Comparison of Japanese and Korean TAC System for Future Expansion

As fisheries resources in the East China Sea, the Yellow Sea and the Japan Sea have the tendency to decrease, the purpose of this study is to identify the problems of the co-management by comparing the Total Allowable Catch (TAC) system between Japan and the Republic of Korea (Korea) in the executed sea areas. Japan, Korea, and China ratified the United Nations Convention on the Law of the Sea in 1996. The TAC system has been implemented by Japan from 1997 and Korea from 1999. While China is still examining the TAC system, Japan is allocated TAC for each administrative division as a fisheries management policy. The TAC of Korea is allocated for only the main fisheries that catch a lot of fish stocks. Common mackerel, sardine and snow crab are agitation for the fish stock targets of Japan and Korea. The target sea areas are EEZ and the provisional sea in both Japan and Korea. In general, the catch from EEZ and provisional sea areas are parts of the TAC. But in reality, the haul of one country in the other country’s EEZ and the provisional sea areas is excluded from its own TAC. Therefore, it is necessary to establish the co-management system for the effective use of resource, for example, the one that can control the catch of migratory fish species.Keywords: Sea of Japan, Fisheries Economics, Co-management, Yellow Sea, TAC System, Japan, Korea, East China Sea, International: Cooperation in Fisheries and Aquacultur

Medium-chain fatty acids suppress lipotoxicity-induced hepatic fibrosis via the immunomodulating receptor GPR84

食事性肥満から肝炎発症に関わる制御因子の同定 --中鎖脂肪酸油による予防・GPR84標的NASH治療薬の可能性--. 京都大学プレスリリース. 2023-01-18.Medium-chain triglycerides (MCTs), which consist of medium-chain fatty acids (MCFAs), are unique forms of dietary fat with various health benefits. G protein–coupled 84 (GPR84) acts as a receptor for MCFAs (especially C10:0 and C12:0); however, GPR84 is still considered an orphan receptor, and the nutritional signaling of endogenous and dietary MCFAs via GPR84 remains unclear. Here, we showed that endogenous MCFA-mediated GPR84 signaling protected hepatic functions from diet-induced lipotoxicity. Under high-fat diet (HFD) conditions, GPR84-deficient mice exhibited nonalcoholic steatohepatitis (NASH) and the progression of hepatic fibrosis but not steatosis. With markedly increased hepatic MCFA levels under HFD, GPR84 suppressed lipotoxicity-induced macrophage overactivation. Thus, GPR84 is an immunomodulating receptor that suppresses excessive dietary fat intake–induced toxicity by sensing increases in MCFAs. Additionally, administering MCTs, MCFAs (C10:0 or C12:0, but not C8:0), or GPR84 agonists effectively improved NASH in mouse models. Therefore, exogenous GPR84 stimulation is a potential strategy for treating NASH

