BackgroundCurry, one of the most popular foods in Japan, contains spices that are rich in potentially antioxidative compounds, such as curcumin and eugenol. Oxidative stress is thought to impair endothelial function associated with atherosclerosis, a leading cause of cardiovascular events. The aim of this study was to determine whether a single consumption of curry meal would improve endothelial function in healthy men.MethodsFourteen healthy male subjects (BMI 23.7 ± 2.7 kg/m2; age 45 ± 9 years) were given a single serving of curry meal or spice-free control meal (180 g of curry or control and 200 g of cooked rice; approximately 500 kcal in total) in a randomized, controlled crossover design. Before and 1 hr after the consumption, fasting and postprandial flow-mediated vasodilation (FMD) responses and other parameters were measured.ResultsThe consumption of the control meal decreased FMD from 5.8 ± 2.4% to 5.1 ± 2.3% (P = 0.039). On the other hand, the consumption of the curry meal increased FMD from 5.2 ± 2.5% to 6.6 ± 2.0% (P = 0.001), and the postprandial FMD after the curry meal was higher than that after the control meal (P = 0.002). Presence of spices in the curry did not alter significantly the systemic and forearm hemodynamics, or any biochemical parameters including oxidative stress markers measured.ConclusionsThese findings suggest that the consumption of curry ameliorates postprandial endothelial function in healthy male subjects and may be beneficial for improving cardiovascular health.Trial registrationUMIN Clinical Trials Registry 000012012.

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Background The aim of this study was to evaluate protective effects of endurance exercise training against diabetic kidney disease (DKD) with muscle weakness by using male spontaneously diabetic Torii (SDT) fatty rats as type 2 diabetic animal models with obesity, hypertension, and hyperlipidemia. Methods Eight-week-old SDT fatty rats (n = 12) and Sprague–Dawley (SD) rats (n = 10) were randomly divided into exercise (Ex; SDT-Ex: n = 6, SD-Ex: n = 5) and sedentary groups (SDT-Cont: n = 6, SD-Cont: n = 5), respectively. Each group underwent regular treadmill exercise four times a week from ages 8 to 16 weeks. Results The exercise attenuated hypertension and hyperlipidemia and prevented increases in renal parameter levels without affecting blood glucose levels. In the SDT fatty rats, it prevented induction of renal morphological abnormalities in the interstitium of the superficial and intermediate layers of the cortex. Downregulated expression of endothelial nitric oxide synthase in the glomerulus of the SDT fatty rats was significantly upregulated by the exercise. The exercise upregulated the renal expressions of both medium-chain acyl-CoA dehydrogenase and peroxisome proliferator-activated receptor γ coactivator-1α related to fatty acid metabolism. It increased muscle strength and both muscle weight and cross-sectional area of type IIb muscle fibers in the extensor digitorum longus muscle in the SDT fatty rats. Conclusion Endurance exercise training in type 2 diabetes ameliorates DKD by improving endothelial abnormality and enhancing fatty acid metabolism in addition to attenuated hypertension, hyperlipidemia, and muscle weakness independently of blood glucose levels.

Oxaliplatin, a third-generation platinum agent, has been used for the treatment of colon, pancreatic, and stomach cancers in recent years. It carries a reduced risk of acute kidney injury (AKI) compared to the previous platinum agents, including cisplatin and carboplatin. Several cases of oxaliplatin-induced acute tubular necrosis (ATN) have been reported; however, only one case has been reported as acute tubulointerstitial nephritis (ATIN) histopathologically. Here, we present a case of biopsy-proven and dialysis-dependent ATIN, which dramatically resolved with steroid therapy. The patient was a 67-yearold male who had undergone chemotherapy for colon adenocarcinoma. He suddenly developed shaking chills, fever, and hot flashes at the end of the 18th 5-fluorouracil (5-FU)/l-leucovorin/oxaliplatin administration, and was admitted to our hospital. On the 4th day of hospitalization, severe renal dysfunction (creatinine 6.5 mg/dL) was observed. As oliguria continued, we initiated hemodialysis therapy on the 6th day of hospitalization. Drug-induced ATIN was strongly suspected due to the history of multiple exposures to oxaliplatin with allergic reaction and sterile pyuria. We began steroid therapy on the 8th day of hospitalization. Subsequently, renal biopsy was performed and the diagnosis of ATIN was made. The patient's renal function gradually improved, and 6 months later, it had returned to baseline. Our case demonstrates that we should consider not only ATN, but also ATIN, as potential presentations of oxaliplatin-induced AKI.

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