Grounded in self-determination theory and work–home enrichment theory, the present study investigates how maternal work engagement relates to adolescent academic achievement, focusing on the potential mediating roles of maternal support, as perceived by both mothers and adolescents, and adolescent academic engagement. The sample consisted of 237 mother–adolescent dyads, in which mothers were white-collar employees (Mage = 44.59, SD = 4.44) and adolescents were high school students aged 14 to 18 years (Mage = 15.66, SD = 1.08). Consistent with the proposed serial mediation model, maternal work engagement was indirectly associated with adolescent academic achievement through adolescents’ perceptions of maternal support and their academic engagement. These findings highlight the interconnections between work and family domains and underscore the importance of adolescents’ subjective experiences in understanding the transmission of work-related resources within families.
The aim of this study is to formulate and empirically test a theoretically grounded convergence equation for financial development. Building on the Solow framework, we derive a testable convergence equation for financial development and estimate it using the System GMM methodology. We examine a panel dataset covering 160 countries, both at the global level and within three income groups, spanning the years 1990 to 2024. Key findings can be outlined as follows: (i) there is robust evidence of unconditional convergence in financial development across the global sample and within all three income groups; (ii) when major macroeconomic controls are introduced, the analysis also confirms the existence of conditional convergence; (iii) the influence of macroeconomic variables on financial development convergence differs across income categories; (iv) trade openness is a significant driver in high-income and upper-middle-income economies, whereas inflation plays a central role in lower-middle and upper-middle-income economies; (v) institutional quality has a statistically significant impact on financial development convergence, but only within upper-middle-income countries. Overall, the study provides robust evidence of financial development convergence and highlights the key macroeconomic and institutional factors shaping the convergence process across income groups.
Maternal nutrition influences offspring brain development, and omega-3 fatty acids have been linked to neuroprotection. However, their effects on acute responses to traumatic brain injury (TBI) in adult offspring have not been examined. Wistar rat dams (n = 21) received fish oil (0.5 g/kg/day), flaxseed oil (0.5 g/kg/day), or water by gavage during lactation (postnatal days (PND): 1–21). Adult male offspring (n = 32; 8 per group) underwent diffuse TBI using the modified Marmarou weight-drop model. Electrocorticography (ECoG) was recorded at baseline, 24 h, and 72 h post-injury. Somatosensory evoked potentials (SSEPs) were measured on day 3, and thalamic tissue was analyzed by immunohistochemistry for NeuN, S100, and GFAP. TBI induced significant prolongation of N2 (p < 0.05) and P3 (p < 0.01) SSEP latencies versus controls, along with significantly reduced thalamic NeuN expression (p < 0.001) and increased S100 (p < 0.01) and GFAP (p < 0.01) immunoreactivity. In the fish oil group, P3 latency was significantly shorter than in TBI (p < 0.05), and NeuN expression was significantly higher (p < 0.05), indicating preserved neuronal integrity. In the flaxseed oil group, GFAP immunoreactivity was significantly lower than in TBI (p < 0.01); however, NeuN did not differ from TBI and was significantly lower than Control (p < 0.05), and S100 was significantly higher than Control (p < 0.05), indicating incomplete normalization. N2 latency did not differ significantly between supplementation groups and TBI. ECoG spectral power analysis revealed no significant intergroup differences across any frequency band (all p > 0.05). These exploratory findings suggest that the two omega-3 sources exerted marker-specific differential effects rather than uniform neuroprotection: maternal fish oil supplementation was associated with preserved thalamic neuronal integrity and shorter late-latency cortical processing time, whereas flaxseed oil was associated with reduced astrocytic GFAP activation. Given the modest sample, and the acute 72-hour observation window, all findings should be regarded as preliminary and hypothesis-generating. Larger, adequately powered, sex-stratified studies with biochemical validation and longer follow-up are needed to confirm these results.
