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Capacitation is an important event in the completion of fertilization by mammalian sperm. Cholesterol efflux is a trigger of capacitation. In general, cholesterol acceptors of albumin and β-cyclodextrins are used to induce capacitation during in vitro fertilization. Previously, we reported that methyl-β-cyclodextrin (MBCD), which is composed of seven glucoses, had a higher ability to induce capacitation than bovine serum albumin (BSA) in frozen–thawed mouse sperm. Comparison of albumin and cyclodextrins is helpful for understanding the mechanism of capacitation. In this study, we examined the effects of albumin, MBCD, and a different type of cyclodextrin, dimethyl-α-cyclodextrin (DMACD), which is composed of six glucoses, on several events of sperm capacitation. We showed that DMACD induced sperm capacitation and promoted fertilization ability. The time required to increase the fertilization rate differed among BSA, MBCD, and DMACD. BSA and MBCD enhanced cholesterol and phospholipid efflux, whereas DMACD enhanced only phospholipid efflux. BSA, MBCD, and DMACD increased sperm membrane fluidity, rearrangement of the lipid raft, and the acrosome reaction. These findings suggest that phospholipid efflux is a novel trigger of capacitation. Increasing the choice of sperm capacitation inducers may be useful for improving in vitro fertilization (IVF) techniques not only in mice, but also in various species in which it has been difficult to produce embryos by IVF.

Liquid-liquid phase separation (LLPS) is involved in various dynamic biological phenomena. In epithelial cells, dynamic regulation of junctional actin filaments tethered to the apical junctional complex (AJC) is critical for maintaining internal homeostasis against external perturbations; however, the role of LLPS in this process remains unknown. Here, after identifying a multifunctional actin nucleator, cordon bleu (Cobl), as an AJC-enriched microtubule-associated protein, we conducted comprehensive in vitro and in vivo analyses. We found that apical microtubules promoted LLPS of Cobl at the AJC, and Cobl actin assembly activity increased upon LLPS. Thus, microtubules spatiotemporally regulated junctional actin assembly for epithelial morphogenesis and paracellular barriers. Collectively, these findings established that LLPS of the actin nucleator Cobl mediated dynamic microtubule-actin cross-talk in junctions, which fine-tuned the epithelial barrier.

Head and forehead hyperhidrosis (HFH) is a disease that causes a large amount of sweating from the head region, and it significantly reduces patients' quality of life. Only a few reports have shown the effectiveness of botulinum toxin type A (BTX-A) local injection therapy (BTX-A therapy) for HFH. To clarify the benefits of BTX-A for HFH, BTX-A therapy was performed in 15 patients, and its efficacy was evaluated. The amount of sweating was measured by the ventilation capsule method and Minor's iodine-starch test. Evaluation was also performed using the Hyperhidrosis Disease Severity Scale (HDSS) and the Dermatology Life Quality Index (DLQI). In most cases, a remarkable antiperspirant effect was observed from 2 weeks after the injection, and the effect lasted for approximately 30 weeks. HDSS and DLQI improved along with the decrease in sweating. Two patients (13.3%) complained of transient mild ptosis. There were no serious side-effects. This study showed that BTX-A therapy is a safe and effective treatment for HFH.

Despite increasing interest in and use of nanoparticles (NP), the environmental consequences of using NP are poorly understood because most relevant studies have not taken the effects of natural coatings on NP into consideration. The aim of this study was to improve our understanding of the fates of NP in aquatic systems. The fates of silver NP (AgNP) capped with citrate and polyethylene glycol dispersed in ecotoxicological matrices in the presence of environmentally relevant components of natural water (humic substances and extracellular polymeric substances) were investigated. Interactions between AgNP and natural organic matter were evaluated by ultracentrifugation and electrophoretic mobility measurements to assess AgNP dissolution. Humic substances and extracellular polymeric substances both decreased the dissolution rate. The natural organic matter (humic substances and extracellular polymeric substances) provided conditions in which the medium stabilized the NP. The dissolution rate depended on the coating type (citrate or polyethylene glycol), dissolved organic carbon concentration, and particle concentration. The presence of algae and Daphnia affected AgNP conversion, demonstrating the value of research that takes environmentally relevant matrices into consideration. The results improve our understanding of the factors that affect the bioavailabilities of AgNP and therefore improve our ability to evaluate AgNP toxicity. Studies of other NP using the same strategy will improve our understanding of the fates of nanomaterials in the environment and biota.

