Biology subjects

Liu, X.

Publications and source records attributed to Liu, X..

At least 433 records · Page 24Linked to original sources

bioRxiv2025

Multi-omics evaluation of cell lines as models for metastatic prostate cancer

Cell lines are indispensable tools in prostate cancer research yet their suitability as models for distance metastasis remains incompletely characterized. Here, we conduct a systematic evaluation study using large-scale public multi-omics data. We reveal substantial genomic differences between cell lines and metastatic patient samples, and meanwhile pinpoint cell lines which more closely resemble metastatic prostate cancer. Notably, hypermutation significantly influences the tumor microenvironment, underscoring the importance of considering mutational burden in model selection. Surprisingly, the widely used PC3 cell line exhibits poor transcriptomic similarity to any prostate cancer subtype, revealing a previously unrecognized limitation. Furthermore, we find existing engineered stem-like cell lines fail to faithfully recapitulate the transcriptomic profiles of mesenchymal stem-like prostate cancer, whereas selected organoids exhibit higher fidelity. Our study provides guidance for cell line selection in metastatic prostate cancer research and highlights the urgent need to develop improved cell lines for the mesenchymal stem-like subtype.

bioinformatics↗

bioRxiv2025

AtlasAgent: Vision language model and Agent-guided Framework for Evaluation of Atlas-scale Single-cell Integration

As single-cell omics transitions into the era of AI-virtual cells (AIVC), where large-scale single-cell data integration becomes prevalent, the computational demands of integration evaluation emerge as critical scalability bottlenecks. Traditional integration evaluation pipelines, requiring metrics like k-nearest-neighbor batch effect test (kBET) and Local Inverse Simpsons Index (iLISI) employed by state-of-the-art scIB method, often demand large computational resources and long runtimes, making them infeasible for large scale integration studies. Herein, we present AtlasAgent, the first vision-language model (VLM)-powered and AI agent framework to accelerate atlas-scale integration evaluation at unprecedented speed and scale. We systematically evaluate batch correction quality, biological signal preservation and overcorrection risks using chain-of-thought reasoning in conjunction with few-shot and zero-shot prompting strategies. AtlasAgent completes evaluation within 32 seconds, in contrast to scIBs runtime of 5.55 hours in GPU, while identifying the scIB-determint best integration methods within the top-3 in 88.3% of the time, lowering evaluation time from hours to seconds while preserving alignment with domain expert reasoning. AtlasAgent pioneers the use of VLMs to realize scalable and rapid integration evaluation at atlas scale.

bioinformatics↗

bioRxiv2025

Genome-Wide Investigation of Transcription Factor Occupancy and Dynamics Using cFOOT-seq

Gene regulation relies on the precise binding of transcription factors (TFs) at regulatory elements, but simultaneously detecting hundreds of TFs on chromatin is challenging. We developed cFOOT-seq, a cytosine deaminase-based TF footprinting assay, for high-resolution, quantitative genome-wide assessment of TF binding in both open and closed chromatin, even with small cell numbers. By utilizing the dsDNA deaminase SsdAtox, cFOOT-seq converts accessible cytosines to uracil while preserving genomic integrity, making it compatible with techniques like ATAC-seq for sensitive and cost-effective detection of TF occupancy at single-molecule and single-cell level. Our approach enables the delineation of TF footprints, quantification of occupancy, and examination of chromatin influences. Notably, cFOOT-seq, combined with FootTrack analysis, predicts TF occupancy dynamics. We demonstrate its application in capturing cell type-specific TFs, analyzing TF dynamics during reprogramming, and revealing TF dependencies on chromatin remodelers. Overall, cFOOT-seq represents a robust approach for investigating the genome-wide dynamics of TF occupancy and elucidating the cis-regulatory architecture underlying gene regulation.

molecular biology↗

bioRxiv2025

mTORC1-Dependent Regulation of the CCL24-CCR3 Axis Controls Granuloma Formation and Maintenance in Sarcoidosis

Sarcoidosis is a chronic granulomatous disease marked by persistent inflammation and immune cell aggregation, yet its molecular underpinnings remain incompletely understood, hindering the development of effective targeted therapies. Here, we report that deletion of TSC1 or TSC2 in mice using a Fsp1-Cre leads to spontaneous formation of sarcoid-like granulomas, driven by hyperactivation of the mTORC1 pathway in fibroblasts and interstitial macrophages. Through inflammatory cytokine/chemokine array, we identified CCL24, a chemokine ligand for CCR3, as a key immunoregulatory molecule downregulated in both our murine model and sarcoid cohort plasma. Mechanistically, mTORC1 suppresses CCL24 expression via aberrant STAT3 signaling in fibroblasts and promotes CCR3 expression in interstitial macrophages, uncovering a novel regulatory axis in granuloma formation and maintenance. Pharmacological inhibition using rapamycin and azithromycin markedly attenuated granuloma burden and normalized CCL24-CCR3 signaling, underscoring the therapeutic relevance of this axis. Together, our study establishes a mechanistic link between mTORC1 activation, CCL24-CCR3 dysregulation, and granuloma persistence, offering not only a new insight into molecular mechanisms in sarcoidosis but also identifying promising targets for clinical intervention.

