The prevalence, incidence, and admission rate of diagnosed schizophrenia spectrum disorders in Korea, 2008-2017: A nationwide population-based study using claims big data analysis.

This study estimated the prevalence and incidence rate of schizophrenia, schizotypal, and delusional disorders (SSDD) in Korea from 2008 to 2017 and analyzed the hospital admission rate, re-admission rate, and hospitalization period. It used the Korean nationwide National Health Insurance Service claims database. SSDD patients who had at least one visit to Korea's primary, secondary, or tertiary referral hospitals with a diagnosis of SSDD, according to the International Classification of Diseases, 10th Revision (ICD-10), were identified as SSDD cases if coded as F20-F29. Data were analyzed using frequency statistics. Results showed that the 12-month prevalence rate of SSDD increased steadily from 0.40% in 2008 to 0.45% in 2017. Analysis of the three-year cumulative prevalence rate of SSDD showed an increase from 0.51% in 2011 to 0.54% in 2017. In 2017, the five-year cumulative prevalence rate was 0.61%, and the 10-year cumulative prevalence rate was 0.75%. The hospital admission rate among SSDD patients decreased from 2008 (30.04%) to 2017 (28.53%). The incidence of SSDD was 0.05% and no yearly change was observed. The proportion of SSDD inpatients whose first hospital visit resulted in immediate hospitalization was 22.4% in 2017. Epidemiological indicators such as prevalence, incidence, and hospitalization rate play an important role in planning social and financial resource allocation. Therefore, efforts to produce more accurate epidemiological indicators are very important and this study's findings could have a significant social impact.

Associations Between Private Health Insurance and Medical Care Utilization for Musculoskeletal Disorders: Using the Korea Health Panel Survey Data for 2014 to 2015.

In South Korea, people may increase their medical coverage by purchasing private health insurance to augment low coverage provided by the National Health Insurance (NHI). Frequent and excessive use of medical care by those with private health insurance is an issue, especially for musculoskeletal disorders that require excessive care and contribute to moral hazard. In South Korea, since private health insurance is structurally linked to the scope of coverage with public health insurance, this increased use of medical care may adversely affect public health insurance finances. This study aimed to analyze the effects of private health insurance on medical care use for patients with musculoskeletal disorders. We used the Korea Health Panel 2014 to 2015 data that included 5622 participants who used medical care for musculoskeletal disorders in 2015. Two groups were created: those who purchased private health insurance (n = 3588) and those without private insurance (n = 2034). We compared their medical utilization using logistic regression, negative binomial regression, and multiple linear regression to determine the associations of private health insurance with medical care use. Medical expenditures by private health insurance purchasers were higher than those of non-purchasers for outpatient care (P < .001), but no differences were found for inpatient care. Our findings suggest that the expansion of private health insurance further burdened the NHI financially, ultimately increasing the burden of medical expenses for the population. Research should implement demonstration studies with different groups of diseases.

Niacin and Selenium Attenuate Brain Injury After Cardiac Arrest in Rats by Up-Regulating DJ-1-Akt Signaling.

OBJECTIVES: To determine neuroprotective effects and mechanism of the combination therapy of niacin and selenium in cardiac arrest rats. DESIGN: Prospective laboratory study. SETTING: University laboratory. SUBJECTS: Rat cortex neurons and male Sprague-Dawley rats (n = 68). INTERVENTIONS: In rat cortex neurons underwent 90 minutes of oxygen-glucose deprivation and 22.5 hours of reoxygenation, effects of the combination therapy of niacin (0.9 mM) and selenium (1.5 µM) were investigated. The role of DJ-1 was determined using DJ-1 knockdown cells. In cardiac arrest rats, posttreatment effects of the combination therapy of niacin (360 mg/kg) and selenium (60 µg/kg) were evaluated. MEASUREMENTS AND MAIN RESULTS: In oxygen-glucose deprivation and 22.5 hours of reoxygenation cells, combination therapy synergistically activated the glutathione redox cycle by a niacin-induced increase in glutathione reductase and a selenium-induced increase in glutathione peroxidase activities and reduced hydrogen peroxide level. It increased phosphorylated Akt and intranuclear Nuclear factor erythroid 2-related factor 2 expression and attenuated neuronal injury. However, these benefits were negated by DJ-1 knockdown. In cardiac arrest rats, combination therapy increased DJ-1, phosphorylated Akt, and intranuclear nuclear factor erythroid 2-related factor 2 expression, suppressed caspase 3 cleavage, and attenuated histologic injury in the brain tissues. It also improved the 7-day Neurologic Deficit Scales from 71.5 (66.0-74.0) to 77.0 (74.-80.0) (p = 0.02). CONCLUSIONS: The combination therapy of clinically relevant doses of niacin and selenium attenuated brain injury and improved neurologic outcome in cardiac arrest rats. Its benefits were associated with reactive oxygen species reduction and subsequent DJ-1-Akt signaling up-regulation.

