Effects of strategies to improve general practitioner-nurse collaboration and communication in regard to hospital admissions of nursing home residents (interprof ACT): study protocol for a cluster randomised controlled trial.

BACKGROUND: In Germany, up to 50% of nursing home residents are admitted to a hospital at least once a year. It is often unclear whether this is beneficial or even harmful. Successful interprofessional collaboration and communication involving general practitioners (GPs) and nurses may improve medical care of nursing home residents. In the previous interprof study, the six-component intervention package interprof ACT was developed to facilitate collaboration of GPs and nurses in nursing homes. The aim of this study is to evaluate the effectiveness of the interprof ACT intervention. METHODS: This multicentre, cluster randomised controlled trial compares nursing homes receiving the interprof ACT intervention package for a duration of 12 months (e.g. comprising appointment of mutual contact persons, shared goal setting, standardised GPs' home visits) with a control group (care as usual). A total of 34 nursing homes are randomised, and overall 680 residents recruited. The intervention package is presented in a kick-off meeting to GPs, nurses, residents/relatives or their representatives. Nursing home nurses act as change agents to support local adaption and implementation of the intervention measures. Primary outcome is the cumulative incidence of hospitalisation within 12 months. Secondary outcomes include admissions to hospital, days admitted to hospital, use of other medical services, prevalence of potentially inappropriate medication and quality of life. Additionally, health economic and a mixed methods process evaluation will be performed. DISCUSSION: This study investigates a complex intervention tailored to local needs of nursing homes. Outcomes reflect the healthcare and health of nursing home residents, as well as the feasibility of the intervention package and its impact on interprofessional communication and collaboration. Because of its systematic development and its flexible nature, interprof ACT is expected to be viable for large-scale implementation in routine care services regardless of local organisational conditions and resources available for medical care for nursing home residents on a regular basis. Recommendations will be made for an improved organisation of primary care for nursing home residents. In addition, the results may provide important knowledge and data for the development and evaluation of further strategies to improve outpatient care for elderly care-receivers. TRIAL REGISTRATION: ClinicalTrials.gov NCT03426475 . Initially registered on 7 February 2018.

VCP and PSMF1: Antagonistic regulators of proteasome activity.

Protein turnover and quality control by the proteasome is of paramount importance for cell homeostasis. Dysfunction of the proteasome is associated with aging processes and human diseases such as neurodegeneration, cardiomyopathy, and cancer. The regulation, i.e. activation and inhibition of this fundamentally important protein degradation system, is still widely unexplored. We demonstrate here that the evolutionarily highly conserved type II triple-A ATPase VCP and the proteasome inhibitor PSMF1/PI31 interact directly, and antagonistically regulate proteasomal activity. Our data provide novel insights into the regulation of proteasomal activity.

JunB-CBFbeta signaling is essential to maintain sarcomeric Z-disc structure and when defective leads to heart failure.

In muscle cells, a complex network of Z-disc proteins allows proper reception, transduction and transmission of mechanical and biochemical signals. Mutations in genes encoding different Z-disc proteins such as integrin-linked kinase (ILK) and nexilin have recently been shown to cause heart failure by distinct mechanisms such as disturbed mechanosensing, altered mechanotransduction or mechanical Z-disc destabilization. We identified core-binding factor ß (CBFß) as an essential component for maintaining sarcomeric Z-disc and myofilament organization in heart and skeletal muscle. In CBFß-deficient cardiomyocytes and skeletal-muscle cells, myofilaments are thinned and Z-discs are misaligned, leading to progressive impairment of heart and skeletal-muscle function. Transcription of the gene encoding CBFß mainly depends on JunB activity. In JunB-morphant zebrafish, which show a heart-failure phenotype similar to that of CBFß-deficient zebrafish, transcript and protein levels of CBFß are severely reduced. Accordingly, ectopic expression of CBFß can reconstitute cardiomyocyte function and rescue heart failure in JunB morphants, demonstrating for the first time an essential role of JunB-CBFß signaling for maintaining sarcomere architecture and function.