisintegration of the deuteron at low energies. A pionless effective field theory with di-baryon fields is used for the investigation. Hadronic weak interactions are treated by parity-violating di-baryon-nucleon-nucleon vertices, which have undetermined coupling contants. A parity-violating asymmetry in the process is calculated for the incident photon energy up to 30 MeV. If experimental data for the parity-violating asymmetry become available in the future, we will be able to determine the unknown coupling contants in the parity-violating vertices.Comment: 4 pages. A contribution to APFB2011, August 22-26, 2011, Seoul, Kore

Beta-blockers have no impact on survival in pancreatic ductal adenocarcinoma prior to cancer diagnosis

Previous studies have suggested that β-adrenergic signaling may regulate the growth of various cancers. The aim of our study is to investigate the association between the incidental use of beta-blockers for various conditions on the overall survival of patients with pancreatic ductal adenocarcinoma (PDAC). Patients with histologically-confirmed PDAC between 2007 and 2011 were extracted from Surveillance, Epidemiology, and End Results registry (SEER)-Medicare linked database. Kaplan Meier and multivariable Cox Proportional-Hazard models were used to examine the association between beta-blocker usage before diagnosis and overall survival adjusting for appropriate confounders. As an additional analysis we also examined continuous beta-blocker use before and after diagnosis. From 2007 to 2011, 13,731 patients were diagnosed with PDAC. Of these, 7130 patients had Medicare Part D coverage in the 6-month period before diagnosis, with 2564 (36%) of these patients using beta-blockers in this period. Patients receiving beta-blockers had a mean survival time of 5.1 months compared to 6 months for non-users (p < 0.01). In multivariable analysis, beta-blockers usage was not associated with improved survival (Hazard Ratio (HR) 1.04, 95%, Confidence Interval (CI) 0.98–1.1, p = 0.2). When patients were stratified by conditions with indications for beta-blocker usage, such as hypertension, coronary artery disease and cardiac arrhythmia, differences in survival were insignificant compared to non-users in all groups (p > 0.05). After stratification by receptor selectivity, this lack of association with survival persisted (p > 0.05 for all). As a subgroup analysis, looking at patients with continuous Medicare Part D coverage who used beta-blockers in the 6-month period before and after cancer diagnosis, we identified 7085 patients, of which 1750 (24.7%) had continuous beta blocker use. In multivariable analysis, continuous beta-blockers usage was associated with improved survival (Hazard Ratio (HR) 0.86, 95%, Confidence Interval (CI) 0.8–0.9, p < 0.01). Beta-blocker usage before diagnosis does not confer a survival advantage in patients with PDAC, though continuous use before and after diagnosis did confer a survival advantage. Prospective studies into the mechanism for this advantage are needed

Comparative Lipidomic Analysis Reveals Heat Stress Responses of Two Soybean Genotypes Differing in Temperature Sensitivity

Heat-induced changes in lipidome and their influence on stress adaptation are not well-defined in plants. We investigated if lipid metabolic changes contribute to differences in heat stress responses in a heat-tolerant soybean genotype DS25-1 and a heat-susceptible soybean genotype DT97-4290. Both genotypes were grown at optimal temperatures (OT; 30/20 °C) for 15 days. Subsequently, half of the plants were exposed to heat stress (38/28 °C) for 11 days, and the rest were kept at OT. Leaf samples were collected for lipid and RNA extractions on the 9th and 11th days of stress, respectively. We observed a decline in the lipid unsaturation level due to a decrease in the polyunsaturated linolenic acid (18:3) content in DS25-1. When examined under OT conditions, DS25-1 and DT97-4290 showed no significant differences in the expression pattern of the Fatty Acid Desaturase (FAD) 2-1A, FAD2-2B, FAD2-2C, FAD3A genes. Under heat stress conditions, substantial reductions in the expression levels of the FAD3A and FAD3B genes, which convert 18:2 lipids to 18:3, were observed in DS25-1. Our results suggest that decrease in levels of lipids containing 18:3 acyl chains under heat stress in DS25-1 is a likely consequence of reduced FAD3A and FAD3B expression, and the decrease in 18:3 contributes to DS25-1′s maintenance of membrane functionality and heat tolerance

Deuteron Photodissociation in Ultraperipheral Relativistic Heavy-Ion on Deuteron Collisions