Significance Although the circadian clock is essential for regulating the temporal order of physiological functions, circadian oscillation is strictly suppressed in the early-to-mid–stage embryos in mammalian developmental process. The biological significance controlling the suppression of the circadian clock and its delayed emergence in mammalian embryos has been unknown. Here, we show that the premature expression of the functional circadian components CLOCK/BMAL1 in mouse induced presomitic mesoderm and gastruloids can interfere with the segmentation clock Hes7 oscillation and somitogenesis through the Hes7 transcription and its regulatory pathways. This suggests that the CLOCK/BMAL1 function may need to be suppressed during somitogenesis., In mammals, circadian clocks are strictly suppressed during early embryonic stages, as well as in pluripotent stem cells, by the lack of CLOCK/BMAL1-mediated circadian feedback loops. During ontogenesis, the innate circadian clocks emerge gradually at a late developmental stage, and with these, the circadian temporal order is invested in each cell level throughout a body. Meanwhile, in the early developmental stage, a segmented body plan is essential for an intact developmental process, and somitogenesis is controlled by another cell-autonomous oscillator, the segmentation clock, in the posterior presomitic mesoderm (PSM). In the present study, focusing upon the interaction between circadian key components and the segmentation clock, we investigated the effect of the CLOCK/BMAL1 on the segmentation clock Hes7 oscillation, revealing that the expression of functional CLOCK/BMAL1 severely interferes with the ultradian rhythm of segmentation clock in induced PSM and gastruloids. RNA sequencing analysis implied that the premature expression of CLOCK/BMAL1 affects the Hes7 transcription and its regulatory pathways. These results suggest that the suppression of CLOCK/BMAL1-mediated transcriptional regulation during the somitogenesis may be inevitable for intact mammalian development.

Programmed necrosis, such as necroptosis and pyroptosis, is a highly pro-inflammatory cellular event that is associated with chronic inflammation. Although there are various triggers of pyroptosis and necroptosis in autoimmune tissue inflammation and subsequent lytic forms of cell death release abundant inflammatory mediators, including damage-associated molecular patterns and IL-1β, capable of amplifying autoimmune Th17 effector functions, it remains largely unclear whether the programs play a crucial role in the pathogenesis of autoimmune arthritis. We herein report that Gasdermin D (Gsdmd) and receptor interacting serine/threonine kinase 3 (Ripk3)—key molecules of pyroptosis and necroptosis, respectively—are upregulated in inflamed synovial tissues, but dispensable for IL-1β production and the development of IL-17-producing T helper (Th17) cell-mediated autoimmune arthritis in SKG mice. Gsdmd−/−, Ripk3−/−, or Gsdmd−/−Ripk3−/− SKG mice showed severe arthritis with expansion of arthritogenic Th17 cells in the draining LNs and inflamed joints, which was comparable to that in wild-type SKG mice. Despite the marked reduction of IL-1β secretion from Gsdmd−/− or Ripk3−/− bone marrow-derived DCs by canonical stimuli, IL-1β levels in the inflamed synovium were not affected in the absence of Gsdmd or Ripk3. Our results revealed that T cell-mediated autoimmune arthritis proceeds independently of the pyroptosis and necroptosis pathways.

SUMMARYNaive and primed states are distinct states of pluripotency during early embryonic development that can be captured and converted to each other in vitro. To elucidate the regulatory mechanism of pluripotency, we performed a recessive genetic screen of homozygous mutant mouse embryonic stem cells (mESCs) and found that suppression of N-myristoyltransferase (Nmt) promotes naive pluripotency. Disruption of Nmt1 in mESCs conferred resistance to differentiation. Suppression of Nmt in mouse epiblast stem cells (mEpiSCs) promoted the conversion from the primed to the naive state. This effect was independent of Src, which is a major substrate of Nmt and is known to promote differentiation of mESCs. Suppression of Nmt in naive-state human induced pluripotent stem cells (hiPSCs) increased the expression of the naive-state marker. These results indicate that Nmt is a novel target for the regulation of naive pluripotency conserved between mice and humans.

This study examined the effects of sharing schadenfreude with friends on late adolescents’ self-esteem. University students (242 men; 238 women) were presented with scenarios depicting a deserved failure of a superior rival classmate and sharing schadenfreude. Participants’ state self-esteem was measured both before the rival’s misfortune and after sharing schadenfreude and was compared with that of participants presented with the non-sharing scenario. Whereas experiencing schadenfreude enhanced late adolescents’ state self-esteem regardless of the level of envy toward the rival, sharing schadenfreude with a best friend was not associated with further increases in self-esteem. When discussing the very well-deserved misfortune of others, the listener will likely react similarly to the expresser; thus, expressing schadenfreude may not bring about a sense of being understood and accepted by friends.

