Unintended consequences of healthcare reform in South Korea: evidence from a regression discontinuity in time design.

BACKGROUND: To address concerns over the financial stability of South Korea's National Health Insurance (NHI) programme, the government transitioned from an outpatient copayment system to a coinsurance system in 2007. This policy aimed to reduce healthcare overutilization by increasing patients' financial responsibility for outpatient services. METHODS: Using comprehensive data on NHI beneficiaries, this study employs a regression discontinuity in time (RDiT) design to assess the policy's impact on outpatient healthcare utilization and expenditures. We focus on changes in overall outpatient visits, average healthcare cost per visit and total outpatient healthcare expenditures. RESULTS: Our findings indicate that the transition from outpatient copayment to coinsurance led to a substantial increase in outpatient healthcare utilization (up to 90%) while decreasing medical expenditures per visit by 23%. The policy shift incentivized beneficiaries to seek more medical treatments during the grace period and enroll in supplemental private health insurance, which provided access to additional medical services at lower marginal costs. CONCLUSIONS: The policy change and the emergence of supplemental private insurance contributed to moral hazard and adverse selection issues, culminating in South Korea becoming the country with the highest per capita utilization of outpatient health services worldwide since 2012. This study underscores the importance of carefully considering the unintended consequences of policy interventions in the healthcare sector.

Corrigendum to "The effects of transboundary air pollution from China on ambient air quality in South Korea" [Heliyon 5 (12) (2019) e02953].

[This corrects the article DOI: 10.1016/j.heliyon.2019.e02953.].

Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.

Although shikimic acid from Illicium verum has antioxidant, antibacterial, anti-inflammatory, and analgesic effects, the effect of shikimic acid on lipogenesis has not yet been explored. Thus, in the present study, hypolipogenic mechanism of shikimic acid was examined in HepG2, Huh7 and 3T3-L1 adipocyte cells. Shikimic acid showed weak cytotoxicity in HepG2, Huh7 and 3T3-L1 cells, but suppressed lipid accumulation in HepG2, Huh7 and 3T3-L1 cells by Oil Red O staining. Also, shikimic acid attenuated the mRNA expression of de novo lipogenesis related genes such as FAS, SREBP-1c, and LXR-α in HepG2 cells by RT-PCR analysis and suppressed the protein expression of SREBP-1c and LXR-α in HepG2 and 3T3-L1 cells. It should be noted that shikimic acid activated phosphorylation of AMP-activated protein kinase (AMPK)/Aacetyl-coenzyme A carboxylase (ACC) and reduced the expression of MID1 Interacting Protein 1 (MID1IP1) in HepG2, Huh7 and 3T3-L1 cells. Conversely, depletion of MID1IP1 activated phosphorylation of AMPK, while overexpression of MID1IP1 suppressed phosphorylation of AMPK in HepG2 cells. However, AMPK inhibitor compound c did not affect the expression of MID1IP1, indicating MID1IP1 as an upstream of AMPK. Taken together, our findings suggest that shikimic acid has hypolipogenic effect in HepG2 and 3T3-L1 cells via phosphorylation of AMPK/ACC and inhibition of MID1IP1 as a potent candidate for prevention or treatment of fatty liver and hyperlipidemia.

The effects of transboundary air pollution from China on ambient air quality in South Korea.

This paper estimates the effects of wind direction on ambient air quality in South Korea (c.2006-2014) to provide insights into the impacts of the long-range transport of air pollutants from China. I find that the effect of transboundary air pollutants from China accounts for 19 percent of the weekly average PM 10 concentrations, varying 12-30 percent by season. More specifically, winds blowing in the southwest direction have the largest year-round impacts on South Korea's ambient air pollution levels, which is consistent with the direction of emissions from Shanghai resulting in worse South Korean pollution levels. Further, the effects are differentiated seasonally according to the diverse activities that lead to the pollutants. Agricultural strawberry burning and coal-fired heating in northern Chinese cities lead to larger northwest wind effects in summer and winter, respectively. The winds from Shanghai have greater effects in spring due to the influence of dust storms passing from the deserts through mainland China.

