Longitudinal relationship between adolescent emotional self-regulation and prosocial behavior toward powerful people: Disentangling between-person differences from within-person effects.

INTRODUCTION: This study investigated the longitudinal effects between adolescent emotional self-regulation and prosocial behavior toward powerful people (i.e., actions aimed at benefiting or supporting individuals who hold significant influence or authority within a group or society), based on the perspective of positive socialization cycle. METHODS: We recruited 543 Chinese adolescents (284 girls, M age at Time 1 = 11.27 years) and collected three waves of data over 3 years, each approximately 1 year apart (n Time 2 = 449, n Time 3 = 417). Traditional cross-lagged panel model was conducted to test the longitudinal relationship between emotional self-regulation and prosocial behavior toward powerful people. Then, a random-intercept cross-lagged panel model was performed to disentangle the between-person differences from the within-person predictive processes. RESULTS: The results showed that, emotional self-regulation in the previous year was positively associated with prosocial behavior toward powerful people in the next year, whereas earlier prosocial behavior toward powerful people was not predictive of subsequent emotional self-regulation. CONCLUSIONS: Findings advocate the domain-specific nature of self-regulation and prosocial behavior and deepen our understanding of the relationship between the two from the culture-specific perspective. This study also highlights the value of emotional self-regulation intervention as a viable way to promote adolescent prosocial development. Theoretical and empirical implications are discussed.

Federated Learning for Predicting Postoperative Remission of Patients with Acromegaly: A Multicentered study.

BACKGROUND: Decentralized federated learning (DFL) may serve as a useful framework for machine learning (ML) tasks in multicentered studies, maximizing the use of clinical data without data sharing. We aim to propose the first workflow of DFL for ML tasks in multicentered studies, which can be as powerful as those using centralized data. METHODS: A DFL workflow was developed with four steps: registration, local computation, model update, and inspection. A total of 598 participants with acromegaly from PUMCH, and 120 participants from XWH were enrolled. The cohort from PUMCH was further split into five centers. Nine clinical features were incorporated into ML-based models trained based on four algorithms: LR, GBDT, SVM, and DNN. The area under the curve (AUC) of receiver operating characteristic curves was used to evaluate the performance of the models. RESULTS: Models trained based on DFL workflow performed better than most models in LR (P<0.05), all models in DNN, SVM, and GBDT (P<0.05). Models trained on DFL workflow performed as powerful as models trained on centralized data in LR, DNN, and SVM (P>0.05). CONCLUSIONS: We demonstrate that the DFL workflow without data sharing should be a more appropriate method in ML tasks in multicentered studies. And the DFL workflow should be further exploited in clinical researches in other departments and it can encourage and facilitate multicentered studies.

DDIT4 promotes erythroid differentiation and coordinates with SIPA1 to regulate erythroid proliferation in bone marrow of high altitude erythrocytosis.

Erythrocytosis moderately enhances the oxygen-carrying capacity of the blood and is considered a characteristic response of individuals adapting from low-altitude regions to high-altitude regions. Nevertheless, erythrocytosis can also turn excessive and result in maladaptive syndromes, such as high altitude polycythemia (HAPC). The increased differentiation or proliferation of erythroid cells in the bone marrow may be a crucial factor leading to accumulation of peripheral erythroid cells. However, the mechanism of erythroid regulation within the bone marrow of high-altitude erythrocytosis remains insufficiently systematically observed. We utilized single-cell transcription sequencing to characterize bone marrow cells following chronic hypoxic exposure and found that bone marrow erythrocytosis is associated with the accumulation of Baso-E, Poly-E, and Ortho-E cells at the terminal stage of erythroid lineage differentiation. Through analysis of differential gene expression and localization in differentiated cells within the erythroid lineage, we confirmed that DDIT4 expression was localized in advanced differentiated erythroblast including Baso-E, Poly-E and Ortho-E, its expression was significantly enhanced by hypoxia exposure. We demonstrated that overexpression of DDIT4 could promote K562 cell differentiation, and through the IP pull-down interaction protein profile, we found that DDIT4 might participate in regulating the cell cycle by interacting with SIPA1 to promote the proliferation of erythroid cells and may be involved in HAPC.