In bone marrow, special microenvironments, known as niches, are essential for the maintenance of hematopoietic stem cells (HSCs). A population of mesenchymal stem cells, termed CXC chemokine ligand 12 (CXCL12)-abundant reticular (CAR) cells or leptin receptor-expressing cells are the major cellular component of HSC niches. The molecular regulation of HSC niche properties is not fully understood. The role of Runx transcription factors, Runx1 and Runx2 in HSC cellular niches remains unclear. Here we show that Runx1 is predominantly expressed in CAR cells and that mice lacking both Runx1 and Runx2 in CAR cells display an increase in fibrosis and bone formation with markedly reduced hematopoietic stem and progenitor cells in bone marrow. In vitro, Runx1 is induced by the transcription factor Foxc1 and decreases fibrotic gene expression in CAR cells. Thus, HSC cellular niches require Runx1 or Runx2 to prevent their fibrotic conversion and maintain HSCs and hematopoiesis in adults.

Background: Peripheral intravenous injection of gemcitabine often causes vascular pain; however, preventive measures have not yet been established. Objectives: This study focused on identifying predictive factors for gemcitabine-induced vascular pain. Methods: We retrospectively analyzed risk factors for developing vascular pain in patients with pancreatic cancer receiving gemcitabine infusions at our institution. Infusions were divided into groups according to presence or absence of vascular pain symptoms, and variables were compared. Odds ratios for risk factors were calculated using logistic regression analyses. Results: Overall, 272 patients with pancreatic cancer were subjected to 725 gemcitabine infusions, and of these, 18.4% (n = 50) experienced vascular pain. There were significant differences in the gemcitabine dose ( P = 0.025), dose of gemcitabine/body surface area (BSA; P = 0.004), concentration of gemcitabine ( P = 0.025), and hot pack use ( P = 0.011) between the vascular pain and no vascular pain groups. Multivariable analyses indicated that gemcitabine dose/BSA and lack of hot pack use were risk factors for developing vascular pain. Moreover, on administration of a higher dosage (>930 mg/m2), the incidence of vascular pain in patients using a hot pack (6.7%) was significantly lower than that in patients not provided a hot pack (16.2%). Conclusions and Relevance: High gemcitabine dosages and lack of hot pack use were predictive factors for gemcitabine-induced vascular pain in patients with pancreatic cancer. Patients receiving gemcitabine treatment should apply a hot pack to the injection site. Scrupulous clinical attention is required for patients presenting with these risk factors to improve pain management.

Conformational conversion of the cellular prion protein, PrPC, into the abnormally folded isoform, PrPSc, is a key pathogenic event in prion diseases. However, the exact conversion mechanism remains largely unknown. Transgenic mice expressing PrP with a deletion of the central residues 91&ndash, 106 were generated in the absence of endogenous PrPC, designated Tg(PrP∆91&ndash, 106)/Prnp0/0 mice and intracerebrally inoculated with various prions. Tg(PrP∆91&ndash, 106)/Prnp0/0 mice were resistant to RML, 22L and FK-1 prions, neither producing PrPSc∆91&ndash, 106 or prions in the brain nor developing disease after inoculation. However, they remained marginally susceptible to bovine spongiform encephalopathy (BSE) prions, developing disease after elongated incubation times and accumulating PrPSc∆91&ndash, 106 and prions in the brain after inoculation with BSE prions. Recombinant PrP∆91-104 converted into PrPSc∆91&ndash, 104 after incubation with BSE-PrPSc-prions but not with RML- and 22L&ndash, PrPSc-prions, in a protein misfolding cyclic amplification assay. However, digitonin and heparin stimulated the conversion of PrP∆91&ndash, 104 into PrPSc∆91&ndash, 104 even after incubation with RML- and 22L-PrPSc-prions. These results suggest that residues 91&ndash, 106 or 91&ndash, 104 of PrPC are crucially involved in prion pathogenesis in a strain-dependent manner and may play a similar role to digitonin and heparin in the conversion of PrPC into PrPSc.