ショウガイジ オ モツ ハハオヤ ノ セイシンテキ ケンコウド 2 ニュウヨウジキ ト ガクレイキ ノ ヒカク

本研究の目的は、障害児を持つ母親の精神的健康度の現状を明らかにし、必要な支援内容に関する指針を得ることである。 対象者はE県の通園事業・通園施設を利用する乳幼児の母親247名とE県立養護学校に通学する児童を持つ母親98名である。母親の属性(年齢、就労状況、世帯構造等)と、「育児ストレス・コーピング」、「育児バーンアウト」、「孤独感」について調査し分析した。さらに、同研究(I)で明らかにした他の指標(「母親の健康関連QOL」「育児ソーシャルサポート」「父親の育児サポート認知」「育児負担感」)との関連性について分析した。また、乳幼児と児童の母親の違いについて分析し、障害児を持つ母親の精神的健康度を高めるための示唆を得た。 障害児を持つ母親の健康関連QOLを高めるためには、乳幼児を持つ母親の場合、育児ソーシャルサポートが逃避的コーピングを回避し、さらに父親の育児サポートが調整的コーピング行動を惹起し、育児負担感や、育児バーンアウト、孤独感を抑制することが示された。一方、児童の母親の場合は健康関連QOLと育児ソーシャルサポートや、父親の育児サポートとは直接的な関連性がないことが明らかになった。しかし、育児負担感や育児バーンアウト、孤独感とは強い相関が認められた。また、育児負担感を軽減し育児バーンアウトを抑制するためには、父親の育児サポートが大きな要因となっていることが明らかになった。また、孤独感は児童の母親の場合は全ての尺度と関連があったが、乳幼児の場合は、父親のサポート認知とは関連が認められないという違いが見られた。The purpose of this study is to investigate condition of mental health on mothers who have disabled preschool/school age children and to provide useful information for developing the assistance guideline for them. 247 mothers who utilize nursery schools for the disabled and 98 mothers who use schools for the disabled attended this study. Questionnaire was consisted of attributes of mothers (age, employment condition, family structure), coping type to parenting stress, parenting burnout, and loneliness. After analyzing these data, following findings were found. For mothers who have preschool disabled children, parenting-related social supports prevented their negative coping (i.e. escape). And parenting support from fathers reduce their parenting stress, parenting burnout and loneliness. For mothers who have school age disabled children, parenting-related social support and parenting support from fathers do not have positive influences on their condition of mental health

ショウガイジ オ モツ ハハオヤ ノ セイシンテキ ケンコウド 1 ニュウヨウジキ ト ガクレイキ ノ ヒカク

本研究の目的は、障害児を持つ母親の精神的健康度の現状を明らかにし、必要な支援内容に関する指針を得ることである。 対象者はE県の通園事業、通園施設を利用する乳幼児の母親247名とE県立養護学校に通学する児童を持つ母親98名である。母親の属性(年齢、就労状況、世帯構造等)と子どもの属性(年齢、性、障害の種類と程度)および「母親の健康関連QOL」、「育児ソーシャルサポート」、母親による「父親の育児サポート認知」、「育児負担感」を調査し分析した。さらに乳幼児と児童の母親の違いについて考察した。 その結果、障害児を持つ母親のQOLを高めるためには、母親の育児負担感を軽減する必要があることが示された。また、児童の母親にとっては父親の育児サポートが育児負担感を軽減することが示唆された。乳幼児の母親のQOLは、育児ソーシャルサポート、父親のサポートによって高められることが示された。The purpose of this study is to examine the level of mental health of mothers with disabled children in order to develop guidelines for the assistance necessary to help them. The subjects were 247 mothers with disabled infants utilizing the institutes of nursery schools for disabled infants in E prefecture and 98 mothers of disabled children attending an E prefectural school for the disabled. This study examined and analyzed the attributes of mothers (age, employment status and household structure), the attributes of children (age, sex, and degree and kind of disability),the quality of life (QOL) of mothers, the social support for raising children, the level of support from fathers, and the parenting stress of mother. This study also examined the difference between mothers of children and those of infants. The results of this study indicate that to increase the QOL of mothers, parenting stress of mother need to be reduced. Moreover, this study suggests that the QOL of mothers be improved by the support of fathers and the social support for raising disabled children

Involvement of Gut Microbial Metabolites Derived from Diet on Host Energy Homeostasis

Due to the excess energy intake, which is a result of a high fat and high carbohydrate diet, dysfunction of energy balance leads to metabolic disorders such as obesity and type II diabetes mellitus (T2DM). Since obesity can be a risk factor for various diseases, including T2DM, hypertension, hyperlipidemia, and metabolic syndrome, novel prevention and treatment are expected. Moreover, host diseases linked to metabolic disorders are associated with changes in gut microbiota profile. Gut microbiota is affected by diet, and nutrients are used as substrates by gut microbiota for produced metabolites, such as short-chain and long-chain fatty acids, that may modulate host energy homeostasis. These free fatty acids are not only essential energy sources but also signaling molecules via G-protein coupled receptors (GPCRs). Some GPCRs are critical for metabolic functions, such as hormone secretion and immune function in various types of cells and tissues and contribute to energy homeostasis. The current studies have shown that GPCRs for gut microbial metabolites improved host energy homeostasis and systemic metabolic disorders. Here, we will review the association between diet, gut microbiota, and host energy homeostasis

