Contributions of nursing students during their clinical practice in primary care: Adaptation and validation of a scale

Aim: To adapt the 'Nursing Student Contributions to Clinical Settings' scale (CEEEC, Spanish acronym), designed for specialized care and to evaluate the validity and reliability of a measure in the primary health care setting. Additionally, a description of the contributions of nursing students to primary health care in Spain is presented, based on the perception of preceptor nurses. Methods: A multicenter cross-sectional study was conducted in Spain, involving a committee of nursing experts who participated in a Delphi panel (n = 5) and cognitive interviews (n = 5) and a sample of nursing preceptors (n = 300) from 57 primary health care centers (2019-2020). The CEEEC was reviewed by experts for the conceptual semantic adequacy of the 24 items for its application in primary health care. Nurse preceptors' responses to the CEEEC scale were used to study the validity and reliability of the measure, including factor analysis, convergent validity with the Health Sciences-Evidence Based Practice scale and a matched test-retest over a three-week interval. Results: According to the consensus of experts, the CEEEC scale is valid for primary health care with minimal modifications (change "patient" to "user"). Based on the analysis of responses to the scale, the corrected item-total correlations of the 24 items were ≥ 0.40 and were grouped into a single factor, explaining 46.3% of the variance. The Cronbach's alpha value was 0.95. Regarding convergent validity, there was a positive correlation between the CEEEC scale and the score of the Health Sciences-Evidence Based Practice scale (Pearson's coefficient= 0.33; p < 0.001). The overall intraclass correlation coefficient was 0.91. Finally, the mean CEEEC score was 61.9 points (range 0-96). The two most positive contributions were 'Nursing students enable nursing professionals to perform their teaching role' and 'Nursing students become future professionals who know the healthcare facility'. Conclusions: The CEEEC scale provides a valid and reliable measure of nursing students' contributions to primary health care. Nursing students' contributions to Spanish primary health care were positive, especially towards the nursing profession and healthcare organizations.This work was supported by grants by Instituto de Salud Carlos III, Spanish State Secretary of R+D+I, Fondo Europeo de Desarrollo Regional (FEDER) and Fondo Social Europeo (FSE) [grant number PI18/00086] and Instituto de Investigación Sanitaria del Principado de Asturias (ISPA). The study funders had no role in the study design and in the collection, analysis, and interpretation of data, and the authors have sole responsibility for the manuscript content.S

Epilepsy in Neurodegenerative Diseases: Related Drugs and Molecular Pathways

Alzheimer’s disease; Huntington’s disease; Parkinson’s diseaseEnfermedad de Alzheimer; Enfermedad de Huntington; Enfermedad de ParkinsonMalaltia d'Alzheimer; Malaltia de Huntington; Malaltia de ParkinsonEpilepsy is a chronic disease of the central nervous system characterized by an electrical imbalance in neurons. It is the second most prevalent neurological disease, with 50 million people affected around the world, and 30% of all epilepsies do not respond to available treatments. Currently, the main hypothesis about the molecular processes that trigger epileptic seizures and promote the neurotoxic effects that lead to cell death focuses on the exacerbation of the glutamate pathway and the massive influx of Ca2+ into neurons by different factors. However, other mechanisms have been proposed, and most of them have also been described in other neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, or multiple sclerosis. Interestingly, and mainly because of these common molecular links and the lack of effective treatments for these diseases, some antiseizure drugs have been investigated to evaluate their therapeutic potential in these pathologies. Therefore, in this review, we thoroughly investigate the common molecular pathways between epilepsy and the major neurodegenerative diseases, examine the incidence of epilepsy in these populations, and explore the use of current and innovative antiseizure drugs in the treatment of refractory epilepsy and other neurodegenerative diseases.A.C. acknowledges the support of the Spanish Ministry of Science, Innovation and Universities under the grant Juan de la Cierva (FJC2018-036012-I). Authors acknowledge the support of the Instituto de Salud Carlos III (ISCIII) Acción Estratégica en Salud, integrated into the Spanish National R+D+I Plan and financed by ISCIII Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER “Una manera de hacer Europa”) grant PI17/01474 awarded to M.B. Boada, grant PI19/00335 awarded to M.M. and the European Social Fund (ESF “Investing in your future”) for the Sara Borrell Contract (CD19/00232) to SA-L; M.E. acknowledges the support of the Spanish Ministry of Economy and Competitiveness under the project SAF2017-84283-R, and CIBERNED under project CB06/05/0024. E.B.S. acknowledges the support of the Portuguese Science and Technology Foundation (FCT) for the strategic fund (UIDB/04469/2020). A.R. acknowledges the support of CIBERNED (Instituto de Salud Carlos III (ISCIII)), the EU/EFPIA Innovative Medicines Initiative Joint Undertaking, ADAPTED Grant Nº 115975, from EXIT project, EU Euronanomed3 Program JCT2017 Grant Nº AC17/00100, from PREADAPT project. Joint Program for Neurodegenerative Diseases (JPND) Grant No. AC19/00097, and from grants PI13/02434, PI16/01861 BA19/00020, and PI19/01301. Acción Estratégica en Salud, integrated in the Spanish National RCDCI Plan and financed by Instituto de Salud Carlos III (ISCIII)- Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER—“Una manera de Hacer Europa”), by Fundación bancaria “La Caixa” and Grífols SA (GR@ACE project)

