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Aim A history of suicide attempts is a well‐established predictor of future suicidal behavior; however, longitudinal evidence from real‐world emergency settings remains limited. Because age and self‐poisoning/overdose are readily available at emergency presentation and may inform post‐discharge care, we examined whether age and overdose at the index suicide attempt predict medically attended suicide reattempts after emergency admission. Methods We conducted a multicenter retrospective cohort study of 1038 patients admitted to emergency departments after suicide attempts between 2020 and 2025 at three tertiary hospitals in Japan (Dokkyo Medical University Hospital, Jichi Medical University Hospital, and Hachinohe City Hospital). Patients were followed longitudinally to identify suicide reattempts requiring medical attention. Time‐to‐event analyses were performed using Kaplan–Meier methods and Cox proportional hazards models. Age (< 40 vs. ≥ 40 years) and sex were included as baseline covariates, and overdose at the index attempt was examined as an explanatory variable. Sensitivity analyses were performed using a stricter definition of overdose (overdose alone). Results During follow‐up, 58 medically attended suicide reattempts were identified. Kaplan–Meier analyses showed higher cumulative reattempt risk in females and in patients aged 39 years or younger. In Cox proportional hazards models, age ≥ 40 years was associated with a lower risk of suicide reattempt, whereas overdose at the index attempt was associated with a significantly increased risk of suicide reattempt. These findings were consistent in sensitivity analyses. Conclusion Younger age and overdose at the index suicide attempt were independently associated with an increased risk of medically attended suicide reattempt. Assessment of the initial suicide method may help identify patients requiring intensive post‐discharge monitoring. A multicenter cohort of 1038 patients admitted to three Japanese tertiary emergency hospitals after suicide attempts was followed to identify medically attended suicide reattempts. Cox proportional hazards models showed that overdose at the index attempt increased the risk of reattempt, while age ≥ 40 years was protective; findings were consistent in sensitivity analyses.

Background Recent prescribing practices have shifted from benzodiazepines (BZs) toward non‐GABAergic hypnotics, including dual orexin receptor antagonists (DORAs) and melatonin receptor agonists (MRAs). We examined whether hypnotics involved in suicide attempts changed over time in a context‐dependent manner. Methods We conducted a multicenter retrospective cohort study of consecutive patients presenting with suicide attempts at three hospitals in Japan between April 2020 and March 2025. Hypnotics involved in attempts were identified from empty medication packages collected at presentation. Annual proportions of BZs and non‐GABAergic hypnotics (OMs: DORAs and MRAs) were analyzed using Cochran–Armitage trend tests under three conditions: (1) all suicide attempts, (2) overdose‐related attempts, and (3) overdose‐related attempts involving a hypnotic. Additional analyses separated DORAs from MRAs. Results Among 1111 suicide attempt encounters, 648 were overdose‐related. OM involvement increased significantly over time across all denominators. In contrast, BZ involvement declined significantly only among overdose‐related attempts. When OMs were disaggregated, DORA involvement showed a significant upward trend using overdose‐related attempts as the denominator (χ2 = 7.3048, p = 0.006877) and using all suicide attempts as the denominator (χ2 = 7.6384, p = 0.005714). MRA (ramelteon) involvement did not show significant temporal change in either analysis. Overall, the increase in OM involvement was primarily attributable to DORAs. Conclusion Hypnotics involved in suicide attempts changed in a context‐dependent manner during the study period. The increase in non‐GABAergic hypnotics was driven by DORAs, whereas reductions in BZ involvement were detectable only in overdose‐related contexts. These findings suggest that evolving hypnotic availability may influence the profile of medications involved in self‐poisoning. Temporal changes in hypnotics involved in suicide attempts showed context‐dependent shifts. Dual orexin receptor antagonists increased significantly, while benzodiazepine involvement declined only in overdose‐related attempts. Melatonin receptor agonists showed no significant trend during 2020.

Cancer cells adapt to various stress conditions by optimizing gene expression profiles via transcriptional and translational regulation. However, whether and how EXOSC9, a component of the RNA exosome complex, regulates adaptation to stress conditions and tumorigenicity in cancer cells remain unclear. Here, we examined the effects of EXOSC9 depletion on cancer cell growth under various stress conditions. EXOSC9 depletion attenuated growth and survival under various stress conditions in cancer cells. Interestingly, this also decreased the number of P-bodies, which are messenger ribonucleoprotein particles (mRNPs) required for stress adaptation. Meanwhile, EXOSC2/EXOSC4 depletion also attenuated P-body formation and stress resistance with decreased EXOSC9 protein. EXOSC9-mediated stress resistance and P-body formation were found to depend on the intact RNA-binding motif of this protein. Further, RNA-seq analyses identified 343 EXOSC9-target genes, among which, APOBEC3G contributed to defects in stress resistance and P-body formation in MDA-MB-231 cells. Finally, EXOSC9 also promoted xenografted tumor growth of MDA-MB-231 cells in an intact RNA-binding motif-dependent manner. Database analyses further showed that higher EXOSC9 activity, estimated based on the expression of 343 target genes, was correlated with poorer prognosis in some cancer patients. Thus, drugs targeting activity of the RNA exosome complex or EXOSC9 might be useful for cancer treatment.