A Novel Cyanine-Based Fluorescent Dye for Targeted Mitochondrial Imaging in Neurotoxic Conditions and In Vivo Brain Studies.

Mitochondrial dysfunction is a key feature of neurodegenerative diseases, often preceding symptoms and influencing disease progression. However, real-time in vivo imaging of mitochondria in the brain is limited by existing dyes like MitoTrackers, which struggle with poor tissue penetration, phototoxicity, and inability to cross the blood-brain barrier (BBB). This study introduces Cy5-PEG4, a novel mitochondrial-targeting dye that overcomes these limitations, enabling high-resolution, non-invasive imaging of mitochondrial dynamics. Cy5-PEG4 effectively labels mitochondria in primary neuronal cells exposed to the SARS-CoV-2 RNYIAQVD peptide, revealing dose-dependent alterations in mitochondrial function that may contribute to COVID-19-related neurodegeneration. Importantly, Cy5-PEG4 crosses the BBB without causing neuroinflammation or toxicity, making it a safe tool for in vivo brain imaging and detailed studies of mitochondrial responses. In 3D cultured cells, Cy5-PEG4 captures dynamic changes in mitochondrial distribution and morphology as cell structures mature, highlighting its potential in neurobiological research, diagnostics, and therapeutic development. These findings support Cy5-PEG4 as a powerful tool for studying disease progression, identifying early biomarkers, and evaluating therapeutic strategies in neurodegenerative disorders and COVID-19.

Disulfide-Rich Self-Assembling Peptides Based on Aromatic Amino Acid.

Aromatic residues in assembling peptides play a crucial role in driving peptide self-assembly through π-π stacking and hydrophobic interactions. Although various aromatic capping groups have been extensively studied, systematic investigations into the effects of single aromatic amino acids in assembling peptides remain limited. In this study, the influence of aromatic-aromatic interactions on disulfide-rich assembling peptides is systematically investigated by incorporating three different aromatic amino acids. Their folding propensity, self-assembling properties, and rheological behaviors are evaluated. These results indicate that different aromatic-aromatic interactions have a significant effect on self-assembly abilities, as determined by critical aggregation concentration (CAC) measurements. Furthermore, the biocompatibility of these hydrogels is assessed, and their potential for 3D cell culture is explored. The injectable F1-ox hydrogel demonstrate excellent biocompatibility for SHED and NIH3T3 cells and exhibit a porous structure that facilitates nutrient and cellular metabolic waste exchange. This work provides new insights into the molecular design of peptide-based biomaterials, with a focus on the impact of aromatic residues on disulfide-rich assembling peptides.

Thermally stable C2-symmetric α-diimine nickel precatalysts for ethylene polymerization: semicrystalline to amorphous PE with high tensile and elastic properties.

In α-diimine nickel catalyst-mediated ethylene polymerization, adjusting catalytic parameters such as steric and electronic factors, as well as spectator ligands, offers an intriguing approach for tailoring the thermal and physical properties of the resulting products. This study explores two sets of C2-symmetric α-diimine nickel complexes-nickel bromide and nickel chloride-where ortho-steric and electronic substituents, as well as nickel halide, were varied to regulate simultaneously chain walking, chain transfer, and the properties of the polymers produced. These complexes were activated in situ with Et2AlCl, resulting in exceptionally high catalytic activities (in the level of 106-107 g (PE) mol-1 (Ni) h-1) under all reaction conditions. Nickel bromide complexes, with higher ortho-steric hindrance, exhibited superior catalytic activity compared to their less hindered counterparts, whereas the reverse was observed for complexes containing chloride. Increased steric hindrance in both sets of complexes facilitated higher polymer molecular weights and promoted chain walking reactions at lower reaction temperature (40 °C), while the effect became less pronounced at higher temperature (100 °C). However, the electron-withdrawing effect of ortho-substituents hindered the rate of monomer insertion, chain propagation, and chain walking reactions, leading to the synthesis of semi-crystalline polyethylene with an exceptionally high melt temperature of 134.6 °C and a high crystallinity of up to 31.9%. Most importantly, nickel bromide complexes demonstrated significantly higher activity compared to their chloride counterparts, while the latter yielded polymers with higher molecular weights and increased melt temperatures. These high molecular weights, coupled with controlled branching degrees, resulted in polyethylenes with excellent tensile strength (up to 13.9 MPa) and excellent elastic properties (up to 81%), making them suitable for a broad range of applications.

