Publications by authors named "Yi Chuan Cheng"

Central nervous system lesions often cause permanent motility defects in mammals since the injured neurons cannot regenerate. In contrast, lower vertebrates like zebrafish can regenerate lost neurons and restore motor function. This study investigates the efficacy of SC79, a pan-Akt activator, and A674563, a selective Akt1 inhibitor, as potential therapeutic agents for promoting spinal cord recovery post-injury.

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Notch signaling is a conserved pathway crucial for nervous system development. Disruptions in this pathway are linked to neurodevelopmental disorders, neurodegenerative diseases, and brain tumors. genes, major downstream targets of Notch, are commonly used as markers for Notch activation.

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Traumatic injury to the spinal cord can lead to significant, permanent disability. Mammalian spinal cords are not capable of regeneration; in contrast, adult zebrafish are capable of such regeneration, fully recovering motor function. Understanding the mechanisms underlying zebrafish neuroregeneration may provide useful information regarding endogenous regenerative potential and aid in the development of therapeutic strategies in humans.

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Neural progenitor cells are self-renewable, proliferative, and multipotent cell populations that generate diverse types of neurons and glia to build the nervous system. Transcription factors play critical roles in regulating various cellular processes; however, the transcription factors that regulate the development of neural progenitors are yet to be identified. In the present study, we demonstrated that zebrafish is expressed in the neural progenitor cells of the neuroectoderm.

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Home-based yoga practice has not been approved as a method for alleviating premenstrual symptoms in Taiwan. This study was a cluster randomized trial. A total of 128 women self-reporting at least one premenstrual symptom were enrolled in the study, of which there were 65 participants in the experimental group and 63 participants in the control group.

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Microglial activation-induced neuroinflammation contributes to onset and progression of sporadic and hereditary Parkinson's disease (PD). Activated microglia secrete pro-inflammatory and neurotoxic IL-1β, IL-6 and TNF-α, which subsequently promote neurodegeneration. Formyl peptide receptor-1 (FPR1) of CNS microglia functions as pattern recognition receptor and is activated by N-formylated peptides, leading to microglial activation, induction of inflammatory responses and resulting neurotoxicity.

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Bone morphogenetic protein (BMP) signaling regulates neural induction, neuronal specification, and neuronal differentiation. However, the role of BMP signaling in neural progenitors remains unclear. This is because interruption of BMP signaling before or during neural induction causes severe effects on subsequent neural developmental processes.

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Objective: The aim of this study was to explore mothers' perceived level of stress one month after hospital discharge following the birth of singleton and multiple preterm infants.

Design: A cross-sectional design was used to compare mother's perceived stress in two groups of postpartum mothers and the relationship of the theoretical antecedents and these variables.

Setting: A neonatal intensive care unit in a medical center in Taiwan.

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Coinfection with and results in higher mortality in animal studies. However, the pathogenesis and interplay between and in bloodstream infections (BSIs) is unclear. This study determines the clinical features and outcomes of mixed / (CA/SA) BSIs and biofilm formation on pathogenesis during coinfection.

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Background/aim: This study aimed to explore RGS2 as a regulator of melanoma cell growth.

Materials And Methods: Effect of RGS2 over-expression was analyzed in three melanoma cell lines, and Rgs2 knockdown was performed in zebrafish.

Results: RGS2 was differentially expressed among the cell lines.

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Parkinson's disease (PD), the most common neurodegenerative motor disorder, is currently incurable. Although many studies have provided insights on the substantial influence of genetic factors on the occurrence and development of PD, the molecular mechanism underlying the disease is largely unclear. Previous studies have shown that point mutations in the phospholipase A2 group VI gene (PLA2G6) correlate with young-onset dystonia-parkinsonism type 14 (PARK14).

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A novel three-dimensional Cd coordination framework, namely, poly[{μ-bis[4-(2-methylimidazol-1-yl)phenyl] ether-κN:N}(μ-naphthalene-1,4-dicarboxylato-κO:O,O)cadmium(II)], [Cd(CHO)(CHNO)] or [Cd(1,4-NDC)(BMIOPE)], where 1,4-HNDC is naphthalene-1,4-dicarboxylic acid and BMIOPE is bis[4-(2-methylimidazol-1-yl)phenyl] ether, has been prepared and characterized by single-crystal X-ray diffraction, elemental analysis, IR spectroscopy and thermogravimetric analysis. The compound displays a novel fourfold interpenetrating diamond-like network. In addition, it not only shows a strong fluorescence emission in the solid state, but also exhibits excellent photocatalytic activity for the degradation of methylene blue (MB) at room temperature.

