Effects of DDGS as a replacement for SBM in Boer grower rations

With the U.S. goat industry, up 211%, from 1.25 million head in 2002 to 2.64 million head in 2017, goat producers and the industry are looking for a new cost effective way of feeding. Other research projects have shown great results of feeding DDGS to sheep, but there is very limited data for goat producers to base recommendations for potential inclusion of DDGS in a goat diet. Thus, the objective of this experiment was to evaluate the efficacy of DDGS as a replacement for soybean meal(SBM) in a Boer goat diet. During this 47 day trial, 48 meat goat kids (approximately 70 d of age) were housed at the Kansas State University Sheep and Meat Goat Center with 3 goats per pen and 4 pens per treatment. The goats were separated into one of the four experimental diets: 1) 0% SBM replaced by DDGS; 2) 33% SBM replaced by DDGS; 3) 66% SBM replaced by DDGS; and 4) 100% SBM replaced by DDGS. All four diets were pelleted, which contained roughages, thus no supplemental forage was needed. Goats and feeders were weighed weekly to determine ADG, ADFI, and G:F. At the conclusion of the experiment, two goats out of each pen were taken to a USDA inspected facility to be slaughtered and to collect carcass data. All data was analyzed using the GLIMMIX procedure of SAS with pen serving as the experimental unit and 0.05 as the alpha value. In conclusion, the treatments did not affect(P>0.10) ADG or ADFI, but did impact (P>0.005) G:F. This was due to a linear improvement (P0.10) of DDGS on hot carcass weight, yield, loin eye area, or fat depth at the 13th rib. In summary, goats can be fed DDGS without detrimental growth or carcass effects

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