In ultraperipheral relativistic deuteron on heavy-ion collisions, a photon emitted from the heavy nucleus may dissociate the deuterium ion. We find deuterium breakup cross sections of 1.38 barns for deuterium-gold collisions at a center of mass energy of 200 GeV per nucleon, as studied at the Relativistic Heavy Ion Collider, and 2.49 barns for deuterium-lead collisions at a center of mass energy of 6.2 TeV, as proposed for the Large Hadron Collider. This cross section includes an energy-independent 140 mb contribution from hadronic diffractive dissociation. At the LHC, the cross section is as large as that of hadronic interactions. The estimated error is 5%. Deuteron dissociation could be used as a luminosity monitor and a `tag' for moderate impact parameter collisions.Comment: Final version, to appear in Phys. Rev. C. Diffractive dissociation included 10 pages with 3 figure

Adverse Reactions to Wheat or Wheat Components

Wheat is an important staple food globally, providing a significant contribution to daily energy, fiber, and micronutrient intake. Observational evidence for health impacts of consuming more whole grains, among which wheat is a major contributor, points to significant risk reduction for diabetes, cardiovascular disease, and colon cancer. However, specific wheat components may also elicit adverse physical reactions in susceptible individuals such as celiac disease (CD) and wheat allergy (WA). Recently, broad coverage in the popular and social media has suggested that wheat consumption leads to a wide range of adverse health effects. This has motivated many consumers to avoid or reduce their consumption of foods that contain wheat/gluten, despite the absence of diagnosed CD or WA, raising questions about underlying mechanisms and possible nocebo effects. However, recent studies did show that some individuals may suffer from adverse reactions in absence of CD and WA. This condition is called non-celiac gluten sensitivity (NCGS) or non-celiac wheat sensitivity (NCWS). In addition to gluten, wheat and derived products contain many other components which may trigger symptoms, including inhibitors of α-amylase and trypsin (ATIs), lectins, and rapidly fermentable carbohydrates (FODMAPs). Furthermore, the way in which foods are being processed, such as the use of yeast or sourdough fermentation, fermentation time and baking conditions, may also affect the presence and bioactivity of these components. The present review systematically describes the characteristics of wheat-related intolerances, including their etiology, prevalence, the components responsible, diagnosis, and strategies to reduce adverse reactions

K-ras Mutation Targeted to Gastric Tissue Progenitor Cells Results in Chronic Inflammation, an Altered Microenvironment, and Progression to Intraepithelial

Chronic infectious diseases, such as Helicobacter pylori infection, can promote cancer in a large part through induction of chronic inflammation. Oncogenic K-ras mutation in epithelial cells activates inflammatory pathways, which could compensate for a lack of infectious stimulus. Gastric histopathology and putative progenitor markers [doublecortin and calcium/calmodulin-dependent protein kinase-like 1 (Dcamkl1) and keratin 19 (K19)] in K19-K-ras-V12 (K19-kras) transgenic mice were assessed at 3, 6, 12, and 18 months of age, in comparison with Helicobacter felis–infected wild-type littermates. Inflammation was evaluated by reverse transcription–PCR of proinflammatory cytokines, and K19-kras mice were transplanted with green fluorescent protein (GFP)–labeled bone marrow. Both H. felis infection and K-ras mutation induced upregulation of proinflammatory cytokines, expansion of Dcamkl1+ cells, and progression to oxyntic atrophy, metaplasia, hyperplasia, and high-grade dysplasia. K19-kras transgenic mice uniquely displayed mucous metaplasia as early as 3 months and progressed to high-grade dysplasia and invasive intramucosal carcinoma by 20 months. In bone marrow–transplanted K19-kras mice that progressed to dysplasia, a large proportion of stromal cells were GFP+ and bone marrow–derived, but only rare GFP+ epithelial cells were observed. GFP+ bone marrow–derived cells included leukocytes and CD45− stromal cells that expressed vimentin or α smooth muscle actin and were often found surrounding clusters of Dcamkl1+ cells at the base of gastric glands. In conclusion, the expression of mutant K-ras in K19+ gastric epithelial cells can induce chronic inflammation and promote the development of dysplasia.National Institutes of Health (U.S.) (Grant NIH 5R01 CA120979-02)National Institutes of Health (U.S.) (Grant R01 DK060694)National Institutes of Health (U.S.) (Grant U01 CA143056)National Institutes of Health (U.S.) (Grant P30 DK050306)Uehara Memorial Foundatio