Cloning and Nucleotide Sequenceof the Genes Encoding Restriction-Modification System from Acidophilic Bacterium Acidocella facilis 22M

The gene encoding the Afa22MI restriction-modification system recognizing the sequence 5'-CGATCG-3' was cloned from Acidocella facilis 22M and sequenced. The cloned DNA fragment contained three genes encoding the Afa22MI methylase (M.Afa22MI) , the putative restriction endonuclease Afa22MI (R.Afa22MI) and a very short patch repair endonuclease (Afa22MI vsr) . M. Afa22MI gene has the conserved motifs of C5-cytosine methyltransferase. Afa22MI vsr gene was localized upstream of M. Afa22MI gene in opposite orientation, and an open reading frame of R. Afa22MI has about 53% sequence similarity to the amino acid sequence for the variable region of M.XorⅡ. Afa22MI vsr has about 66% sequence similarity to the amino acid sequence of XorII vsr which was associated M. XorII.CGATCGを認識する Afa22MI 制限修飾系遺伝子を好酸性細菌 Acidocella facilis 22M より、クローニングし、塩基配列を決定した。その結果、C5-シトシンメチラーゼに特徴的なモチーフが保存された。M.Afa22MI 遺伝子、その上流に、M.Afa22MI 遺伝子とは逆方向に、 very short patch repair endonuclease 様タンパク質遺伝子（Afa22MI vsr）、制限酵素（R.Afa22MI）遺伝子と推定されるオープンリーディングフレームが見出された。M.Afa22MI の推定アミノ酸配列は、Xanthomonas oryzae pv. oryzae 由来 M.XorII の配列と全体で約63%、veriable region 内で約53%の高い配列類似性を示した。また、Afa22MI usr の推定アミノ酸配列も、M.XorIIに付随する XorII vsr の配列と約66%の高い類似性を示した

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