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INTRODUCTION: Support care aims to improve the experience of patients. m-health is one of the tools recently developed to promote patient empowerment. The objective of this study was to evaluate the appreciation of an m-health application to enhance prostatectomy path for patients suffering from prostate cancer. METHOD: A prospective monocentric study was conducted in the urology department of the University Hospital of Rennes from February to April 2023. MyCHU application was optimized by integrating information sheets in the postoperative period after prostatectomy on sphincter rehabilitation exercises, erectile dysfunction and urinary incontinence. The questionnaire used to evaluate the usability of "MyCHU" application was the System Usability Scale (SUS). Semi-structured interviews explored the patients' feelings about the content of the information sheets and the impact on their empowerment regarding sexual disorders. RESULTS: Twelve patients participated in this study and 7 agreed to complete an interview The average SUS score was 75.58, which indicate an high usability. Patients appreciated the fact that the application structured their healthcare pathway by centralizing information. The information sheets were clear and accurate. The impact on their empowerment was positive, with a gain in their ability to take ownership of the therapies. CONCLUSION: The role of digital technology in health care has been growing in recent years. Our study has shown the interest that mobile application can bring to the patient who undergoes prostatectomy. It increases his empowerment and favor the dialogue with his surgeon.
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Proteins of the tetraspanin superfamily participate in the formation of plasma membrane signaling complexes; recent evidence implicates neuronal tetraspanins in axon growth and target recognition. We used a degenerate PCR screen to identify cDNAs encoding tetraspanins expressed in the embryonic spinal cord. Two cDNAs identified apparently represent chick homologues of NAG-2 (cnag) and CD9 (chCD9). A third clone encodes a novel tetraspanin (neurospanin). All three mRNAs are widely expressed but exhibit developmentally distinct patterns of expression in the nervous system. Both neurospanin and cnag exhibit high relative expression in nervous tissue, including brain, spinal cord and dorsal root ganglia (DRG).
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Antígenos CD/metabolismo , Encéfalo/embriología , Glicoproteínas de Membrana , Proteínas de la Membrana/química , Proteínas de la Membrana/metabolismo , Proteínas del Tejido Nervioso/metabolismo , Neuronas Aferentes/metabolismo , Médula Espinal/embriología , Secuencia de Aminoácidos , Animales , Antígenos CD/genética , Northern Blotting , Embrión de Pollo , Clonación Molecular , Hibridación in Situ , Proteínas de la Membrana/genética , Datos de Secuencia Molecular , Proteínas del Tejido Nervioso/genética , ARN Mensajero/metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Homología de Secuencia de Aminoácido , Tetraspanina 29 , Tetraspaninas , Factores de Tiempo , Distribución TisularRESUMEN
Several distinct classes of proteins positively regulate axonal growth; some of these are known to activate the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) signaling cascade, at least in nonneuronal cells. We have found that N-cadherin, as well as laminin (LN) and basic fibroblast growth factor (bFGF), can activate ERK in embryonic chick retinal neurons. Additionally, adhesion of retinal neurons to LN or N-cadherin substrates induced a redistribution of ERK from the cytoplasm toward the plasma membrane. Neurite outgrowth induced by bFGF, LN, or N-cadherin was strongly inhibited by treatment with inhibitors of ERK kinase activation, but not by an inhibitor of p38 MAPK. We conclude (1) that N-cadherin and LN can activate ERK in retinal neurons and (2) that activation of ERK is required for full neurite outgrowth induced by these proteins. Our results suggest that ERK activation is one point of convergence for signaling pathways generated by a variety of axon growth inducers.
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Proteínas Quinasas Dependientes de Calcio-Calmodulina/metabolismo , Isoenzimas/metabolismo , Proteínas Quinasas Activadas por Mitógenos , Neuritas/enzimología , Transducción de Señal/fisiología , Células 3T3/citología , Células 3T3/enzimología , Animales , Anticuerpos , Factor Neurotrófico Derivado del Encéfalo/farmacología , Cadherinas/farmacología , Proteínas Quinasas Dependientes de Calcio-Calmodulina/análisis , Proteínas Quinasas Dependientes de Calcio-Calmodulina/antagonistas & inhibidores , Proteínas Quinasas Dependientes de Calcio-Calmodulina/inmunología , Membrana Celular/enzimología , Células Cultivadas , Embrión de Pollo , Activación Enzimática/efectos de los fármacos , Activación Enzimática/fisiología , Inhibidores Enzimáticos/farmacología , Factor 2 de Crecimiento de Fibroblastos/farmacología , Flavonoides/farmacología , Técnica del Anticuerpo Fluorescente , Laminina/farmacología , Ratones , Proteína Quinasa 1 Activada por Mitógenos , Proteína Quinasa 3 Activada por Mitógenos , Proteína Básica de Mielina/farmacología , Neuritas/efectos de los fármacos , Neuronas/citología , Neuronas/enzimología , Neuronas/ultraestructura , Retina/citología , Especificidad por Sustrato , Proteínas Quinasas p38 Activadas por MitógenosRESUMEN
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