This study proposed that, among older adults, higher support and lower strain received from each of the four relational sources (spouse/partner, children, family, and friends) were associated with reduced loneliness and improved well-being and that loneliness might mediate the relationship between support/strain and well-being. Structural equation modeling was conducted using a national sample of adults aged 50 years and older (N = 7,367) from the Health and Retirement Study. Findings indicated that support from spouse/partner and friends alleviated loneliness, while strain from all the four sources intensified loneliness; higher support and lower strain from various sources directly and indirectly improved well-being, with indirect effects mediated through reduced loneliness. It was concluded that, in later life, various sources of support/strain engender distinct effects on loneliness and well-being, and loneliness serves as one of the psychological pathways linking support/strain to well-being.
BACKGROUND With limited numbers of intensive care unit (ICU) beds available, increasing patient acuity is expected to contribute to episodes of inpatient deterioration on general wards. OBJECTIVE To prospectively validate a predictive algorithm for clinical deterioration in general–medical ward patients, and to conduct a trial of real‐time alerts based on this algorithm. DESIGN Randomized, controlled crossover study. SETTING/PATIENTS Academic center with patients hospitalized on 8 general wards between July 2007 and December 2011. INTERVENTIONS Real‐time alerts were generated by an algorithm designed to predict the need for ICU transfer using electronically available data. The alerts were sent by text page to the nurse manager on intervention wards. MEASUREMENTS Intensive care unit transfer, hospital mortality, and hospital length of stay. RESULTS Patients meeting the alert threshold were at nearly 5.3‐fold greater risk of ICU transfer (95% confidence interval [CI]: 4.6‐6.0) than those not satisfying the alert threshold (358 of 2353 [15.2%] vs 512 of 17678 [2.9%]). Patients with alerts were at 8.9‐fold greater risk of death (95% CI: 7.4‐10.7) than those without alerts (244 of 2353 [10.4%] vs 206 of 17678 [1.2%]). Among patients identified by the early warning system, there were no differences in the proportion of patients who were transferred to the ICU or who died in the intervention group as compared with the control group. CONCLUSIONS Real‐time alerts were highly specific for clinical deterioration resulting in ICU transfer and death, and were associated with longer hospital length of stay. However, an intervention notifying a nurse of the risk did not result in improvement in these outcomes. Journal of Hospital Medicine 2013;8:236–242. © 2013 Society of Hospital Medicine
Although there have been numerous reports describing the isolation of liver progenitor cells from adult liver, their exact origin has not been clearly defined; and the role played by mature hepatocytes as direct contributors to the hepatic progenitor cell pool has remained largely unknown. Here we report strong evidence that mature hepatocytes in culture have the capacity to dedifferentiate into a population of adult liver progenitors without genetic or epigenetic manipulations. By using highly-purified mature hepatocytes, which were obtained from untreated, healthy rat liver and labeled with fluorescent dye PKH2, we found that hepatocytes in culture gave rise to a population of PKH2-positive liver progenitor cells. These cells, Liver Derived Progenitor Cells or LDPCS, which share phenotypic similarities with oval cells, were previously reported to be capable of forming mature hepatocytes both in culture and in animals. Studies done at various time points during the course of dedifferentiation cultures revealed that hepatocytes rapidly transformed into liver progenitors within one week through a transient oval cell-like stage. This finding was supported by lineage-tracing studies involving double-transgenic AlbuminCreXRosa26 mice expressing β-galactosidase exclusively in hepatocytes. Cultures set up with hepatocytes obtained from these mice resulted in generation of β-galactosidase-positive liver progenitor cells demonstrating that they were a direct dedifferentiation product of mature hepatocytes. Additionally, these progenitors differentiated into hepatocytes in vivo when transplanted into rats that had undergone retrorsine pretreatment and partial hepatectomy. Conclusion Our studies provide strong evidence for the unexpected plasticity of mature hepatocytes to dedifferentiate into progenitor cells in culture; and this may potentially have a significant impact on the treatment of liver diseases requiring liver or hepatocyte transplantation.
VACTERL association is a condition comprising multisystem congenital malformations, causing severe physical disability in affected individuals. It is typically defined by the concurrence of at least three of the following component features: vertebral anomalies (V), anal atresia (A), cardiac malformations (C), tracheo-oesophageal fistula (TE), renal dysplasia (R) and limb abnormalities (L). Vertebral anomaly is one of the most important and common defects that has been reported in approximately 60–95% of all VACTERL patients. Recent breakthroughs have suggested that genetic factors play an important role in VACTERL association, especially in those with vertebral phenotypes. In this review, we summarised the genetic studies of the VACTERL association, especially focusing on the genetic aetiology of patients with vertebral anomalies. Furthermore, genetic reports of other syndromes with vertebral phenotypes overlapping with VACTERL association are also included. We aim to provide a further understanding of the genetic aetiology and a better evidence for genetic diagnosis of the association and vertebral anomalies.
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