Nutrition policy in South Korea

Since 1970s, the economic and social development in South Korea, as well as dietary pattern, has undergone various changes. Concerns for the decreased nutrition quality and physical activities among Koreans, especially young population, call for a need of a holistic approach in national food and nutrition policy. The National Health Promotion Act of 1995 included national interventions and programs to deal with nutrition-related chronic diseases and obesity prevention. A nation-wide monitoring system, which includes nutrition and health examination survey, is being built and run by the Ministry of Health and Welfare and its affiliated organizations every three years. The Korea Food and Drug Administration (KFDA) is another key agency undertaking national food and nutrition policies. The KFDA recently promulgated the national strategic plans for improving food safety and nutrition, focusing on children. Nutrition labelling policy for processed food is managed by KFDA and various education programs are developed and disseminated to enhance the awareness of nutrition labelling. The agency also makes standards and regulates foods for special dietary uses and health functional food. The Rural Development Administration (RDA) is responsible for maintaining the food composition database. Finally, the National School Lunch Program is mainly governed by the Ministry of Education and Human Resources Development. The above central government agencies along with regional health centers are making efforts to promote the healthy eating habits in addition to constructing healthy environment by making laws and programs and by research and social marketing

Perceptions of medical students toward assessors in interprofessional education

Purpose This study aims to establish if medical students think it is fair to be assessed by nursing professors in interprofessional education (IPE) and why. Methods Eighty-seven third-year medical students who participated in the IPE in 2022 submitted self-reflection essays. They were asked how they perceived the assessors, and 86 medical students responded to content analyses. Results Sixty-seven students (77.9%) agreed to be assessed by nursing professors. They believed that interprofessional assessment is possible because it is an IPE. They also believed that this was an opportunity to be assessed from various perspectives. Nineteen students (22.1%) objected because the assessment criteria may be different and nursing professors would not understand the learning experiences of medical students. Conclusion Regarding the reasons medical students oppose it, IPE developers should supplement the development of assessment criteria and understand learners’ experiences during planning assessment

Pro-survival function of the mitochondrial Hsp90 homolog, TRAP1, in cancer cells and insight into cancer therapy

Department Of Biological SciencesHeat shock protein (Hsp90) is an ATP dependent chaperone that regulates folding of a wide range of client proteins or substrates, which are involved in cellular signaling pathways for tumorigenesis. The most of Hsp90 is localized in cytoplasm but mitochondrial Hsp90 homologue, tumor necrosis factor receptor-associated protein 1 (TRAP1), has been reported. The TRAP1 is highly elevated in many cancer cell types and human cancer patients compared to normal cells. TRAP1 plays important roles in tumorigenesis including the neoplastic metabolic shift to aerobic glycolysis, tumor cell invasion and metastatasis, inhibition of cell death and development of drug resistance. A class of TRAP1 inhibitors, named gamitrinibs (GA mitochondrial matrix inhibitors), has been developed through combinatorial chemistry. Gamitrinib consist of geldanamycin, a competitive inhibitor of the ATPase pocket of Hsp90 and TRAP1, conjugated with tandem repeats of tetracyclic guanidinium or triphenylphosphonium for mitochondrial targeting. Gamitrinib not only trigger massive cell death in cultured cancer cells in vitro but also strongly suppress tumor growth in various cancer xenograft or genetic mouse model in vivo. The gamitrinib induced cytotoxicity is attributed to the reactivation of cyclophilin D (CypD), an opener of the permeability transition pore (PTP) located in the mitochondrial inner membrane. PTP opening by CypD activation is often suppressed in cancer cells to avoid cell death by interaction with mitochondrial Hsp90s even under stressful cellular environment. Furthermore, gamitrinibs have been shown to induce organelle-specific stress response and dysregulation of bioenergetics in mitochondria of cancer cells. Resistance to cell death in the presence of stressful stimuli is one of hallmarks of cancer cells acquired during multistep tumorigenesis, and knowledge of the molecular mechanism of stress adaptation can be exploited to develop cancer-selective therapeutics. Mitochondria and the endoplasmic reticulum (ER) are physically interconnected organelles that can sense and exchange various stress signals. Although there have been many studies on stress propagation from the ER to mitochondria, reverse stress signals originating from mitochondria have not been well reported. In this study, we showed that mitochondrial heat shock protein 90 (Hsp90) suppresses mitochondria-initiated calcium-mediated stress signals propagating into the ER in cancer cells. Mitochondrial Hsp90 inhibition with gamitrinib triggers the calcium signal by opening the mitochondrial permeability transition pore and, in turn, the ER ryanodine receptor, via calcium-induced calcium release. Subsequent depletion of ER calcium activates unfolded protein responses in the ER, thereby increasing the expression of a pro-apoptotic transcription factor, CEBP homologous protein (CHOP). Combined treatment of the ER stressor thapsigargin with the mitochondrial Hsp90 inhibitor gamitrinib augments interorganelle stress signaling by elevating CHOP expression, and showed synergistic cytotoxic activity exclusively in cancer cells in vitro and in vivo. Collectively, the mitochondrial Hsp90s confer apoptosis resistance to cancer cells by suppressing the mitochondria-initiated calcium-mediated interorganelle stress response. Next, the mitochondria stress inducer, gamibrinib has been exploited, for combination cancer therapy with clinical cancer drug doxorubicin (DOX). DOX, an anthracycline antibiotic with the trade name Adrimycin, is one of the most effective anticancer drugs and has been widely used to treat cancer patients in various combination chemotherapeutic regimens. The antitumor activities of DOX and closely related anthracycline analogs are primarily attributed to DNA damage resulting from the inhibition of DNA topoisomearse II. DOX has also been reported to increase oxygen derived free radicals, which contributes not only to its anticancer activities but also induce a major side effect, irreversible cardiomyopathy in the patients. To mitigate the cardiotoxic side effects of DOX, we explored the efficacy of combination treatment of DOX with gamitrinib. The combination treatment with DOX and gamitrinib showed synergistically increased anticancer activities at suboptimal cytotoxic dose in vitro and in vivo, without augmenting the cardiotoxic side effects. The mechanism of the action is involved in stimulation of cellular stress signaling mediating JNK of CHOP pathways and activation of proapoptotic protein Bim. Depending on cellular context of disparate cancer cell types, the combination treatment induced CHOP and Bim expression and phosphorylation of JNK and Bim, which leads to enhance accumulation of Bim and Bad in the mitochondria. These mechanisms were independent of ROS production and synergistically enhanced apoptosis exclusively in cancer cells in vitro and in vivo. In summary, combined treatment of TRAP1 inhibitors can unleash the full potential of the anticancer activity of various anticancer drugs.ope

