"Comprehensive Care" Concept in Nursing: Systematic Review.

Introduction. Integrated health care is a concept widely used in the planning and organisation of nursing care. It is a highly topical concept, but at the same time it is deeply rooted in the theory and models of Nursing right from its inception as a science. There is no clear, agreed definition that describes it. Objective. To systematise the knowledge available on the concept of "comprehensive care" in Nursing from the point of view of nursing care, its domains and characteristics. Methods. A literature search has been carried out in several languages (Spanish, Portuguese, English and Romanian) in the databases Web of Science, Scopus, Medline, PubMed, Cochrane and Dialnet, covering the period between 2013 and 2019. The search terms used were: comprehensive health care, health and nursing. Prospero register 170327. Results. Sixteen documents were identified, which grouped 8 countries, mainly Brazil, being the country with the highest output on this context– 10 documents were found within the qualitative paradigm and 6 quantitative ones. The concept "Comprehensive" ; is commonly used to refer to comprehensive nursing care techniques, protocols, programmes and plans, covering care in all aspects of the individual as a complement to or independent of the clinical needs arising from health care. Conclusion. The definition of features pertaining to the concept "Comprehensive Care" ; encourages the use and standardisation of nursing care plans, improving patient follow-up, the detection of new risk factors, complications and new health problems not related to the reason for admission. This increases the capacity for prevention and improves the patient’s quality of life, and their primary and/or family caregivers, which translates into lower costs in the health system.post-print871 K

Disminución de reingresos tras una hospitalización por exacerbación de EPOC a través de un modelo de atención domiciliaria

To decrease readmissions at 30 and 90 days post-discharge from a hospital admission for chronic obstructive pulmonary disease exacerbation (COPDE)through the home care model ofthe Ambulatory Chronic Respiratory Care Unit (ACRCU), increase patient survival at one year, and validate our readmission risk scale (RRS). Materials and methods: This was an observational study, with a prospective data collection and a retrospective data analysis. A total of 491 patients with a spirometry diagnosis of chronic obstructive pulmonary disease (COPD) requiring hospitalisation for an exacerbation were included in the study. Subjects recruited within the first year (204 cases) received conventional care (CC). In the following year a home care (HC) programme was implemented and of those recruited that year (287) 104 were included in the ACRCU, administered by a specialised nurse. Results: In the group of patients included in the home care model of the Ambulatory Chronic Respiratory Care Unit(ACRCU) a lower number of readmissions was observed at 30 and 90 days after discharge (30.5% vs. 50%, p = 0.012 and 47.7% vs. 65.2%, p = 0.031, respectively) and a greater one-year survival (85.3% vs. 59.1%, p < 0.001). The validation of our RRS revealed that the tool’s capacity to predict readmissions at both 30 and 90 days was not high (AUC = 0.69 and AUC = 0.66, respectively). The inclusion of exacerbator or fragile COPD patients in the ACRCU could achieve a decrease in readmissions and an increase in survival. The number of episodes of exacerbation within the 12 months prior to the hospital admission is the variable that best predicts the risk of readmissionDisminuir los reingresos a los 30 y 90 días tras el alta por un ingreso hospitalario por exacerbación de enfermedad pulmonar obstructiva crónica (EPOC) a través del modelo de atención domiciliaria de la Unidad de Cuidados Crónicos Respiratorios Ambulatorios (UCCRA), aumentar la supervivencia al año y validar nuestra escala de riesgo de reingreso (ERR). Estudio observacional con recogida prospectiva de datos. Se incluyó en el estudio a un total de 491 pacientes con diagnóstico espirométrico de enfermedad pulmonar obstructiva crónica que requirieron hospitalización por una agudización. Los sujetos reclutados dentro del primer año (204 casos) recibieron atención convencional (AC). Al año siguiente se implementó un programa de atención domiciliaria (AD) y de los pacientes reclutados ese año (287), 104 fueron incluidos en la UCCRA con seguimiento de una enfermera especializada. En el grupo de pacientes incluidos en el modelo de atención domiciliaria de la UCCRA se observó un menor número de reingresos a los 30 y 90 días tras el alta (30,5% vs 50%, p = 0,012 y 47,7% vs. 65,2%, p = 0,031, respectivamente) y una mayor supervivencia al año (85,3% vs. 59,1%, p < 0,001). La validación de nuestra ERR reveló que la capacidad de la misma para predecir reingresos tanto a los 30 como a los 90 días no era alta (AUC = 0,69 y AUC = 0,66, respectivamente). La inclusión de pacientes con EPOC agudizadores o frágiles en la UCCRA podría conseguir una disminución de los reingresos y una aumento de la supervivencia. El número de agudizaciones en los 12 meses previos al ingreso hospitalario es la variable que mejor predice el riesgo de reingres