High-content phenotypic analysis of a C. elegans recombinant inbred population identifies genetic and molecular regulators of lifespan.

Lifespan is influenced by complex interactions between genetic and environmental factors. Studying those factors in model organisms of a single genetic background limits their translational value for humans. Here, we mapped lifespan determinants in 85 C. elegans recombinant inbred advanced intercross lines (RIAILs). We assessed molecular profiles-transcriptome, proteome, and lipidome-and life-history traits, including lifespan, development, growth dynamics, and reproduction. RIAILs exhibited large variations in lifespan, which correlated positively with developmental time. We validated three longevity modulators, including rict-1, gfm-1, and mltn-1, among the top candidates obtained from multiomics data integration and quantitative trait locus (QTL) mapping. We translated their relevance to humans using UK Biobank data and showed that variants in GFM1 are associated with an elevated risk of age-related heart failure. We organized our dataset as a resource that allows interactive explorations for new longevity targets.

Different responses of larval fatty acid profiles to cryopreservation in two commercially important bivalves.

Larval cryopreservation techniques have been established in Pacific oysters and Mediterranean mussels. Although initial cryopreservation protocols for both species differed slightly in Ficoll PM 70 (FIC) concentration, better post-thaw larval survivability was produced in mussels than oysters. Furthermore, the post-thaw survivability in the latter could be improved significantly by the addition of lipids and antioxidants to the cryoprotectant agent. These findings have generated a unique opportunity to investigate the cryo-functions of both endogenous and exogenous fatty acids (FAs) in bivalves as mammalian studies indicated that lipid compositions could contribute the interspecific difference in gamete and embryo cryopreservation. Our study showed that the higher survivability of post-thaw larvae in mussels (65% vs. 34% in oysters) could be attributed to their higher proportion of total polyunsaturated fatty acids (PUFAs), especially C22:6, and higher resistance of FA profiles to cryopreservation. In oysters, on the other hand, their FA profiles were very sensitive to cryopreservation, with saturated FAs and PUFAs being significantly increased (from 37 to 41%) and decreased (from 35% to ~ 32%), respectively. Although exogenous lipids could significantly improve the survivability of post-thaw oyster larvae from 34 to 51%, their supplementation did not alter the response pattern of endogenous FA profiles to cryopreservation.

Atomization by Acoustic Levitation Facilitates Contactless Microdroplet Reactions.

Microdroplet chemistry is now well-known to be able to remarkably accelerate otherwise slow reactions and trigger otherwise impossible reactions. The uniqueness of the microdroplet is attributable to either the air-water interface or solid-liquid interface, depending on the medium that the microdroplet is in contact with. To date, the importance of the solid-liquid interface might have been confirmed, but the contribution from the air-water interface seems to be elusive due to the lack of method for generating contactless microdroplets. In this study, we used a droplet atomization method with acoustic levitation. Upon manipulation of the acoustic field, the levitated parent droplet can be further atomized into progeny microdroplets. With this method, only the air-water interface was present, and a large variety of reactions were successfully tested. We anticipate that this study can be an advance toward the understanding of the air-water interfacial processes of microdroplet chemistry.

Transcription factor EB (TFEB) promotes autophagy in early brain injury after subarachnoid hemorrhage in rats.

