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Effects of household washing methods and post-ripening on the residue dissipation of the systemic fungicides mandestrobin and metconazole in Persimmons
Calcined oyster shell powder as a lime substitute in earthen building materials
Why Seeding Works When Nucleation Barriers Vanish
Toxicity assessment in preclinical histopathology via class-aware Mahalanobis distance for known and novel anomalies
Unlocking Gd(III) Anisotropy: Determining the Zero-Field Splitting Axes to Enhance Spin-Label Structural Analysis
Toward clinically relevant automated corneal biomanufacturing with human-derived FBS alternatives
Abstract The replacement of animal-derived components from cell culture protocols is essential for the development of human-compatible and clinically translatable systems. Fetal bovine serum (FBS) is still widely used for cell expansion, although its xenogeneic origin and batch variability limit regulatory compliance. In this study, human platelet lysate (hPL) and human serum (HS) were assessed as low-serum (2%) alternatives to FBS during the subculture phase of bone marrow-derived mesenchymal stromal cells (BM-MSC) prior to keratocyte differentiation for corneal tissue engineering. BM-MSC were gradually adapted over four days to 2% FBS, hPL, or HS, maintained for seven days, and then transferred to serum-free keratocyte differentiation medium for 14 days in either two-dimensional (2D) or three-dimensional (3D) cultures in 30 wt% riboflavin-arginine-triggered gelatin methacryloyl (RA-GelMA) hydrogels crosslinked under visible blue light. To demonstrate the applicability of this approach in corneal tissue engineering, differentiation was evaluated by immunofluorescence and quantitative PCR in 2D cultures, and by immunofluorescence in 3D cultures. Both hPL and HS maintained metabolic activity, supported keratocyte-associated marker expression, and suppressed α-SMA, performing comparably to FBS, thereby supporting their use as clinically compliant, human-derived alternatives for xeno-reduced corneal biomanufacturing.
Valence-Shell Electrons and Ionic Radius as Descriptors for Multisite Doping of RuO <sub>2</sub> for Durable Zn-Air Batteries
Response of maize varieties to soil acidity under field conditions in Western Ethiopia
Electrostatic Confinement of Plasma Electrons by Water Microdroplets Enables Dinitrogen Oxidation
Sex-related neuropsychiatric recovery from maternal perinatal depression and expression of monoamine and amino acid neurotransmitter levels in specific brain regions of adult offspring
Bioinspired Carbon Radical Catalysis
Design of a triplex fluorescence aptasensor for a culture-free diagnosis of peritoneal dialysis-related peritonitis
Enantio- and <i>Z</i> / <i>E</i> -Stereodivergent Ni/Pd Dual Catalysis for Trisubstituted Alkenes Featuring α-Chiral Carbonyls
Ideology and free speech values predict content moderation preferences: cross-national evidence across targets of hate speech
Abstract With over 4 billion people using social media platforms daily, decisions about what content to allow or moderate have profound implications for global public discourse, democratic deliberation, and users’ psychological well-being. This study examines cross-national variation in content moderation preferences by exposing participants in 10 countries to a standardized example of hate speech: a hateful post modeled on text that X (formerly Twitter) had cited in its content moderation guidelines. Across contexts, exposure to such content triggers widespread support for intervention, with minimal differences based on the experimentally varied identity of the target. However, significant variation emerges across countries. The United States stands out for its comparatively lower support for moderation of hate speech, while countries like France, Brazil, and South Africa exhibit much stronger demand. Within most countries, political ideology predicts support: individuals on the right are less likely to endorse removal or suspension than those on the left. Crucially, values around freedom of speech versus harm prevention consistently shape preferences across all contexts. Those who prioritize prevention from harm are markedly more likely to support hard forms of moderation (e.g., account suspension and content take-downs). These findings highlight that moderation preferences are shaped less by the specific target than by individuals’ deeper commitments regarding free expression and harm prevention.
Concise Total Synthesis of (+)-Shearilicine: A Machine Learning-Assisted Strategy for Ligand Optimization of an Enantioselective Palladium-Catalyzed α-Arylation
Vacuolar H <sup>+</sup> -ATPase Preserves Cardiolipin Homeostasis Through the Lysosomal-Mitochondrial Axis to Restrain Cardiac Aging
BACKGROUND: Cardiac aging involves progressive mitochondrial dysfunction, contributing to heart failure. Cardiolipin (CL), essential for mitochondrial function, is increasingly depleted in aging cardiomyocytes, promoting mitochondrial decline. Lysosomal degradation relies on v-ATPase (vacuolar-type H+-ATPase)–mediated acidification, and although lysosomes regulate phospholipid metabolism, their roles in CL homeostasis during aging remains unclear. This study examines whether v-ATPase dysfunction drives age-related cardiac changes by disrupting CL metabolism and mitochondrial function. METHODS: To investigate underlying mechanisms and causality, we use RNA sequencing, targeted lipidomics, immunofluorescence microscopy, (co)immunoprecipitation, proximity ligation assays, subcellular fractionation, mitochondrial respiration analysis and echocardiography, a cardiolipin synthase-1 ( Crsl1 ) knockout mouse model, and 2 v-ATPase knockout models. In addition, we assess whether a nutraceutical intervention targeting v-ATPase dysfunction can mitigate heart failure in aging mouse models and elderly people. RESULTS: Our present findings reveal a sequence of events driving age-related cardiomyopathy: declining cardiac nicotinamide adenine dinucleotide levels impair v-ATPase–mediated lysosomal acidification by weakening the interaction between nicotinamide adenine dinucleotide–dependent glycolytic enzyme aldolase and v-ATPase. This disruption increases lysosomal membrane permeability by reducing lysosomal acidification, allowing cathepsin B to leak into mitochondria. There, cathepsin B disrupts mitochondrial CRLS1 (cardiolipin synthase I), impairing CL synthesis and remodeling. The resulting CL deficiency causes mitochondrial oxidative stress and programmed cell death, leading to mitochondrial and cardiac dysfunction. Genetic or chemical inhibition of v-ATPase and of CRLS1 in mouse models reproduce these age-related defects, highlighting their central roles in cardiac aging. Restoring nicotinamide adenine dinucleotide levels rescues lysosomal acidification and CL metabolism, protecting against age-related cardiomyopathy in rodents and humans. CONCLUSIONS: Augmenting v-ATPase–mediated lysosomal acidification offers novel therapeutic strategies to combat age-related cardiomyopathy by rewiring CL homeostasis.