The transcription factor Foxp3 plays crucial roles for Treg cell development and function. Conserved non-coding sequences (CNSs) at the Foxp3 locus control Foxp3 transcription, but how they developmentally contribute to Treg cell lineage specification remains obscure. Here, we show that among Foxp3 CNSs, the promoter-upstream CNS0 and the intergenic CNS3, which bind distinct transcription factors, were activated at early stages of thymocyte differentiation prior to Foxp3 promoter activation, with sequential genomic looping bridging these regions and the promoter. While deletion of either CNS0 or CNS3 partially compromised thymic Treg cell generation, deletion of both completely abrogated the generation and impaired the stability of Foxp3 expression in residual Treg cells. As a result, CNS0 and CNS3 double-deleted mice succumbed to lethal systemic autoimmunity and inflammation. Thus, hierarchical and coordinated activation of Foxp3 CNS0 and CNS3 initiates and stabilizes Foxp3 gene expression, thereby crucially controlling Treg cell development, maintenance, and consequently immunological self-tolerance.

Cell type-specific gene expression is driven by the interplay between lineage-specific transcription factors and cis-regulatory elements to which they bind. Adaptive immunity relies on RAG-mediated assembly of T cell receptor (TCR) and immunoglobulin (Ig) genes. Although Rag1 and Rag2 expression is largely restricted to adaptive lymphoid lineage cells, it remains unclear how Rag gene expression is regulated in a cell lineage-specific manner. Here, we identified three distinct cis-regulatory elements, a T cell lineage-specific enhancer (R-TEn) and the two B cell-specific elements, R1B and R2B By generating mice lacking either R-TEn or R1B and R2B, we demonstrate that these distinct sets of regulatory elements drive the expression of Rag genes in developing T and B cells. What these elements have in common is their ability to bind the transcription factor E2A. By generating a mouse strain that carries a mutation within the E2A binding site of R-TEn, we demonstrate that recruitment of E2A to this site is essential for orchestrating changes in chromatin conformation that drive expression of Rag genes in T cells. By mapping cis-regulatory elements and generating multiple mouse strains lacking distinct enhancer elements, we demonstrate expression of Rag genes in developing T and B cells to be driven by distinct sets of E2A-dependent cis-regulatory modules.

Objectives:The objective of this study is to provide road centerline data for professionals of disaster medicine areas who are often beginners in GIS use.Methods:Newly developed vector tile format data were converted into shapefile format data, then were organized as second level medical districts to which medical professionals are accustomed.Results:Road centerline data in Japan is being prepared to release from Association for Promotion of Infrastructure Geospatial Information Distribution free of charge.Conclusion:Professionals of disaster medicine areas increased their accessibility of GIS. Logistic planning for evacuation activities and dispatching of rescue teams were improved.

Cell sorting via flow cytometry is a powerful tool to select subpopulations of cells in many biological fields. Selection of fertilisation-prone sperm is a critical step to ensure a stable and high fertilisation rate in in vitro fertilisation (IVF). However, a combination of conventional cell sorting and IVF system has not been established because of severe mechanical damages to the sperm during the sorting process. A cell sorter with microfluidics chip technology that lessens cell damage during cell sorting may address this problem. We evaluated the effects of microfluidics chip cell sorting on the sperm using the parameters, such as motility and fertility, and found this cell sorting method had minimal harmful effect on the sperm. Then, sperm were selected by a marker for acrosome reaction and showed higher fertilisation rate than that of the population of acrosome-intact sperm. Embryo derived from these sperm developed normally. These results indicated that microfluidics chip cell sorting can select fertile sperm to improve IVF technique.

The field of genome editing was founded on the establishment of methods, such as the clustered regularly interspaced short palindromic repeat (CRISPR) and CRISPR-associated protein (CRISPR/Cas) system, used to target DNA double-strand breaks (DSBs). However, the efficiency of genome editing also largely depends on the endogenous cellular repair machinery. Here, we report that the specific modulation of targeting vectors to provide 3′ overhangs at both ends increased the efficiency of homology-directed repair (HDR) in embryonic stem cells. We applied the modulated targeting vectors to produce homologous recombinant mice directly by pronuclear injection, but the frequency of HDR was low. Furthermore, we combined our method with the CRISPR/Cas9 system, resulting in a significant increase in HDR frequency. Thus, our HDR-based method, enhanced homologous recombination for genome targeting (eHOT), is a new and powerful method for genome engineering.

