RESUMEN
Strumpellin/Wiskott-Aldrich syndrome protein and SCAR homologue (WASH) complex subunit 5 (WASHC5) is a core component of the WASH complex, and its mutations confer pathogenicity for hereditary spastic paraplegia (HSP) type SPG8, a rare neurodegenerative gait disorder. WASH complex activates actin-related protein-2/3-mediated actin polymerization and plays a pivotal role in intracellular membrane trafficking in endosomes. In this study, we examined the role of strumpellin in the regulation of structural plasticity of cortical neurons involved in gait coordination. Administration of a lentivirus containing a strumpellin-targeting short hairpin RNA (shRNA) to cortical motor neurons lead to abnormal motor coordination in mice. Strumpellin knockdown using shRNA attenuated dendritic arborization and synapse formation in cultured cortical neurons, and this effect was rescued by wild-type strumpellin expression. Compared with the wild-type, strumpellin mutants N471D or V626F identified in patients with SPG8 exhibited no differences in rescuing the defects. Moreover, the number of F-actin clusters in neuronal dendrites was decreased by strumpellin knockdown and rescued by strumpellin expression. In conclusion, our results indicate that strumpellin regulates the structural plasticity of cortical neurons via actin polymerization.
Asunto(s)
Actinas , Paraplejía Espástica Hereditaria , Animales , Ratones , Actinas/metabolismo , Endosomas/metabolismo , Marcha , Neuronas/metabolismo , ARN Interferente Pequeño/metabolismo , Paraplejía Espástica Hereditaria/genética , Paraplejía Espástica Hereditaria/metabolismoRESUMEN
The balance between the actions of protein kinases and phosphatases is crucial for neuronal functions, including synaptic plasticity. Although the phosphorylation and dephosphorylation of neuronal proteins are regulated by synaptic plasticity, no systematic analyses of this have yet been conducted. We performed a phosphoproteomic analysis of hippocampal synaptic plasticity using a nano-Acquity/Synapt LC-MS/MS system. Neuronal proteins were extracted from hippocampal tissues and cultured neurons exposed to long-term potentiation (LTP) or long-term depression (LTD). Filter-aided sample preparation (FASP) was performed to remove residual anionic detergents for complete tryptic digestion. Phosphopeptides were then enriched using TiO2 chromatography, followed by immunoaffinity chromatography with an anti-phosphotyrosine antibody. Among the 1500 phosphopeptides identified by LC-MS/MS, 374 phosphopeptides were detected simultaneously in both hippocampal tissues and cultured neurons. Semi-quantification counting the number of spectra of each phosphopeptide showed that 42 of 374 phosphopeptides changed significantly depending on synaptic plasticity. In conclusion, a new proteomic method using sequential enrichment of phosphopeptides and semi-quantification enabled the phosphoproteomic analysis of hippocampal synaptic plasticity.
Asunto(s)
Fosfopéptidos , Proteómica , Cromatografía Liquida , Hipocampo/metabolismo , Depresión Sináptica a Largo Plazo/fisiología , Plasticidad Neuronal/fisiología , Fosfopéptidos/química , Proteoma/metabolismo , Proteómica/métodos , Espectrometría de Masas en Tándem/métodosRESUMEN
PURPOSE: The aim of this study was to examine the validity and reliability of the Korean version of the self-efficacy for managing chronic disease 6-item scale (SECD-6-K). METHODS: The English version of the Self-Efficacy for Managing Chronic Disease 6-item Scale first underwent forward and backward translation procedures. The SECD-6-K was then used to collect data from 350 adults diagnosed with chronic diseases. Content, construct, convergent, discriminant, and criterion validity were all evaluated. Reliability was assessed using Cronbach's α. SPSS 25.0 and the data were analyzed using AMOS 26.0 software. RESULTS: The SECD-6-K consists of six items in two domains: disease management and health behavior. The results for construct, convergent, and discriminant validity were good. Exploratory factor analysis produced eigen values between 2.27 and 3.28, with factors total explained cumulative variance of 91.1%. Confirmatory factor analysis supported goodness of fit and reliability for the modified SECD-6-K model. The criterion validity also showed significant correlation with both the Patient Health Questionnaire and 12-item Short-Form Health Survey version 2. Finally, reliability was found to be excellent. CONCLUSION: This study identified the high reliability and validity of SECD-6-K. The SECD-6-K is an appropriate tool for determining Korean patients' self-efficacy in managing their chronic conditions. Therefore, this scale may be used in clinical settings as well as in educational and research settings.
