Effects of Implementing a Brief Family Nursing Intervention With Hospitalized Oncology Patients and Their Families in Germany: A Quasi-Experimental Study.

Family nursing, based on the Calgary Family and Intervention Models, was implemented in a German oncological inpatient unit to promote effective family functioning in the context of cancer care. The objective of this study was to investigate the effects of implementing family nursing care on several psychological and physical outcomes of patients and their family members. A quasi-experimental study with 214 patients with a cancer diagnosis and 122 family members was conducted. Findings indicate that the superiority of family nursing, when compared to traditional care, could not be confirmed with respect to patients' outcomes (psychological burden, social support, satisfaction with care) and family members' outcomes (psychological burden, physical complaints, satisfaction with care). Various factors, such as country-specific structures and challenges in implementing family nursing care on an inpatient unit, may have contributed to these findings. Further replication attempts in similar settings in other countries are needed to shed light on the factors impairing or promoting the implementation of family nursing in practice settings.

[Evaluation of the implementation process of family nursing in oncology]. / Implementation und Evaluation einer familienzentrierten Pflege in der Onkologie.

Evaluation of the implementation process of family nursing in oncology Abstract. BACKGROUND: The confrontation with a life-threatening cancer disease and the resulting consequences are a great burden for patients as well as for their family members. Family nursing based on the Calgary Model was implemented on a German oncological inpatient unit in order to strengthen the family's ability to self-help. AIM: The objectives were a) to systematically record, evaluate and if necessary to modify the implementation process, b) to highlight promoting and inhibiting factors and c) to derive recommendations for transferability to other oncological units. METHODS: The implementation process was examined by means of two group interviews with nurses, five interviews with other members of the treatment team, and observations of, in each case four, family assessments, family interviews and family-related team meetings. RESULTS: Family nursing could be implemented in a modified form. Genograms and ecomaps have become part of the admission interview. In family interviews, needs of the entire family were determined with the help of circular communication. Family-related team meetings were carried out according to an adapted method of the reflecting team. The complete implementation of family nursing was impeded by the lack of professional consulting competences of the nursing staff, the system of nursing care delivery and lack of time. CONCLUSION: An implementation of family nursing in other oncological units is recommended under modified preconditions.

The neuropeptide head activator is a high-affinity ligand for the orphan G-protein-coupled receptor GPR37.

The neuropeptide head activator (HA) is a mitogen for mammalian cell lines of neuronal or neuroendocrine origin. HA signalling is mediated by a G-protein-coupled receptor (GPCR). Orphan GPCRs with homology to peptide receptors were screened for HA interaction. Electrophysiological recordings in frog oocytes and in mammalian cell lines as well as Ca(2+) mobilisation assays revealed nanomolar affinities of HA to GPR37. HA signal transduction through GPR37 was mediated by an inhibitory G protein and required Ca(2+) influx through a channel of the transient receptor potential (TRP) family. It also required activation of Ca(2+)-dependent calmodulin kinase and phosphoinositide 3-kinase. Respective inhibitors blocked HA signalling and HA-induced mitosis in GPR37-expressing cells. HA treatment resulted in internalisation of GPR37. Overexpression of GPR37 led to aggregate formation, retention of the receptor in the cytoplasm and low survival rates of transfected cells, confirming the notion that misfolded GPR37 contributes to cell death, as observed in Parkinson's disease.

Characterization of the VPS10 domain of SorLA/LR11 as binding site for the neuropeptide HA.

The single transmembrane receptor sorLA/LR11 contains binding domains typical for the low-density lipoprotein receptors and a VPS10 domain which, in the related receptor sortilin, binds the neuropeptide neurotensin. SorLA is synthesized as a proreceptor which is processed to the mature form by a furin-like propeptidase. Endogenous sorLA and its hydra homologue HAB bind the neuropeptide head activator (HA). Transiently expressed partial sorLA constructs were investigated for ligand binding. We found that HA binds with nanomolar affinity to the VPS10 domain. The sorLA propeptide also bound to the VPS10 domain, whereas the receptor-associated protein RAP interacted both with the class A repeats and the VPS10 domain. The sorLA propeptide inhibited binding of HA to full-length sorLA and to the VPS10 domain. It also interfered with binding of HA to hydra HAB, which is taken as evidence for a highly conserved tertiary structure of the VPS10 domains of this receptor in hydra and mammals. The propeptide inhibited HA-stimulated mitosis and proliferation in the human neuroendocrine cell line BON and the neuronal precursor cell line NT2. We conclude that sorLA is necessary for HA signaling and function.