Intestinal GPR119 activation by microbiota-derived metabolites impacts feeding behavior and energy metabolism

Objective: The gastrointestinal tract affects physiological activities and behavior by secreting hormones and generating signals through the activation of nutrient sensors. GPR119, a lipid sensor, is indirectly involved in the secretion of incretins, such as glucagon-like peptide-1 and glucose-dependent insulinotropic peptide, by enteroendocrine cells, while it directly stimulates insulin secretion by pancreatic beta cells. Since GPR119 has the potential to modulate metabolic homeostasis in obesity and diabetes, it has attracted interest as a therapeutic target. However, previous studies have shown that the deletion of Gpr119 in mice does not affect glucose homeostasis and appetite in either basal or high-fat diet-fed conditions. Therefore, the present study aimed to explore the role of GPR119 signaling system in energy metabolism and feeding behavior in mice. Methods: Gpr119 knockout (KO) mice were generated using CRISPR-Cas9 gene-editing technology, and their feeding behavior and energy metabolism were evaluated and compared with those of wild type (WT) mice. Results: Upon inducing metabolic stress via food deprivation, Gpr119 KO mice exhibited lower blood glucose levels and a higher body weight reduction compared to WT mice. Although food intake in WT and KO mice were similar under free-feeding conditions, Gpr119 KO mice exhibited increased food intake when they were refed after 24 h of food deprivation. Further, food-deprived Gpr119 KO mice presented shorter post-meal intervals and lower satiety for second and later meals during refeeding, resulting in increased food intake. Associated with this meal pattern, levels of oleoylethanolamide (OEA), an endogenous agonist of GPR119, in the luminal contents of the distal gastrointestinal tract were elevated within 2 h after refeeding. The large-intestinal infusion of OEA prolonged post-meal intervals and increased satiety in the first meal, but not the second meal. On the other hand, infusion of oleic acid increased cecal OEA levels at 2 h from the beginning of infusion, while prolonging post-meal intervals and increasing satiety on the meals that occurred approximately 2 h after the infusion. Cecal OEA levels were low in antibiotic-treated mice, suggesting that the gut microbiota partially synthesizes OEA from oleic acid. Conclusions: Collectively, our results indicate that the activation of gastrointestinal GPR119 by microbiota-produced OEA derived from oleic acid is associated with satiety control and energy homeostasis under energy shortage conditions

Potential Survival Benefit of Anti-Apoptosis Protein: Survivin-Derived Peptide Vaccine with and without Interferon Alpha Therapy for Patients with Advanced or Recurrent Urothelial Cancer—Results from Phase I Clinical Trials

We previously identified a human leukocyte antigen (HLA)-A24-restricted antigenic peptide, survivin-2B80–88, a member of the inhibitor of apoptosis protein family, recognized by CD8+cytotoxic T lymphocytes (CTL). In a phase I clinical trial of survivin-2B80-88 vaccination for metastatic urothelial cancer (MUC), we achieved clinical and immunological responses with safety. Moreover, our previous study indicated that interferon alpha (IFNα) enhanced the effects of the vaccine for colorectal cancer. Therefore, we started a new phase I clinical trial of survivin-2B80–88 vaccination with IFNα for MUC patients. Twenty-one patients were enrolled and no severe adverse event was observed. HLA-A24/survivin-2B80–88 tetramer analysis and ELISPOT assay revealed a significant increase in the frequency of the peptide-specific CTLs after vaccination in nine patients. Six patients had stable disease. The effects of IFNα on the vaccination were unclear for MUC. Throughout two trials, 30 MUO patients received survivin-2B80–88 vaccination. Patients receiving the vaccination had significantly better overall survival than a comparable control group of MUO patients without vaccination (P=0.0009). Survivin-2B80–88 vaccination may be a promising therapy for selected patients with MUC refractory to standard chemotherapy. This trial was registered with UMIN00005859