Subarachnoid hemorrhage (SAH) has high mortality. Early brain injury (EBI) is responsible for unfavorable outcomes for patients with SAH. The protective involvement of autophagy in hemorrhagic stroke has been proposed. The transcription factor EB (TFEB) can increase autophagic flux by promoting autophagosome formation and autophagosome-lysosome fusion, and dysregulation of TFEB activity might induce the development of several diseases. However, the biological functions of TFEB in EBI after SAH remain unknown. We established an animal model of SAH by the modified endovascular perforation method. Expression of TFEB and autophagy required genes was measured by western blotting and immunofluorescence staining. SAH grading, brain water content and neurobehavioral functions were evaluated at 24 h post-SAH. Neuronal apoptosis in cerebral cortex was assessed by TUNEL staining and Fluoro Jade B staining. TFEB was downregulated in SAH rats, and its overexpression reduced brain edema and ameliorated neurological deficits of SAH rats. Additionally, the neuronal apoptosis induced by SAH was inhibited by TFEB overexpression. Moreover, TFEB overexpression promoted autophagy after SAH. TFEB overexpression promotes autophagy to inhibit neuronal apoptosis, brain edema and neurological deficits post-SAH.

Spontaneous Generation of Alkoxide Radical from Alcohols on Microdroplets Surface.

Water microdroplets have been demonstrated to exhibit extraordinary chemical behaviors, including the abilities to accelerate chemical reactions by several orders of magnitude and to trigger reactions that cannot occur in bulk water. One of the most striking examples is the spontaneous generation of hydroxyl radical from hydroxide ions. Alcohols and alkoxide ions, being structurally similar to water and hydroxide ions, might exhibit similar behavior on microdroplets. Here, we report the spontaneous generation of alkoxide radicals from alcohols (RCH2OH) in aqueous microdroplets through quantum chemical calculations, quantum mechanical/molecular mechanical (QM/MM) molecular dynamics (MD) simulations, ab initio MD simulations, and mass spectrometry. Our results show that an electric field (EF) on the order of 10-1 V/Šand partial solvation at the air‒water interface jointly promote the dissociation of RCH2OH into RCH2O- and H3O+ ions. QM/MM MD simulations indicate that RCH2O- can be ionized to produce RCH2O• radicals on the microdroplet surface. Furthermore, partial solvation and the EF collaboratively catalyze the isomerization of the RCH2O• radical into a more stable tautomer, R•CHOH. This study highlights the molecular mechanisms underlying the widespread generation of radicals at the microdroplet surface and provides insights into the importance of fundamental alcohol chemistry in the atmosphere.

Low expression of auxin receptor EcAFB4 confers resistance to florpyrauxifen-benzyl in Echinochloa crus-galli (L.) P. Beauv.

Echinochloa crus-galli (L.) P. Beauv is a monocotyledonous weed that seriously infests rice fields. Florpyrauxifen-benzyl, a novel synthetic auxin herbicide commercialized in China in 2018, is an herbicide for controlling E. crus-galli. However, a suspected resistant population (R) collected in 2012 showed resistance to the previously unused florpyrauxifen-benzyl. Whole-plant dose-response bioassay indicated that the R population evolved high resistance to quinclorac and florpyrauxifen-benzyl. Pretreatment with P450 inhibitors did not influence the GR50 of E. crus-galli to florpyrauxifen-benzyl. The expression of target receptor EcAFB4 was down-regulated in the R population, leading to the reduced response to florpyrauxifen-benzyl (suppresses over-production of ethylene and ABA). We verified this resistance mechanism in the knockout OsAFB4 in Oryza sativa L. The Osafb4 mutants exhibited high resistance to florpyrauxifen-benzyl and moderate resistance to quinclorac. Furthermore, DNA methylation in the EcAFB4 promoter regulated its low expression in the R population after florpyrauxifen-benzyl treatment. In summary, the low expression of the auxin receptor EcAFB4 confers target resistance to the synthetic auxin herbicide florpyrauxifen-benzyl in the R- E. crus-galli.

