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Photocatalytic Defluorination of Perfluorooctanoic Acid by Twisted Linear Polymer Radicals
Limited on-demand water delivery as a managerial strategy to enhance operational flexibility in pressurized irrigation networks
Monitoring in vivo transcription with synthetic serum markers
Distinct RNA Physical Microenvironments Shape Unique Properties and Functions within Biomolecular Condensates
Correction: Synergistic design of gadolinium-doped polyaniline/MWCNT hybrid nanocomposites for high-performance supercapacitors
Pangenome and resequencing analyses reveal flowering evolution and genetic control in Cerasus
Synthesis of Distal 1,4-Diaxial Atropisomers: CPA-Catalyzed Atroposelective (3 + 3)-Annulation via a Desymmetrization Strategy
Retraction Note: Mathematical modeling and statistical analysis of breast cancer drugs using M-polynomial indices for the physical properties
Progressive release of long-stored carbon from tropical peatland disturbances
Abstract Tropical peatlands are globally important, millennia-old carbon sinks, yet unprecedented human-driven degradation is triggering alarming carbon emissions. Comprehensive quantification of carbon dynamics across the disturbance sequence—from peat swamp forests to drained and fire-impacted peatlands—remains a critical knowledge gap. Here we show that over 18 years (1996–2014), drainage and subsequent peat fires released approximately 30–41 kg C m −2 from peatlands in Central Kalimantan, Indonesia, using radiocarbon dating of peat profiles and groundwater dissolved organic carbon. Drainage contributed 5–11 kg C m −2 , primarily from centuries- to millennium-old, previously waterlogged peat. Fires released 23–32 kg C m −2 from peat accumulated over the past 3,000 years, initiating progressive oxidative decomposition of older peat. Extrapolation to Indonesia’s disturbed peatlands suggests a release of 0.81–3.70 Gt C between 1996 and 2014, with ongoing decomposition releasing an additional 0.03–0.08 Gt C annually, accelerating the impact on the global carbon balance.
Artificial MetalloDNAzymes with High-Density, Near-Atomic Precision Organization of Metal Cofactors for Enhanced Bioorthogonal Catalysis
Investigating the emergence of the Brazilian porcupinepox poxvirus in wild Brazilian porcupines (Coendou longicaudatus)
Defective ventral neurogenesis due to midfetal Chd8 mutation drives autistic-like behavior in mice
Abstract Autism spectrum disorder (ASD) is a common neurodevelopmental condition characterized by behavioral abnormalities. Although mouse models have been widely adopted to recapitulate the pathology of ASD, the identification of specific neural abnormalities responsible for autistic-like behavior has remained challenging. Here we provide insight into this causal relation by identifying the critical period and cell type responsible for the development of such behavior in ASD model mice with a Chd8 mutation. We find that Chd8 mutation induced at embryonic day 14.5 gives rise to ASD-like behavioral phenotypes, including abnormal social interaction and increased anxiety-like behavior, as well as to accelerated cell-cycle exit and differentiation in ventral progenitor cells. Restoration of Chd8 expression in ventral progenitor cells ameliorates both the behavioral phenotypes and aberrant ventral differentiation in Chd8 mutant mice. Our findings indicate that Chd8 mutation during the midfetal period—in particular, in ventral progenitor cells—contributes to the development of autistic-like behavior.
Phase Segregation of Colloidal Quantum Dots Driven by Marangoni Vortex Flow for Multi-Component Microfabrication
The anti-interleukin-6 antibody ALD518-P18 mitigates murine kidney ischemia–reperfusion injury
Abstract Interleukin-6 (IL-6) is a key pleiotropic cytokine implicated in kidney injury; however, the therapeutic potential of IL-6 blockade against acute ischemia–reperfusion injury (IRI) remains uncertain, with previous murine studies yielding conflicting results. This study investigated the protective effects of the high-affinity chimeric anti-IL-6 monoclonal antibody, cALD518-P18, in a non-transplant mouse model of warm renal IRI (22 min ischemia, 24 h reperfusion). Male C57BL/6 mice received a single 40 mg/kg dose of cALD518-P18 or an isotype control, administered either intraperitoneally 30 min before ischemia or intravenously immediately after ischemia. At 24 h, control mice exhibited significant kidney dysfunction (serum creatinine, urea), injury, and inflammation, consistent with elevated pro-inflammatory IL-6 trans-signalling (soluble IL-6R (sIL-6R) and tubular STAT3 phosphorylation (pSTAT3)). Treatment with cALD518-P18, in both regimens, significantly protected the kidneys from IRI, demonstrating improved renal function and reduced tissue damage. The antibody attenuated inflammation, endothelial activation and pSTAT3 signalling, significantly downregulating gene expression of the acute tubular stress marker NGAL. These findings confirm the pathogenic role of IL-6 and highlight its early blockade with cALD518-P18 as a promising therapeutic strategy to improve outcomes in acute kidney injury and transplantation.