This study aimed to investigate the prevalence of carbon monoxide (CO) poisoning and the provision of hyperbaric oxygen therapy (HBOT) in South Korea. We used data from the Korea Health Insurance Review and Assessment service. In total, 44,361 patients with CO poisoning were identified across 10 years (2010–2019). The prevalence of CO poisoning was found to be 8.64/10,000 people, with a gradual annual increment. The highest prevalence was 11.01/10,000 individuals, among those aged 30–39 years. In 2010, HBOT was claimed from 15 hospitals, and increased to 30 hospitals in 2019. A total of 4,473 patients received HBOT in 10 years and 2,684 (60%) were treated for more than 2 hours. This study suggested that the prevalence of both CO poisoning and HBOT in Korea gradually increased over the past 10 years, and disparities in prevalence were observed by region.

Purpose: We report the estimated incidence of, and risk factors for, recurrent anterior uveitis in patients with initial acute-onset Vogt-Koyanagi-Harada (VKH) disease using survival analyses. Methods: Patients who were diagnosed with initial acute-onset VKH disease during 2003–2022 at two university hospitals were included. Recurrent anterior uveitis was defined as the first occurrence of the granulomatous anterior uveitis with anterior chamber cells and flare of 2+ or more by the Standardization of Uveitis Nomenclature (SUN) Working Group grading scheme, after the disappearance of conspicuous uveitis and serous retinal detachment for at least 3 months, regardless of systemic or local treatment. The univariate log-rank test and multivariate Cox regression analyses were performed, including patients’ demographic characteristics, underlying diseases, presence of prodromal symptoms, duration of visual symptoms, visual acuity, slit-lamp and fundus findings, and height of serous retinal detachment. The treatment method and response to treatment were also included. Results: The estimated incidence was 39.3% at 10 years. Fifteen of 55 patients (27.3%) had recurrent anterior uveitis during the mean follow-up of 4.5 years. The presence of focal posterior synechiae at the diagnosis increased the risk of recurrent anterior uveitis 6.97-fold compared to the absence of synechiae (95% confidence interval [CI], 2.20–22.11; p < 0.001). Use of systemic high-dose steroid therapy more than 7 days after the development of visual symptoms resulted in a hazard ratio of 4.55 (95% CI, 1.27–16.40; p = 0.020). Conclusions This study reports the estimated incidence and risk factors of recurrent anterior uveitis in VKH disease from survival analyses. However, because of the retrospective nature of this study, it is hard to confirm the consistency of the medical records regarding risk factors, thus, the presence of focal posterior synechiae can be inconclusive as a risk factor. Further studies are warranted.

Background: Although muscles and bones interact with each other through various secretory factors, the role of sclerostin, an osteocyte-secreted factor, on muscle metabolism has not been well studied. We investigated the levels of serum sclerostin in Korean older adults with sarcopenia. Methods: Blood samples were collected from 129 participants who underwent evaluation of muscle mass and function in an outpatient geriatric clinic of a teaching hospital. Sarcopenia and related parameters were determined using cutoff values for the Asian population. Serum sclerostin levels were measured using an enzyme-linked immunosorbent assay. Results: The mean age of the participants was 69.6 years, and 20 participants (15.5%) were classified as having sarcopenia. After adjusting for age, sex, and body mass index, serum sclerostin levels were significantly lower in participants with sarcopenia, low muscle mass, or weak muscle strength (P=0.003 to 0.045). Serum sclerostin levels were positively associated with skeletal muscle index and grip strength after adjusting for confounders (P=0.001 and P=0.003), whereas sarcopenic phenotype score showed a negative association (P=0.006). These increases in muscle mass and strength were also dose dependent as serum sclerostin levels increased (P for trends=0.003 and P for trends=0.015). Higher serum sclerostin levels were associated with lower odds ratio (ORs) for sarcopenia, low muscle mass, and weak muscle strength after adjusting for confounders (OR, 0.27 to 0.50; P<0.001 to 0.025). Conclusion Higher serum sclerostin levels were associated with a lower risk of sarcopenia, low muscle mass, and weak muscle strength in Korean older adults.

Background/Aims: Lumican, a small leucine-rich proteoglycan, has shown osteoprotective effects by synchronously stimulating bone formation and suppressing bone resorption. To clarify the role of lumican in human bone metabolism, the association between lumican concentrations and osteoporosis-related phenotypes was evaluated using bone marrow (BM) samples directly reflecting local microenvironments. Methods: BM aspirates were obtained from 77 patients during hip surgery for either fragility hip fractures (HF) (n = 29) or osteoarthritis (n = 48) and centrifuged. Concentrations of lumican and biochemical bone markers in BM supernatants were measured using enzyme linked immunosorbent assays. Results: After considering confounders, lumican concentrations in BM supernatants were 16.9% lower in patients with HF than in controls, with each increase in the standard deviation of lumican concentration being associated with a 61% lower likelihood of HF. The odds ratios for HF decreased linearly with increasing lumican tertiles in BM, with the odds of having fragility HF markedly lower in participants in the highest than in the lowest lumican tertile. Higher lumican level correlated significantly with higher femur neck bone mineral density and higher bone-specific alkaline phosphatase levels, but not with tartrate-resistant acid phosphatase 5b concentrations, in BM supernatants. Conclusions These data clinically validate previous in vitro and animal experiments showing the beneficial roles of lumican for bone homeostasis and suggest that lumican may contribute to a reduction in fracture risk in humans mainly through its stimulation of bone formation.

