日本と韓国における養子制度の発展と児童福祉 : 社会的養護としての養子縁組を考える

養子縁組とは血縁に依存せず法的に親子関係を創出する制度であり，家庭に恵まれない児童が新たに恒久的な家庭を得る唯一の方法である．しかし，韓国では養子制度が児童福祉に重要な役割を果たしているのに対して，日本では児童福祉政策としての機能をほとんど果たしていない．本研究では「なぜ日韓では社会的養護としての養子縁組の位置づけが大きく異なるのか」という問いを立て，政府統計を駆使して比較可能な長期統計を作成し，両国における制度発展の歴史的経路を明らかにする．分析の結果によると，日本と韓国は戦後の混乱期に児童福祉制度の近代化を図った点で似たような初期条件にあった．しかし，国家の財政力などの違いから発展経路が分かれ，韓国では外国援助団体と政府機関の連携の下に要保護児童対策における養子縁組の役割が拡大していったのに対して，日本では民間事業者と政府機関の連携の下に施設養護が主流となり，養子法の改革が遅れ，現在に至るまで養子縁組は児童福祉として積極的に活用されていない．Child adoption is an institution that permits legal creation of parent-child relations. As such, it is the only means for a child who lost parental care to obtain a new and permanent home. In Korea, child adoption plays an important role in the protection of children in need of care, while in Japan it plays little such role. In this paper, to understand why the roles of child adoption in child welfare systems greatly differ between Korea and Japan, we compile comparable historical statistics and document the paths of institutional development in the two countries. Our analysis shows that both countries shared similar initial conditions in the 1950s, as the governments introduced modern child welfare systems during the turmoil of postwar years. Due to the differences in state fiscal capacity and other factors, however, their paths began to diverge : In Korea, in cooperation with foreign relief organizations, the government promoted child adoption to protect orphaned or abandoned children. By contrast, as child welfare institutions and government agencies formed collaborative relations, institutional care became a dominant mode of child protection in Japan, which delayed an adoption law reform and limited the role of child adoption in the area of child welfare

Paralog Specificity Determines Subcellular Distribution, Action Mechanism, and Anticancer Activity of TRAP1 Inhibitors

Although Hsp90 inhibitors can inhibit multiple tumorigenic pathways in cancer cells, their anticancer activity has been disappointingly modest. However, by forcing Hsp90 inhibitors into the mitochondria with mitochondrial delivery vehicles, they were converted into potent drugs targeting the mitochondrial Hsp90 paralog TRAP1. Here, to improve mitochondrial drug accumulation without using the mitochondrial delivery vehicle, we increased freely available drug concentrations in the cytoplasm by reducing the binding of the drugs to the abundant cytoplasmic Hsp90. After analyzing X-ray cocrystal structures, the purine ring of the Hsp90 inhibitor 2 (BIIB021) was modified to pyrazolopyrimidine scaffolds. One pyrazolopyrimidine, 12b (DN401), bound better to TRAP1 than to Hsp90, inactivated the mitochondrial TRAP1 in vivo, and it exhibited potent anticancer activity. Therefore, the rationale and feasible guidelines for developing 12b can potentially be exploited to design a potent TRAP1 inhibitor

Intranasal Delivery of Anti-Apoptotic siRNA Complexed with Fas-Signaling Blocking Peptides Attenuates Cellular Apoptosis in Brain Ischemia

Ischemic stroke-induced neuronal cell death leads to the permanent impairment of brain function. The Fas-mediating extrinsic apoptosis pathway and the cytochrome c-mediating intrinsic apoptosis pathway are two major molecular mechanisms contributing to neuronal injury in ischemic stroke. In this study, we employed a Fas-blocking peptide (FBP) coupled with a positively charged nona-arginine peptide (9R) to form a complex with negatively charged siRNA targeting Bax (FBP9R/siBax). This complex is specifically designed to deliver siRNA to Fas-expressing ischemic brain cells. This complex enables the targeted inhibition of Fas-mediating extrinsic apoptosis pathways and cytochrome c-mediating intrinsic apoptosis pathways. Specifically, the FBP targets the Fas/Fas ligand signaling, while siBax targets Bax involved in mitochondria disruption in the intrinsic pathway. The FBP9R carrier system enables the delivery of functional siRNA to hypoxic cells expressing the Fas receptor on their surface—a finding validated through qPCR and confocal microscopy analyses. Through intranasal (IN) administration of FBP9R/siCy5 to middle cerebral artery occlusion (MCAO) ischemic rat models, brain imaging revealed the complex specifically localized to the Fas-expressing infarcted region but did not localize in the non-infarcted region of the brain. A single IN administration of FBP9R/siBax demonstrated a significant reduction in neuronal cell death by effectively inhibiting Fas signaling and preventing the release of cytochrome c. The targeted delivery of FBP9R/siBax represents a promising alternative strategy for the treatment of brain ischemia