Asunto(s)
Enfermedad Crónica/terapia , Manejo de la Enfermedad , Autoeficacia , Encuestas y Cuestionarios/normas , Adulto , Humanos , Psicometría , Reproducibilidad de los Resultados , República de Corea , TraducciónRESUMEN
The neural circuits of the infant brain are rapidly established near 6 months of age, but neurodevelopmental disorders can be diagnosed only at the age of 2-3 years using existing diagnostic methods. Early diagnosis is very important to alleviate life-long disability in patients through appropriate early intervention, and it is imperative to develop new diagnostic methods for early detection of neurodevelopmental disorders. We examined the serum level of secretogranin II (SCG2) in pediatric patients to evaluate its potential role as a biomarker for neurodevelopmental disorders. A plasmonic immunosensor performing an enzyme-linked immunosorbent assay (ELISA) on a gold nanodot array was developed to detect SCG2 in small volumes of serum. This nanoplasmonic immunosensor combined with tyramide signal amplification was highly sensitive to detect SCG2 in only 5 µL serum samples. The analysis using the nanoplasmonic immunosensor revealed higher serum SCG2 levels in pediatric patients with developmental delay than in the control group. Overexpression or knockdown of SCG2 in hippocampal neurons significantly attenuated dendritic arborization and synaptic formation. These results suggest that dysregulated SCG2 expression impairs neural development. In conclusion, we developed a highly sensitive nanoplasmonic immunosensor to detect serum SCG2, a candidate biomarker for the early diagnosis of neurodevelopmental disorders.
Asunto(s)
Biomarcadores/sangre , Técnicas Biosensibles/métodos , Inmunoensayo/métodos , Nanopartículas/química , Trastornos del Neurodesarrollo/diagnóstico , Neuronas/patología , Secretogranina II/sangre , Animales , Estudios de Casos y Controles , Niño , Diagnóstico Precoz , Hipocampo/metabolismo , Hipocampo/patología , Humanos , Trastornos del Neurodesarrollo/sangre , Neuronas/metabolismo , RatasRESUMEN
BACKGROUND: With the drastic change in the nursing education environment due to the coronavirus pandemic, several attempts have been made in Korea to help nursing students better adapt to the new learning environment. OBJECTIVE: This study aimed to explore nursing students' experience of online peer tutoring based on the Goal-Reality-Options-Will (GROW) model. DESIGN: A qualitative study using content analysis. SETTINGS: This study was conducted in the department of nursing at two universities in South Korea. PARTICIPANTS: The participants were 14 nursing students who participated as tutors and tutees in the online peer tutoring. METHODS: Three focus group interviews were conducted with the 14 students. Data were transcribed and analyzed using content analysis. RESULTS: Three categories and nine subcategories were extracted. Online peer tutoring allowed participants to learn using a new approach, promoted their efficiency of studying in multiple aspects, and encouraged them to persevere and advance in academics, thus proving its usefulness as an auxiliary strategy to enhance the efficiency of online learning. CONCLUSIONS: Structured online peer tutoring can be a useful tool for enhancing the effectiveness of non-face-to-face education for nursing students. This study's results can serve as meaningful basic data for planning and composing learning activities optimized for the future online nursing education environment.
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Educación en Enfermería , Estudiantes de Enfermería , Humanos , Aprendizaje , Grupo Paritario , Investigación CualitativaRESUMEN
COVID-19 is a respiratory disease caused by a novel coronavirus that quickly spread worldwide, resulting in a global pandemic. Healthcare professionals coming into close contact with COVID-19 patients experience mental health issues, including stress, depression, anxiety, post-traumatic stress disorder, and burnout. This study aimed to explore the experiences of COVID-19-designated hospital nurses in South Korea who provided care for patients based on their lived experiences. Eighteen nurses working in a COVID-19-designated hospital completed in-depth individual telephone interviews between July and September 2020, and the data were analyzed using Giorgi's phenomenological methodology. The essential structure of the phenomenon was growth after the frontline battle against an infectious disease pandemic. Nine themes were identified: Pushed onto the Battlefield Without Any Preparation, Struggling on the Frontline, Altered Daily Life, Low Morale, Unexpectedly Long War, Ambivalence Toward Patients, Forces that Keep Me Going, Giving Meaning to My Work, and Taking Another Step in One's Growth. The nurses who cared for patients with COVID-19 had both negative and positive experiences, including post-traumatic growth. These findings could be used as basic data for establishing hospital systems and policies to support frontline nurses coping with infectious disease control to increase their adaption and positive experiences.
