Kinjo Gakuin University (金城学院大学, Kinjō gakuin daigaku) is a private women's university in Moriyama-ku, Nagoya, Aichi Prefecture, Japan. The predecessor of the school was founded in 1889. It was chartered as a university 1949.Kinjo Gakuin University has 14 undergraduate departments and majors covering a wide range of fields — from human/social science to natural science — and a graduate school in the humanities and in human ecology offering master's and doctoral degrees..
Trichloroethylene (TCE) remains a versatile organic solvent used globally. In recent years, immunological occupational diseases such as hypersensitivity syndrome (HS) and systemic sclerosis (SSc) have attracted attention in terms of the number of patients and the life-threatening consequences. This review summarizes mechanisms underlying HS pathogenesis based on the available literature. TCE-HS is a disease attributable to anti-CYP2E1 autoantibodies and HLA-B13:01 as susceptibility gene and is characterized by systemic skin lesions, severe-to-moderate liver damage, fever above 38 °C, leukocytosis, lymphadenopathy, and human herpesvirus 6 (HHV6) reactivation with elevated inflammatory cytokines, which are all similar to the characteristics of drug-induced HS. TCE-HS occurs on average 1 month after the commencement of exposure to TCE, which is shorter than the corresponding period for SSc. Recent epidemiological and animal studies have clarified the mechanism of pathogenesis: the oxidative metabolites chloral hydrate, dichloroacetyl chloride, and trichloroethanol, which are produced by CYP2E1, amplify the methylation of CD4+ T cells and activate them, resulting in the upregulation of cytokines such as TNF-α. Subsequently, some unidentified but oxidized metabolite haptens are assumed to activate CD8+ T cells with HLA-B*13:01, resulting in the production of anti-CYP2E1 autoantibodies. Subsequently, HHV6 is reactivated, leading to the development of skin and hepatic injuries. Whether skin lesions develop through a pathophysiological mechanism originating from hepatic lesions or by the same mechanism as the development of hepatic lesions remains unclear. Although disease contours have been clarified, further studies are required to elucidate its pathogenesis.
Metallo-β-lactamases (MBLs)-Zn2+-dependent β-lactamases that compromise the efficacy of most β-lactam antibiotics, including carbapenems-are difficult to monitor rapidly with broadly applicable small-molecule probes due to the structural diversity among the MBLs. Fluorescent thiol-based probes that bind to the dinuclear Zn2+ active site would offer a mechanistically different approach for the selective detection and inhibition of MBLs compared to serine β-lactamases (SBLs); however, their performance across genetically divergent MBLs remains poorly defined. To clarify the structural determinants governing probe recognition across different MBLs, we examined the structure-activity relationships using a homologous series of dansyl-based thiol probes, DansylCnSH (n = 2 and 4-6) toward BlaB, a class B MBL of Elizabethkingia meningoseptica, and compared their behavior with those of the clinically relevant MBLs imipenemase-1 (IMP-1) and Verona integron-encoded metallo-β-lactamase 2 (VIM-2). Consistent with the minimal differences in fluorescence enhancement among the series, BlaB inhibition exhibited only modest spacer-length dependence (IC50 = 29-51 μM; apparent inhibition constants (Kiapp) = 3600-5910 nM). In contrast, IMP-1 and VIM-2 showed markedly stronger fluorescence emission and inhibitory potencies (IMP-1: IC50 = 0.7-5.2 μM; Kiapp = 140-1100 nM; VIM-2: IC50 = 1.5-2.1 μM; Kiapp = 286-370 nM), reflecting their distinct active-site architectures. Docking analyses further revealed distinct binding orientations that explain their photophysical behaviors. No fluorescence enhancement or inhibition was observed with the class A SBL Guiana extended-spectrum β-lactamase-3 (GES-3), confirming the high selectivity and specificity of the DansylCnSH series. These findings allow identifying key structural determinants governing selective activation and inhibition of fluorescence from each MBL.
Background: The time from mastication to swallowing is used as an indicator of masticatory and swallowing functions. However, there have been no reports on reasonable eating times associated with eating satisfaction. Clarifying the reasonable time for eating and drinking to achieve eating satisfaction will indicate the level of mastication and swallowing functions that contributes to maintaining an individual’s quality of life. Objective: This study aimed to determine the time from food intake to the end of swallowing that is associated with eating satisfaction. Methods: A cross-sectional survey of 437 community-dwelling older people was conducted. Mastication and swallowing times (SST-MST) were measured using the Saku-Saku Test with a 2 g rice cracker. Food intake difficulty and eating satisfaction were evaluated using a questionnaire. The association between the SST-MST and the difficulty in eating food or eating satisfaction was assessed by sensitivity, specificity, Youden index, sensitivity–specificity ratio, positive likelihood ratio, negative likelihood ratio, odds ratio, and 95% confidence interval. Results: Most indices indicated that a cutoff point of 25 s on the SST-MST was associated with not having difficulty in eating food items. Moreover, when the SST-MST cutoff was set to 25 s, all indices showed a favorable association with eating satisfaction. Conclusions: In community-dwelling older people in their 70s and 80s, an SST-MST of about 25 s for 2 g of rice crackers was modestly associated with eating satisfaction.
Genomic imprinting, an epigenetic mechanism that governs parent-of-origin-specific gene expression, is essential for mammalian development, yet its role in late-stage development remains unclear due to the lethality of parthenogenetic (Pg) embryos. Here, we establish cell replacement with parthenogenote-derived cells (CReP), a blastocyst complementation strategy that enables survival and tissue-specific contribution of Pg-derived cells. By creating tissue-specific niches in recipient embryos, CReP allows targeted incorporation of Pg-derived cells into late-stage tissues. Brain-targeted CReP showed that Pg-derived cells can participate in neural development but exhibit impaired maintenance of neuronal-glial balance, accompanied by increased Notch signaling and reduced expression of the paternally expressed gene Dlk1. Recombinant Dlk1 attenuated Notch activity and shifted neuronal differentiation toward control levels. These findings support a key contribution of the paternal genome to neural stem cell expansion and balanced cell fate decisions, in part through Dlk1-Notch-related pathways. The CReP model provides a powerful platform for investigating genomic imprinting and parental genome contributions in development and disease.
