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Hydrodynamic dispersion drives viral–cellular contact for gene delivery in porous media
Reactive biological processes often hinge on rare collisions between particles whose transport is governed by disparate advective, diffusive, and sedimentary mechanisms. Biological cell–virus encounters offer a uniquely quantifiable instance of this general problem: collisions between particles whose transport is governed by entirely different physical mechanisms, yet whose interactions determine system-level function. In stagnant liquids, nanoscale viral vectors explore space only via slow Brownian diffusion, whereas microscale cells rapidly sediment, producing species separation that suppresses virus-cell interfacial interactions. Here we show that liquid absorption into a dry, macroporous sponge enhances viral–cellular interactions by shifting the system into an advection-dispersion regime that circumvents this sedimentation-diffusion limit. By integrating experimental results with a multiscale simulation model, we demonstrate that the tortuous sponge porosity converts capillary-driven flow into convective mixing, driving orders-of-magnitude increases in viral–cellular collision rates. Coupling these dispersive transport dynamics with a probabilistic capture model reveals that hydrodynamic dispersion accounts for the multifold enhancement in viral–cellular transduction efficiency observed in porous sponges. These results provide a quantitative framework for emergent collision dynamics in complex porous media and establish a generalizable strategy to optimize active transport in spatiotemporally heterogeneous biological systems.
Edge-intelligent vision-based robotic manipulation for real-time pick-and-place in dynamic industrial environments
Correction for Chang et al., Plant pathogenic nematode exosomes remodel vector tracheae to enhance pathogen transmission
Development and validation of a nomogram for predicting the prognosis of lung cancer patients with brain metastases harboring EGFR or ALK mutations: a multicenter retrospective study
Mitofusin-2 in ventral striatal D1 neurons regulates effort-based motivation through sex-specific mitochondrial–synaptic reprogramming
Effort-based motivation varies widely across individuals and affects well-being, yet the molecular and neuronal mechanisms that set motivational capacity remain incompletely understood. Mitochondrial function is emerging as a critical regulator of behavior, and mitofusin-2 (MFN2) is a key mediator of mitochondrial fusion and endoplasmic reticulum–mitochondria coupling. Here, we asked how downregulation of Mfn2 in dopamine receptor type-1-expressing medium spiny neurons (D1-MSNs) contributes to effort-based motivation and stress coping in male and female mice by integrating electrophysiology, neuronal and synaptic morphology, immunohistochemistry, mitochondrial readouts, RNA in situ hybridization, RiboTag, and behavioral analyses. MFN2 deficiency resulted in fragmented dendritic mitochondria and remodeled synaptic inputs in ventral striatal D1-MSNs, with no cellular impact in dorsomedial striatal D1-MSNs. Although MFN2 deficiency elicited sex-dependent synaptic and structural alterations, both sexes showed reduced recruitment of accumbal D1-MSNs during motivated behavior and impaired effort-based motivation and stress coping. Translatome profiling revealed shared depletion of mitochondrial pathways in both sexes, with more pronounced suppression of oxidative phosphorylation and TCA cycle programs in males. Strikingly, only males also exhibited coordinated downregulation of ribosomal programs together with enrichment of synaptic pathways, with high representation of genes regulating glutamate receptor cycling and PSD remodeling, providing a mechanistic framework for the observed synaptic alterations. Pathway-level network inference further supported coupling among mitochondrial, translational, and synaptic programs in males. These findings identify MFN2-dependent mitochondrial integrity in ventral striatal D1-MSNs as a critical determinant of motivational capacity and reveal sex-specific molecular and cellular responses through which mitochondrial dysfunction converges on similar motivational deficits.
Performance evaluation and optimization of powder mixed EDM of Inconel 718 using composite electrodes and the VIKOR method
A population of primary afferent sensory neurons mediates pain relief through nocifensive coping behavior in mice
When exposed to noxious cutaneous stimuli, animals exhibit nocifensive behaviors, including rapid defensive reflexes that limit tissue damage and subsequent coping behaviors—most commonly licking of the affected area—that alleviate pain. Despite its ubiquity, the neural mechanism underlying pain relief through licking remains poorly understood. Here, we demonstrate that Npy2r-Cre + primary sensory neurons in the dorsal root ganglion (DRG), a population of Aβ fibers that includes touch-sensitive, rapidly adapting low-threshold mechanoreceptors, are critical for this process. Mice lacking Npy2r-Cre + neurons exhibited a significant prolongation of coping behavior duration, but not bout frequency, following intraplantar injection of capsaicin or formalin. Conversely, optogenetic activation of Npy2r-Cre + neurons produced attenuating effects on irritant-induced pain. Electrophysiological analyses revealed that Npy2r-Cre + neurons form functional synaptic connections with neurons in the substantia gelatinosa of the spinal dorsal horn (SDH) and that their activation suppressed C fiber-evoked excitation of neurons in lamina I of the SDH, a region implicated in nociceptive transmission to the brain. Together, these findings identify Npy2r-Cre + DRG neurons as a key neural substrate for gating nociceptive transmission in the SDH and mediating pain relief through coping behaviors.
