Browse Articles

Size-Dependent Restructuring of Supported Platinum Cluster Catalysts

Evaluating land degradation and environmental hazards in North delta Egypt using machine learning and GIS approaches

A hybrid statistical–machine learning framework for evaluating geomagnetic storm effects on MisrSat2 satellite power subsystems

Abstract This study introduces a hybrid statistical–machine learning framework to evaluate the impact of the May 2024 geomagnetic storm on the power subsystem of the MisrSat-2 satellite. The proposed framework integrates a multi-tiered statistical approach, employing CUSUM for change point detection, z-score for outlier identification, and event-based analysis, with robust validation through Welch’s t-tests, bootstrapping, and Benjamini–Hochberg false discovery rate (BH-FDR) control. On 10 May, near the storm’s onset, the solar arrays showed modest current deviations, after validation, 13 events solar panel-1 and 17 events solar panel-2 were retained, with the largest cluster between 07:05 and 09:25 UTC. whereas the battery subsystem remained stable and buffered fluctuations, maintaining bus integrity. Event-based analysis confirmed that all deviations were small (< 4%) and within design tolerances. Radiation degradation modeling with EQUFLUX predicted only 0.32% cumulative loss for May 2024, align with the absence of measurable radiation-driven signatures in telemetry. Extending beyond descriptive detection, a Mixture of Experts (MoE) machine learning framework achieved superior predictive accuracy (R 2  = 0.921, MAE = 0.063 A) compared to baseline models providing interpretable validation of statistical findings. The novelty of this research lies in its integrative approach, merging physics-based modelling, robust statistical methods, and interpretable machine learning to provide a scalable framework for anomaly diagnostics and mission assurance in dynamic space environments.

BRCA2 deficiency and replication stress drive APOBEC3-Mediated genomic instability

Abstract BRCA2 plays a critical role in stabilizing stalled replication forks, yet critical gaps remain in understanding how BRCA2 deficiency triggers fork collapse and drives genomic instability. Here, we identify cytidine deaminase APOBEC3B as a key driver of this process. Using a unique uracil-in-DNA probe, we show that BRCA2 loss promotes APOBEC3B-mediated uracil accumulation in single-stranded DNA (U-ssDNA) at stalled forks. These lesions when processed by UNG2 and APE1, trigger fork collapse and release ssDNA fragments into the cytoplasm, activating NF-κB signaling. This in turn upregulates APOBEC3B expression, establishing a self-reinforcing loop that amplifies cytidine deamination at stalled forks and exacerbates genomic instability. Depletion of APOBEC3B, UNG2, or APE1 rescues these defects. Notably, BRCA1-deficient cells do not accumulate U-ssDNA or induce APOBEC3B under replication stress, highlighting a BRCA2-specific vulnerability. Clinically, low APE1 expression correlates with poor survival in patients with BRCA2 -mutant tumors, with high APOBEC3 levels further worsening outcomes. Together, our findings establish that replication stress, whether intrinsic or therapy induced, triggers APOBEC3B overexpression and potentially activates an APOBEC3B-driven mutagenic loop in BRCA2-deficient cells. These results position APOBEC3B, UNG2 and APE1 as critical regulators of BRCA2 -mutant tumor evolution and therapy resistance.

Unveiling the phenylalanine coaggregation mechanism for a deep understanding of phenylketonuria disease

‘A real risk’: the rise of weapons that can act alone

Reinventing Chemiluminescence through Redox-Driven Self-Assembly

Estimating rates of treatment delay for malaria fevers among children in Sub-Saharan Africa 2006–2022

Abstract Late diagnosis and treatment of malaria increase the odds of severe disease by nearly 2.8 times, enhance transmission rates, compromise drug effectiveness, and trigger malaria outbreaks. No continent-wide estimates for malaria treatment delay exist. We estimate delay rates among African children treated for malaria between 2006 and 2022, using 177 nationally representative surveys. We found that 60% [95% UI 45.7–72.8] of treated children experienced >24 h of delay, while 29% [95% UI 18.9–41.2] faced delays exceeding 48 h, affecting 33 million and 16 million children, respectively. Spatiotemporal variability exists across Africa. Somalia has the highest (76% [95% UI 39.7–97.9]) and Tanzania has the lowest (35.3% [95% UI 11.5–53.8]) delay rates. Overall, initial improvements in treatment delay stagnated post-2015, but East Africa showed the most progress, while Central and West Africa experienced increases. Socioeconomic factors and residence influenced delays, with poorer and rural populations facing higher rates. These findings are vital for policymakers to enhance malaria case management, access to effective treatment, and reduce malaria mortality among children.