Mitochondrial Hsp90s suppress calcium-mediated stress signals propagating from mitochondria to the ER in cancer cells

Background: Resistance to cell death in the presence of stressful stimuli is one of the hallmarks of cancer cells acquired during multistep tumorigenesis, and knowledge of the molecular mechanism of stress adaptation can be exploited to develop cancer-selective therapeutics. Mitochondria and the endoplasmic reticulum (ER) are physically interconnected organelles that can sense and exchange various stress signals. Although there have been many studies on stress propagation from the ER to mitochondria, reverse stress signals originating from mitochondria have not been well reported.Methods: After inactivation of the proteins by pharmacologic and genetic methods, the signal pathways were analyzed by fluorescence microscopy, flow cytometry, MTT assay, and western blotting. A mouse xenograft model was used to examine synergistic anticancer activity and the action mechanism of drugs in vivo.Results: We show in this study that mitochondrial heat shock protein 90 (Hsp90) suppresses mitochondria-initiated calcium-mediated stress signals propagating into the ER in cancer cells. Mitochondrial Hsp90 inhibition triggers the calcium signal by opening the mitochondrial permeability transition pore and, in turn, the ER ryanodine receptor, via calcium-induced calcium release. Subsequent depletion of ER calcium activates unfolded protein responses in the ER lumen, thereby increasing the expression of a pro-apoptotic transcription factor, CEBP homologous protein (CHOP). Combined treatment with the ER stressor thapsigargin and the mitochondrial Hsp90 inhibitor gamitrinib augmented interorganelle stress signaling by elevating CHOP expression, and showed synergistic cytotoxic activity exclusively in cancer cells in vitro and in vivo.Conclusions: Collectively, mitochondrial Hsp90s confer cell death resistance to cancer cells by suppressing the mitochondria-initiated calcium-mediated interorganelle stress response.open0

Curcumin induces expression of 15-hydroxyprostaglandin dehydrogenase in gastric mucosal cells and mouse stomach in vivo: AP-1 as a potential target