Genetic alterations of APC and CTNNB1 (beta-catenin) have been identified in a number of human cancers including tumors arising in the colon and liver. Mutations in these genes lead to abnormal accumulation of beta-catenin and constitutive activation of target genes in the Wnt signaling pathway. To clarify the precise role of accumulated beta-catenin in colorectal carcinogenesis, we searched for genes involved in the beta-catenin/Tcf signaling pathway by cDNA microarray. MT1-MMP (membrane-type matrix metalloproteinase) was among 84 genes that were down-regulated after beta-catenin had been depleted by transduction of wild-type APC in SW480 cells. Expression of MT1-MMP was elevated in 22 of 24 colon carcinomas we examined. Reporter assays and an electromobility-shift assay revealed a DNA fragment between -1169 bp and -1163 bp in the 5' flanking region of this gene to be a target of the beta-catenin/Tcf4 complex. Our results indicate that MT1-MMP is a direct down-stream target in the Wnt signaling pathway, and that one of the ways accumulated beta-catenin contributes to colorectal carcinogenesis is by transactivating this gene.

Cytoplasmic polyadenylation element-binding protein 3 (CPEB3) is an RNA-binding protein that plays a pivotal role in the formation of long-term memory. The N-terminal region (residues 1–459) of CPEB3 is a highly aggregative intrinsically disordered region (IDR) that regulates the translation of specific targets, such as AMPA subunits, through mechanisms including liquid-liquid phase separation (LLPS) and the formation of fibrous aggregates. Despite its significance, the underlying mechanisms remain poorly understood. In this study, we present the backbone resonance assignments of residues 101–200 and 294–410 segments of the CPEB3 IDR. In agreement with sequence-based predictions, CPEB3 [101–200] was found to be disordered, whereas two partial α-helices were identified within CPEB3 [294–410].

The Sendai Framework for Disaster Risk Reduction emphasizes the need to rebuild better after a disaster to ensure that the at-risk communities can withstand a similar or stronger shock in the future. In the present work, the authors analyzed the reconstruction paths through a comparative analysis of the perspective of a community in Japan and another in Chile, and their respective local governments. While both countries are at risk to tsunamis, they follow different reconstruction philosophies. Data was gathered through key informant interviews of community members and local government officials, by adapting and modifying the Building Resilience to Adapt to Climate Extremes and Disasters (BRACED) 3As framework to a tsunami scenario. The 3As represent anticipatory, adaptive, and absorptive capacities as well as transformative capacities and respondents were asked to rate this according to their perspectives. It was found that while both communities perceive that much is to be done in recovery, Kirikiri has a more holistic and similar perspective of the recovery with their government officials as compared to Dichato. This shows that community reconstruction and recovery from a disaster requires a holistic participation and understanding.

We studied morphologic changes after sublethal high hydrostatic pressure treatment (HPT) of Escherichia coli K-12 strains in which genes related to the cytoskeleton, cell wall, and cell division had been deleted. Some long filamentous and swelling cells were observed in wild-type bacteria, while some spherical, branched, or collapsed cells were observed in deletion mutants. In particular, ΔzapA and ΔrodZ showed distinguished morphologies. ZapA supports FtsZ, a cytoskeletal protein, forming ring with ZapB. RodZ, a cytoskeletal protein, interacts with MreB, also a cytoskeletal protein, and both factors are necessary for maintaining the rod shape of the cell. These results showed that insufficient formation of FtsZ rings induced cell elongation and that insufficient formation of MreB induced a branched and collapsed cell shape. Therefore, the correct formation of the bacteria cytoskeleton by FtsZ rings and MreB is important for keeping normal cell shape during growth after HPT, and the polymerization of cytoskeletal proteins was a critical target of sublethal HPT. These results indicate that sublethal HPT induces bacterial cell morphologic change and provide important information on the role of genes involved in morphogenesis. Therefore, sublethal HPT may be a good tool for studying the morphogenesis of bacterial cells.

The Epstein-Barr virus (EBV)-encoded latent membrane protein 1 (LMP1) has a significant role in initiating EBV-associated lymphoproliferative disease and EBV-related malignancies. In view of clinical features related to the type of EBV latency, LMP1 may influence invasiveness of EBV associated tumors categorized as types II and III as represented on nasopharyngeal carcinoma (NPC). To screen for genes associated with invasion of epithelial cells transformed by LMP1, Madin-Darby canine kidney (MDCK) epithelial cells were transformed by LMP1. Stable transfection of a LMP1 gene into MDCK cells induced morphological change from cobblestone to a long spindle-shape, reduced cell-cell adhesion and caused high cell motility. Parental MDCK cells, which form spherical cysts in three-dimensional collagen gel matrix, form branching tubules following exposure to hepatocyte growth factor (HGF). MDCK cells transformed by LMP1 showed invasive growth to form branching tubules into collagen gel without HGF-treatment. mRNA differential display and Northern hybridization identified plasminogen activator inhibitor-1 (PAI-1), urokinase type plasminogen activator (uPA) and ets1 as genes upregulated during transformation by LMP1. Expression of a dominant negative type of Etsl in LMP1-transformed cells downregulated uPA expression and cell motility. Deletion of LMP1 cytoplasmic carboxy-terminal activating region 1 (CTAR1) domain abolished transformation, but a deletion mutant lacking CTAR2 domain still retained transforming and uPA-inducing ability. Expression of Ets1 was immunolocalized in tumor cells of NPC tissue which frequently express LMP1. Taken together, it is suggested that LMP1 induces expression of Ets1 which may contribute to invasion of NPC by stimulating cell motility and uPA expression.