Evaluation of antibacterial and antioxidant activities of Sesame (Sesamum indicum) meal protein hydrolysate produced by Bacillus coagulans (IBRC 10807) fermentation

Abstract In this research, sesame meal protein hydrolysate (SPH) was obtained from the sesame protein after hydrolysis by Bacillus coagulans . At first, the peptide concentration test was performed at different times to confirm the protease activity of B. coagulans . The chemical composition and total amino acid contents of sesame meal were determined. Fermentation conditions were optimized using response surface methodology (RSM). The results showed DPPH radical scavenging up to 70%, reducing power up to 0.779, and inhibitory activity against Staphylococcus aureus up to 78%, Escherichia coli up to 60%, Listeria monocytogenes up to 80% and Clostridium perfringens up to 85%. The antioxidant activity of the optimal sample was investigated at concentrations ranging from 10 to 50 mg/mL. The results demonstrated that 50 mg/mL of the SPH had the highest antioxidant activity. Analysis of amino acids by HPLC revealed that glutamic acid and glycine had the highest concentrations, and all essential amino acids were detected. SEM analysis showed smaller heterogeneous particles of protein hydrolysate, which confirmed the hydrolysis process during fermentation. FTIR results showed that different functional groups were formed, which confirmed the hydrolysis of sesame protein. Generally, sesame protein can be a good source in the fermentation system by B. coagulans to produce hydrolysate with antimicrobial and antioxidant properties.

Cascade Mechanochemical Transformation of a Benzobarrelane Polymer

High-frequency FeSiAl-based soft magnetic composites via simultaneously suppressed eddy and hysteresis losses

Abstract Soft magnetic composites present promising solutions for integrated transformers and inductors, but challenges arise at MHz range, where hysteresis and intra-eddy losses result in substantial performance degradation. In this study, we propose a bulk/interface insulation strategy to synthesize FeSiAl:Sn/Al 2 O 3 soft magnetic composite by mutual diffusion of metal atoms, where a ~ 3 um-depth Sn-substituted FeSiAl is obtained in the matrix and an insulating Al 2 O 3 layer is epitaxially grown on FeSiAl surface. The formation of FeSiAl:Sn can not only suppress intra-eddy loss by enhancing electrical resistivity, but also reduce coercivity by mitigating lattice distortion for reducing hysteresis loss. Meanwhile, the in-situ grown Al 2 O 3 layer can reduce inter-eddy loss by electrical isolation between FeSiAl particles. This construction leads to power loss of 47 mW/cm 3 at 100 kHz and 1344 mW/cm 3 at 1 MHz under 50 mT, as well as effective permeability of 60 up to tens of MHz, associated with cut-off frequency of 250.7 MHz. This approach lays the groundwork for the development of high-frequency soft magnetic composites in engineering applications.

Enhanced drug-drug interaction extraction from biomedical text using deep learning-based sentence representations

Selective silencing of antibiotic-tethered ribosomes as a resistance mechanism against aminoglycosides

Abstract Antibiotic resistance is a growing threat, underscoring the need to understand the underlying mechanisms. Aminoglycosides kill bacteria by disrupting translation fidelity, leading to the synthesis of aberrant proteins. Surprisingly, mutations in fusA , a gene encoding translation elongation factor G (EF-G), frequently confer resistance, even though EF-G neither participates in mRNA decoding nor blocks aminoglycoside binding. Here, we show that EF-G resistance variants selectively slow ribosome movement along mRNA when aminoglycosides are bound. This delay increases the chance that the drug dissociates before misreading occurs. Over several elongation cycles, this selective silencing of drug-bound ribosomes prevents error cluster formation, preserving proteome and membrane integrity. As a result, fusA mutations confer resistance early in treatment by preventing self-promoted aminoglycoside uptake. Translation on drug-free ribosomes remains sufficiently rapid to sustain near-normal bacterial growth. The mechanism of selective silencing of corrupted targets reveals a previously unrecognized antibiotic resistance strategy with potential therapeutic implications.

Epidemiological attribution of knee and ankle injuries in firefighters

Bowhead whales can live for more than 200 years — this protein might be why

Bioinspired Carbonic Anhydrase Mimics with Zr–OH Sites and Size-Tunable Nanopockets for Efficient Bidirectional Catalysis of CO ₂ Hydration

Structural characterization of atrial natriuretic peptide amyloid fibrils from patients with atrial fibrillation

Numerical study of the performance of a three-phase horizontal separator under varying water outlet pressures

Magnetocaloric Effect in a Microporous Material Using a Rare-Earth-Free, Hybrid Perovskite

Regulation of ADP-ribosyltransferase activity by ART domain dimerization in PARP15

Abstract PARP15 is a mono-ADP-ribosyltransferase that targets an unknown set of proteins as well as RNA. Its evolutionary relationship with PARP14 suggests roles in antiviral defence; its localization to stress granules points to functions in the regulation of translation. Here we show that the transferase domain of PARP15 dimerizes in solution; the formation of dimers is a prerequisite for catalytic activity and monomeric mutant variants of the domain are inactive. In cells, dimer-disrupting mutations abrogate catalytic activity and alter the subcellular localization of the full-length protein. Using biophysical methods, including X-ray crystallography and HDX-MS, we provide evidence for a regulatory mechanism by which dimerization enables correct target engagement rather than NAD + co-substrate binding, and by which the two protomers of the dimer operate independently of one another. Together, our results uncover a regulatory mechanism in a PARP family enzyme.