Purpose: A pilot project using epinephrine at the scene under medical control is currently underway in Korea. This study aimed to determine whether prehospital epinephrine administration is associated with improved survival and neurological outcomes in out-of-hospital cardiac arrest (OHCA) patients who received epinephrine during cardiopulmonary resuscitation (CPR) in the emergency department. Materials and Methods: This retrospective observational study used a nationwide multicenter OHCA registry. Patients were classified into two groups according to whether they received epinephrine at the scene or not. The associations between prehospital epinephrine use and outcomes were assessed using propensity score (PS)-matched analysis. Multivariable logistic regression analysis was performed using PS matching. The same analysis was repeated for the subgroup of patients with non-shockable rhythm. Results: PS matching was performed for 1084 patients in each group. Survival to discharge was significantly decreased in the patients who received prehospital epinephrine [odds ratio (OR) 0.415, 95% confidence interval (CI) 0.250–0.670, p<0.001]. However, no statistical significance was observed for good neurological outcome (OR 0.548, 95% CI 0.258–1.123, p=0.105). For the patient subgroup with non-shockable rhythm, prehospital epinephrine was also associated with lower survival to discharge (OR 0.514, 95% CI 0.306–0.844, p=0.010), but not with neurological outcome (OR 0.709, 95% CI 0.323–1.529, p=0.382). Conclusion Prehospital epinephrine administration was associated with decreased survival rates in OHCA patients but not statistically associated with neurological outcome in this PS-matched analysis. Further research is required to investigate the reason for the detrimental effect of epinephrine administered at the scene.

Background: Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods: Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reversetranscription polymerase chain reaction, Western blot, viability, and migration analyses were performed for experimental research. Results: Recombinant aldosterone treatment suppressed muscle differentiation from mouse C2C12 myoblasts in a dose-dependent manner, and consistently reduced the expression of myogenic differentiation markers. Furthermore, aldosterone significantly increased intracellular reactive oxygen species (ROS) levels in myotubes, and treatment with N-acetyl cysteine, a potent biological thiol antioxidant, reversed the decrease of myotube area, myotube area per myotube, nucleus number per myotube, and fusion index due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular ROS generation during myogenesis and markedly attenuated the suppression of in vitro myogenesis by aldosterone. Conclusion These findings support the hypothesis that hypersecretion of aldosterone, like PA, directly contributes to muscular deterioration and suggest that antioxidants and/or MR antagonists could be effective therapeutic options to reduce the risk of sarcopenia in these patients.

Background: Despite clinical evidence indicating poor muscle health in subjects with primary aldosteronism (PA), it is still unclear whether the role of aldosterone in muscle metabolism is direct or mediated indirectly via factors, such as electrolyte imbalance or impaired glucose uptake. As one approach to clarify this issue, we investigated the effect of aldosterone on in vitro myogenesis and the potential mechanism explaining it. Methods: Myogenesis was induced in mouse C2C12 myoblasts with 2% horse serum. Immunofluorescence, quantitative reversetranscription polymerase chain reaction, Western blot, viability, and migration analyses were performed for experimental research. Results: Recombinant aldosterone treatment suppressed muscle differentiation from mouse C2C12 myoblasts in a dose-dependent manner, and consistently reduced the expression of myogenic differentiation markers. Furthermore, aldosterone significantly increased intracellular reactive oxygen species (ROS) levels in myotubes, and treatment with N-acetyl cysteine, a potent biological thiol antioxidant, reversed the decrease of myotube area, myotube area per myotube, nucleus number per myotube, and fusion index due to aldosterone through decreasing oxidative stress. A binding enzyme-linked immunosorbent assay confirmed that mineralocorticoid receptor (MR) interacted with aldosterone in C2C12 myoblasts, while eplerenone, an MR inhibitor, blocked aldosterone-stimulated intracellular ROS generation during myogenesis and markedly attenuated the suppression of in vitro myogenesis by aldosterone. Conclusion These findings support the hypothesis that hypersecretion of aldosterone, like PA, directly contributes to muscular deterioration and suggest that antioxidants and/or MR antagonists could be effective therapeutic options to reduce the risk of sarcopenia in these patients.

