ABSTRACT
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.
ABSTRACT
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).
Subject(s)
Antigens, CD/metabolism , Brain/embryology , Membrane Glycoproteins , Membrane Proteins/chemistry , Membrane Proteins/metabolism , Nerve Tissue Proteins/metabolism , Neurons, Afferent/metabolism , Spinal Cord/embryology , Amino Acid Sequence , Animals , Antigens, CD/genetics , Blotting, Northern , Chick Embryo , Cloning, Molecular , In Situ Hybridization , Membrane Proteins/genetics , Molecular Sequence Data , Nerve Tissue Proteins/genetics , RNA, Messenger/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Sequence Homology, Amino Acid , Tetraspanin 29 , Tetraspanins , Time Factors , Tissue DistributionABSTRACT
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.
Subject(s)
Calcium-Calmodulin-Dependent Protein Kinases/metabolism , Isoenzymes/metabolism , Mitogen-Activated Protein Kinases , Neurites/enzymology , Signal Transduction/physiology , 3T3 Cells/cytology , 3T3 Cells/enzymology , Animals , Antibodies , Brain-Derived Neurotrophic Factor/pharmacology , Cadherins/pharmacology , Calcium-Calmodulin-Dependent Protein Kinases/analysis , Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors , Calcium-Calmodulin-Dependent Protein Kinases/immunology , Cell Membrane/enzymology , Cells, Cultured , Chick Embryo , Enzyme Activation/drug effects , Enzyme Activation/physiology , Enzyme Inhibitors/pharmacology , Fibroblast Growth Factor 2/pharmacology , Flavonoids/pharmacology , Fluorescent Antibody Technique , Laminin/pharmacology , Mice , Mitogen-Activated Protein Kinase 1 , Mitogen-Activated Protein Kinase 3 , Myelin Basic Protein/pharmacology , Neurites/drug effects , Neurons/cytology , Neurons/enzymology , Neurons/ultrastructure , Retina/cytology , Substrate Specificity , p38 Mitogen-Activated Protein KinasesABSTRACT
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