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    α β フホウワ エステル アヨビ ホウコウゾク ニトロ カゴウブツ ノ パラジウム ショクバイ ニヨル キンイツ カンゲン

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    Abstracts Aromatic nitro-compounds are not normally reduced by sodium borohydride in aqueous solution or alcoholic solution. The present paper described the use of dichlorobis(triphenylphosphine)palladium (II) as catalysts for this reaction. In a nitrogen atomosphere, nitrobenzene was smoothly reduced at 60℃ by sodium borohydride, using triphenylphosphine palladium complex as catalysts to aniline (63%) accompanied by a small amount of hydrazobenzene (3%). In the same conditions, both azoxybenzene and azobenzene were reduced to hydrazobenzene, benzylideneaniline gave benzylaniline (85%), and ethyl cinnamate was led to ethyl hydrocinnamate (75%).  芳香族ニトロ化合物とα,β不飽和酸のエステルは一般には水素化ホウ素ナトリウムにより,そのニトロ基および炭素-炭素二重結合は還元されない。触媒量のパラジウム錯体の存在で芳香族のニトロ基,α,β不飽和エステルの二重結合が水素化ホウ素ナトリウムによって還元されると云う結果がえられたことを報告する。ニトロベンゼソは窒素雰囲気下ジクロロービス(トリフエニルホスヒン)パラジウム(II)の存在で水素下ホウ素ナトリウムにより還元されアニリン(63%)とヒドラゾベソゼン(3%)を生ずる。アゾベンゼンおよびアゾオキシベンゼンは同一条件下でそれぞれヒドラゾベンゼソを生ずる。ベンジリデンアニリンはベンジルアニリンに桂皮酸エチルエステルは同様にヒドロ桂皮酸エチルエステルに還元された

    Empagliflozin in Patients with Chronic Kidney Disease

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    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
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