Publications by authors named "J Y Ko"

4,483 Publications

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Alopecia Areata Treatment Patterns, Healthcare Resource Utilization, and Comorbidities in the US Population Using Insurance Claims.

Adv Ther 2021 Jul 22. Epub 2021 Jul 22.

Yale School of Medicine, New Haven, CT, USA.

Introduction: Alopecia areata (AA) is an autoimmune disorder causing sudden, non-scarring hair loss. There are currently no drugs approved for AA treatment. This study assessed prevalence of comorbidities, treatments, and healthcare costs and resource utilization among patients with AA in the USA.

Methods: Patients diagnosed with AA between January 2011 and December 2018 were identified in IBM MarketScan Research Databases. Eligible patients had no other hair loss-related disorders and were continuously enrolled with medical and pharmacy benefits at least 12 months before and after AA diagnosis. Descriptive statistics were used to summarize comorbid conditions, treatments related to AA or other autoimmune/inflammatory conditions, and all-cause and AA-specific healthcare costs and resource utilization identified from claims data.

Results: A total of 68,121 patients with AA were identified. Mean (SD) age was 40.3 (17.8) years and 61.0% were female. The most common comorbidities included hyperlipidemia (22.4%), hypertension (21.8%), thyroid disorders (13.1%), contact dermatitis or eczema (10.8%), depression (9.5%), and anxiety (8.4%). Comorbid autoimmune diseases included atopic dermatitis (2.8%), psoriasis (2.1%), chronic urticaria (1.5%), and rheumatoid arthritis (1.1%). During the 12-month follow-up period, 37,995 patients (55.8%) were prescribed treatment for their AA or other comorbid autoimmune/inflammatory disease; 44.9% of treated patients were prescribed therapy within 7 days of AA diagnosis. Of patients receiving treatment, 80.3% received topical steroids and 30.0% received oral steroids. Mean (SD) total healthcare costs were $11,241.21 ($43,839.69) for all-causes and $419.12 ($1534.99) for AA. AA-related expenses were driven by outpatient and prescription costs.

Conclusion: Patients with AA have a high comorbidity burden and lack of treatment. Current AA treatments, including systemic therapies other than oral steroids, were not frequently utilized in this study population. Healthcare costs incurred by patients with AA went beyond AA-related expenses. Longitudinal data are needed to better understand treatment trajectories and the disease burden in patients with AA.
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http://dx.doi.org/10.1007/s12325-021-01845-0DOI Listing
July 2021

Npas4 regulates IQSEC3 expression in hippocampal somatostatin interneurons to mediate anxiety-like behavior.

Cell Rep 2021 Jul;36(3):109417

Department of Brain and Cognitive Sciences, Daegu Gyeongbuk Institute of Science and Technology (DGIST), 333 Techno Jungangdae-Ro, Hyeonpoong-Eup, Dalseong-Gun, Daegu 42988, Korea. Electronic address:

Activity-dependent GABAergic synapse plasticity is important for normal brain functions, but the underlying molecular mechanisms remain incompletely understood. Here, we show that Npas4 (neuronal PAS-domain protein 4) transcriptionally regulates the expression of IQSEC3, a GABAergic synapse-specific guanine nucleotide-exchange factor for ADP-ribosylation factor (ARF-GEF) that directly interacts with gephyrin. Neuronal activation by an enriched environment induces Npas4-mediated upregulation of IQSEC3 protein specifically in CA1 stratum oriens layer somatostatin (SST)-expressing GABAergic interneurons. SST interneuron-specific knockout (KO) of Npas4 compromises synaptic transmission in these GABAergic interneurons, increases neuronal activity in CA1 pyramidal neurons, and reduces anxiety behavior, all of which are normalized by the expression of wild-type IQSEC3, but not a dominant-negative ARF-GEF-inactive mutant, in SST interneurons of Npas4-KO mice. Our results suggest that IQSEC3 is a key GABAergic synapse component that is directed by Npas4 and ARF activity, specifically in SST interneurons, to orchestrate excitation-to-inhibition balance and control anxiety-like behavior.
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http://dx.doi.org/10.1016/j.celrep.2021.109417DOI Listing
July 2021

Biocompatible Nanotransfer Printing Based on Water Bridge Formation in Hyaluronic Acid and Its Application to Smart Contact Lenses.