This paper proposes a novel knowledge-guided learning model for low-light image enhancement. The developed pipeline improves image visibility by addressing noise and contrast issues, detail preservation, and color balancing. This is achieved by integrating denoising and Retinex techniques with vision transformers. Given as little as a single low-light input image, a set of intermediate exposures are generated by means of gamma transform, which serve as inputs to an ensemble of ten transformer models to produce enhanced outputs. An adaptive exposure selection process is then applied based on a composite image quality score. Finally, the selected outputs are fused in a multi-scale manner using weight maps based on contrast, saturation, and well-exposedness features. Extensive experiments on benchmark datasets, LOL-v1, LOL-v2-Real, LOL-v2-Synthetic, and a unified dataset, demonstrate that the proposed method is competitive with state-of-the-art techniques and shows a significant advantage when processing images captured in extremely low-light conditions. In addition, the developed method is successfully applied to the image dehazing problem without any further optimization.
Therapeutic resistance to tyrosine kinase inhibitors (TKIs) remains a major challenge in the clinical management of chronic myeloid leukemia (CML). The transcription factor STAT5A, a principal downstream effector of BCR::ABL1, has emerged as a key transcriptional regulator implicated in the development of TKI resistance. This study aims to functionally validate the role of STAT5A in TKI-resistant CML by employing CRISPR/Cas9-mediated gene knockout and assessing the downstream molecular and phenotypic alterations. We hypothesized that selective disruption of STAT5A would restore apoptotic sensitivity and TKI responsiveness in resistant CML models. Additionally, we sought to integrate bioinformatic transcriptional network analyses to confirm whether STAT5A directly regulates the genes modulated by its deletion, thus reinforcing its mechanistic relevance as a therapeutic target. STAT5A was knocked out using CRISPR/Cas9 in K562 cells and their TKI-resistant derivatives (K562/Ima-Res, K562/Pon-Res). Western blot analysis confirmed effective depletion of STAT5A protein following CRISPR/Cas9 editing, validating that the observed phenotypic and transcriptional changes were attributable to successful STAT5A knockout. Post-editing, XTT assays were performed to assess cell viability, followed by Annexin V/PI staining for apoptosis and PI-based flow cytometry for cell cycle analysis. RT-qPCR was used to quantify the expression of key genes involved in the JAK/STAT pathway (JAK2, STAT3, CISH) and apoptosis/DNA damage responses (TP53, ATM, CASP3, CASP8). In silico analyses were conducted using TRRUST and Harmonizome/ChEA3 to confirm whether the genes modulated by STAT5A deletion were direct transcriptional targets. For additional validation, expression matrices from GSE207627 and GSE208314 were reanalyzed to confirm STAT5A-centered pathway alterations in resistant CML datasets. STAT5A knockout significantly reduced cell viability and induced apoptosis across all CML cell models, accompanied by G0/G1 cell cycle arrest. RT-qPCR revealed altered expression of both JAK/STAT components (JAK2, STAT3, CISH) and apoptosis-related genes (TP53, ATM, CASP3, CASP8). Transcriptional target analysis confirmed that several of these genes—such as CDKN2B, BCL2L1, and CCND1—are direct STAT5A targets, reinforcing the functional consequences of STAT5A loss. Integration of these findings suggests that STAT5A knockout reprograms both intrinsic (CASP3, TP53, ATM) and extrinsic (CASP8, BCL2L1) apoptotic pathways, thereby restoring chemosensitivity. CISH dysregulation further suggested compensatory feedback within the signaling network. CRISPR/Cas9-mediated STAT5A disruption effectively reverses TKI resistance in CML cells by reprogramming apoptotic and proliferative signaling. These findings identify STAT5A as a mechanistically validated and clinically actionable target, supporting its potential for combination strategies with TKIs or STAT5 inhibitors such as pimozide. Integration of transcriptional network analysis supports the mechanistic basis of these effects. STAT5A emerges as a compelling therapeutic target, meriting further investigation in preclinical models and patient-derived samples to evaluate its translational potential. Future validation in patient-derived CD34⁺ CML models may advance STAT5A-based therapeutic design.