Epilepsy in neurodegenerative diseases: related drugs and molecular pathways

Epilepsy is a chronic disease of the central nervous system characterized by an electrical imbalance in neurons. It is the second most prevalent neurological disease, with 50 million people affected around the world, and 30% of all epilepsies do not respond to available treatments. Currently, the main hypothesis about the molecular processes that trigger epileptic seizures and promote the neurotoxic effects that lead to cell death focuses on the exacerbation of the glutamate pathway and the massive influx of Ca2+ into neurons by different factors. However, other mechanisms have been proposed, and most of them have also been described in other neurodegenerative diseases, such as Alzheimers disease, Parkinsons disease, Huntingtons disease, or multiple sclerosis. Interestingly, and mainly because of these common molecular links and the lack of effective treatments for these diseases, some antiseizure drugs have been investigated to evaluate their therapeutic potential in these pathologies. Therefore, in this review, we thoroughly investigate the common molecular pathways between epilepsy and the major neurodegenerative diseases, examine the incidence of epilepsy in these populations, and explore the use of current and innovative antiseizure drugs in the treatment of refractory epilepsy and other neurodegenerative diseases.Acknowledges the support of the Spanish Ministry of Science, Innovation and Universities under the grant Juan de la Cierva (FJC2018-036012-I). Authors acknowledge the support of the Instituto de Salud Carlos III (ISCIII) Acción Estratégica en Salud, integrated into the Spanish National R+D+I Plan and financed by ISCIII Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER “Una manera de hacer Europa”) grant PI17/01474 awarded to M.B. Boada and grant PI19/00335 awarded to M.M.; M.E. acknowledges the support of the Spanish Ministry of Economy and Competitiveness under the project SAF2017- 84283-R, and CIBERNED under project CB06/05/0024. E.B.S. acknowledges the support of the Portuguese Science and Technology Foundation (FCT) for the strategic fund (UIDB/04469/2020). A.R. acknowledges the support of CIBERNED (Instituto de Salud Carlos III (ISCIII)), the EU/EFPIA Innovative Medicines Initiative Joint Undertaking, ADAPTED Grant Nº 115975, from EXIT project, EU Euronanomed3 Program JCT2017 Grant Nº AC17/00100, from PREADAPT project. Joint Program for Neurodegenerative Diseases (JPND) Grant No. AC19/00097, and from grants PI13/02434, PI16/01861 BA19/00020, and PI19/01301. Acción Estratégica en Salud, integrated in the Spanish National RCDCI Plan and financed by Instituto de Salud Carlos III (ISCIII)- Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER—“Una manera de Hacer Europa”), by Fundación bancaria “La Caixa” and Grífols SA (GR@ACE project)info:eu-repo/semantics/publishedVersio

Epilepsy in Neurodegenerative Diseases: Related Drugs and Molecular Pathways

Epilepsy is a chronic disease of the central nervous system characterized by an electrical imbalance in neurons. It is the second most prevalent neurological disease, with 50 million people affected around the world, and 30% of all epilepsies do not respond to available treatments. Currently, the main hypothesis about the molecular processes that trigger epileptic seizures and promote the neurotoxic effects that lead to cell death focuses on the exacerbation of the glutamate pathway and the massive influx of Ca2+ into neurons by different factors. However, other mechanisms have been proposed, and most of them have also been described in other neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, or multiple sclerosis. Interestingly, and mainly because of these common molecular links and the lack of effective treatments for these diseases, some antiseizure drugs have been investigated to evaluate their therapeutic potential in these pathologies. Therefore, in this review, we thoroughly investigate the common molecular pathways between epilepsy and the major neurodegenerative diseases, examine the incidence of epilepsy in these populations, and explore the use of current and innovative antiseizure drugs in the treatment of refractory epilepsy and other neurodegenerative diseases. Keywords: Alzheimer's disease; Huntington's disease; Parkinson's disease; epilepsy; multiple sclerosis; neurodegenerative diseases

Auxin response factors ARF6 and ARF8 promote jasmonic acid production and flower maturation

Pollination in flowering plants requires that anthers release pollen when the gynoecium is competent to support fertilization. We show that i

The polygenic risk for bipolar disorder influences brain regional function relating to visual and default state processing of emotional information