Disease-specific quality of life and associated health outcomes among children with diabetes in Khartoum state, sudan: a cross-sectional study
Correction for Cao et al., Cenozoic geoclimatic changes drove the evolutionary dynamics of floristic endemism on the Qinghai–Tibet Plateau
Cytochrome b gene heteroplasmy associated with QoI fungicide resistance in Venturia inaequalis populations from Northwestern Himalayas
Divergent philosophical commitments in neuroscience: Evidence from a global survey
The mind–brain relationship is a foundational yet underexplored dimension of contemporary neuroscience, shaping research framing, data interpretation, and public communication. We conducted a large-scale international survey of 2,657 neuroscientists to assess their views on the mind–brain problem, free will, and the future of the discipline. Our results reveal a complex and sometimes paradoxical worldview. While 64% of participants endorse reductive physicalism—the view that mental activity is fully reducible to brain function—only 17.5% reject free will. Despite estimating that current knowledge covers only a limited portion of brain structure and function (30%), respondents express marked optimism about the future of neuroscience, including the prospect of fully understanding the human being and mental disorders through neuroscience, and even achieving mind reading and mental uploading. A principal component analysis identified five latent dimensions, some of which vary systematically across sociodemographic and disciplinary factors. These findings indicate that neuroscientists hold diverse philosophical commitments that diverge from common narratives of hard determinism. The prevalence of neuroessentialist views further highlights the need for sustained interdisciplinary dialogue to address the conceptual, ethical, and societal implications of neuroscientific progress.
Physicochemical analysis and comparative toxicity of Juniperus phoenicea L. essential oil against Planococcus citri and Planococcus ficus
Endosomal TPC1–mediated Ca <sup>2+</sup> nanodomains regulate transferrin receptor trafficking and iron homeostasis
Two-pore channel 1 (TPC1) is an endosomal Na + /Ca 2+ -selective channel implicated in membrane trafficking, endosome tubulation, and excitability, but how TPC1 regulates membrane trafficking is unknown. Using TPC1-null human cells, we demonstrate that TPC1 drives transferrin receptor (TfR) trafficking and recycling via Ca 2+ , and not Na + fluxes or endosomal pH changes, since channel-targeted Ca 2+ -buffers inhibited trafficking, whereas a Na + -deficient Ca 2+ -permeable TPC1 mutant fully supported trafficking. TPC1 was unique since other Ca 2+ sources did not support TfR trafficking. TPC1 activity depended on the lipid PI(3,5)P 2 , since trafficking was impaired by a lipid-insensitive TPC1 or inhibitors of lipid synthesis. Finally, a corollary of this reduced TfR trafficking is an iron-deficiency and storage phenotype in TPC1-deficient HeLa cells and mice. Our findings highlight endosomes as unique Ca 2+ stores mobilized by a phosphoinositide-induced TPC1 channel that generates local Ca 2+ nanodomains crucial for maintaining TfR trafficking and consequent iron homeostasis.
Deterioration behavior and model of alkali-activated fly ash-slag concrete under freeze–thaw cycles
Abstract Concrete components in highways and bridges are susceptible to freeze–thaw deterioration in cold regions, compromising their service safety. Alkali-activated fly ash-slag concrete (AAFSC), which fully replaces Portland cement with industrial by-products, offers promising environmental and application benefits. However, research on its freeze–thaw damage remains limited, hindering its use in cold-region infrastructure. This study presents a systematic experimental and theoretical investigation into the freeze–thaw deterioration of AAFSC. For the first time, the damage process is described within the Kachanov–Rabotnov evolution framework, establishing an exponential damage model with well-defined physical boundary conditions—extending continuum damage mechanics to freeze–thaw action in concrete. The model quantitatively captures damage progression in AAFSC and demonstrates broad applicability across various concrete types reported in the literature. This work provides important guidance for predicting the freeze–thaw durability of AAFSC-based transportation infrastructure components in cold regions.
