Inquiries into Wheat Streak Mosaic Virus and Other WSM Associated Viruses

Wheat Streak Mosaic WSM) is a complex disease found to cause severe impact on wheat yield. Wheat streak mosaic virus (WSMV Triticum Mosaic Virus (TMV) and Wheat Mosaic Virus (WMOV) are all transmitted by Aceria tosichella, the wheat cun mite, and have been reported as the viruses associated with WSM. There is a research project on the genetic composition of the associated viruses as well as determining any novel viruses that may be involved in the disease. The process has begun with the virus assessment of neid samples by RT-PCR and sanger Sequencing in a different study, the potential of a common Insect in wheat fields. Rhopalosiphum padi, the Bird cherry oat aphid, to be a vector for WSMV was Investigated. R. Daar was found to be not a vector of WSMV through RT-PCR. The other proiect screened some wid-relative wheat plants for WSMV resistance Various lines of Aeglos tauschii, a landrace wheat, were tested for viral resistance by assessing the viral copy number by RT-PCR. The Initial result has demonstrated that one of the four selected lines may have promising tolerance The preliminary tests performed for each Inquiry provides Insight to Improving the respective experiment design for further understanding of how concerned parties such as farmers may better combat the disease

PIECE OF PI: NOVEL GENETICS FOR SNOW MOLD TOLERANCE IN PI 173438

Winter wheat is an economically significant commodity in the Pacific Northwest (PNW) and one of the few crops whose yields are impacted by snow mold, a fungal disease with multiple causal agents. To date, cultural controls and tolerant varieties have remained the best methods to manage the disease. However, since initial breeding efforts began in the 1940s, genetic diversity for snow mold tolerance has remained limited in local varieties. The winter wheat landrace PI 173438 has been evaluated for snow mold tolerance in the PNW but has not yet been used in local breeding programs. This project investigated PI 173438 for novel quantitative trait loci (QTL) associated with snow mold tolerance and recovery using a doubled haploid mapping population developed from a cross between PI 173438 and a susceptible Washington State University breeding line WA 8137. In the QTL analysis using linkage mapping, six QTL were found in association with snow mold tolerance traits, with five of the QTL originating from PI 173438. A QTL was found on chromosome 1D that has not been reported before. The remaining QTL occurred on chromosomes that were previously reported to have snow mold tolerant QTL, some of which may be identical. Several of the linked markers to these QTL were suitable for testing via marker-assisted selection using a KASP assay on two separate, but related populations. This revealed no significant differences amongst the three or four QTL that could be tested. Such results continue to indicate the complexity of snow mold tolerance and breeding for this trait using molecular markers. PI 173438 has also been found to have resistance to other diseases and may possess other useful genetics for future studies of other biotic stresses or economically important traits. The PI 173438/WA 8137 doubled haploid mapping population was characterized and submitted to the NLGRP to aid in future research

Empagliflozin in Patients with Chronic Kidney Disease

Background The effects of empagliflozin in patients with chronic kidney disease who are at risk for disease progression are not well understood. The EMPA-KIDNEY trial was designed to assess the effects of treatment with empagliflozin in a broad range of such patients. Methods We enrolled patients with chronic kidney disease who had an estimated glomerular filtration rate (eGFR) of at least 20 but less than 45 ml per minute per 1.73 m(2) of body-surface area, or who had an eGFR of at least 45 but less than 90 ml per minute per 1.73 m(2) with a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of at least 200. Patients were randomly assigned to receive empagliflozin (10 mg once daily) or matching placebo. The primary outcome was a composite of progression of kidney disease (defined as end-stage kidney disease, a sustained decrease in eGFR to < 10 ml per minute per 1.73 m(2), a sustained decrease in eGFR of & GE;40% from baseline, or death from renal causes) or death from cardiovascular causes. Results A total of 6609 patients underwent randomization. During a median of 2.0 years of follow-up, progression of kidney disease or death from cardiovascular causes occurred in 432 of 3304 patients (13.1%) in the empagliflozin group and in 558 of 3305 patients (16.9%) in the placebo group (hazard ratio, 0.72; 95% confidence interval [CI], 0.64 to 0.82; P < 0.001). Results were consistent among patients with or without diabetes and across subgroups defined according to eGFR ranges. The rate of hospitalization from any cause was lower in the empagliflozin group than in the placebo group (hazard ratio, 0.86; 95% CI, 0.78 to 0.95; P=0.003), but there were no significant between-group differences with respect to the composite outcome of hospitalization for heart failure or death from cardiovascular causes (which occurred in 4.0% in the empagliflozin group and 4.6% in the placebo group) or death from any cause (in 4.5% and 5.1%, respectively). The rates of serious adverse events were similar in the two groups. Conclusions Among a wide range of patients with chronic kidney disease who were at risk for disease progression, empagliflozin therapy led to a lower risk of progression of kidney disease or death from cardiovascular causes than placebo