Coenzyme Q10 Improves the Post-Thaw Sperm Quality in Dwarf Surfclam Mulinia lateralis.

Previous studies have shown that post-thaw sperm performance is affected by multiple stressors during cryopreservation, such as those induced by physical, chemical, mechanical and physiological changes. One of these is the balance disturbance between the antioxidant defense system and reactive oxygen species (ROS) production. This study investigated whether this disturbance could be alleviated by the addition of different antioxidants to cryoprotective solution [8% dimethyl sulfoxide (DMSO) in 1 µm filtered seawater] optimized for the sperm in dwarf surf clam Mulinia lateralis, the model bivalve species used in many different types of studies. Results showed that the addition of 20 µM coenzyme Q10 (Q10) to 8% DMSO achieved a D-stage larval rate similar to that of the fresh control at a sperm-to-egg ratio at least 50% less than the 8% DMSO treatment alone. The addition of other antioxidants (glycine, melatonin and polyvinylpyrrolidone) did not have any positive effects. The improvement in post-thaw sperm quality by Q10 could be due to its ability to significantly decrease ROS production and lipid peroxidation and significantly increase the motility, plasma membrane integrity, mitochondrial membrane potential, acrosome integrity, DNA integrity and activities of catalase and glutatione. In this study, 37 fatty acids (FAs) were quantified in dwarf surf clam sperm, with 21 FAs being significantly impacted by the cryopreservation with 8% DMSO. Thirteen of these 21 FAs were changed due to the addition of 20 µM Q10 to 8% DMSO, with approximately half of them being improved significantly toward the levels of fresh control, while the remaining half extended further from the trends shown with 8% DMSO treatment. However, no significant difference was found in the percentage of each FA category sum and the ratio of unsaturated/saturated FAs between the two treated groups. In conclusion, the antioxidant Q10 has shown the potential to further improve the sperm cryopreservation technique in bivalves.

ASB3 expression aggravates inflammatory bowel disease by targeting TRAF6 protein stability and affecting the intestinal microbiota.

E3 ubiquitin ligase (E3) plays a vital role in regulating inflammatory responses by mediating ubiquitination. Previous studies have shown that ankyrin repeat and SOCS box-containing protein 3 (ASB3) is involved in immunomodulatory functions associated with cancer. However, the impact of ASB3 on the dynamic interplay of microbiota and inflammatory responses in inflammatory bowel disease (IBD) is unclear. Here, we systematically identify the E3 ligase ASB3 as a facilitative regulator in the development and progression of IBD. We observed that ASB3 exhibited significant upregulation in the lesions of patients with IBD. ASB3-/- mice are resistant to dextran sodium sulfate-induced colitis. IκBα phosphorylation levels and production of proinflammatory factors IL-1ß, IL-6, and TNF-α were reduced in the colonic tissues of ASB3-/- mice compared to WT mice. This colitis-resistant phenotype was suppressed after coprophagic microbial transfer and reversed after combined antibiotics removed the gut commensal microbiome. Mechanistically, ASB3 specifically catalyzes K48-linked polyubiquitination of TRAF6 in intestinal epithelial cells. In contrast, in ASB3-deficient organoids, the integrity of the TRAF6 protein is shielded, consequently decelerating the onset of intestinal inflammation. ASB3 is associated with dysregulation of the colitis microbiota and promotes proinflammatory factors' production by disrupting TRAF6 stability. Strategies to limit the protein level of ASB3 in intestinal epithelial cells may help in the treatment of colitis. IMPORTANCE: Ubiquitination is a key process that controls protein stability. We determined the ubiquitination of TRAF6 by ASB3 in intestinal epithelial cells during colonic inflammation. Inflammatory bowel disease patients exhibit upregulated ASB3 expression at focal sites, supporting the involvement of degradation of TRAF6, which promotes TLR-Myd88/TRIF-independent NF-κB aberrant activation and intestinal microbiota imbalance. Sustained inflammatory signaling in intestinal epithelial cells and dysregulated protective probiotic immune responses mediated by ASB3 collectively contribute to the exacerbation of inflammatory bowel disease. These findings provide insights into the pathogenesis of inflammatory bowel disease and suggest a novel mechanism by which ASB3 increases the risk of colitis. Our results suggest that future inhibition of ASB3 in intestinal epithelial cells may be a novel clinical strategy.

