老年患者出院后跌倒发生率及影响因素的调查研究

目的了解老年人出院后1年内累积跌倒发生率及其影响因素。方法2019年5月至2020年8月,对重庆市一所三级甲等医院的出院老年患者进行前瞻性调查研究。采用中文版跌倒风险自评量表、衰弱评估量表(FRAIL scale)和9项患者健康问卷(Patient Health Questionnaire-9,PHQ-9)、Barthel指数评定量表(Bar-thel index,BI)调查出院老年人跌倒风险、衰弱、抑郁、自理能力状况并在其出院后电话追踪1年。应用累积发生率函数估计老年人出院后1年内跌倒的累积发生率,利用竞争风险模型中部分分布风险函数探讨跌倒的危险因素。结果共有1077例老年患者参与此研究,出院后1、6、12个月跌倒累计发生率分别为4.45%、9.03%和10.80%。出院时伴有抑郁和衰弱的老年人在出院后1、6、12个月的跌倒累计发生率分别26.19%、49.93%、58.53%和21.59%、41.67%、48.73%,远高于没有抑郁和衰弱的老年人(P<0.05)。出院时伴有抑郁、衰弱、Barthel指数得分61~80分、住院时间>20 d、随访时间内再次入院、由他人照料和跌倒风险是影响老人出院后1年内跌倒的因素。结论住院老年人出院后1年内跌倒发生率随出院时间的延长具有累积效应,且受多种因素影响,未来构建预出院老年人跌倒预防策略时应关注这些影响因素,并重点关注老年人抑郁和衰弱。

Bone morphogenetic protein 4 (BMP4) promotes hepatic glycogen accumulation and reduces glucose level in hepatocytes through mTORC2 signaling pathway

Liver is an important organ for regulating glucose and lipid metabolism.Recent studies have shown that bone morphogenetic proteins(BMPs)may play important roles in regu-lating glucose and lipid metabolism.Inour previous studies,we demonstrated that BMP4 signif-icantly inhibits hepatic steatosis and lowers serum triglycerides,playing a protective role against the progression of non-alcoholic fatty liver disease(NAFLD).However,the direct impact of BMP4 on hepatic glucose metabolism is poorly understood.Here,we investigated the regulatory roles of BMP4 in hepatic glucose metabolism.Through a comprehensive analysis of the 14 types of BMPs,we found that BMP4 was one of the most potent BMPs in promoting hepatic glycogen accumulation,reducing the level of glucose in hepatocytes and effecting the expression of genes related to glucose metabolism.Mechanistically,we demonstrated that BMP4 reduced the hepatic glucose lewels through the activation of mTORC2 signaling pathway in vitro and in wivo.Collectively,our findings strongly suggest that BMP4 may play an essential role in regulating hepatic glucose metabolism.This knowledge should aid us to understand the molecular pathogenesis of NAFLD,and may lead to the development of novel therapeutics by exploiting the inhibitory effects of BMPs on hepatic glucose and lipid metabolism.

Reversibly immortalized keratinocytes(iKera)facilitate re-epithelization and skin wound healing:Potential applications in cell-based skin tissue engineering

Skin injury is repaired through a multi-phase wound healing process of tissue granulation and re-epithelialization.Any failure in the healing process may lead to chronic non-healing wounds or abnormal scar formation.Although significant progress has been made in developing novel scaffolds and/or cell-based therapeutic strategies to promote wound healing,effective management of large chronic skin wounds remains a clinical challenge.Keratinocytes are critical to re-epithelialization and wound healing.Here,we investigated whether exogenous keratinocytes,in combination with a citrate-based scaffold,enhanced skin wound healing.We first established reversibly immortalized mouse keratinocytes(iKera),and confirmed that the iKera cells expressed keratinocyte markers,and were responsive to UVB treatment,and were non-tumorigenic.In a proof-of-principle experiment,we demonstrated that iKera cells embedded in citrate-based scaffold PPCN provided more effective re-epithelialization and cutaneous wound healing than that of either PPCN or iKera cells alone,in a mouse skin wound model.Thus,these results demonstrate that iKera cells may serve as a valuable skin epithelial source when,combining with appropriate biocompatible scaffolds,to investigate cutaneous wound healing and skin regeneration.