Reversal of glyphosate inhibition of Sandersonia aurantiaca flower senescence with aromatic amino acids

Abstract Glyphosate (N-(phosphonomethyl) glycine) is a broad spectrum post-emergence herbicide. This herbicide inhibits the shikimate pathway enzyme EPSP synthase (5-enol pyruvylshikimate 3-phosphate synthase), thereby interfering with aromatic amino acid metabolism. During preliminary investigations with inhibitors of protein and amino acid biosynthesis, we noticed that vase solutions containing glyphosate altered the normal pattern of Sandersonia aurantiaca flower senescence. Further studies showed that although glyphosate (2 mM) was toxic to all green tissue on the flower stem, the senescence of mature flowers (no green tissue) was delayed. Glyphosate-treated flowers did not fade but stayed a bright orange colour and the compressive strength of the flowers was greater (the flowers were less wilted) than the control flowers that were held in water. Treatment of flowers with vase solutions of phenylalanine (2 mM) and tyrosine (2 mM) in the presence of glyphosate reversed the beneficial effect that glyphosate treatment had on flower senescence. The data indicate that a lack of aromatic amino acids may be the cause of delayed fading and wilting of glyphosate-treated sandersonia flowers

palmitoyltransferase homologues

oleracea: cloning broccoli LSD1, Bax inhibitor and serin

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