VCAM-1 mediates proximal tubule-immune cell cross talk in failed tubule recovery during AKI-to-CKD transition.

Studies in animal models have suggested a linkage between the inflammatory response to injury and subsequent nephron loss during the acute kidney injury (AKI) to chronic kidney disease (CKD) transition. Failure of normal repair during the CKD transition correlates with de novo expression of vascular cell adhesion protein-1 (VCAM-1) by a subset of injured proximal tubule cells. This study identified the role of VCAM-1 expression in promoting the failed repair state. Single-cell transcriptome analysis of patients with AKI and CKD and whole kidney RNA and protein analyses of mouse models of CKD confirmed a marked increase of VCAM-1 expression in the proximal tubules of injured kidneys. In immortalized mouse proximal tubular cells and primary cultured renal cells (PCRCs), VCAM-1 expression was induced by proinflammatory cytokines including tumor necrosis factor (TNF)-α and interleukin (IL)-1ß. Analyses of bulk RNA sequencing of TNF-α-treated primary cultured renal cells or pseudo-bulk RNA sequencing of biopsies from Kidney Precision Medicine Project datasets indicated activation of NF-κB and an enrichment of inflammatory response and cell adhesion pathways in VCAM-1-positive cells. Pharmacological inhibition of NF-κB signaling or genetic deletion of myeloid differentiation factor 88 and TIR domain-containing adapter-inducing interferon-ß suppressed TNF-α- and IL-1ß-induced VCAM-1 expression in vitro. TNF-α stimulation or overexpression of VCAM-1 significantly increased splenocyte adhesion to the mouse proximal tubular monolayer in culture. These results demonstrate that persistence of proinflammatory cytokines after AKI can induce NF-κB-dependent VCAM-1 expression by proximal tubule cells, mediating increased immune cell adhesion to the tubule and thus promoting further tubule injury and greater risk of progression from AKI to CKD.NEW & NOTEWORTHY We demonstrated the induction of VCAM-1 and its biological function in proximal tubules. We found that proinflammatory cytokines (TNF-α and IL-1ß) significantly induced VCAM-1 expression via NF-κB signaling pathway. TNF-α treatment or overexpression of VCAM-1 in immortalized MPT cells increased CD45+ splenocyte adhesion. Pharmacological inhibition of NF-κB or genetic deletion of Vcam1 suppressed TNF-α-induced splenocyte adhesion in vitro, suggesting that VCAM-1 mediates proximal tubular-immune cell cross talk in failed tubule recovery during AKI-to-CKD transition.

ACMSD inhibition corrects fibrosis, inflammation, and DNA damage in MASLD/MASH.

