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Energy restriction and iron supplementation improve iron status in women with obesity regardless of red meat consumption: a randomized controlled trial
Abstract Iron deficiency without anemia (IDNA) may be linked to obesity-related inflammation. Weight reduction and heme-iron intake from red meat are proposed to improve iron status. This randomized controlled trial (NCT06104800) assessed the impact of a low-calorie, high-protein diet with red meat (RM) compared to a low-calorie, high-protein diet without red meat (WR) over 60 days on iron concentrations in women with obesity and IDNA receiving oral iron supplementation. Fifty-two females were randomized (26 per group); 45 completed the study. After intervention, serum iron increased for both groups: RM 55.8 ± 27.0 µg/dL to 69.8 ± 30.5 µg/dL, p = 0.05; WR 65.3 ± 28.4 µg/dL to 76.8 ± 45.6 µg/dL, p = 0.27. However, group-by-time analysis showed no significant differences between dietary interventions ( p = 0.55). Additional significant improvements ( p < 0.05) in secondary and exploratory outcomes included ferritin, transferrin, unsaturated iron-binding capacity, uric acid, and fat mass. In conclusion, no statistically significant benefit of red meat consumption over other dietary iron sources, when combined with oral iron supplementation, was demonstrated for improving iron status in women with obesity and IDNA.
Full scale optimization of an anaerobic/aerobic/anoxic process for nitrogen removal from low-strength municipal wastewater
Paired analysis of meconium and neonatal hair reveals distinct biomarker profiles of prenatal exposure to trace metal elements
Superconductivity in kagome metals due to soft loop-current fluctuations
Abstract We demonstrate that soft fluctuations of translation symmetry-breaking loop currents provide a mechanism for unconventional superconductivity in kagome metals that naturally addresses the multiple superconducting phases observed under pressure. Focusing on the rich multi-orbital character of these systems, we show that loop currents involving both vanadium and antimony orbitals generate low-energy collective modes that couple efficiently to electrons near the Fermi surface and mediate attractive interactions in two distinct unconventional pairing channels. While loop-current fluctuations confined to vanadium orbitals favor chiral d + i d superconductivity, which spontaneously breaks time-reversal symmetry, the inclusion of antimony orbitals stabilizes an s ± state that is robust against disorder. We argue that these two states are realized experimentally as pressure increases and the antimony-dominated Fermi surface sheet undergoes a Lifshitz transition.
Hallucination risk and trustworthiness of generative AI systems based on IVMPF-MABAC decision-making strategies
Unravelling the bi-functional role of cation-regulated surface hydroxyl kinetics in Pt-catalyzed alcohol fuel cells
Nurse practitioners’ competencies for occupational health services in primary care units, Thailand: a qualitative study
Molecular basis of allosteric regulation and pharmaceutical targeting of protein kinase Cβ
Abstract Protein kinase C (PKC) isozymes are ubiquitous kinases that direct diverse cellular pathways and are important drug targets for the treatment of cancer and neurological diseases. PKCs are auto-regulating enzymes governed by phospholipid and Ca 2+ signals via a mechanism that has remained enigmatic due to a paucity of structural information. Herein we present a series of structures of the full-length human PKCβI and PKCβII isozymes. These structures reveal the molecular basis by which PKCs maintain an auto-inhibited state, convert to a defined and ordered active conformation via a “lipid-lever” mechanism of allosteric activation, and how isoform-specific differences alter their allosteric regulatory mechanisms. We show that endoxifen, a recently identified PKCβI inhibitor, can alter the allosteric regulatory mechanism of PKCβI, providing a proof of concept for allosteric regulators of PKCs. Collectively, our data describe a foundational molecular model of second messenger-mediated allosteric regulation of PKCs that underpins PKC function, misregulation, and mechanisms of inhibition.
Foliar silicon enhances drought resilience and productivity in buckwheat by stabilizing photosynthetic performance
DGAT: a dual-graph attention network for inferring spatial protein landscapes from transcriptomics
Sustainable high-throughput microwell spectrophotometric methods for avapritinib quality control via charge-transfer complexation
(3R, 7S)-11-hydroxy-jasmonic acid is a major oxidative shunt product of jasmonic acid catabolism in Arabidopsis thaliana
A membrane-bound nuclease directly cleaves phage DNA during genome injection
Abstract From mammals to bacteria, the direct recognition and cleavage of viral nucleic acids is a potent defence strategy against viral infection, but it requires mechanisms for distinguishing self from non-self 1,2 . In bacteria, CRISPR–Cas and restriction-modification systems achieve this discrimination by recognizing specific DNA sequences or DNA modifications, respectively. Alternative mechanisms probably remain to be discovered. Here, we characterize SNIPE, an anti-bacteriophage defence system that constitutively localizes to the bacterial cell membrane in Escherichia coli to block phage λ infection. Using radiolabelled phage DNA and time-lapse microscopy to track phage genomes, we demonstrate that SNIPE directly cleaves phage DNA during genome injection. Based on proximity labelling, we find that SNIPE associates with host proteins essential for λ genome entry and with the λ tape measure protein, which facilitates λ genome injection across the inner membrane. SNIPE also defends against diverse siphoviruses, probably through direct interactions with their tape measure proteins. Our findings establish SNIPE as a widespread bacterial defence system that exploits the spatial organization of phage genome injection to specifically target viral DNA, representing a previously unknown strategy for distinguishing self from non-self in prokaryotic immune systems.
Exploring the spatiotemporal evolution and spatial correlation network characteristics of cultivated land carbon emissions in China
Flow-mediated endothelial remodeling and inflammation drive developmental vascular susceptibility in ldlr loss of function
Abstract Atherosclerosis, the leading cause of cardiovascular disease, is associated with aberrant lipid metabolism, endothelial dysfunction, and chronic inflammation, yet its early manifestations and mechanisms remain incompletely understood. As low-density lipoprotein receptor loss of function is the most common monogenic cause of atherosclerosis, we employed low-density lipoprotein receptor knockout ( ldlr -/-) zebrafish to investigate the developmental origins of atherosclerotic cardiovascular disease. Single-cell RNA-sequencing under differential flow conditions in embryonic ldlr -/- zebrafish identified a population of disproportionately stressed endothelial cells marked by overexpression of heat shock protein 70 ( hsp70 ). Hsp70 is induced in stressed endothelial cells in a flow-dependent manner in zebrafish and a subset of human endothelial cells, and its activation is associated with disrupted remodeling angiogenesis in vivo. Genetic and pharmacological studies demonstrated that hsp70 upregulation inhibits vascular apoptosis and ciliogenesis, leading to altered angiogenic remodeling. Concurrently, pro-inflammatory processes, including enhanced myelopoiesis and thrombogenicity, are amplified at early stages in ldlr -/- zebrafish, which also exhibit impaired regenerative angiogenesis and heightened neutrophil recruitment post-vascular injury. Our findings reveal how abnormalities in flow-mediated endothelial remodeling and inflammation converge during embryogenesis to drive vascular susceptibility to hemodynamic and other stressors in ldlr loss of function.