Artistic visions shape and respond to Mars missions
COVLIAS 3.5: integration of attention-based segmentation technique with fuzzy dilated convolutional neural networks for improved classification of chest X-ray scans for multiclass pneumonia diagnosis
Abstract This study aims to improve pneumonia diagnosis by integrating attention-based U-Net models for lung segmentation with fuzzy logic-enhanced CNNs for classification. This approach addresses the limitations of inadequate modelling of complex spatial relationships in medical images. The underutilization of fuzzy logic with dilated convolutions has restricted the extraction of multiscale features. We utilized 18,608 chest X-ray (CXR) images. Subsequently, these images were segmented using four models namely: U-Net, Attention U-Net, Pruned U-Net and U-Net++. Fuzzy logic system was used to process the segmented data. Additionally, we show that the dilated CNN architecture for improved classification performance. In lung segmentation, our experimental results indicate that Attention U-Net (AU) achieved 1% better mean accuracy, 2% better mean Jaccard and Dice than U-Net, pruned U-Net and U-Net++. In the classification, the model has demonstrated 10% better mean accuracy over augmented U-Net and Attention U-Net based segmented data. ROCs have shown that augmented effect has 15% better AUC in bacterial pneumonia class. Additionally, we saw a 4% improvement with fuzzy logic. The integration of fuzzy dilated CNN with Attention U-Net segmentation presents a 1% better accuracy compared to U-Net. Best AUC achieved was 0.98 in bacterial pneumonia. Our findings underscore the critical role of attention mechanisms and augmentation in enhancing medical image analysis. The integration of Attention U-Net for segmentation and fuzzy dilated CNN for multi-class classification significantly improves diagnostic accuracy and reliability. This approach has the potential to revolutionize pneumonia diagnosis, leading to better patient outcomes and more efficient healthcare delivery.
Hydration and hydrolysis define antibiotic resistance conferred by macrolide esterases
Macrolides are an antibiotic class widely used in both human and veterinary medicine, and function by interfering with protein synthesis. Regrettably, numerous strategies for evading the antibiotic properties of macrolides have been found in bacteria, including enzyme-mediated inactivation. These mechanisms are now widely disseminated among pathogenic, animal-associated, and environmental bacteria making them a One Health issue. Macrolide esterases, which hydrolyze the macrolactone’s ester bond, confer one such resistance mechanism. Two types of macrolide esterases have thus far been identified, the well-studied erythromycin esterases and the recently discovered Est-type enzymes that belong to the α/β-hydrolase superfamily. We present detailed structure–function studies for four diverse Est type esterases: which only share 44 to 66% sequence identity (EstT Sf , EstT St , EstT Bc , and EstX Ec ). In addition to resistance profiling and substrate specificity studies, we present structures for all four enzymes, including structures for EstT Bc and EstX Ec in complex with tylosin and tylvalosin macrolides, posthydrolysis. Complementing the data with mutational and kinetic studies allowed for a detailed analysis of the structural basis for macrolide–enzyme interactions. Combined, the data suggest that promiscuous binding and imprecise positioning, mediated by a water-cage, dictate substrate specificity for Est-type macrolide resistance enzymes. These insights may prove beneficial for next-generation antibiotic development.
Genomic surveillance of multidrug-resistant Enterobacterales in a long-term care facility in Northern Italy based on a point prevalence screening
Homer condensates orchestrate YAP–Wnt signaling crosstalk downstream of the Crumbs polarity complex
The Hippo pathway governs cell growth, proliferation, and differentiation and is frequently deregulated in cancer. Yes-associated protein (YAP) is the central transcriptional coactivator of the Hippo pathway and interacts with β-catenin to coordinate YAP–Wnt signaling crosstalk. Both pathways are modulated by diverse upstream signals including mechanical cues, cell density, and cell polarity, yet how such signals are integrated remains poorly understood. Here, we demonstrate that Homer scaffolding proteins coordinate YAP and Wnt signaling downstream of the Crumbs polarity complex. Homers interact directly via their EVH1 domains with the Crumbs component PATJ and the NDR kinase scaffold Furry-like (FRYL). Homers antagonize FRYL to promote YAP activation while cooperating with FRYL to enhance Wnt/β-catenin signaling, revealing pathway-selective regulation. PATJ, in contrast, recruits Homers to the cortex and restrains YAP activity. We further show that Homers form biomolecular condensates in nonpolarized epithelial and colorectal cancer cells, whose assembly and signaling properties are differentially modulated by PATJ and FRYL. Whereas FRYL promotes the formation of cytoplasmic droplets, PATJ drives the assembly of phase-separated compartments at or near the plasma membrane. Collectively, our findings establish Homer-driven phase separation as a tunable signaling mechanism to translate polarity cues into transcriptional output.