Farnesiferol c induces apoptosis via regulation of L11 and c-Myc with combinational potential with anticancer drugs in non-small-cell lung cancers.

Though Farnesiferol c (FC) has been reported to have anti-angiogenic and antitumor activity, the underlying antitumor mechanism of FC still remains unclear. Thus, in the present study, we investigated the apoptotic mechanism of FC in human H1299 and H596 non-small lung cancer cells (NSCLCs). FC significantly showed cytotoxicity, increased sub-G1 accumulation, and attenuated the expression of Bcl-2, Bcl-xL, Survivin and procaspase 3 in H1299 and H596 cells. Furthermore, FC effectively suppressed the mRNA expression of G1 arrest related genes such as Cyclin D1, E2F1 transcription factor and CDC25A by RT-PCR. Interestingly, FC inhibited the expression of c-Myc, ribosomal protein L11 (L11) and nucleolin (NCL) in H1299 and H596 cells. Of note, silencing of L11 by siRNA transfection enhanced the expression of c-Myc through a negative feedback mechanism, while c-Myc knockdown downregulated L11 in H1299 cells. Additionally, combined treatment of FC and puromycin/doxorubicin promoted the activation of caspase 9/3, and attenuated the expression of c-Myc, Cyclin D1 and CDK4 in H1299 cells compared to single treatment. Taken together, our findings suggest that FC induces apoptosis and G1 arrest via regulation of ribosomal protein L11 and c-Myc and also enhances antitumor effect of puromycin or doxorubicin in NSCLCs.

Development of a death education curriculum model for the general public using DACUM method.

In order to analyze tasks of the death education curriculum for the public, DACUM method was used. A committee for DACUM was gathered and a survey was conducted on professors of health care, humanities and social sciences for an interdisciplinary study. In the survey used to verify the model for death education for the public, a compilation based on difficulty and importance factor shows that the 27 tasks including the psychological changes in terminally ill or suicidal patients, healing of stress, acceptance and understanding of death and suicide prevention were identified as needing to be included in the curriculum. The data thus concluded will have to be reviewed when they are applied to actual education to revise the education program to make it more appropriate.

Upregulation of death receptor 5 and activation of caspase 8/3 play a critical role in ergosterol peroxide induced apoptosis in DU 145 prostate cancer cells.

BACKGROUND: Though ergosterol peroxide (EP) derived from Neungyi mushrooms (Sarcodon aspratus) was known to have cytotoxic, apoptotic, anti-inflammatory and antimycobacterial effects, the underlying molecular mechanism of EP still remains unclear. Thus, in the present study, the apoptotic mechanism of EP was elucidated in DU 145 prostate cancer cells. METHODS: Cell viability of prostate cancer cells was measured by MTT assay. To see whether EP induces the apoptosis, FACS, western blot and TUNEL assay were performed. To determine the role of Death receptor (DR) 5 molecules in EP-induced apoptosis in DU 145 prostate cancer cells, the silencing of DR 5 was performed by using siRNAs. RESULTS: EP showed significant cytotoxicity against DU 145, PC 3, M2182 prostate cancer cells. Also, EP effectively increased the sub G1 population and terminal deoxynucleotidyl transferase DUTP nick end labeling (TUNEL) positive cells in DU 145 prostate cancer cells. Furthermore, western blotting revealed that EP cleaved poly (ADP-ribose) polymerase (PARP) and caspase 8/3, attenuated the expression of fluorescence loss in photobleaching (FLIP), Bcl-XL and Bcl-2 as well as activated Bax, Fas-associated death domain (FADD) and DR 5 in a concentration dependent manner in DU 145 prostate cancer cells. Conversely, caspase 8 inhibitor Z-IETD-FMK blocked the apoptotic ability of EP to cleave PARP and an increase of sub G1 population in DU 145 prostate cancer cells. Likewise, the silencing of DR 5 suppressed the cleavages of PARP induced by EP in DU 145 prostate cancer cells. CONCLUSION: Overall, our findings suggest that ergosterol peroxide induces apoptosis via activation of death receptor 5 and caspase 8/3 in DU 145 prostate cancer cells as a cancer chemopreventive agent or dietary factor.