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Wavelength-responsive in situ redox chemistry enables stable CO2 photocatalysis
Plasticity in the structure and assembly of proteasomes
ChunkyBERT: a novel technique for multiclass political bias detection in news media
Abstract With the increasing use of digital platforms for spread of information, political news has some of the most skewed sources which has confused people on what are facts and what are biased reportings. While most modern methods of finding bias in media use advanced Machine Learning algorithms and deep Learning techniques, such techniques heavily rely on manually generated features as sentiment analysis and lexical frequency which are tedious and time consuming. Hence we propose a novel method using Bidirectional Encoder Representations from Transformers (BERT) for ascertaining political media bias, mainly classifying articles into left-wing, centrist and right-wing inclinations via incorporation of the complete text. The suggested method includes dividing long political articles into segments of a set length. These are encoded separately using a pre-trained BERT model. A Transformer encoder then aggregates these segment-level embeddings, along with an attention pooling mechanism. This lets the model focus on and use the parts of the text that best show political bias for classification tasks. The experiments showed a highest validation accuracy of 86.22% and a validation AUC-ROC of 0.96, which is better than standard methods. This research gives a way to scale the detection of political bias, with potential uses in journalism, media monitoring, and improving digital literacy tools.
Cobalt-Catalyzed Selective Cross-Addition of Two Similar Acrylates for the Synthesis of Adipates and Glutarates
Sgk1 upregulation in hippocampus-projecting amygdala neurons underlies the delayed onset of PTSD-like avoidance behavior
Abstract Excessive avoidance is a core symptom of post-traumatic stress disorder (PTSD), yet its underlying circuit mechanisms remain poorly understood. Here, using a mouse model of PTSD induced by inescapable footshock, we observed a delayed and prolonged increase in avoidance behavior associated with selective activation of basolateral amygdala (BLA) projection neurons (PNs) targeting ventral hippocampus (BLA→vHPC PNs), but not nucleus accumbens, in both sexes. This projection-specific activation results from enhanced neuronal excitability and excitatory transmission driven by glucocorticoid receptor (GR) signaling. Among the cascade of GR signaling molecules, we identified serum- and glucocorticoid-regulated kinase 1 (Sgk1) as a key downstream mediator linking stress exposure to the hyperactivation of BLA→vHPC PNs and PTSD-like avoidance behavior. Manipulating Sgk1 expression bidirectionally regulates neuronal activity and susceptibility to stress-induced avoidance. These findings underscore the critical role of projection-specific upregulation of Sgk1 in BLA PNs in the pathogenesis of PTSD-like avoidance behavior.
Mechanisms of DNA methyltransferase 3A1-mediated DNA methylation of nucleosomes
Multi-platform profiling reveals host- and cell -type-specific pseudorabies virus gene expression
Abstract Pseudorabies virus (PRV) is an alphaherpesvirus that follows a conserved immediate-early → early → late transcriptional cascade, yet how this program adapts to diverse cell types is unclear. We profiled PRV transcription in four permissive cell lines—two epithelial (porcine kidney PK-15 and rat kidney NRK), one glial (rat glioma C6), and one neuron-like (rat PC-12)—at six time points (1–12 h post-infection). Host-dependent differences peaked early in infection, particularly for the regulators ie180 , ep0 , and us1 . ie180 showed strong species bias, with high expression in PK-15 but minimal in rodent lines, whereas ep0 and us1 varied quantitatively by cell type, with C6 and PC-12 showing marked early us1 activation. Combining long-read direct cDNA and direct RNA sequencing with 5′-capped CAGE-seq resolved viral transcription boundaries and identified 94 previously unannotated transcripts, including 5′ UTR isoforms, polygenic RNAs, and noncoding transcripts. Differential transcript usage analysis revealed extensive isoform remodeling across conditions, with late infection showing shifts from long or polygenic isoforms toward shorter forms. Together, these results provide the first multi-host, isoform-resolved temporal atlas of PRV transcription and show that the canonical cascade is conserved yet quantitatively tuned by host species and cell-type background.
