Publications by authors named "Young Jae Moon"

Background/objectives: Interleukin 13 receptor alpha 2 (IL-13Rα2) is a receptor with a high affinity for IL-13 and is involved in the progression of human cancers. However, studies on the role of IL-13Rα2 in osteosarcoma are limited. Therefore, this study aimed to investigate the expression and roles of IL-13Rα2 in the progression of osteosarcoma.

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PAK4 and PD-L1 have been suggested as novel therapeutic targets in human cancers. Moreover, PAK4 has been suggested to be a molecule closely related to the immune evasion of cancers. Therefore, this study evaluated the roles of PAK4 and PD-L1 in the progression of osteosarcomas in 32 osteosarcomas and osteosarcoma cells.

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  • The absence of dystrophin protein in boys with Duchenne Muscular Dystrophy (DMD) leads to heart problems, but common mouse models don't show these issues until they are older, making it hard to study early cardiac effects.
  • The mdx mouse model with a DBA/2J genetic background (D2-) demonstrates early heart dysfunction, revealing increased inflammation and fibrosis as key contributors to juvenile cardiomyopathy.
  • Activating the N-formyl peptide receptor 2 (FPR2) can reduce chronic inflammation and fibrosis, offering a potential new treatment strategy to prevent heart problems in young D2-mdx mice with DMD.
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  • Despite efforts to address forward head posture (FHP), effective screening and diagnostic methods are still lacking; this study introduces a new noninvasive approach using body angle measurements alongside radiological assessments.
  • A total of 145 adolescents were screened, measuring the forward neck tilt angle (FNTA) with a device called the POM-Checker and analyzing various sagittal alignment parameters through standing lateral radiographs.
  • The preliminary diagnostic model developed showed a high agreement rate (95.35%) and was 100% effective in identifying participants needing further radiographic evaluation, indicating that FNTA is a crucial factor in diagnosing FHP.
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Posttraumatic osteoarthritis is primarily characterized by articular cartilage destruction secondary to trauma or fracture events. Even while intra-articular scar tissue can be observed following ankle fractures, little is known about its nature and molecular events linking its biological activity and cartilage deterioration. Here, we investigated scar tissue's histological and molecular characteristics, and its relationship with localized articular cartilage alterations consistent with early osteoarthritic degeneration.

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Aging is an independent risk factor for recurrent tearing after surgical repair of rotator cuff ruptures around the tendon-to-bone area. However, aging signature factors and related mechanisms involved in the healing of the rotator cuff are still unknown. We hypothesized that differences in proteins involved in the rotator cuff according to age may affect tendon-to-bone healing.

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Background: Supracondylar humerus (SCH) fractures in children have been traditionally categorized according to the Wilkins-modified Gartland classification scheme, which is solely based on the degree of displacement. As this classification does not consider fracture patterns in the coronal or sagittal plane, the relationship between the fracture pattern and prognosis in SCH fractures remains unclear. Therefore, the purpose of this study was to evaluate the relationship between the fracture level and prognosis of pediatric SCH fractures.

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Periodontitis is an inflammatory disease caused by microorganisms that induce the destruction of periodontal tissue. Inflamed and damaged tissue produces various inflammatory cytokines, which activate osteoclasts and induce alveolar bone loss and, eventually, tooth loss. Sirt6 expression suppresses inflammation and bone resorption; however, its role in periodontitis remains unclear.

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Lack of dystrophin expression is the underlying genetic basis for Duchenne muscular dystrophy (DMD). However, disease severity varies between patients, based on specific genetic modifiers. D2-mdx is a model for severe DMD that exhibits exacerbated muscle degeneration and failure to regenerate even in the juvenile stage of the disease.

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Lack of dystrophin is the genetic basis for the Duchenne muscular dystrophy (DMD). However, disease severity varies between patients, based on specific genetic modifiers. D2- is a model for severe DMD that exhibits exacerbated muscle degeneration and failure to regenerate even in the juvenile stage of the disease.

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Dysferlinopathy covers a spectrum of muscle disorder categorized by two major phenotypes, namely Miyoshi muscular dystrophy type 1 (MMD1, OMIM #254130) and limb-girdle muscular dystrophy autosomal recessive 2 (LGMDR2, OMIM #253601), and two minor symptoms, including asymptomatic hyperCKemia and distal myopathy with anterior tibial onset (DMAT, OMIM #606768). We report the first Korean MMD1 misdiagnosed as Becker muscular dystrophy (BMD), which was caused by a combination of compound heterozygous c.663 + 1G > C and p.

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The use of long-term and high-dose bisphosphate is associated with severely suppressed bone turnover and the delayed union of fractures. However, therapeutic methods to overcome the negative effects of bisphosphonate use are lacking. Bone morphogenetic proteins (BMPs) are powerful osteoinductive proteins.

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Article Synopsis
  • Malignant hyperthermia (MH) is a rare genetic disorder affecting muscle calcium regulation, triggered by certain anesthetics like sevoflurane in individuals with the susceptibility.
  • A 14-year-old Korean boy with MH and multi-minicore myopathy displayed symptoms such as severe flexion contractures and was successfully treated with intravenous dantrolene and sodium bicarbonate during a surgical procedure.
  • Genetic testing revealed a novel mutation in the RYR1 gene linked to MH, and tests indicated his B lymphocytes had abnormal calcium responses, highlighting the condition's complexity and expanding understanding of its clinical presentation.
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  • Expanding skeletal muscle's capacity for exercise may help combat obesity-related metabolic diseases by converting muscle fibers into slower-twitch, oxidative types.
  • The study highlights Sirt6, an anti-aging enzyme, as crucial for this conversion, showing that activating Sirt6 can mimic exercise benefits.
  • Experiments in mice demonstrate that manipulating Sirt6 affects muscle fiber types, boosts energy production, and enhances exercise performance, suggesting its potential as a target for improving muscle health.
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Background: Malrotation after nailing of femoral shaft fractures occurs in about 25% of cases. It can cause substantial functional problems. The lesser trochanter (LT) profile has been used to assess rotational alignment.