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Candida albicans bloodstream infection (BSI) is epidemiologically important because of its increasing frequency and serious outcome. Strain typing and delineation of the species are essential for understanding the phylogenetic relationship and clinical significance. Microsatellite CAI genotyping and multilocus sequence typing (MLST) were performed on 285 C.

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This article focuses on the unique needs and concerns of nursing educators and nursing students in the face of the COVID-19 pandemic. During social distancing, interacting with other human beings has been restricted. This would undermine the experiential learning of nursing students.

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Alzheimer's disease (AD) is a neuronal dementia with progressive memory loss. Amyloid-beta (Aβ) peptides has major effect in the neurodegenerative disorder, which are thought to promote mitochondrial dysfunction in AD brains. Anti-AD drugs acting upon the brain are generally difficult to develop, often cause serious side effects or lack therapeutic efficacy.

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Herein, positively surface-charged silver nanoparticles (AgNPs) capped with trimethylchitosan nitrate (TMCN) were synthesized using an environmentally friendly method. Nano-sized TMCN-AgNPs (~80 nm) with high zeta potential (>30 mV) provide sufficient static repulsion to stabilize colloid AgNPs in aqueous solutions without aggregation for >3 months. In in vitro cell cycle assays, TMCN-AgNPs showed low cytotoxicity towards L929 cells.

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Background And Purpose: It is essential to develop a reliable predictive serum biomarker for Parkinson's disease (PD). The accumulation of alpha-synuclein (αSyn) and up-regulated expression of Rab35 participate in the etiology of PD. The purpose of this investigation was to determine whether the combined assessment of serum αSyn and Rab35 is a useful predictive biomarker for PD.

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Ischemic stroke arising from the sudden blockage of arteries in the brain, is a common and serious brain damaging problem worldwide, often leading to disability or death. The oxygen glucose deprivation (OGD) model was created to improve understanding of hypoxia- and hypoglycemia-induced neuronal cell injury, and provide an in vitro surrogate to assess novel treatments for cerebral hypoxia-ischemia. AMP-activated protein kinase (AMPK) is a critical neuroprotective regulator of energy homeostasis, metabolism and cell survival.

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MicroRNAs (miRs) downregulate or upregulate the mRNA level by binding to the 3'-untranslated region (3'UTR) of target gene. Dysregulated miR levels can be used as biomarkers of Parkinson's disease (PD) and could participate in the etiology of PD. In the present study, 45 brain-enriched miRs were evaluated in serum samples from 50 normal subjects and 50 sporadic PD patients.

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Recent studies have suggested that DDX3 functions in antiviral innate immunity, but the underlying mechanism remains elusive. We previously identified target mRNAs whose translation is controlled by DDX3. Pathway enrichment analysis of these targets indicated that DDX3 is involved in various infections and inflammation.

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Background: Many molecules and signaling pathways involved in neural development play a role in neurodegenerative diseases and brain tumor progression. Peroxisome proliferator-activated receptor (PPAR) proteins regulate the differentiation of tissues and the progression of many diseases. However, the role of these proteins in neural development is unclear.

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PARK14 patients with homozygous (D331Y) PLA2G6 mutation display motor deficits of pure early-onset Parkinson's disease (PD). The aim of this study is to investigate the pathogenic mechanism of mutant (D331Y) PLA2G6-induced PD. We generated knockin (KI) mouse model of PARK14 harboring homozygous (D331Y) PLA2G6 mutation.

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Peroxisome proliferator-activated receptor gamma (PPARγ) belongs to a family of ligand-activated nuclear receptors known to regulate many crucial physiological and pathological conditions. Indeed, altered PPARγ transcriptional activity contributes to metabolic syndromes (obesity and hyperglycemia associated with type 2 diabetes mellitus), stroke and neurodegenerative diseases. Various studies suggest that PPARγ agonists influence neuronal deficits in Alzheimer's Disease (AD) patients and rodent models of AD.

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Objective: The purpose of this study was to investigate the effectiveness of preterm infant learning portfolios in enabling mothers to develop infant care knowledge and skills, as well as confidence in their abilities.

Design: This study used a quasi-experimental design.

Setting And Participants: The sample consisted of 52 mothers with preterm infants recruited at a neonatal intermediate unit of a medical centre in central Taiwan.

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Hexanucleotide repeat expansions in the C9orf72 gene are a common genetic cause of familial and sporadic amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). However, the function of C9orf72 in neural development and the pathogenic mechanism underlying neurodegeneration are unknown. We found that disrupting C9orf72 expression by using C9orf72 constructs that lack the complete DENN domain result in reduced GTPase activity in zebrafish embryos, demonstrating the indispensability of the complete DENN domain.

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