Bifunctional D−π–A Ligand Directs Self-Organized Interface Passivation for Efficient Perovskite Photovoltaics
Loss of luminal lineage drives resistance to next-generation ERα antagonists in pretreated ER+ HER2− locally-advanced or metastatic breast cancer
Abstract Next-generation selective estrogen receptor-α (ERα) antagonist/degraders (SERDs) are being developed for ER-positive breast cancer (ER + BC), with intentions of improving outcomes for patients. In recent clinical trials of metastatic ER + BC, next-generation SERDs demonstrated clinical activity, and elacestrant received an approval for advanced ESR1 -mutant disease. However, responses to these drugs were highly heterogeneous: across trials and independent of ESR1 status, 30–50% of patients progressed by their first follow-up scan while other patients sustained benefit for 2 years or more. Here, we interrogate the basis for heterogeneous responses by comparing biopsies from non-responding patients (NR; progression-free survival <2 months) and responding patients (Resp; PFS ≥ 2 months) who received the next-generation SERD giredestrant. While Resp tumors maintain high dependency on ERα signaling, NR tumors exhibit loss of luminal lineage identity and by extension, ERα dependence. NR tumors instead up-regulate multiple ERα-independent proliferative pathways, such as EGFR/MAPK and Hippo/TEAD, which may represent targetable dependencies in NR disease. Modeling resistance and lineage plasticity in vitro, we find that giredestrant-resistant ER + BC cell lines exhibit profound shifts in chromatin accessibility, with the transcription factors, FOXA1 and FOXM1, implicated in gene expression of NR-upregulated proliferative pathways.
Structure of Acinetobacter baumannii cytochrome bo3 ubiquinol oxidase
LOC100912399 regulates osteogenic differentiation of bone marrow mesenchymal stem cells through modulating p38MAPK signaling-mediated oxidative stress and apoptosis
Abstract This study aims to investigate the role and underlying mechanism of the long non-coding RNA (lncRNA) LOC100912399 in regulating osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), with a specific focus on its involvement in oxidative stress-induced apoptosis via the p38 mitogen-activated protein kinase (p38MAPK) signaling pathway. BMSCs were isolated from the tibiae and fibulae of Sprague-Dawley (SD) rat pups and cultured to the third passage. Cell purity was confirmed by flow cytometric analysis of surface markers (CD45, CD29, CD106, CD90, CD11b), and multilineage differentiation potential was verified using Alizarin Red S (osteogenic), Oil Red O (adipogenic), and Alcian Blue (chondrogenic) staining. At 90% confluence, BMSCs were transduced with lentiviral vectors for LOC100912399 overexpression (Lv-LOC100912399) or knockdown (Sh-LOC100912399), alone or in combination with p38MAPK pathway inhibition or overexpression (Lv-p38MAPK), followed by exposure to oxidative stress for 48 h. Apoptosis was evaluated by Annexin V/PI staining, cell viability by CCK-8 assay, and gene expression by quantitative real-time PCR (qRT-PCR). Protein levels of oxidative stress-related enzymes (MnSOD, CAT, GPx), apoptosis-related factors (Bcl-2, Bax, p-p38MAPK), and osteogenic markers (RUNX2, OPN, ALP) were determined by Western blot. High-purity BMSCs (> 99%) were successfully isolated and characterized. Overexpression of LOC100912399 significantly promoted oxidative stress-induced apoptosis, reduced cell viability, downregulated antioxidant enzyme expression, increased the Bax/Bcl-2 ratio, and inhibited osteogenic differentiation ( P < 0.05). Conversely, knockdown of LOC100912399 enhanced antioxidant capacity, suppressed apoptosis, and upregulated osteogenic marker expression ( P < 0.05). These effects were further modulated by either p38MAPK overexpression or inhibition, indicating that LOC100912399 functions, at least in part, through the p38MAPK signaling pathway. LOC100912399 regulates oxidative stress and apoptosis in BMSCs via the p38MAPK signaling pathway, thereby influencing osteogenic differentiation. Targeting LOC100912399 may represent a potential therapeutic strategy for enhancing bone formation under oxidative stress-related conditions such as osteoporosis.
Evidence of Two-Dimensional Porous Ice at Room Temperature
TNF alpha unmasks enteric malate aspartate shuttle dysfunction bridging Parkinson disease and intestinal inflammation
Abstract Gastrointestinal dysfunction often precedes motor symptoms in Parkinson’s disease (PD), suggesting the enteric nervous system (ENS) is central to early pathogenesis. How α-synuclein contributes to ENS dysfunction, and how inflammation modulates this, remains unclear. Here we show that Tumor Necrosis Factor alpha enhances α-synuclein accumulation in induced pluripotent stem cell-derived enteric neurons and glia, and impairs the malate-aspartate shuttle, a key pathway for mitochondrial energy production. This drives a metabolic shift toward glutamine oxidation in patient cells. This metabolic impairment reduces overall mitochondrial function, which is partially rescued by the neuroprotective compound Chicago-Sky-Blue 6B. Furthermore, transcriptomic and histological analyses of human gut tissue from inflammatory bowel disease patients reveal that inflammation-associated metabolic suppression and α-synuclein upregulation occur beyond PD, representing general hallmarks of intestinal inflammation. These findings highlight a conserved metabolic vulnerability in the ENS and establish patient-derived enteric lineages as a robust platform to model inflammatory ENS pathology.