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CK2α/CSNK2A1 is involved in cancer progression by phosphorylating various signaling molecules. Considering the role of CSNK2A1 in cancer progression and the phosphorylation of SIRT6 and the role of SIRT6 in chemoresistance through the DNA damage repair pathway, CSNK2A1 and SIRT6 might be involved in resistance to conventional anti-cancer therapies. We evaluated the expression of CSNK2A1 and phosphorylated SIRT6 in the 37 osteosarcoma patients and investigated the effects of CSNK2A1 and the phosphorylation of SIRT6 on Ser338 on resistance to the anti-cancer effects of doxorubicin.

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Accelerating wound healing with minimized bacterial infection has become a topic of interest in the development of the new generation of tissue bio-adhesives. In this study, we fabricated a hydrogel system (MGC-g-CD-ic-TCS) consisting of triclosan (TCS)-complexed beta-cyclodextrin (β-CD)-conjugated methacrylated glycol chitosan (MGC) as an antibacterial tissue adhesive. Proton nuclear magnetic resonance (H NMR) and differential scanning calorimetry (DSC) results showed the inclusion complex formation between MGC-g-CD and TCS.

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Background: IL4Rα and IL13Rα1 are constituents of the type II IL4 receptor. Recently, IL4Rα and IL13Rα1 were reported to have roles in cancer progression and suggested as potential prognostic markers. However, studies on IL4Rα and IL13Rα1 in soft-tissue sarcomas have been limited.

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Background: SIRT6 has diverse roles in cells, and the role of SIRT6 in tumorigenesis is controversial. Considering the role of SIRT6 as an inducer of DNA damage repair, it might be involved in resistance to anti-cancer therapy.

Methods: We evaluated the prognostic significance of SIRT6 in 37 osteosarcomas and investigated the therapeutic efficacy of SIRT6 on the anticancer effects of doxorubicin, olaparib, and ATM inhibitor.

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Ischemic osteonecrosis (ION) can produce permanent deformity and osteoarthritis in the femoral head and other joints. No biologic treatment has been established, and the molecular mechanisms involved in the pathogenesis of ION have not been elucidated. In this work, we found that treatment with sirtuin6 (Sirt6) suppressed inflammatory cytokines, bone resorption, progression of osteoarthritis, and reduced bone deformity in an ION mouse model.

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Osteoporosis is a degenerative disease characterized by reduced bone mass, in which deregulated bone remodeling by osteoclasts and osteoblasts is a main pathogenesis. Although recently tussilagone, a major active component of flower buds of Tussilago farfara, has been shown to inhibit osteoclastogenesis, its effect on estrogen deficiency-induced osteoporosis remains unknown. This study examined the effect of tussilagone on bone loss in ovariectomized mice and further explored its impact on osteoclast apoptosis and osteoblast formation in addition to osteoclastogenesis.

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In syndesmosis injury, whether the syndesmosis screw should be removed prior to weight-bearing remains controversial. The aim of this study was to compare the functional outcome between removed screw and retained groups and between recurrence of diastasis and no diastasis groups.Fifty-six patients who had undergone open reduction and internal fixation due to syndesmosis injury were retrospectively evaluated and divided into four groups: (A) removed syndesmotic screw before weight-bearing (postoperative 3 months, n = 28), (B)retained (n = 28), (C) recurrence of diastasis (n = 9), and (D) no diastasis (n = 47).

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In this study, we aimed to identify a candidate drug that can activate endogenous Angiopoietin 1 (Ang1) expression via drug repositioning as a pharmacological treatment for avascular osteonecrosis. After incubation with 821 drugs from the Food and Drug Administration (FDA)-approved drug library, Ang1 expression in U2OS cell culture media was examined by ELISA. Metformin, the first-line medication for treatment of type 2 diabetes, was selected as a candidate for in vitro and in vivo experimental evaluation.

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Osteosarcoma (OSA) is a difficult cancer to treat due to its tendency for relapse and metastasis; advanced methods are therefore required for OSA treatment. In this study, we prepared a local drug-delivery system for OSA treatment based on doxorubicin·hydrochloride (DOX·HCl)/cisplatin (CP)-loaded visible light-cured glycol chitosan (GC) hydrogel/(2-hydroxypropyl)-beta-cyclodextrin (GDHCP), and compared its therapeutic efficiency with that of DOX·HCl- and CP-loaded GC hydrogels (GD and GHCP). Because of diffusion driven by concentration gradients in the swollen matrix, the three hydrogels showed sustained releases of DOX·HCl and CP over 7 days, along with initial 3-h bursts.

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Background: FAM83H was initially identified as a protein essential for dental enamel formation. Recent reports have shown that FAM83H is also involved in the progression of human cancers in conjunction with tumor-associated molecules, such as MYC and β-catenin. However, the role of FAM83H in sarcoma has not yet been investigated.

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