Genome-wise association studies have identified a number of common single-nucleotide polymorphisms (SNPs), each of small effect, associated with risk to bipolar disorder (BD). Several risk-conferring SNPs have been individually shown to influence regional brain activation thus linking genetic risk for BD to altered brain function. The current study examined whether the polygenic risk score method, which models the cumulative load of all known risk-conferring SNPs, may be useful in the identification of brain regions whose function may be related to the polygenic architecture of BD. We calculated the individual polygenic risk score for BD (PGR-BD) in forty-one patients with the disorder, twenty-five unaffected first-degree relatives and forty-six unrelated healthy controls using the most recent Psychiatric Genomics Consortium data. Functional magnetic resonance imaging was used to define task-related brain activation patterns in response to facial affect and working memory processing. We found significant effects of the PGR-BD score on task-related activation irrespective of diagnostic group. There was a negative association between the PGR-BD score and activation in the visual association cortex during facial affect processing. In contrast, the PGR-BD score was associated with failure to deactivate the ventromedial prefrontal region of the default mode network during working memory processing. These results are consistent with the threshold-liability model of BD, and demonstrate the usefulness of the PGR-BD score in identifying brain functional alternations associated with vulnerability to BD. Additionally, our findings suggest that the polygenic architecture of BD is not regionally confined but impacts on the task-dependent recruitment of multiple brain regions

Structural and Functional Brain Correlates of Cognitive Impairment in Euthymic Patients with Bipolar Disorder

Introduction Cognitive impairment in the euthymic phase is a well-established finding in bipolar disorder. However, its brain structural and/or functional correlates are uncertain. Methods Thirty-three euthymic bipolar patients with preserved memory and executive function and 28 euthymic bipolar patients with significant memory and/or executive impairment, as defined using two test batteries, the Rivermead Behavioural Memory Test (RBMT) and the Behavioural Assessment of the Dysexecutive Syndrome (BADS), plus 28 healthy controls underwent structural MRI using voxel-based morphometry (VBM). Twenty-seven of the cognitively preserved patients, 23 of the cognitively impaired patients and 28 controls also underwent fMRI during performance of the n-back working memory task. Results No clusters of grey or white matter volume difference were found between the two patient groups. During n-back performance, the cognitively impaired patients showed hypoactiva- tion compared to the cognitively preserved patients in a circumscribed region in the right dorsolateral prefrontal cortex. Both patient groups showed failure of de-activation in the medial frontal cortex compared to the healthy controls. Conclusions Cognitive impairment in euthymic bipolar patients appears from this study to be unrelated to structural brain abnormality, but there was some evidence for an association with altered prefrontal function

What we learn about bipolar disorder from large-scale neuroimaging:Findings and future directions from the ENIGMA Bipolar Disorder Working Group

MRI-derived brain measures offer a link between genes, the environment and behavior and have been widely studied in bipolar disorder (BD). However, many neuroimaging studies of BD have been underpowered, leading to varied results and uncertainty regarding effects. The Enhancing Neuro Imaging Genetics through Meta-Analysis (ENIGMA) Bipolar Disorder Working Group was formed in 2012 to empower discoveries, generate consensus findings and inform future hypothesis-driven studies of BD. Through this effort, over 150 researchers from 20 countries and 55 institutions pool data and resources to produce the largest neuroimaging studies of BD ever conducted. The ENIGMA Bipolar Disorder Working Group applies standardized processing and analysis techniques to empower large-scale meta- and mega-analyses of multimodal brain MRI and improve the replicability of studies relating brain variation to clinical and genetic data. Initial BD Working Group studies reveal widespread patterns of lower cortical thickness, subcortical volume and disrupted white matter integrity associated with BD. Findings also include mapping brain alterations of common medications like lithium, symptom patterns and clinical risk profiles and have provided further insights into the pathophysiological mechanisms of BD. Here we discuss key findings from the BD working group, its ongoing projects and future directions for large-scale, collaborative studies of mental illness

Genomic Characterization of Host Factors Related to SARS-CoV-2 Infection in People with Dementia and Control Populations: The GR@ACE/DEGESCO Study

Emerging studies have suggested several chromosomal regions as potential host genetic factors involved in the susceptibility to SARS-CoV-2 infection and disease outcome. We nested a COVID-19 genome-wide association study using the GR@ACE/DEGESCO study, searching for susceptibility factors associated with COVID-19 disease. To this end, we compared 221 COVID-19 confirmed cases with 17,035 individuals in whom the COVID-19 disease status was unknown. Then, we performed a meta-analysis with the publicly available data from the COVID-19 Host Genetics Initiative. Because the APOE locus has been suggested as a potential modifier of COVID-19 disease, we added sensitivity analyses stratifying by dementia status or by disease severity. We confirmed the existence of the 3p21.31 region (LZTFL1, SLC6A20) implicated in the susceptibility to SARS-CoV-2 infection and TYK2 gene might be involved in COVID-19 severity. Nevertheless, no statistically significant association was observed in the COVID-19 fatal outcome or in the stratified analyses (dementia-only and non-dementia strata) for the APOE locus not supporting its involvement in SARS-CoV-2 pathobiology or COVID-19 prognosis