Altered benzo[a]pyrene adduct formation in nucleosomes establishes distinct mutational patterns in lung cancer
Particle dissolution rate controls macrophage response and drug release from mesoporous silica inhalation carriers
Abstract Mesoporous silica particles (MSPs) are promising micronized carriers for pulmonary drug delivery, combining excellent aerodynamic properties with the ability to dissolve into nanoparticles in lung fluid, enabling intracellular drug transport. In this study, we evaluated the interactions between three MSPs with distinct dissolution profiles in lung fluid and human macrophage models (primary M1, M2, and dTHP-1 cells). Following 4-hour exposure, all MSPs maintained high mitochondrial activity above the IC 50 threshold, regardless of concentration, up to 1 mg/mL. MSPs did not induce TNF-α release, indicating a minimal immunological response. However, in simulated lung fluid, MSPs dissolved into nanoparticles exhibited greater toxicity than their microparticle counterparts. Toxicity correlated with dissolution rate: faster-dissolving particles were more toxic at short exposure times, while all MSPs reached similar toxicity levels after 24 h, independent of medium composition. Albumin, the predominant lung fluid protein, was found to mitigate particle toxicity, enhancing biocompatibility. Drug release studies revealed that faster-dissolving particles produced a rapid but unstable supersaturated drug solution, whereas slower-dissolving particles offered a more sustained release profile, supporting its potential for prolonged pulmonary therapy. The lowest observed adverse effect level (LOAEL) in vitro was determined to be 0.06 mg/mL for all the MSPs. This concentration maintained mitochondrial activity, oxidative stress and cell membrane integrity above 70%. These findings highlight the translational potential of MSPs as dual-scale carriers for targeted pulmonary delivery, combining effective drug release with favorable safety profiles.
Reentrant superconductivity in a naturally occurring Josephson junction array tuned by radio-frequency power
Roads and detours for CAR T cell therapy in autoimmune diseases
Mechanistic insights into Na+ pumping by KR2: Distinct roles of Asp102 and Asn112 coupled with retinal distortion in two O intermediates
Comparative analysis of compressible solver schemes for underexpanded jet aerodynamics with Schlieren validation
Abstract The accurate prediction of compressible high-speed jet flows remains a critical challenge in computational aerodynamics due to the strong coupling between shock waves, expansion fans, shear-layer turbulence, and mixing processes downstream of nozzles. While density-based (DB) solvers are conventionally used for supersonic and transonic regimes, pressure-based (PB) solvers have recently gained attention for their reduced computational cost; however, their suitability for underexpanded jet modeling remains insufficiently explored. This study provides a systematic evaluation of PB and DB solvers available in ANSYS Fluent for simulating compressible flow discharged from an axisymmetric convergent nozzle over a range of nozzle pressure ratios (PR = 1.92–5). Experimental Schlieren flow visualization was conducted using a custom optical setup to qualitatively assess shock structures and validate near-field flow features. Numerical simulations employed compressible Reynolds Average Navier-Stokes (RANS) formulations with a standard k–ε turbulence model, structured quadrilateral meshes, and consistent boundary conditions for both solvers. Validation against published measurements demonstrated that both solvers accurately predict Mach disk formation and the streamwise location of the first shock cell, with a maximum deviation of 4.5% in peak Mach number. For PR > 1.92, both solvers captured the characteristic diamond shock pattern and the progressive increase in shock cell strength and spacing; the first shock cell occurred at X/De ≈ 1.09, 1.57, and 2 for PR = 3, 4, and 5, respectively. While PB and DB solvers exhibited comparable performance in resolving centerline Mach number and pressure oscillations, the DB solver overpredicted turbulent kinetic energy in the far-field subsonic region due to its known sensitivity at low Mach numbers. Discharge coefficients predicted by both solvers showed close agreement, with differences < 0.2%. Results demonstrate that the PB solver, despite being traditionally associated with incompressible and low-speed flows, can reliably model underexpanded supersonic jets at significantly reduced numerical cost. The findings provide practical guidance for CFD practitioners seeking cost-effective tools for compressible nozzle flow modeling and contribute to broader discussions on solver strategy selection for high-speed aerodynamic simulations.