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To overcome organ shortage, expanded criteria donors, including elderly deceased donors (DDs), should be considered. We analyzed outcomes of kidney transplantation (KT) from elderly DDs in a nationwide study. In total, data of 1049 KTs from DDs using the database of Korean Organ Transplantation Registry (KOTRY) were retrospectively analyzed based on the age of DDs age ≥60 years vs. less then 60 years. Clinical information, graft status, and adverse events were reviewed in DDs and recipients. The mean age of the 1006 DDs was 51.04±10.54 years, and 21.5% of donors were aged ≥60 years. Elderly DDs had a significantly higher prevalence of diabetes and hypertension and higher Kidney Donor Risk Index (KDRI) and Kidney Donor Profile Index (KDPI). The mean age of the recipients was 47.45±14.87 years. Patients who received KT from elderly DDs were significantly older (53.12±15.14 vs. 45.88±14.41, P less then 0.001) and had a higher rate of diabetes (41.9 vs. 24.4%, P less then 0.001). Graft outcomes were not significantly different. Renal function was similar between the groups at the time of discharge and at 6 months, 1 year, and 2 years after KT. The rate of delayed graft function (DGF) was not significantly different. Smad inhibitor Risk factors of DGF were significantly different in DDs aged ≥60 years and less then 60 years. In the multivariable model, male sex (odds ratio 3.99, 95% confidence interval 1.42-11.22; P = 0.009) and KDRI (12.17, 2.23-66.34; P = 0.004) were significant risk factors for DGF in DDs aged ≥60 years. In DDs aged less then 60 years, thymoglobulin induction (2.62, 1.53-4.48; P less then 0.001) and continuous renal replacement therapy (3.47, 1.52-7.96; P = 0.003) were significant factors. Our data indicated that graft outcomes, including renal function and DGF, were similar for elderly DDs and DDs aged less then 60 years. Elderly DDs might be considered tolerable donors for KT, with active preoperative surveillance.Viruses and their hosts are locked in an evolutionary race where resistance to infection is acquired by the hosts while viruses develop strategies to circumvent these host defenses. Forming one arm of the host defense armory are cell autonomous restriction factors like Fv1. Originally described as protecting laboratory mice from infection by murine leukemia virus (MLV), Fv1s from some wild mice have also been found to restrict non-MLV retroviruses, suggesting an important role in the protection against viruses in nature. We surveyed the Fv1 genes of wild mice trapped in Thailand and characterized their restriction activities against a panel of retroviruses. An extra copy of the Fv1 gene, named Fv7, was found on chromosome 6 of three closely related Asian species of mice Mus caroli, M. cervicolor, and M. cookii. The presence of flanking repeats suggested it arose by LINE-mediated retroduplication within their most recent common ancestor. A high degree of natural variation was observed in both Fv1 and Fv7 and, on top of positive selection at certain residues, insertions and deletions were present that changed the length of the reading frames. These genes exhibited a range of restriction phenotypes, with activities directed against gamma-, spuma-, and lentiviruses. It seems likely, at least in the case of M. caroli, that the observed gene duplication may expand the breadth of restriction beyond the capacity of Fv1 alone and that one or more such viruses have recently driven or continue to drive the evolution of the Fv1 and Fv7 genes.Background In individuals below 65 years of age, primary prevention programs have not been successful in reducing the risk of cardiovascular disease (CVD) and death. However, no large study to our knowledge has previously evaluated the effects of prevention programs in individuals aged 65 years or older. The present cohort study evaluated the risk of CVD in a primary prevention program for community-dwelling 70-year-olds. Method and findings In 2012-2017, we included 3,613 community-dwelling 70-year-olds living in Umeå, in the north of Sweden, in a health survey and multidimensional prevention program (the Healthy Ageing Initiative [HAI]). Classic risk factors for CVD were evaluated, such as blood pressure, lipid levels, obesity, and physical inactivity. In the current analysis, each HAI participant was propensity-score-matched to 4 controls (n = 14,452) from the general Swedish population using national databases. The matching variables included age, sex, diagnoses, medication use, and socioeconomic factors.tional design and that changes in blood pressure and lipid levels likely were influenced by regression towards the mean. Conclusions In this study, a primary prevention program was associated with a lower risk of CVD in community-dwelling 70-year-olds. With the limitation of this being an observational study, the associations may partly be explained by improved control of classic risk factors for CVD with the program.Recent discoveries from large-scale genome-wide association studies (GWASs) explain a larger proportion of the genetic variability to BMI and obesity. The genetic risk associated with BMI and obesity can be assessed by an obesity-specific genetic risk score (GRS) constructed from genome-wide significant genetic variants. The aim of our study is to examine whether the duration and exclusivity of breastfeeding can attenuate BMI increase during childhood and adolescence due to genetic risks. A total sample of 5,266 children (2,690 boys and 2,576 girls) from the Avon Longitudinal Study of Parents and Children (ALSPAC) was used for the analysis. We evaluated the role of breastfeeding (exclusivity and duration) in modulating BMI increase attributed to the GRS from birth to 18 years of age. The GRS was composed of 69 variants associated with adult BMI and 25 non-overlapping SNPs associated with pediatric BMI. In the high genetic susceptible group (upper GRS quartile), exclusive breastfeeding (EBF) to 5 months reduces BMI by 1.14 kg/m2 (95% CI, 0.37 to 1.91, p = 0.0037) in 18-year-old boys, which compensates a 3.9-decile GRS increase. In 18-year-old girls, EBF to 5 months decreases BMI by 1.53 kg/m2 (95% CI, 0.76 to 2.29, p less then 0.0001), which compensates a 7.0-decile GRS increase. EBF acts early in life by delaying the age at adiposity peak and at adiposity rebound. EBF to 3 months or non-exclusive breastfeeding was associated with a significantly diminished impact on reducing BMI growth during childhood. EBF influences early life growth and development and thus may play a critical role in preventing overweight and obesity among children at high-risk due to genetic factors.