Clinical relevance of the transcriptional signature regulated by CDC42 in colorectal cancer

CDC42 is an oncogenic Rho GTPase overexpressed in colorectal cancer (CRC). Although CDC42 has been shown to regulate gene transcription, the specific molecular mechanisms regulating the oncogenic ability of CDC42 remain unknown. Here, we have characterized the transcriptional networks governed by CDC42 in the CRC SW620 cell line using gene expression analysis. Our results establish that several cancer-related signaling pathways, including cell migration and cell proliferation, are regulated by CDC42. This transcriptional signature was validated in two large cohorts of CRC patients and its clinical relevance was also studied. We demonstrate that three CDC42-regulated genes offered a better prognostic value when combined with CDC42 compared to CDC42 alone. In particular, the concordant overexpression of CDC42 and silencing of the putative tumor suppressor gene CACNA2D2 dramatically improved the prognostic value. The CACNA2D2/CDC42 prognostic classifier was further validated in a third CRC cohort as well as in vitro and in vivo CRC models. Altogether, we show that CDC42 has an active oncogenic role in CRC via the transcriptional regulation of multiple cancer-related pathways and that CDC42-mediated silencing of CACNA2D2 is clinically relevant. Our results further support the use of CDC42 specific inhibitors for the treatment of the most aggressive types of CRCThis work has been supported by grants to JCL from Ministerio de Ciencia e Innovación (SAF2008- 03750, RD06-0020-0016 and RD12/0036/0019) and to DGO Cancer Institute New South Wales (2017/CDF625). FVM is a National Breast Cancer Foundation/Cure Cancer Australia Foundation Postdoctoral Training Fellow

Efectividad de la estrategia educativa para la prevención de la violencia y el maltrato infantil en el currículo del Grado de Enfermería

Objetivo: Determinar la efectividad de la estrategia educativa «libro fórum» para la prevención de la violencia y el maltrato infantil dentro del itinerario curricular del alumno de Grado de Enfermería, en la Universidad Francisco de Vitoria, durante el curso académico 2018-2019. Método: Estudio cuasiexperimental, longitudinal y prospectivo. Se realizaron dos mediciones, una previa a la intervención educativa y otra posterior. La variable dependiente fue el resultado cuantitativo posterior a esta. La variable de intervención elegida fue una estrategia educativa basada en el «libro fórum» titulado La mirada de Sara Nosly. Relatos para prevenir el maltrato infantil. Para la captación de información se realizó una base de datos en el programa SPSS v24. En el análisis inferencial se utilizó la t de Student para muestras relacionadas y ANOVA para conocer la diferencia entre grupos. Resultados: La evaluación global pretest (promedio ± desviación estándar) fue 7,82 ± 1,02; posteriormente a la intervención el promedio fue 9,16 ± 0,80. De acuerdo con el análisis estadístico, se observó una significación estadística positiva tras la intervención ([t = 14,44] p < 0,001). Conclusión: La estrategia educativa «libro fórum» es efectiva para el desarrollo de competencias sobre maltrato infantil en la formación de los alumnos, lo que favorece la prevención de este fenómeno de gran impacto social.2019-2

UNR/CDSE1 expression as prognosis biomarker in resectable pancreatic ductal adenocarcinoma patients: A proof-of-concept

Pancreatic ductal adenocarcinoma is an aggressive form of pancreatic cancer and the fourth leading cause of cancer-related death. When possible, curative approaches are based on surgical resection, though not every patient is a candidate for surgery. There are clinical guidelines for the management of these patients that offer different treatment options depending on the clinical and pathologic characteristics. However, the survival rates seen in this kind of patients are still low. The CDSE1 gene is located upstream of NRAS and encodes an RNA-binding protein termed UNR. The aim of this study was to analyze UNR expression and its correlation with outcome in patients with resectable pancreatic ductal adenocarcinoma (PDAC). For this, samples from resectable PDAC patients who underwent duodenopancreatectomy were used to evaluate UNR protein expression by immunohistochemistry using a tissue microarray. Here, we observed that low UNR expression was significantly associated with shorter progression-free survival after surgery (P = 0.010). Moreover, this prognostic marker remained significant after Cox proportional hazards model (P = 0.036). We further studied the role of CDSE1 expression in patient’s prognosis using data from public repositories (GEO and TGCA), confirming our results. Interestingly, CDSE1 expression correlated with that of genes characteristic of an immunogenic molecular subtype of pancreatic cancer. Based on these findings, UNR may be considered a potential prognostic biomarker for resectable PDAC and may serve to guide subsequent adjuvant treatment decisionsThis work has been carried out with the support of the RNA-Reg CONSOLIDER Network CSD2009-00080 (J.M.-U. and J.G.-F.), and Spanish Health Research Project Funds PI16/ 01468 from ªInstituto de Salud Carlos IIIº (A.C. and J.G.-F.), both of the Spanish Ministry of Economy, Industry and Competitivenes

