Astrupbennett2657

3% vs. 4.7%, p<0.001). However, there was no significant difference between young-old and non-older groups (58.8% vs. 41.2%, p=0.145). Middle-old to oldest-old age and osteoporosis were associated with an increased incidence of femoral intertrochanteric fractures (p<0.001, p=0.004).

A higher incidence of femoral intertrochanteric fractures from minor falls was found among middle-old to oldest-old patients compared to that in young-old patients. Therefore, physicians should perform more thorough physical examinations and radiograph reading in middle-old to oldest-old patients even if the patients do not complain of pain.

A higher incidence of femoral intertrochanteric fractures from minor falls was found among middle-old to oldest-old patients compared to that in young-old patients. Therefore, physicians should perform more thorough physical examinations and radiograph reading in middle-old to oldest-old patients even if the patients do not complain of pain.

Long-term care is a burden on individuals, families, and society. It is important to find ways to delay the onset of disability to lessen the burden of long-term care in aging societies. Fracture is one of the risk factors that affect physical functions and make older people dependent. This study aimed to examine how much more often older adults who experienced fractures initiated long-term care compared to those who did not, and whether the risk of entering long-term care differed significantly by fracture site.

The analyses included insurants aged 65 years and over from the Korean National Health Insurance Service-senior cohort study (2002-2013). Cox proportional hazard models were used to calculate the hazard ratios of the first certification of initiation of long-term care after fracture, by fracture site, and for multiple recurrent fractures.

The incidence rate of initial long-term care beneficiaries was approximately 2.5 times higher when older people had experienced fractures; these individuals entered long-term care beneficiary status 3 years earlier compared to those who had no fracture events. SLF1081851 datasheet Lower extremity fracture and multiple recurrent fractures more than doubled the risk for long-term care.

Additional attention to fracture sites in prevention and rehabilitation settings is warranted to reduce disability and the related long-term care burden.

Additional attention to fracture sites in prevention and rehabilitation settings is warranted to reduce disability and the related long-term care burden.The gut microbiome is deeply associated with both skeletal muscle and brain function. In particular, gut microbiome dysbiosis may accelerate age-related diseases by affecting these systems. Although there is increasing evidence of the correlations between the gut microbiome and skeletal muscle and brain, it remains unclear whether changes in the gut microbiome due to exercise training can lead to healthy aging. This review covers the current status of gut microbiome-related research and future directions related to aging (e.g., physical frailty and cognitive dysfunction) as well as the effect of exercise training on both. We reviewed relevant literature including original articles and reviews identified from searches of the PubMed, Google Scholar, SCOPUS, EBSCOHost, ScienceDirect, Cochrane Library, and EMBASE databases using the following terms 'gut microbiome', 'exercise', 'physical frailty', and 'cognitive dysfunction'. We identified a strong positive correlation between cognitive dysfunction or physical frailty and the gut microbiome. Furthermore, exercise had a significant effect on the composition of the gut microbiome. These results suggest that exercise training can prevent physical frailty or cognitive dysfunction by altering the gut microbiome. However, the exact mechanism by which these effects occur is not yet clear. Further studies are needed to determine whether exercise training can prevent age-related diseases by balancing the gut microbiome.Sarcopenia, the loss of skeletal muscle mass and function with age, was first recognized as a disease in the International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) (M62.84) and has recently attracted attention as aged populations increase. However, the diagnostic criteria for sarcopenia remain controversial and there are as yet no US Food and Drug Administration-approved medications for sarcopenia. Given that both intrinsic and extrinsic factors contribute to sarcopenia onset and development, understanding the mechanism of sarcopenia is important for the development of therapeutic strategies. In this review, we described a variety of drugs for sarcopenia under investigation, including myostatin/ActR2 signaling inhibitors, exercise mimetics, anabolic hormones, and natural compounds. However, the combination of non-drug therapies with exercise and nutritional supplements are also needed as more easily accessible intervention strategies against sarcopenia rather than pharmacological treatments alone. Many approaches to develop therapeutic methods to overcome sarcopenia may lead to healthy aging.The accumulation of misfolded proteins in the endoplasmic reticulum (ER) defines a condition called ER stress that induces the unfolded protein response (UPR). The UPR in mammalian cells attenuates protein synthesis initiation, which prevents the piling up of misfolded proteins in the ER. Mammalian cells rely on Protein Kinase RNA-Like Endoplasmic Reticulum Kinase (PERK) phosphorylation of eIF2α to arrest protein synthesis, however, plants do not have a PERK homolog, so the question is whether plants control translation in response to ER stress. We compared changes in RNA levels in the transcriptome to the RNA levels protected by ribosomes and found a decline in translation efficiency, including many UPR genes, in response to ER stress. The decline in translation efficiency is due to the fact that many mRNAs are not loaded onto polyribosomes (polysomes) in proportion to their increase in total RNA, instead some of the transcripts accumulate in stress granules (SGs). The RNAs that populate SGs are not derived from the disassembly of polysomes because protein synthesis remains steady during stress.