Asunto(s)
COVID-19/enfermería , Enfermeras y Enfermeros , Hospitales , Humanos , Pandemias , República de Corea/epidemiologíaRESUMEN
PTPRT has been known to regulate synaptic formation and dendritic arborization of hippocampal neurons. PTPRT-/- null and PTPRT-D401A mutant mice displayed enhanced depression-like behaviors compared with wild-type mice. Transient knockdown of PTPRT in the dentate gyrus enhanced the depression-like behaviors of wild-type mice, whereas rescued expression of PTPRT ameliorated the behaviors of PTPRT-null mice. Chronic stress exposure reduced expression of PTPRT in the hippocampus of mice. In PTPRT-deficient mice the expression of GluR2 (also known as GRIA2) was attenuated as a consequence of dysregulated tyrosine phosphorylation, and the long-term potentiation at perforant-dentate gyrus synapses was augmented. The inhibitory synaptic transmission of the dentate gyrus and hippocampal GABA concentration were reduced in PTPRT-deficient mice. In addition, the hippocampal expression of GABA transporter GAT3 (also known as SLC6A11) was decreased, and its tyrosine phosphorylation was increased in PTPRT-deficient mice. PTPRT-deficient mice displayed reduced numbers and neurite length of newborn granule cells in the dentate gyrus and had attenuated neurogenic ability of embryonic hippocampal neural stem cells. In conclusion, our findings show that the physiological roles of PTPRT in hippocampal neurogenesis, as well as synaptic functions, are involved in the pathogenesis of depressive disorder.
Asunto(s)
Depresión , Neurogénesis , Animales , Giro Dentado , Hipocampo , Ratones , Ratones Noqueados , Neurogénesis/genética , Neuronas , SinapsisRESUMEN
Given the prevalence and undesirable consequences of smartphone dependency among adolescents, it is necessary to explore the influencing factors of adolescent smartphone dependency. The aim of this study was to examine the intergenerational transmission of mother-adolescent smartphone dependency and the mediating role of negative parenting, moderated by adolescent gender. Data for 2541 middle school students (mean aged = 13 years)-mother dyads were obtained from the first wave of the Korean Children and Youth Panel Survey 2018 (KCYPS 2018). The moderated mediation model using Hayes PROCESS macro (Model 14) was employed to test the study hypothesis. The moderated mediation model revealed that maternal smartphone dependency was associated with adolescent smartphone dependency. Perceived negative parenting mediated this link and adolescent gender moderated the relationship between negative parenting and adolescent smartphone dependency, especially for adolescent girls. Our findings showed that both maternal smartphone dependency and negative parenting were determinants of adolescent smartphone dependency, suggesting that both factors were important for understanding these issues. Moreover, the mediating role of negative parenting (between maternal and adolescent smartphone dependency) implies that parental education programs designed to improve negative parenting may reduce adolescent smartphone dependency, especially for adolescent girls.
Asunto(s)
Conducta Adictiva , Relaciones Madre-Hijo , Responsabilidad Parental , Teléfono Inteligente , Adolescente , Femenino , Identidad de Género , Humanos , Masculino , Madres , Encuestas y CuestionariosRESUMEN
KIF1A is a brain-specific anterograde motor protein that transports cargoes towards the plus-ends of microtubules. Many variants of the KIF1A gene have been associated with neurodegenerative diseases and developmental delay. Homozygous mutations of KIF1A have been identified in a recessive subtype of hereditary spastic paraplegia (HSP), SPG30. In addition, KIF1A mutations have been found in pure HSP with autosomal dominant inheritance. Here we report the first case of familial complicated HSP with a KIF1A mutation transmitted in autosomal dominant inheritance. A heterozygous p.T258M mutation in KIF1A was found in a Korean family through targeted exome sequencing. They displayed phenotypes of mild intellectual disability with language delay, epilepsy, optic nerve atrophy, thinning of corpus callosum, periventricular white matter lesion, and microcephaly. A structural modeling revealed that the p.T258M mutation disrupted the binding of KIF1A motor domain to microtubules and its movement along microtubules. Assays of peripheral accumulation and proximal distribution of KIF1A motor indicated that the KIF1A motor domain with p.T258M mutation has reduced motor activity and exerts a dominant negative effect on wild-type KIF1A. These results suggest that the p.T258M mutation suppresses KIF1A motor activity and induces complicated HSP accompanying intellectual disability transmitted in autosomal dominant inheritance.