Niacin and Selenium Attenuate Sepsis-Induced Lung Injury by Up-Regulating Nuclear Factor Erythroid 2-Related Factor 2 Signaling.

OBJECTIVES: To determine whether the combination therapy of niacin and selenium attenuates lung injury and improves survival during sepsis in rats and whether its benefits are associated with the activation of the glutathione redox cycle and up-regulation of nuclear factor erythroid 2-related factor 2. DESIGN: Prospective laboratory study. SETTING: University laboratory. SUBJECTS: Human lung microvascular endothelial cells and male Sprague-Dawley rats (n = 291). INTERVENTION: In lipopolysaccharide-exposed cells, the dose-related effects of niacin and selenium were assessed, and the therapeutic effects of the combination therapy of niacin (0.9 mM) and selenium (1.5 µM) were evaluated. The role of nuclear factor erythroid 2-related factor 2 was determined using nuclear factor erythroid 2-related factor 2 knockdown cells. In endotoxemic and cecal ligation and puncture with antibiotics rats, the therapeutic effects of the posttreatments of clinically relevant doses of niacin (360 mg/kg) and selenium (60 µg/kg) were evaluated. MEASUREMENTS AND MAIN RESULTS: Combination therapy reduced the hydrogen peroxide level via the synergistic activation of the glutathione redox cycle, which involves niacin-induced increases in glutathione reductase activity, and reduced the glutathione level and a selenium-induced increase in glutathione peroxidase activity. Combination therapy contributed to the up-regulation of nuclear factor erythroid 2-related factor 2, enhancement of glutathione synthesis, and down-regulation of nuclear factor κB signaling, but nuclear factor erythroid 2-related factor 2 knockdown inhibited the enhancement of glutathione synthesis and down-regulation of the nuclear factor κB pathway. The therapeutic effects of combination therapy on endotoxemic rats were consistent with those on lipopolysaccharide-exposed cells. In addition, the posttreatment of combination therapy attenuated lung injury and improved survival in endotoxemic and cecal ligation and puncture with antibiotics rats. However, individual therapies of niacin or selenium failed to achieve these benefits. CONCLUSIONS: The combination therapy of niacin and selenium attenuated lung injury and improved survival during sepsis. Its therapeutic benefits were associated with the synergistic activation of the glutathione redox cycle, reduction of hydrogen peroxide level, and up-regulation of nuclear factor erythroid 2-related factor 2.

The therapeutic effect and mechanism of niacin on acute lung injury in a rat model of hemorrhagic shock: Down-regulation of the reactive oxygen species-dependent nuclear factor κB pathway.

BACKGROUND: The purpose of the current study was to investigate the protective effect of niacin on acute lung injury by the down-regulation of the nuclear factor κB (NF-κB) pathway in hemorrhagic shock (HS) rats. METHODS: HS was induced in male Sprague-Dawley rats by withdrawing blood to maintain a mean arterial pressure of 20 mm Hg to 25 mm Hg for 40 minutes. The rats were resuscitated by the reinfusion of the drawn blood, and a vehicle (HS), a low-dose of niacin (360 mg/kg, HS + LD-NA), or a high dose of niacin (1,080 mg/kg, HS + HD-NA) were administered orally. The survival of the subjects was observed for 72 hours, and a separate set of animals was killed at 6 hours after HS induction. We measured cytoplasmic phosphorylated inhibitor κB-α and inhibitor κB-α expressions, nuclear NF-κB p65 expression, NF-κB p65 DNA-binding activity, MEK partner 1 activity, tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-8, nicotinamide adenine dinucleotide (NAD+), reduced nicotinamide adenine dinucleotide phosphate, reduced glutathione, glutathione disulfide, malondialdehyde levels, and histologic damage in the lung tissue. We also measured TNF-α, IL-6, and IL-8 levels in the serum. RESULTS: The survival rates of the sham, HS, HS + LD-NA, and HS + HD-NA groups were 6 of 6 (100%), 0 of 9 (0%), 1 of 9 (11.1%), and 3 of 9 (33.3%), respectively. A high dose of niacin increased lung NAD+, nicotinamide adenine dinucleotide phosphate levels, and glutathione-glutathione disulfide ratios; decreased lung malondialdehyde levels; down-regulated the NF-κB pathway; suppressed TNF-α, IL-6, and IL-8 levels in the lung tissue and serum; and attenuated histologic lung damage. CONCLUSION: A high dose of niacin attenuated lung inflammation, suppressed proinflammatory cytokine release, reduced histologic lung damage, and improved survival after HS in rats. Its therapeutic benefits were associated with the down-regulation of the reactive oxygen species-dependent NF-κB pathway.