Purpose: This study aimed to investigate the abnormal and borderline ABIs for predicting coronary re-intervention and mortality in patients with coronary artery disease (CAD). Materials and Methods: Data from a previous study were obtained and used to investigate the prevalence of peripheral arterial disease among Korean patients with CAD (n=285) in 2010. All patients underwent follow-up coronary angiography as scheduled (asymptomatic: 2-, 5-, and 7-month intervals) or as clinically indicated (symptomatic). Results: In total, 33 patients had an abnormal ABI (ab-ABI: <1.0 or >1.4), and 252 had a normal ABI (nl-ABI: 1.0≤ABI≤1.4). The mean follow-up was 47 months. The mortality was significantly higher in the ab-ABI group than in the nl-ABI group (18.2% vs. 6.7%, P=0.0233). MACEs were significantly more common in the ab-ABI group (60.6% vs. 34.5%, P=0. 0036). Moreover, the ab-ABI group had a greater CAD progression than the nl-ABI group (48.5% vs. 31.3%, P=0.0496). The incidence of clinically indicated coronary re-intervention was significantly higher in the ab-ABI group than in the nl-ABI group (33.3% vs. 13.1%, P=0.0025). After adjusting for age, diabetes, dyslipidemia, dialysis, smoking, and obesity, the incidence of clinically indicated re-intervention was significantly higher in the ab-ABI group than in the nl-ABI group (HR, 2.80; 95% CI, 1.24 to 6.34). Conclusion Abnormal and borderline ABI significantly increased the incidence of clinically indicated coronary revascularization and all-cause mortality during a 4-year follow-up among patients with CAD. Hence, ABI could be used to stratify extremely high-risk patients with CAD who may require aggressive surveillance or treatment.

PURPOSE: Lung Cancer Subcommittee of Korean Radiation Oncology Group (KROG) has recently launched a prospective clinical trial (KROG 17-06) of hippocampus-sparing whole brain radiotherapy (HS-WBRT) with simultaneous integrated boost (SIB) in treating multiple brain metastases from non-small cell lung cancer. In order to improve trial quality, dummy run studies among the participating institutions were designed. This work reported the results of two-step dummy run procedures of the KROG 17-06 study. MATERIALS AND METHODS: Two steps tested hippocampus contouring variability and radiation therapy planning compliance. In the first step, the variation of the hippocampus delineation was investigated for two representative cases using the Dice similarity coefficients. In the second step, the participating institutions were requested to generate a HS-WBRT with SIB treatment plan for another representative case. The compliance of the treatment plans to the planning protocol was evaluated. RESULTS: In the first step, the median Dice similarity coefficients of the hippocampus contours for two other dummy run cases changed from 0.669 (range, 0.073 to 0.712) to 0.690 (range, 0.522 to 0.750) and from 0.291 (range, 0.219 to 0.522) to 0.412 (range, 0.264 to 0.598) after providing the hippocampus contouring feedback. In the second step, with providing additional plan priority and extended dose constraints to the target volumes and normal structures, we observed the improved compliance of the treatment plans to the planning protocol. CONCLUSION: The dummy run studies demonstrated the notable inter-institutional variability in delineating the hippocampus and treatment plan generation, which could be decreased through feedback from the trial center.
Brain ; Carcinoma, Non-Small-Cell Lung ; Compliance ; Hippocampus ; Lung Neoplasms ; Neoplasm Metastasis ; Prospective Studies ; Radiation Oncology ; Radiotherapy

BACKGROUND: Current dilemma working with surgically-induced OA (osteoarthritis) model include inconsistent pathological state due to various influence from surrounding tissues. On the contrary, biochemical induction of OA using collagenase II has several advantageous points in a sense that it does not involve surgery to induce model and the extent of induced cartilage degeneration is almost uniform. However, concerns still exists because biochemical OA model induce abrupt destruction of cartilage tissues through enzymatic digestion in a short period of time, and this might accompany systemic inflammatory response, which is rather a trait of RA (rheumatoid arthritis) than being a trait of OA. METHODS: To clear the concern about the systemic inflammatory response that might be caused by abrupt destruction of cartilage tissue, OA was induced to only one leg of an animal and the other leg was examined to confirm the presence of systemic degenerative effect. RESULTS: Although the cartilage tissues were rapidly degenerated during short period of time upon biochemical induction of OA, they did not accompanied with RA-like process based on the histology data showing degeneration of articular cartilage occurred only in the collagenase-injected knee joint. Scoring evaluation data indicated that the cartilage tissues in non-induced joint remained intact. Neutrophil count transiently increase between day 8 and day 16, and there were no significant change in other complete blood count profile showing a characteristics of OA disease. CONCLUSION: These study shows that biochemically induced cartilage degeneration truly represented uniform and reliable OA state.
Animals* ; Blood Cell Count ; Cartilage ; Cartilage, Articular ; Clothing ; Collagenases* ; Digestion ; Inflammation ; Joints ; Knee Joint ; Leg ; Models, Animal* ; Neutrophils ; Osteoarthritis* ; Regeneration