BACKGROUND & AIMS: Recent findings reveal the importance of tryptophan-initiated de novo nicotinamide adenine dinucleotide (NAD+) synthesis in the liver, a process previously considered secondary to biosynthesis from nicotinamide. The enzyme α-amino-ß-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD), primarily expressed in the liver and kidney, acts as a modulator of de novo NAD+ synthesis. Boosting NAD+ levels has previously demonstrated remarkable metabolic benefits in mouse models. In this study, we aimed to investigate the therapeutic implications of ACMSD inhibition in the treatment of metabolic dysfunction-associated steatotic liver disease/steatohepatitis (MASLD/MASH). METHODS: In vitro experiments were conducted in primary rodent hepatocytes, Huh7 human liver carcinoma cells and induced pluripotent stem cell-derived human liver organoids (HLOs). C57BL/6J male mice were fed a western-style diet and housed at thermoneutrality to recapitulate key aspects of MASLD/MASH. Pharmacological ACMSD inhibition was given therapeutically, following disease onset. HLO models of steatohepatitis were used to assess the DNA damage responses to ACMSD inhibition in human contexts. RESULTS: Inhibiting ACMSD with a novel specific pharmacological inhibitor promotes de novo NAD+ synthesis and reduces DNA damage ex vivo, in vivo, and in HLO models. In mouse models of MASLD/MASH, de novo NAD+ biosynthesis is suppressed, and transcriptomic DNA damage signatures correlate with disease severity; in humans, Mendelian randomization-based genetic analysis suggests a notable impact of genomic stress on liver disease susceptibility. Therapeutic inhibition of ACMSD in mice increases liver NAD+ and reverses MASLD/MASH, mitigating fibrosis, inflammation, and DNA damage, as observed in HLO models of steatohepatitis. CONCLUSIONS: Our findings highlight the benefits of ACMSD inhibition in enhancing hepatic NAD+ levels and enabling genomic protection, underscoring its therapeutic potential in MASLD/MASH. IMPACT AND IMPLICATIONS: Enhancing NAD+ levels has been shown to induce remarkable health benefits in mouse models of metabolic dysfunction-associated steatotic liver disease/steatohepatitis (MASLD/MASH), yet liver-specific NAD+ boosting strategies remain underexplored. Here, we present a novel pharmacological approach to enhance de novo synthesis of NAD+ in the liver by inhibiting α-amino-ß-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD), an enzyme highly expressed in the liver. Inhibiting ACMSD increases NAD+ levels, enhances mitochondrial respiration, and maintains genomic stability in hepatocytes ex vivo and in vivo. These molecular benefits prevent disease progression in both mouse and human liver organoid models of steatohepatitis. Our preclinical study identifies ACMSD as a promising target for MASLD/MASH management and lays the groundwork for developing ACMSD inhibitors as a clinical treatment.

The role expectations of young women as wives after breast cancer treatment: A qualitative study.

Objectives: Through the reflection of young breast cancer women on their selves and identities, we explored expectations of the wife role that they need to fulfill to return to their families, aimed to provide a reference basis for medical professionals to develop interventions related to cancer family rehabilitation. Methods: Descriptive phenomenological methods and purposive sampling were used. Young breast cancer patients and their spouses were selected for semi-structured face-to-face interviews in the study from March to April 2023 at the department of breast surgery and oncology center of a Class A tertiary hospital in Xuzhou City, China. The interviews were transcribed verbatim and analyzed using Colaizzi's phenomenological approach. Results: Twenty patients and six spouses were interviewed. The mean patient age was (35.95 ± 3.36) years, and the mean spouse was (37.67 ± 5.28) years. Young breast cancer patients were concerned about three main wife expectations during their treatment and rehabilitation: preserving self-love and self-esteem (paying attention to physical health, embracing the disease, and regaining confidence in female characters); adjustment of conjugal relationships (harmonious and effective couple communication, providing support for marriage and love, and creating a beautiful married life together); assisting in family recovery (relieving stress on spouses from caregiving and finances, and management of daily household chores). Conclusions: The wife role expectations of young breast cancer women and their spouses encompass three core aspects: self, couple, and family. Self-esteem and self-love are the most fundamental expectations of the wife role, while adjusting the couple's relationship and assistance in family rehabilitation represent higher expectations. This study can help healthcare professionals and cancer families gain a more comprehensive understanding of the wife role expectations for young cancer women, thereby enabling the development of couple-centered interventions to promote patient recovery and enhance the resilience of marriages and families.

Uncovering the Size-Dependent Thermal Solid Transformation of Akaganéite.

