Publications by authors named "Young M Oh"

MicroRNAs play a crucial role in directly reprogramming (converting) human fibroblasts into neurons. Specifically, miR-9/9* and miR-124 (miR-9/9*-124) display neurogenic and cell fate-switching activities when ectopically expressed in human fibroblasts by erasing fibroblast identity and inducing a pan-neuronal state. These converted neurons maintain the biological age of the starting fibroblasts and thus provide a human neuron-based platform to study cellular properties in aged neurons and model adult-onset neurodegenerative disorders using patient-derived cells.

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Article Synopsis
  • Aging is a significant risk factor in neurodegenerative diseases, and studying neuronal aging in controlled backgrounds can help understand the relationship between aging and neurodegeneration.
  • In Huntington's disease, researchers found that the protein RCAN1 increases with age and its reduction can protect against neuron degeneration in affected individuals.
  • Targeting RCAN1, either through genetic modification or the drug G2-115, enhances neuronal resilience by improving gene accessibility linked to longevity and autophagy.
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Spinal epidural hematoma (SEH) is exceedingly rare, especially in children. Acute cervical epidural hematoma presents suddenly, with progressive neurologic deficits. However, it is difficult to diagnose in infants, which results in delayed diagnosis.

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Article Synopsis
  • Aging contributes to neurodegenerative disorders; studying neurons in a controlled environment can help uncover how aging influences diseases like Huntington's.
  • Researchers analyzed gene expression changes in striatal medium spiny neurons from different ages, finding that an increase in the protein RCAN1 is linked to neuronal aging and neurodegeneration.
  • By reducing RCAN1 levels in Huntington's disease models, the neurons showed improved health due to enhanced gene activity related to longevity and autophagy, suggesting that targeting RCAN1 could be a therapeutic strategy.
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Huntington disease (HD) is an inherited neurodegenerative disease with adult-onset clinical symptoms. However, the mechanism by which aging triggers the onset of neurodegeneration in HD patients remains unclear. Modeling the age-dependent progression of HD with striatal medium spiny neurons (MSNs) generated by direct reprogramming of fibroblasts from HD patients at different disease stages identifies age-dependent decline in critical cellular functions such as autophagy/macroautophagy and onset of neurodegeneration.

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Purpose: Using simulation in continuing professional development (CPD) courses for local practitioners is uncommon in Korea. The aim of our study was to evaluate the responses of the local practitioners for a simulation-based short CPD course.

Methods: Following the targeted needs assessment of local practitioners, we developed and implemented a 3-hour simulation-based CPD course for the first 5 minutes of cardiac arrest in the resource-limited local clinics.

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Huntington's disease (HD) is an inherited neurodegenerative disorder with adult-onset clinical symptoms, but the mechanism by which aging drives the onset of neurodegeneration in patients with HD remains unclear. In this study we examined striatal medium spiny neurons (MSNs) directly reprogrammed from fibroblasts of patients with HD to model the age-dependent onset of pathology. We found that pronounced neuronal death occurred selectively in reprogrammed MSNs from symptomatic patients with HD (HD-MSNs) compared to MSNs derived from younger, pre-symptomatic patients (pre-HD-MSNs) and control MSNs from age-matched healthy individuals.

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Background: In patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary interventions (pPCI), longer door-to-balloon (DTB) time is known to be associated with an unfavorable outcome. A percentage of patients with acute coronary occlusion present with atypical electrocardiographic (ECG) findings, known as STEMI-equivalents. We investigated whether DTB time for STEMI-equivalent patients was delayed.

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Prion diseases are mortal neurodegenerative pathologies that are caused by the accumulation of abnormal prion protein (PrPSc) in the brain. Recent advances reveal that calcineurin may play a critical role in regulating nuclear factor kappa B (NF-κB) in the calcium-calmodulin pathway. However, the exact mechanism by calcineurin remains unclear.

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It has been reported that valproic acid (VPA) combined with therapeutic hypothermia can improve survival and neurologic outcomes in a rat asphyxial cardiac arrest model. However, neuroprotective mechanisms of such combined treatment of valproic acid with hypothermia remains unclear. We hypothesized that epigenetic regulation of HSP70 by histone acetylation could increase HSP70-mediated neuroprotection suppressed under hypothermia.

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Background: To evaluate the associations between glycated hemoglobin (HbA1c) at admission and 6-month mortality and outcomes after out-of-hospital cardiac arrest (OHCA) treated by hypothermic targeted temperature management (TTM).

Methods: This single-center retrospective cohort study included adult OHCA survivors who underwent hypothermic TTM from December 2011 to December 2019. High HbA1c at admission was defined as a level higher than 6%.

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Background: Paricalcitol is known to attenuate ischemic-reperfusion injury of various organs. However, it is not known whether paricalcitol prevents neuronal injury after global cerebral ischemia. The purpose of this study is to investigate the neuroprotective effect of paricalcitol in a rat model of transient global cerebral ischemia.

