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Lessons from Portugal on effects of cutting research funding
Vulnerability of amphibians to global warming
Abstract Amphibians are the most threatened vertebrates, yet their resilience to rising temperatures remains poorly understood1,2. This is primarily because knowledge of thermal tolerance is taxonomically and geographically biased3, compromising global climate vulnerability assessments. Here we used a phylogenetically informed data-imputation approach to predict the heat tolerance of 60% of amphibian species and assessed their vulnerability to daily temperature variations in thermal refugia. We found that 104 out of 5,203 species (2%) are currently exposed to overheating events in shaded terrestrial conditions. Despite accounting for heat-tolerance plasticity, a 4 °C global temperature increase would create a step change in impact severity, pushing 7.5% of species beyond their physiological limits. In the Southern Hemisphere, tropical species encounter disproportionally more overheating events, while non-tropical species are more susceptible in the Northern Hemisphere. These findings challenge evidence for a general latitudinal gradient in overheating risk4–6 and underscore the importance of considering climatic variability in vulnerability assessments. We provide conservative estimates assuming access to cool shaded microenvironments. Thus, the impacts of global warming will probably exceed our projections. Our microclimate-explicit analyses demonstrate that vegetation and water bodies are critical in buffering amphibians during heat waves. Immediate action is needed to preserve and manage these microhabitat features.
Prevalence and risk factors of undiagnosed age-related macular degeneration: the Korea National Health and Nutrition Examination Survey 2017–2020
Experimental study on dynamic evolutions of airflow in the ventilation network under the effect of mine gas outburst disasters
Microbes can capture carbon and degrade plastic — why aren’t we using them more?
Bio-inspired coral reef-like NiCo-LDH nanostructure fabricated on carbon felt for high performance flexible supercapacitor
Study on the mechanism of hsa_circ_0074763 regulating the miR-3667-3P/ACSL4 axis in liver fibrosis
Abstract This study aimed to investigate the involvement of hsa_circ_0074763 in the activation of HSCs (hepatic stellate cells ) and liver fibrosis. Additionally, it aimed to conduct a preliminary analysis of the molecular mechanism targeting miR-3667-3p/ACSL4 (Long-chain acyl-CoA synthetase 4), thereby providing novel molecular targets for liver fibrosis. The GEO database was utilized to identify differentially expressed hsa_circ_0074763 and determined its subcellular localization in LX-2 cells using fluorescence in situ hybridization. Bioinformatics analysis was employed for result prediction, and the interaction between hsa_circ_0074763 and miR-3667-3P was confirmed using dual-luciferase reporter gene assay. ACSL4 mediated ferroptosis was detected with kit. Hsa_circ_0074763 exhibits high expression levels in the fibrosis model. Validation through dual-luciferase reporter gene assays confirms the interaction between hsa_circ_0074763 and miR-3667-3P. Functional cell experiments demonstrate that overexpression of hsa_circ_0074763 promotes proliferation of LX-2 cells, elevates inflammation levels, and inhibits apoptosis. Additionally, ACSL4 has been identified as a direct target of miR-3667-3P, with overexpression of hsa_circ_0074763 counteracting the inhibitory effect on ACSL4 by suppressing miR-3667-3P. Overexpression of ACSL4 increased the expression levels of ROS (Lipid Oxidation), Iron (Ferro Orange) and MDA (Malondialdehyde), and decreased the expression levels of GPX4 (Glutathione peroxidase 4) and GSH (Glutathione). Our finding suggests that overexpression of hsa_circ_0074763 likely enhances the HSC activation through modulation of the miR-3667-3P/ACSL4 axis. Therefore, hsa_circ_0074763 holds potential as a therapeutic target for liver fibrosis.
Lesotho matters
Effects of whole brain proton irradiation at conventional or ultra-high dose rate (FLASH), in adult male Sprague Dawley rats
Analysis and identification of the temperature field of dam leakage based on infrared thermal imaging
Climate change will send home insurance spiralling. Here’s how to control costs
Multimodal medical image fusion combining saliency perception and generative adversarial network
A novel approach to prepare a composite of hydroxyapatite with cellulose nanocomposites by novel methods including theoretical studies
Fasting for weight loss is all the rage: what are the health benefits?
Static training improves insulin resistance in skeletal muscle of type 2 diabetic mice via the IGF-2/IGF-1R pathway
Development and evaluation of curcumin nano-niosomes for glioma-targeted therapy
Abstract Glioma remains a significant global health challenge, and is characterized by a persistently high mortality rate. Chemotherapy is a common treatment for glioma, but many anticancer drugs exhibit poor permeability across the blood–brain barrier (BBB) and fail to reach tumor tissues adequately, while also exerting toxic effects on normal cells. To address these issues, this study investigated the use of niosomes (Nio), which are biocompatible, biodegradable, and non-immunogenic, to encapsulate curcumin (Cur) and enhance its delivery to glioma tissues. Niosomes were prepared using the non-ionic surfactant sorbitan monostearate (Span 60) and cholesterol as carrier materials, and subsequently modified with transferrin (TF) to facilitate receptor-mediated transport across the BBB. The resulting TF-modified curcumin niosomes (TF-Cur-Nio) demonstrated enhanced targeting of brain tumors, improved anti-glioma efficacy, and favorable in vivo safety. These findings suggest that the TF-Cur-Nio delivery system has significant potential for advancing glioma treatment by overcoming the limitations of conventional chemotherapy and improving drug delivery to the brain.