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Turbocharged ‘killer’ cells show promise for autoimmune disease

Interfacial ion-electron conversion enhanced moisture energy harvester

Newly established forests dominated global carbon sequestration change induced by land cover conversions

Publisher Correction: Comprehensive evaluation of phosphoproteomic-based kinase activity inference

Integrative spatial omics reveals distinct tumor-promoting multicellular niches and immunosuppressive mechanisms in Black American and White American patients with TNBC

Abstract Racial disparities in the clinical outcomes of triple-negative breast cancer (TNBC) have been well-documented, but the underlying biological mechanisms remain poorly understood. To investigate these disparities, we employed a multi-omic approach integrating imaging mass cytometry and spatial transcriptomics to characterize the tumor microenvironment (TME) in self-identified Black American (BA) and White American (WA) TNBC patients. Our analysis revealed that the TME in BA patients is marked by a network of endothelial cells, macrophages, and mesenchymal-like cells, which correlates with reduced patient survival. In contrast, the WA TNBC microenvironment is enriched in T-cells and neutrophils, indicative of T-cell exhaustion and suppressed immune responses. Ligand-receptor and pathway analyses further demonstrated that BA TNBC tumors exhibit a relatively “immune-cold” profile, while WA TNBC tumors display features of an “inflamed” TME, suggesting the evolution of a unique immunosuppressive mechanism. These findings provide insight into racially distinct tumor-promoting and immunosuppressive microenvironments, which may contribute to the observed differences in clinical outcomes among BA and WA TNBC patients.

A collective intelligence model for swarm robotics applications

Motor learning refines thalamic influence on motor cortex

China pours money into brain chips that give paralysed people more control

Rare find: interstellar visitor seen blazing through our Solar System

A kinase mediator of rhizobial symbiosis and immunity in Medicago

Signatures of chiral superconductivity in rhombohedral graphene

Close-in planet induces flares on its host star

Association of Post Kala-Azar Dermal Leishmaniasis pathogenesis with prolonged sunlight (ultraviolet radiations) exposure in VL endemic population of Bihar

Chronic haloperidol exposure impairs neurodevelopment via Notch1 signaling in human stem cell-derived brain organoids

Stepwise ATP translocation into the endoplasmic reticulum by human SLC35B1

Abstract ATP generated in the mitochondria is exported by an ADP/ATP carrier of the SLC25 family1. The endoplasmic reticulum (ER) cannot synthesize ATP but must import cytoplasmic ATP to energize protein folding, quality control and trafficking2,3. It was recently proposed that a member of the nucleotide sugar transporter family, termed SLC35B1 (also known as AXER), is not a nucleotide sugar transporter but a long-sought-after ER importer of ATP4. Here we report that human SLC35B1 does not bind nucleotide sugars but indeed executes strict ATP/ADP exchange with uptake kinetics consistent with the import of ATP into crude ER microsomes. A CRISPR–Cas9 cell-line knockout demonstrated that SLC35B1 clusters with the most essential SLC transporters for cell growth, consistent with its proposed physiological function. We have further determined seven cryogenic electron microscopy structures of human SLC35B1 in complex with an Fv fragment and either bound to an ATP analogue or ADP in all major conformations of the transport cycle. We observed that nucleotides were vertically repositioned up to approximately 6.5 Å during translocation while retaining key interactions with a flexible substrate-binding site. We conclude that SLC35B1 operates by a stepwise ATP translocation mechanism, which is a previously undescribed model for substrate translocation by an SLC transporter.

Intercellular adhesion molecule-1 protects against adipose tissue inflammation and insulin resistance but promotes liver disease activity in western-diet fed mice

Abstract Metabolic dysfunction associated steatotic liver disease (MASLD) presents a growing global health problem. Disease progression is promoted not only by hepatic leukocyte accumulation but also by inflammatory signals from adipose tissue and an altered gut microbiome. To determine the contribution of intercellular adhesion molecule-1 (ICAM-1) to MASLD pathogenesis, male mice with an ICAM-1 mutation (Icam1tmBay) and wild type (WT) mice were compared in 12 and 24-week feeding experiments with a Western-style diet (WD) containing 40 kcal% fat, 20 kcal% fructose, and 2% cholesterol. WD-induced MASLD was accompanied by increased ICAM-1 expression in liver, epididymal white adipose tissue (EWAT), and intestine in WT mice. WD-fed Icam1tmBay mice exhibited increased circulating neutrophils, higher frequencies of inflammatory leukocytes in EWAT, and a worsened glucose tolerance when compared to WT mice. In contrast, the mutation resulted in reduced WD-induced liver disease activity and less accumulation of intrahepatic leukocytes. WD-feeding caused substantial changes in fecal microbiota with decreased microbial diversity that differed between the mouse strains. In conclusion, ICAM-1 positively regulates adipose tissue homeostasis and protects from insulin resistance but promotes liver damage in diet-induced obesity. This points to organ-specific roles for ICAM-1 and the potential of liver-specific targeting of ICAM-1 for treatment of MASLD.

Broadband time domain diffuse optical characterization of human cadaver bone from 500 to 1100 nm

Electroporation-mediated functional analysis method of genes in the giant insect Trypoxylus dichotomus

FeNO as a biomarker of interstitial and fibrotic pulmonary sequelae in patients admitted for severe SARS-CoV-2 pneumonia

Effect of harvest time on sugar content and carotenoid composition in different sweet maize hybrids

Abstract Sweet maize (Zea mays convar. saccharata var. rugosa) is valued for its high sugar content, which gradually converts to starch during kernel maturation. This study evaluated the yield and biochemical composition of five super sweet maize hybrids (D, M, G, S, and N) across four harvest dates (July 19, July 26, August 2, and August 9) over two consecutive growing seasons. Seventeen key nutritional parameters—including sugars, minerals, and carotenoids—were significantly affected by both hybrid and harvest time (p < 0.05). The M hybrid showed the highest levels of β-carotene (5.61 µg/g), phosphorus (3.45 mg/g), and magnesium (1.96 mg/g), while the S hybrid had the greatest concentrations of lutein (2.84 µg/g), zeaxanthin (2.71 µg/g), and β-cryptoxanthin (1.79 µg/g). The D hybrid recorded the highest sucrose content (78.5 mg/g), and the N hybrid was superior in dry matter (32.7%) and fructose (61.4 mg/g). Harvest timing also had a significant impact: early harvest (July 19) resulted in peak concentrations of β-carotene (5.89 µg/g), potassium (4.17 mg/g), and glucose (84.2 mg/g), whereas late harvest (August 9) favored hybrid-specific nutrient accumulation. Principal Component Analysis (PCA) revealed that the first two components explained 75.82% of the total variance, with glucose and potassium identified as key discriminating traits. These findings highlight the critical role of genotype selection and harvest timing in optimizing the nutritional quality and market value of sweet maize under temperate growing conditions.