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Diagnostics and characterization of nanoparticles in dusty glow discharge plasma
Ras-related protein 2 limits vascular smooth muscle cell phenotypic switching and abdominal aortic aneurysm development
Single-base station positioning for photovoltaic power plant inspection UAVs based on PPP-B2b signal
Selection and transmission of the gut microbiome alone can shift mammalian behavior
Abstract Animals live in partnership with their gut microbiota, and these microbial communities often shift when hosts adapt to new environments. While it is well known that the microbiome can influence traits ranging from metabolism to behavior, a key question remains unresolved: can host traits under natural selection be transmitted solely through the microbiome, without changes to the host genome? Here we experimentally demonstrate that selection on a behavioral trait in mice significantly shifts the host trait over time through microbiome transmission alone. We first identify locomotor activity as transmissible through the gut microbiome, using fecal transfers from wild-derived mouse strains into germ-free male recipients. Building on this, we carry out four rounds of one-sided microbiome selection, serially transferring microbiomes from low-activity donors to independently bred male germ-free mice. Only this selection line, not the randomly chosen control line, shows a decrease in locomotion toward the end of the experiment. Reduced activity is linked to enrichment of Lactobacillus and its metabolite indolelactic acid, and administration of either alone is sufficient to suppress locomotion. These findings demonstrate that microbiome selection and transmission can shape mammalian behavior, independent of host genomic evolution. Our work highlights the role of microbiome-mediated trait inheritance in shaping host ecology and evolution.
Prediction of adverse left ventricular remodeling by culprit lesion features in patients with LAD-related myocardial infarction
Multi-view deep learning framework for the detection of chest X-rays compatible with pediatric pulmonary tuberculosis
Progressively altered genes in colorectal carcinogenesis link oncogenesis immune cycle and tumor microenvironment
Abstract The adenoma-adenocarcinoma pathway represents a crucial mechanism underlying the development of colorectal precancerous lesions, encompassing approximately 85%-90% of colorectal cancer (CRC). Elucidating the molecular mechanisms underlying colorectal cancer progression is of paramount importance for achieving early and accurate diagnosis as well as effective treatment. We collected peripheral blood mononuclear cells (PBMC) from healthy controls, adenoma patients, and adenocarcinoma patients, and performed transcriptomic profiling to characterize dynamic gene expression during carcinogenesis. Diagnostic potential was assessed using receiver operating characteristic (ROC) analysis, and a random-forest model was trained to classify disease status. The screening identified genes with consistent expression changes as potential early diagnostic markers, and further exploration of their functions and significance in CRC is conducted through analysis of the TCGA database. The findings revealed that the progression of precancerous lesions in the “Normal-Adenoma-Cancer” (N-A-C) sequence was accompanied by a sustained enhancement of the immune response. Notably, HECW2, WARS1, SLC16A3, SECTM1, IFITM3, ADAMTSL4, FCGR1A, F2RL1, OPLAH, SERPINA1, FCGR1CP showed consistent upregulation with promising diagnostic performance. In our PBMC cohort, the random-forest classifier achieved an accuracy of 93.62%, indicating potential for distinguishing cancer from precancerous lesions. The bioinformatics analysis revealed a significant association of these genes with DNA methyltransferase, DNA mismatch repair, m6A regulator, tumor mutational burden (TMB) and microsatellite instability (MSI). Furthermore, a detailed analysis was further performed on WARS1. In the “N-A-C” sequence, WARS1 exhibited a significant upregulation in both blood and tissues, demonstrating a positive correlation with augmented infiltration of immune cells, activation of stromal and immune responses, as well as heightened activity during the cancer immune cycle. However, it demonstrates a declining trend in the progression of CRC from stage I to IV, which may be intricately associated with the metastasis of CRC. The WARS1 can serve as a reliable indicator of the immune response in CRC, thereby demonstrating its potential to impede tumorigenesis or metastasis.
The successful impossible radical ring-opening copolymerization of thionolactones and methacrylates via an auxiliary third comonomer
Public values in public R&D through natural language processing
Temporal fingerprints for identity matching across fully encrypted domains
Predicted peptide scaffolds for drug screening in endometrial cancer organoids
DirectRM: integrated detection of landscape and crosstalk between multiple RNA modifications using direct RNA sequencing
Impact compression test and dynamic triaxial unified strength criterion for concrete under freeze–thaw cycle action
Visualizing alkali metal aggregation-induced coordination in CO2 activation on copper
An exploratory study of physicians’ familiarity, knowledge, and willingness to prescribe pre-exposure prophylaxis in the MENA region
The global biomass of mammals since 1850
Spectroscopic quantification of cyclopentolate using an erythrosine-based resonance rayleigh scattering strategy: application to ophthalmic formulations
Abstract Cyclopentolate (CYP), an antimuscarinic (anticholinergic) agent, is pharmacologically employed in ophthalmology to induce cycloplegia (temporary paralysis of the ciliary muscle) and mydriasis (pupil dilation) for diagnostic and therapeutic procedures, including ocular examinations and surgeries. This study establishes a spectrofluorimetric method for quantifying CYP in ophthalmic solutions based on Resonance Rayleigh Scattering (RRS) signal modulation. The approach exploits the formation of an ion-associate complex between CYP and the dye erythrosine, which induces a measurable RRS enhancement. Critical experimental parameters governing the complexation and subsequent RRS response were systematically investigated and optimized. Under these established optimal conditions, a linear correlation existed between the enhanced RRS intensity and CYP concentration across the range of 40 to 1500 ng/mL. The method demonstrated a detection limit (LOD) of 13 ng/mL and a quantification limit (LOQ) of 39.5 ng/mL. Successful application to the assay of cyclopentolate in commercial eye drop formulations confirmed the method’s accuracy and precision. This RRS-based methodology utilizing erythrosine presents a straightforward, rapid, cost-effective, and environmentally favorable option for routine quality control and monitoring of CYP in pharmaceutical preparations.
Structural basis of apoptosis induction by the mitochondrial voltage-dependent anion channel
Abstract The voltage-dependent anion channel (VDAC) is the main gateway for metabolites across the mitochondrial outer membrane. VDAC oligomers are connected to apoptosis induced by various stimuli. However, the mechanistic and structural basis of apoptosis induction by VDAC remains poorly understood. Here, using cryo-EM and NMR we show that VDAC1 oligomerization or confinement in small lipid nanodiscs triggers the exposure of its N-terminal α-helix (VDAC1-N) which becomes available for partner protein binding. NMR and X-ray crystallography data show that VDAC1-N forms a complex with the BH3 binding groove of the anti-apoptotic Bcl2 protein BclxL. Biochemical assays demonstrate that VDAC1-N exhibits a pro-apoptotic function by promoting pore formation of the executor Bcl2 protein Bak via neutralization of BclxL. This mechanism is reminiscent of BH3-only sensitizer Bcl2 proteins that are efficient inducers of Bax/Bak-mediated mitochondrial outer membrane permeabilization and ultimately apoptosis. The VDAC pathway most likely responds to mitochondrial stress or damage.