Priorities for the professional development of registered nurses in nursing homes: a Delphi study

Objective: to establish a consensus on the care and professional development needs of registered nurses (RNs) employed by UK care homes. Design: two-stage, online modified Delphi study. Setting and participants: a panel (n = 352) of individuals with experience, expertise or interest in care home nursing: (i) care home nurses and managers; (ii) community healthcare professionals (including general practitioners, geriatricians, specialist and district nurses); and (iii) nurse educators in higher education. Results: RNs employed by nursing homes require particular skills, knowledge, competence and experience to provide high-quality care for older residents. The most important responsibilities for the nursing home nurse were: promoting dignity, personhood and wellbeing, ensuring resident safety and enhancing quality of life. Continuing professional development priorities included personal care, dementia care and managing long-term conditions. The main barrier to professional development was staff shortages. Nursing degree programmes were perceived as inadequately preparing nurses for a nursing home role. Nursing homes could improve by providing supportive learning opportunities for students and fostering challenging and rewarding careers for newly RNs. Conclusion: if nurses employed by nursing homes are not fit for purpose, the consequences for the wider health and social-care system are significant. Nursing homes, the NHS, educational and local authorities need to work together to provide challenging and rewarding career paths for RNs and evaluate them. Without well-trained, motivated staff, a high-quality care sector will remain merely an aspiration

An International Comparison of the Effect of Policy Shifts to Organ Donation Following Cardiocirculatory Death (DCD) on Donation Rates After Brain Death (DBD) and Transplantation Rates

During the past decade an increasing number of countries have adopted policies that emphasize donation after cardiocirculatory death (DCD) in an attempt to address the widening gap between the demand for transplantable organs and the availability of organs from donation after brain death (DBD) donors. In order to examine how these policy shifts have affected overall deceased organ donor (DD) and DBD rates, we analyzed deceased donation rates from 82 countries from 2000–2010. On average, overall DD, DBD and DCD rates have increased over time, with the proportion of DCD increasing 0.3% per year (p = 0.01). Countries with higher DCD rates have, on average, lower DBD rates. For every one-per million population (pmp) increase in the DCD rate, the average DBD rate decreased by 1.02 pmp (95% CI: 0.73, 1.32; p<0.0001). We also found that the number of organs transplanted per donor was significantly lower in DCD when compared to DBD donors with 1.51 less transplants per DCD compared to DBD (95% CI: 1.23, 1.79; p<0.001). Whilst the results do not infer a causal relationship between increased DCD and decreased DBD rates, the significant correlation between higher DCD and lower DBD rates coupled with the reduced number of organs transplanted per DCD donor suggests that a national policy focus on DCD may lead to an overall reduction in the number of transplants performed

Clinical characteristics and prognosis of cardiac amyloidosis defined by mass spectrometry-based proteomics in an Australian cohort.

Cardiac amyloidosis has a very poor prognosis, but it is the nature of the involved precursor protein that ultimately dictates treatment and survival. We report the clinical characteristics and survival of 47 cardiac amyloid patients across 2 Australian centres including 39 patients evaluated for definitive amyloid subtype utilising laser microdissection and tandem mass spectrometry (LMD-MS). A quarter of patients (n=12) were classified as wild type transthyretin amyloidosis (ATTRwt), 33 patients as light or heavy chain amyloidosis (AL or AH), and 2 as hereditary mutant transthyretin amyloidosis (ATTRv). Greater left ventricular hypertrophy (IV septum 22 vs. 15 mm, p=0.005) and history of cardiac arrhythmia (75% vs. 31%, p=0.016) were significantly associated with ATTRwt patients compared with AL/AH patients. AL patients demonstrated significantly shorter median survival compared to ATTRwt patients (3.5 vs. 37 months, (P=0.007)). New York heart association (NYHA) class III-IV symptoms or plasma cells ≥ 10% at diagnosis, were the only independent predictors of worse survival in AL patients on multivariate analysis. In the era of novel therapies for both AL amyloid and ATTR, identification of the correct amyloid subtype is essential in making therapeutic decisions and providing accurate prognostic information to patients. This article is protected by copyright. All rights reserved

The intrahepatic signalling niche of hedgehog is defined by primary cilia positive cells during chronic liver injury

Background & Aims: In vertebrates, canonical Hedgehog (Hh) pathway activation requires Smoothened (SMO) translocation to the primary cilium (Pc), followed by a GLI-mediated transcriptional response. In addition, a similar gene regulation occurs in response to growth factors/cytokines, although independently of SMO signalling. The Hh pathway plays a critical role in liver fibrosis/regeneration; however, the mechanism of activation in chronic liver injury is poorly understood. This study aimed to characterise Hh pathway activation upon thioacetamide (TAA)- induced chronic liver injury in vivo by defining Hh-responsive cells, namely cells harbouring Pc and Pc-localised SMO. Methods: C57BL/6 mice (wild-type or Ptc1+/_) were TAA-treated. Liver injury and Hh ligand/pathway mRNA and protein expression were assessed in vivo. SMO/GLI manipulation and SMO dependent/ independent activation of GLI-mediated transcriptional response in Pc-positive (Pc+) cells were studied in vitro. Results: In vivo, Hh activation was progressively induced following TAA. At the epithelial-mesenchymal interface, injured hepatocytes produced Hh ligands. Progenitors, myofibroblasts, leukocytes and hepatocytes were GLI2+. Pc+ cells increased following TAA, but only EpCAM+/GLI2+ progenitors were Pc+/SMO+. In vitro, SMO knockdown/hGli3-R overexpression reduced proliferation/viability in Pc+ progenitors, whilst increased proliferation occurred with hGli1 overexpression. HGF induced GLI transcriptional activity independently of Pc/SMO. Ptc1+/_ mice exhibited increased progenitor, myofibroblast and fibrosis responses. Conclusions: In chronic liver injury, Pc+ progenitors receive Hh ligand signals and process it through Pc/SMO-dependent activation of GLI-mediated transcriptional response. Pc/SMO-independent GLI activation likely occurs in Pc_/GLI2+ cells. Increased fibrosis in Hh gain-of-function mice likely occurs by primary progenitor expansion/proliferation and secondary fibrotic myofibroblast expansion, in close contact with progenitors