Chronic kidney disease (CKD) is associated with increased risk of cardiovascular disease (CVD), and may also lead to an increase in medical expenditures. The effect of CKD on individual and population medical expenditures was examined in a Japanese cohort study. The participants included 4026 Japanese National Health Insurance beneficiaries aged 40-74 years living in one city, who had no history of major CVD. They were classified into three categories according to their glomerular filtration rate (GFR) at the baseline survey, and their total medical expenditures were followed-up for 3 years. The arithmetic and geometric means of the cumulative medical expenditures were calculated for each category. The geometric mean was also expressed after adjusting for several confounding factors using analysis of covariance. The CKD-related medical expenditures attributable to the participants with mild (60pGFRo90) or moderate (30pGFRo60) kidney dysfunction were compared with those of participants with normal (GFRX90) kidney function. There was a negative correlation between the GFR category and the arithmetic and geometric means of personal medical expenditures (adjusted geometric mean: GFRX90, 167 879 yen; 60pGFRo90, 210 660 yen; and 30pGFRo60, 330 050 yen). The CKD-related medical expenditures accounted for 11.5 and 6.5% of the total medical expenditures for the participants with mild and moderate kidney dysfunction, respectively. The prevention of mild CKD is very important for containing medical expenditures. Appropriate strategies, such as regular creatinine measurement, are needed for early detection of CKD.
Branched-chain amino acids (BCAAs) and IGF-I, the secretion of which is stimulated by growth hormone (GH), prevent muscle atrophy. mTOR plays a pivotal role in the protective actions of BCAA and IGF-1. The pathway by which BCAA activates mTOR is different from that of IGF-1, which suggests that BCAA and GH work independently. We tried to examine whether BCAA exerts a protective effect against dexamethasone (Dex)-induced muscle atrophy independently of GH using GH-deficient spontaneous dwarf rats (SDRs). Unexpectedly, Dex did not induce muscle atrophy assessed by the measurement of cross-sectional area (CSA) of the muscle fibers and did not increase atrogin-1, MuRF1 and REDD1 expressions, which are activated during protein degradation. Glucocorticoid (GR) mRNA levels were higher in SDRs compared to GH-treated SDRs, indicating that the low expression of GR is not the reason of the defect of Dex’s action in SDRs. BCAA did not stimulate the phosphorylation of p70S6K or 4E-BP1, which stimulate protein synthesis. BCAA did not decrease the mRNA level of atrogin-1 or MuRF1. These findings suggested that Dex failed to modulate muscle mass and that BCAA was unable to activate mTOR in SDRs because these phosphorylations of p70S6K and 4E-BP1 and the reductions of these mRNAs are regulated by mTOR. In contrast, after GH supplementation, these responses to Dex were normalized and muscle fiber CSA was decreased by Dex. BCAA prevented the Dex-induced decrease in CSA. BCAA increased the phosphorylation of p70S6K and decreased the Dex-induced elevations of atrogin-1 and Bnip3 mRNAs. However, the amount of mTORC1 components including mTOR was not decreased in the SDRs compared to the normal rats. These findings suggest that GH increases mTORC1 activity but not its content to recover the action of BCAA in SDRs and that GH is required for actions of Dex and BCAA in muscles.
). On the fifth post-injection day, they were again given an intravenous injection with 40 mmol kg 21 of the same USPIO, and MR angiography (MRA) was performed.The signal-to-noise ratio (SNR) in regions of interest in the wall of the upper abdominal aorta was calculated on coronal images. Specimens from the same level of the aorta were subjected to iron staining and RAM-11 immunostaining and used for histopathological study. For statistical analysis of the MRA and histopathological findings, we used analysis of variance [Tukey's honest significant difference (HSD) test].Results: In 9-month-old rabbits, the SNR was significantly lower than in rabbits of the other ages (p , 0.01), and the area of RAM-11 (DAKO Corporation, Glostrup, Denmark) and iron uptake in the aortic wall was significantly larger (RAM-11, p , 0.01; iron, p , 0.05). These areas were the smallest in 3-month-old rabbits. Conclusion: Histopathologically, the number of macrophages was the greatest in 9-month-old rabbits. Our findings indicate that the SNR on MRI scans reflects the number of macrophages in the aortic wall of WHHL rabbits. Advances in knowledge: USPIO-enhanced MRI visualized the accumulation of macrophages in early atherosclerotic plaques of WHHL rabbits in the course of natural progression.
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