Cell type-specific gene expression is driven by the interplay between lineage-specific transcription factors and cis-regulatory elements to which they bind. Adaptive immunity relies on RAG-mediated assembly of T cell receptor (

In this study, the association between extracting benefits from negative experiences and identity development was explored by focusing on differences in benefit-finding domains. Participants (508 undergraduates) recalled a past event they considered to be the most influential in terms of creating their current identity, regardless of whether the event was negative or positive, and then completed the Centrality of Event Scale, Identity Scale, and items regarding benefit-finding. Consequently, the benefit-finding domain of ‘personal growth’ and the pattern of extracting sufficient benefits in various different domains were determined to be associated with high identity achievement. Furthermore, it was also suggested that negative experiences result in higher identity achievement than positive experiences, provided sufficient benefits are successfully extracted from various different domains.

Bone marrow is the tissue filling the space between bone surfaces. Hematopoietic stem cells (HSCs) are maintained by special microenvironments known as niches within bone marrow cavities. Mesenchymal cells, termed CXC chemokine ligand 12 (CXCL12)-abundant reticular (CAR) cells or leptin receptor-positive (LepR+) cells, are a major cellular component of HSC niches that gives rise to osteoblasts in bone marrow. However, it remains unclear how osteogenesis is prevented in most CAR/LepR+ cells to maintain HSC niches and marrow cavities. Here, using lineage tracing, we found that the transcription factor early B-cell factor 3 (Ebf3) is preferentially expressed in CAR/LepR+ cells and that Ebf3-expressing cells are self-renewing mesenchymal stem cells in adult marrow. When Ebf3 is deleted in CAR/LepR+ cells, HSC niche function is severely impaired, and bone marrow is osteosclerotic with increased bone in aged mice. In mice lacking Ebf1 and Ebf3, CAR/LepR+ cells exhibiting a normal morphology are abundantly present, but their niche function is markedly impaired with depleted HSCs in infant marrow. Subsequently, the mutants become progressively more osteosclerotic, leading to the complete occlusion of marrow cavities in early adulthood. CAR/LepR+ cells differentiate into bone-producing cells with reduced HSC niche factor expression in the absence of Ebf1/Ebf3. Thus, HSC cellular niches express Ebf3 that is required to create HSC niches, to inhibit their osteoblast differentiation, and to maintain spaces for HSCs.

// Takuya Tsubaki 1 , Tetsuya Kadonosono 1 , Shimon Sakurai 1 , Tadashi Shiozawa 1 , Toshiki Goto 1 , Shiori Sakai 1 , Takahiro Kuchimaru 1 , Takeharu Sakamoto 2 , Hitomi Watanabe 3 , Gen Kondoh 3 and Shinae Kizaka-Kondoh 1 1 School of Life Science and Technology, Tokyo Institute of Technology, Yokohama 226-8501, Japan 2 Division of Molecular Pathology, Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo 108-8639, Japan 3 Laboratory of Integrative Biological Science, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan Correspondence to: Shinae Kizaka-Kondoh, email: skondoh@bio.titech.ac.jp Keywords: myeloid-derived suppressor cells; cancer microenvironment; tumor immunology; angiogenesis; tumor-associated macrophage Received: November 11, 2017 Accepted: January 19, 2018 Published: January 29, 2018 ABSTRACT The immunosuppressive tumor microenvironment is a hallmark of cancer. Myeloid-derived suppressor cells (MDSCs) are CD11b + Gr-1 + tumor-infiltrating immature myeloid cells that strongly mediate tumor immunosuppression. The CD11b + Gr-1 + cells are a heterogeneous cell population, and the impacts of each subpopulation on tumor progression are not yet completely understood. In the present study, we identified a novel subpopulation of CD11b + Gr-1 + cells from murine lung carcinoma tumors according to their strongly adherent abilities. Although strong adherent activity is a unique property of macrophages, their marker expression patterns are similar to those of MDSCs; thus, we named this novel subpopulation MDSC-like adherent cells (MLACs). Unlike known MDSCs, MLACs lack the ability to suppress cytotoxic T lymphocytes and differentiate into tumor-associated macrophages (TAMs), but could still directly facilitate tumor growth and angiogenesis through secreting CCL2, CXCL1/2/5, PAI-1, MMPs, and VEGFA. Furthermore, MLACs recruited MDSCs via the secretion of CCL2/5 and CXCL1/2/5, thereby enhancing the immunosuppressive tumor microenvironment and promoting TAMs-mediated tumor progression. Our findings suggest that MLACs may function as an initiator of the immunosuppressive tumor microenvironment and highlight a new therapeutic target to prevent the onset or delay malignant progression.