Prevention of Alzheimer's disease pathology by cannabinoids: Neuroprotection mediated by blockade of microglial activation

Alzheimer's disease (AD) is characterized by enhanced β-amyloid peptide (βA) deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits. Cannabinoids are neuroprotective agents against excitotoxicity in vitro and acute brain damage in vivo. This background prompted us to study the localization, expression, and function of cannabinoid receptors in AD and the possible protective role of cannabinoids after βA treatment, both in vivo and in vitro. Here, we show that senile plaques in AD patients express cannabinoid receptors CB1 and CB2, together with markers of microglial activation, and that CB1-positive neurons, present in high numbers in control cases, are greatly reduced in areas of microglial activation. In pharmacological experiments, we found that G-protein coupling and CB1 receptor protein expression are markedly decreased in AD brains. Additionally, in AD brains, protein nitration is increased, and, more specifically, CB1 and CB2 proteins show enhanced nitration. Intracerebroventricular administration of the synthetic cannabinoid WIN55,212-2 to rats prevent βA-induced microglial activation, cognitive impairment, and loss of neuronal markers. Cannabinoids (HU-210, WIN55,212-2, and JWH-133) block βA-induced activation of cultured microglial cells, as judged by mitochondrial activity, cell morphology, and tumor necrosis factor-α release; these effects are independent of the antioxidant action of cannabinoid compounds and are also exerted by a CB2-selective agonist. Moreover, cannabinoids abrogate microglia-mediated neurotoxicity after βA addition to rat cortical cocultures. Our results indicate that cannabinoid receptors are important in the pathology of AD and that cannabinoids succeed in preventing the neurodegenerative process occurring in the disease.Peer Reviewe

Choline kinase inhibition induces exacerbated endoplasmic reticulum stress and triggers apoptosis via CHOP in cancer cells

11 p.-6 fig.Endoplasmic reticulum (ER) is a central organelle in eukaryotic cells that regulates protein synthesis and maturation.Perturbation of ER functions leads to ER stress, which has been previously associated with a broad variety of diseases. ER stress is generally regarded as compensatory, but prolonged ER stress has been involved in apoptosis induced by several cytotoxic agents. Choline kinase a (ChoKa), the first enzyme in the Kennedy pathway, is responsible for the generation of phosphorylcholine (PCho) that ultimately renders phosphatidylcholine. ChoKa overexpression and high PCho levels have been detected in several cancer types. Inhibition of ChoKa has demonstrated antiproliferative and antitumor properties; however, the mechanisms underlying these activities remain poorly understood. Here, we demonstrate that ChoKa inhibitors (ChoKIs), MN58b and RSM932A, induce cell death in cancer cells (T47D,MCF7, MDA-MB231, SW620 and H460), through the prolonged activation of ER stress response. Evidence of ChoKIs-induced ER stress includes enhanced production of glucose-regulated protein, 78 kDa (GRP78), protein disulfide isomerase, IRE1a, CHOP, CCAAT/enhancer-binding protein beta (C/EBPb) and TRB3. Although partial reduction of ChoKa levels by small interfering RNA was not sufficient to increase the production of ER stress proteins, silencing of ChoKa levels also show a decrease in CHOP overproduction induced by ChoKIs, which suggests that ER stress induction is due to a change in ChoKa protein folding after binding to ChoKIs. Silencing of CHOP expression leads to a reduction in C/EBPb, ATF3 and GRP78 protein levels and abrogates apoptosis in tumor cells after treatment with ChoKIs, suggesting that CHOP maintains ER stress responses and triggers the pro-apoptotic signal. Consistent with the differential effect of ChoKIs in cancer and primary cells previously described, ChoKIs only promoted a transient and moderated ER stress response in the non-tumorogenic cells MCF10A. In conclusion, pharmacological inhibition of ChoKa induces cancer cell death through a mechanism that involves the activation of exaggerated and persistent ER stress supported by CHOP overproduction.This work has been funded by the following grants:Comunidad de Madrid (S2010/BMD-2326), Ministerio de Economía y Competitividad (SAF2011-29699, RD06-0020-0016 and RD12/0036/0019) and EU no.259737. ESL is a Sara Borell fellow under the program ISCIII/MICINN.Peer reviewe