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It is known that the behavior of a drug released from a supporting carrier is influenced by the surrounding environment and the carrier. In this study, we investigated the drug behavior of a swellable electrospun nanofibrous membrane. Nanofibrous mats with different swelling ratios were prepared by mixing cellulose acetate (CA) and polyurethane (PU).

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Magnesium (Mg) and its alloys have attracted much attention as a promising candidate for degradable implant applications however the rapid corrosion of magnesium inside the human body greatly limits its use as an implant material. Therefore, coating the alloy surface with a multifunctional film is a promising way to overcome the drawbacks. Here we propose for the first time a multifunction layer coating to enhance the cell viability, antibacterial property and decelerated corrosion rates to act as a novel material to be used for degradable implant Applications.

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Injured peripheral sensory neurons switch to a regenerative state after axon injury, which requires transcriptional and epigenetic changes. However, the roles and mechanisms of gene inactivation after injury are poorly understood. Here, we show that DNA methylation, which generally leads to gene silencing, is required for robust axon regeneration after peripheral nerve lesion.

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We have successfully extracted cellulose nanocrystals (CNCs) from seaweed by removing unwanted materials via our modified process. The prepared CNCs were mixed with two biocompatible polymers (polyethylene oxide (PEO)/Eudragit S100). We used the most popular electrospinning method to fabricate a micro/nano-net membrane.

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Neuronal hyperexcitability is one of the major characteristics of fragile X syndrome (FXS), yet the molecular mechanisms of this critical dysfunction remain poorly understood. Here we report a major role of voltage-independent potassium (K)-channel dysfunction in hyperexcitability of CA3 pyramidal neurons in knock-out (KO) mice. We observed a reduction of voltage-independent small conductance calcium (Ca)-activated K (SK) currents in both male and female mice, leading to decreased action potential (AP) threshold and reduced medium afterhyperpolarization.

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The ability to convert human somatic cells efficiently to neurons facilitates the utility of patient-derived neurons for studying neurological disorders. As such, ectopic expression of neuronal microRNAs (miRNAs), miR-9/9 and miR-124 (miR-9/9-124) in adult human fibroblasts has been found to evoke extensive reconfigurations of the chromatin and direct the fate conversion to neurons. However, how miR-9/9-124 break the cell fate barrier to activate the neuronal program remains to be defined.

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Background: Hyper-IgE syndrome (HIES) caused by loss-of-function (LOF) mutations in STAT3 gene (STAT3 LOF HIES) is associated with dental and facial abnormalities in addition to immunological defects. The role of STAT3 in the pathogenesis of the dental/facial features is, however, poorly elucidated.

Objectives: Since mechanism of cellular resorption of mineralized tissues such as bone and teeth are similar, we attempted to study the expression of genes involved in bone homeostasis in STAT3 LOF HIES.

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We have investigated the effect of flow rate on shear stress and in turn thrombus formation on a lab-on-a-chip with a microchannel that is suitable for cell culture and growth. Using a combination of Arduino UNO, Arduino Motor Shield, and a SERVO stepper motor, we created a pump system that closely mimics the in vivo conditions of the human body. With this system, we achieved continuous flow of blood and observed attached platelets at the bottom of the collagen coated microslide, confirming that with shear stress, thrombus formation increases.

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Objectives: Neutrophil gelatinase-associated lipocalin (NGAL) is secreted by various tissues in pathologic states. Previous studies reported that post-cardiac arrest serum NGAL levels correlate with short-term neurologic outcomes and survival. The aim of this study was to examine the associations between NGAL levels post-cardiac arrest and long-term outcomes and survival.

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This paper presents a wearable electrophysiological interface with enhanced immunity to motion artifacts. Anti-artifact schemes, including a patch-type modular structure and real-time automatic level adjustment, are proposed and verified in two wireless system prototypes of a patch-type electrocardiogram (ECG) module and an electromyogram (EMG)-based robot-hand controller. Their common ExG readout integrated circuit (ROIC), which is reconfigurable for multiple physiological interfaces, is designed and fabricated in a 0.

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Article Synopsis
  • Mitochondria play crucial roles in both cellular and organismal immunity, but their exact contributions remain unclear.
  • The mitochondrial chaperone HSP-60 enhances anti-bacterial immunity by activating the p38 MAP kinase signaling pathway, specifically in the intestine and neurons.
  • The study identifies that by stabilizing key proteins involved in this immune pathway, HSP-60 boosts resistance to pathogenic bacteria like PA14, suggesting a conserved mechanism across species.
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H3K36 methylation by Set2 targets Rpd3S histone deacetylase to transcribed regions of mRNA genes, repressing internal cryptic promoters and slowing elongation. Here we explore the function of this pathway by analysing transcription in yeast undergoing a series of carbon source shifts. Approximately 80 mRNA genes show increased induction upon SET2 deletion.

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