The circadian clock, which regulates cellular physiology, such as energy metabolism, resides in each cell level throughout the body. Recently, it has been elucidated that the cellular circadian clock is closely linked with cellular differentiation. Moreover, the misregulation of cellular differentiation in mouse embryonic stem cells (ESCs) induced abnormally differentiated cells with impaired circadian clock oscillation, concomitant with the post-transcriptional suppression of CLOCK proteins. Here, we show that the circadian molecular oscillation is disrupted in dysdifferentiation-mediated mouse kidney tumors induced by partial in vivo reprogramming, resembling Wilms tumors. The expression of CLOCK protein was dramatically reduced in the tumor cells despite the Clock mRNA expression. We also showed that a similar loss of CLOCK was observed in human Wilms tumors, suggesting that the circadian molecular clockwork may be disrupted in dysdifferentiation-mediated embryonal tumors such as Wilms tumors, similar to the in vivo reprogramming-induced mouse kidney tumors. These results support our previous reports and may provide a novel viewpoint for understanding the pathophysiological nature of cancers through the correlation between cellular differentiation and circadian clock.

Made available in DSpace on 2018-12-11T16:50:10Z (GMT). No. of bitstreams: 0 Previous issue date: 2017-09-01. Added 1 bitstream(s) on 2021-07-15T15:02:30Z : No. of bitstreams: 1 S1413-41522017000500961.pdf: 290918 bytes, checksum: cec293ea8894a0bfae450608dda8791e (MD5) Metals are often evaluated in fresh water as dissolved solutions, assuming that the toxic effect is caused only by water (respiration and contact). However, toxicity studies in food and water, in a concomitant way, as occurs in the environment, are less discussed. In this study, zinc and cadmium toxicity was evaluated through the exposure of Ceriodaphnia dubia to contaminated food and water. The species of green algae Raphidocelis subcapitata was exposed for 96h to concentrations of Zn (0,18 and 0,27 mg.L-1) and Cd (0,001 and 0,0015 mg.L-1). The results were statistically analyzed by means of Analysis of Variance (Kruskal-Wallis). Algae were used as food source for C. dubia, during chronic exposure (eight days) in the same concentrations described. Subsequently, neonates (F1 generation) were introduced in non-contaminated water and food in order to ascertain their biological recovery capacity. The number of newborns by individuals, morphology of newborns, and quantification of metals in biological tissue were evaluated. The results showed that the tested concentrations did not inhibit the growth of R. subcapitata, while C. dubia had chronic toxicity, with reduction in the reproductive rate in both generations, for both metals. The results allowed the conclusion that, even at relatively low concentrations, the metals zinc and cadmium can alter the reproductive patterns of freshwater invertebrates, compromising the aquatic ecosystem and its resilience. Thus, considering the toxic effects of these metals and their interference in the biological system, new ecotoxicological tests should be performed to allow a better understanding of the behavior of these substances in organisms. Ciências Ambientais pela Universidade Estadual Paulista “Júlio de Mesquita Filho” (UNESP) Pesquisadora no Laboratório Toxicologia de Contaminantes Ambientais e Histologia da UNESP Ciências Ambientais pela UNESP Pesquisadora no Laboratório Toxicologia de Contaminantes Ambientais e Histologia da UNESP Ciências Ambientais pela UNESP Pesquisadora no Laboratório de Química da UNESP Ciências Ambientais Departamento de Toxicologia Ambiental da Universidade Estadual Paulista “Júlio de Mesquita Filho” (UNESP) Ciências Ambientais pela Universidade Estadual Paulista “Júlio de Mesquita Filho” (UNESP) Pesquisadora no Laboratório Toxicologia de Contaminantes Ambientais e Histologia da UNESP Ciências Ambientais pela UNESP Pesquisadora no Laboratório Toxicologia de Contaminantes Ambientais e Histologia da UNESP Ciências Ambientais pela UNESP Pesquisadora no Laboratório de Química da UNESP Ciências Ambientais Departamento de Toxicologia Ambiental da Universidade Estadual Paulista “Júlio de Mesquita Filho” (UNESP)

Which types of benefit finding in negative events central to identity lead to higher identity achievement? This study examined the relationships between the identity centrality of negative events, benefit finding, and identity achievement, with consideration of differences between benefit-finding domains. Participants included 245 undergraduates, who recalled a previous negative event and completed the Identity Scale, Centrality of Event Scale, and items regarding benefit finding. Path analysis showed that benefit finding regarding personal growth consistently correlated with identity achievement, while the effects of recognizing warmth in others were unstable depending on event category. The findings demonstrated the role of benefit finding regarding personal growth in promoting identity achievement and buffering the original adverse impact of negative events on identity.