15-Hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes the conversion of oncogenic prostaglandin E-2 to non-tumerigenic 15-keto prostaglandin E-2. In the present study, we found that curcumin, a yellow coloring agent present in the rhizome of Curcuma Tonga Linn (Zingiberaceae), induced expression of 15-PGDH at the both transcriptional and translational levels in normal rat gastric mucosal cells. By using deletion constructs of 15-PGDH promoter, we were able to demonstrate that activator protein-1 (AP-1) is the principal transcription factor responsible for regulating curcumin-induced 15-PGDH expression. Curcumin enhanced the expression of c-jun and cFos that are functional subunits of AP-1, in the nuclear fraction of cells. Silencing of c-jun suppressed curcumin-induced expression of 15-PGDH. Moreover, the chromatin immunoprecipitation assay revealed curcumin-induced binding of c-Jun to the AP-1 consensus sequence present in the 15-PGDH promoter. Curaimin increased phosphorylation of ERK1/2 and JNK. and pharmacologic inhibition of these kinases abrogated the curcumin-induced phosphorylation of clun and 15-PGDH expression. In contrast, tetrahydrocurcumin which lacks the alpha,beta-unsaturated carbonyl group failed to induce 15-PGDH expression, suggesting that the electrophilic carbonyl group of curcumin is essential for its induction of 15-PGDH expression. Curcumin restored the expression of 15-PGDH which is down-regulated by Helicobater pylori through suppression of DNA methyltransferase 1. In addition, oral administration of curcumin increased the expression of 15-PGDH and its regulators such as p-ERK1/2, p-JNK and c-Jun in the mouse stomach. Taken together, these findings suggest that curcumin-induced upregulation of 15-PGDH may contribute to chemopreventive effects of this phytochemical on inflammation-associated gastric carcinogenesis. (C) 2020 Elsevier Inc. All rights reserved.

Novel involvement of leukotriene B4 receptor 2 through ERK activation by PP2A down-regulation in leukotriene B4-induced keratin phosphorylation and reorganization of pancreatic cancer cells

AbstractPerinuclear reorganization via phosphorylation of specific serine residues in keratin is involved in the deformability of metastatic cancer cells. The level of leukotriene B4 is high in pancreatic cancers. However, the roles of LTB4 and its cognate receptors in keratin reorganization of pancreatic cancers are not known. LTB4 dose-dependently induced phosphorylation and reorganization of Keratin 8 (K8) and these processes were reversed by LY255283 (BLT2 antagonist). BLT2 agonists such as Comp A and 15(S)-HETE also induced phosphorylation of serine 431 in K8. Moreover, Comp A-induced K8 phosphorylation and reorganization were blocked by LY255283. Gene silencing of BLT2 suppressed Comp A-induced K8 phosphorylation and reorganization in PANC-1 cells. Over-expression of BLT2 promoted K8 phosphorylation. Comp A promoted the migration of PANC-1 cells in a dose-dependent manner, and LY255283 blocked Comp A-induced migration, respectively. PD98059 (ERK inhibitor) suppressed Comp A-induced phosphorylation of serine 431 and reorganization of K8. Gene silencing of BLT2 suppressed the expression of pERK, and over-expression of BLT2 increased the expression of pERK even without Comp A. Comp A induced the expression of active ERK (pERK) and BLT2. These inductions were blocked by PD98059. Comp A decreased PP2A expression and hindered the binding of PP2A to the K8, leading to the activation of ERK. PD98059 suppressed the Comp A-induced migration of PANC-1 cells and BLT2 over-expression-induced migration of PANC-1 cells. Overall, these results suggest that BLT2 is involved in LTB4‐induced phosphorylation and reorganization through ERK activation by PP2A downregulation, leading to increased migration of PANC‐1 cells

Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review

Insulin resistance and pancreatic beta cell dysfunction are major contributors to the pathogenesis of diabetes. Various conditions play a role in the pathogenesis of pancreatic beta cell dysfunction and are correlated with endoplasmic reticulum (ER) stress. Pancreatic beta cells are susceptible to ER stress. Many studies have shown that increased ER stress induces pancreatic beta cell dysfunction and diabetes mellitus using genetic models of ER stress and by various stimuli. There are many reports indicating that ER stress plays an important role in the impairment of insulin biosynthesis, suggesting that reduction of ER stress could be a therapeutic target for diabetes. In this paper, we reviewed the relationship between ER stress and diabetes and how ER stress controls insulin biosynthesis

カンコク ヘナム グン ノ ベイサク ノウカ ニ オケル キコウ ヘンドウ ノ ニンシキ ニ カンスル ブンセキ

本研究では韓国ヘナム郡の米作農家における気候変動の認識に関して分析した。ロジットモデルとプロビットモデルを用いて、気候変動の認識の決定要素を検定した。結果として、米作農家の気候変動の認識は高いこと(83.6%)が示された。年齢については負の値であり、高齢者であるほど認識が少ない。つまり若年層が強く気候変動を認識していた。教育については正の値であり、高学歴であるほど強く気候変動を認識していた。そして気候情報の入手については正の値であり、情報アクセスを改善することによって、強く気候変動を認識させることができると分かった。本研究から気候変動情報、教育、訓練における適切な政策プログラムが提供される。This study analyzes perception to climate change of rice farmers in Haenam district, Korea. A logit model and a probit model are used to examine the determinants of perception to climate change. The results indicate that rice farmers\u27 perception of climate change appear to be high(83.6 percent). The findings indicate that age, education and access to climate information have a significant impact on perception to climate change. This study provides some appropriate policy program of information on climate change, education and training