ACS Appl Mater Interfaces 2021 Jul 20. Epub 2021 Jul 20.

Department of Mechanical Engineering, Korea Advanced Institute of Science and Technology (KAIST), 291 Daehak-ro, Yuseong-gu, Daejeon, 34141, South Korea.

Many conventional micropatterning and nanopatterning techniques employ toxic chemicals, rendering them nonbiocompatible and unsuited for biodevice production. Herein the formation of water bridges on the surface of hyaluronic acid (HA) films is exploited to develop a transfer-based nanopatterning method applicable to diverse structures and materials. The HA film surface, made deformable via water bridge generation, is brought into contact with a functional material and subjected to thermal treatment, which results in film shrinkage, allowing a robust pattern transfer. The proposed biocompatible method, which avoids the use of extra chemicals, enables the transfer of nanoscale, microscale, and thin-film structures as well as functional materials such as metals and metal oxides. A nanopatterned HA film is transferred onto a moisture-containing contact lens to fabricate smart contact lenses with unique optical characteristics of rationally designed optical nanopatterns. These lenses demonstrated binocular parallax-induced stereoscopy via nanoline array polarization and acted as cutoff filters, with nanodot arrays, capable of treating Irlen syndrome.
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http://dx.doi.org/10.1021/acsami.1c06225DOI Listing
July 2021

Elastic Properties of Taurine Single Crystals Studied by Brillouin Spectroscopy.

Int J Mol Sci 2021 Jul 1;22(13). Epub 2021 Jul 1.

Division of Materials Science, University of Tsukuba, Tsukuba 305-8573, Japan.

The inelastic interaction between the incident photons and acoustic phonons in the taurine single crystal was investigated by using Brillouin spectroscopy. Three acoustic phonons propagating along the crystallographic -axis were investigated over a temperature range of -185 to 175 °C. The temperature dependences of the sound velocity, the acoustic absorption coefficient, and the elastic constants were determined for the first time. The elastic behaviors could be explained based on normal lattice anharmonicity. No evidence for the structural phase transition was observed, consistent with previous structural studies. The birefringence in the -plane indirectly estimated from the split longitudinal acoustic modes was consistent with one theoretical calculation by using the extrapolation of the measured dielectric functions in the infrared range.
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http://dx.doi.org/10.3390/ijms22137116DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267836PMC
July 2021

Increased GM-CSF-producing NCR ILC3s and neutrophils in the intestinal mucosa exacerbate inflammatory bowel disease.

Clin Transl Immunology 2021 8;10(7):e1311. Epub 2021 Jul 8.

Laboratory of Mucosal Immunology Department of Biomedical Sciences Seoul National University College of Medicine Seoul Korea.

Objectives: Inflammatory bowel disease (IBD) is characterised by dysregulated mucosal immune responses associated with genetic, environmental and microbial factors. Recent therapies targeting key inflammatory mediators such as tumor necrosis factor (TNF)-α emphasise the importance of innate immunity in the development of IBD.

Methods: We examined the distribution of innate immune cells such as innate lymphoid cells (ILCs) and myeloid cells in the intestinal epithelium from children diagnosed as IBD and murine models of colitis induced by dextran sulphate sodium (DSS) or an anti-CD40 antibodies.

Results: We found an increased number of type 3 ILCs (ILC3s) that do not express the natural cytotoxicity receptor (NCR) and neutrophils, in both human IBD patients and colitis-induced mice. A co-culture experiment of neutrophils with NCR ILC3s revealed that NCR ILC3s stimulate neutrophils by producing granulocyte-macrophage colony-stimulating factor (GM-CSF). Furthermore, a blockade of GM-CSF could inhibit the development of IBD by inhibiting neutrophil activity.

Conclusion: The NCR ILC3: GM-CSF: neutrophil axis could contribute to the development of IBD.
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http://dx.doi.org/10.1002/cti2.1311DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8264747PMC
July 2021
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