Investigating the structural evolution and phase transformation of iron oxides is crucial for gaining a deeper understanding of geological changes on diverse planets and preparing oxide materials suitable for industrial applications. In this study, in-situ heating techniques are employed in conjunction with transmission electron microscopy (TEM) observations and ex-situ characterization to thoroughly analyze the thermal solid-phase transformation of akaganéite 1D nanostructures with varying diameters. These findings offer compelling evidence for a size-dependent morphology evolution in akaganéite 1D nanostructures, which can be attributed to the transformation from akaganéite to maghemite (γ-Fe2O3) and subsequent crystal growth. Specifically, it is observed that akaganéite nanorods with a diameter of ∼50 nm transformed into hollow polycrystalline maghemite nanorods, which demonstrated remarkable stability without arresting crystal growth under continuous heating. In contrast, smaller akaganéite nanoneedles or nanowires with a diameter ranging from 20 to 8 nm displayed a propensity for forming single-crystal nanoneedles or nanowires through phase transformation and densification. By manipulating the size of the precursors, a straightforward method is developed for the synthesis of single-crystal and polycrystalline maghemite nanowires through solid-phase transformation. These significant findings provide new insights into the size-dependent structural evolution and phase transformation of iron oxides at the nanoscale.

Association between serum uric acid levels and diabetic peripheral neuropathy in type 2 diabetes: a systematic review and meta-analysis.

Background: The evidence supporting a connection between elevated serum uric acid (SUA) levels and diabetic peripheral neuropathy (DPN) is controversial. The present study performed a comprehensive evaluation of this correlation by conducting a systematic review and meta-analysis of relevant research. Method: PubMed, Web of Science (WOS), Embase, and the Cochrane Library were searched for published literature from the establishment of each database to January 8, 2024. In total, 5 cohort studies and 15 cross-sectional studies were included, and 2 researchers independently screened and extracted relevant data. R 4.3.0 was used to evaluate the included literature. The present meta-analysis evaluated the relationship between SUA levels and the risk of DPN in type 2 diabetes (T2DM) by calculating the ratio of means (RoM) and 95% confidence intervals (CIs) using the method reported by JO Friedrich, and it also analyzed continuous outcome measures using standardized mean differences (SMDs) and 95% CIs to compare SUA levels between DPN and non-DPN groups. Funnel plot and Egger's test were used to assess publication bias. Sensitivity analysis was conducted by sequentially removing each study one-by-one. Results: The meta-analysis included 20 studies, with 12,952 T2DM patients with DPN and 16,246 T2DM patients without DPN. There was a significant correlation between SUA levels and the risk of developing DPN [odds ratio (OR) = 1.23; 95% CI: 1.07-1.41; p = 0.001]. Additionally, individuals with DPN had higher levels of SUA compared to those without DPN (SMD = 0.4; 95% CI: -0.11-0.91; p < 0.01). Conclusion: T2DM patients with DPN have significantly elevated SUA levels, which correlate with a heightened risk of peripheral neuropathy. Hyperuricemia (HUA) may be a risk indicator for assessing the risk of developing DPN in T2DM patients. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO, identifier CRD42024500373.

Systems genetics of metabolic health in the BXD mouse genetic reference population.

Susceptibility to metabolic syndrome (MetS) is dependent on genetics, environment, and gene-by-environment interactions, rendering the study of underlying mechanisms challenging. The majority of experiments in model organisms do not incorporate genetic variation and lack specific evaluation criteria for MetS. Here, we derived a continuous metric, the metabolic health score (MHS), based on standard clinical parameters and defined its molecular signatures in the liver and circulation. In human UK Biobank, the MHS associated with MetS status and was predictive of future disease incidence, even in individuals without MetS. Using quantitative trait locus analyses in mice, we found two MHS-associated genetic loci and replicated them in unrelated mouse populations. Through a prioritization scheme in mice and human genetic data, we identified TNKS and MCPH1 as candidates mediating differences in the MHS. Our findings provide insights into the molecular mechanisms sustaining metabolic health across species and uncover likely regulators. A record of this paper's transparent peer review process is included in the supplemental information.