immunology↗

bioRxiv2025

Cell-resolved high-dimensional imaging analysis, therapeutic modeling, and a Phase Ib clinical study validate BCL-2 as a target across heterogeneous CRPC subtypes

BCL-2 has been implicated in prostate cancer (PCa) progression and development of castration-resistant disease (CRPC). However, it remains unclear how the BCL-2- and AR-expressing PCa cell populations evolve across the PCa continuum, how AR molecularly regulates BCL-2 and whether BCL-2 represents a common therapeutic target in heterogeneous CRPC. Importantly, BCL-2 inhibitors have yet to be approved for treating PCa patients. Here we first show the selective induction of BCL-2 by AR pathway inhibitors (ARPIs) in both patient specimens and xenograft models. Vectra-based quantitative multiplex immunofluorescence (qmIF) and image mass cytometry (IMC) analyses with single-cell resolution reveal markedly expanded BCL-2+ (AR+ or AR-) PCa cell populations in CRPC. Mechanistically, AR represses BCL-2 transcription through genomic binding via several AR binding sites and ARPIs relieve this repression, leading to BCL-2 upregulation. Comprehensive therapeutic studies in cells, organoids and xenografts establish that castration-induced BCL-2 is not merely associated with resistance but represents a shared and actionable vulnerability as the BCL-2 inhibitor ABT-199 potently suppressed the growth of multiple subtypes of CRPC. A Phase Ib clinical trial (NCT03751436) combining enzalutamide and BCL-2 inhibitor venetoclax demonstrated reduced circulating tumor cells in responding patients. Together, our findings elucidate the AR+/-BCL-2+/- PCa cell subpopulation dynamics during PCa progression, reveal a direct mechanistic link between AR inhibition and BCL-2-mediated resistance, and provide a strong rationale for targeting BCL-2 from the outset to eliminate emerging resistant subpopulations, inhibit treatment-induced cellular heterogeneity and plasticity, and improve therapeutic outcomes in CRPC.

cancer biology↗

bioRxiv2025

The cryo-EM-delineated mechanism underlying mimicry of CXCR4 agonism enables widespread stem cell neuroprotection in a mouse model of ALS

G-protein coupled receptors (GPCRs) are transmembrane proteins that mediate a range of signaling functions and, therefore, offer targets for a number of therapeutic interventions. Chemokine receptor CXCR4, a GPCR, plays versatile roles in normal and abnormal physiological processes. Synthetic CXCR4 antagonists have been extensively studied and approved for the clinical treatment of cancer and other diseases. We recently elucidated the structural mechanisms underlying CXCR4 antagonism using cryogenic electron microscopy (cryo-EM). CXCR4 agonism by synthetic molecules is an unanticipated therapeutic intervention we recently unveiled. The structural mechanisms underlying those actions remain poorly understood yet could help elucidate a new class of drugs. Here we demonstrate a synthetic dual-moiety strategy that combines simplified agonistic and antagonistic moieties taken from natural agonistic and antagonistic chemokines, respectively, to design de novo peptide mimics of biological function of natural CXCR4 agonist SDF-1. Two peptides so generated, SDV1a and SDVX1 were shown to mimic the action of SDF-1 in activating CXCR4 signaling pathways and cell migration. The structural mechanism of these peptides in the mimicry of CXCR4 agonism was illustrated by cryo-EM structures of CXCR4 bound and activated by the peptides in the presence of G protein, revealing common interactions with the receptor by these peptides in comparison with SDF-1 that explain their close mimicry and conformational changes leading to CXCR4 signal activation. The therapeutic benefit of one of these peptides, SDV1a, was demonstrated in the SOD1G93A mouse model of the spinal motor neuron degenerative disease, amyotrophic lateral sclerosis (ALS) wherein the success of neuroprotective actions of transplanted human neural stem cells (hNSCs) is directly correlated with the expanse of diseased neuroaxis traversed by the donor cells; SDV1a enabled broader neuroprotective coverage while also permitting a much less invasive route of cell administration for extending life. Taken together, these results provide insights into the structural determinants of therapeutic CXCR4 agonism which may allow the design of adjunctive drugs that improve cell-based treatments of central nervous system (CNS) diseases.

neuroscience↗

bioRxiv2025

SMCHD1 compacts DNA directly in an ATP-regulated manner

Structural maintenance of chromosome (SMC) complexes play crucial roles in genome organization by DNA loop extrusion. SMCHD1 is a non-canonical SMC protein important for X-inactivation, imprinting and the silencing of specific autosomal genes. While it is known to be a repressor, little is known about its structure or mechanism of action. Here, we show that the SMCHD1 homodimer is flexible and dynamic in solution. This flexibility is conferred by its yet uncharacterized linker domain, which can alter its length by dynamically switching between compact and extended conformations. Interestingly, we observed that SMCHD1 can directly bridge and compact DNA, independently of other proteins, forming large protein-DNA clusters. SMCHD1 contains a GHKL ATPase domain and SMC hinge domain, however each domain alone is insufficient for DNA compaction. DNA compaction rate decreases when the linker domain is removed. The coiled-coil domain does not affect compaction rate but facilitates interaction with a partner protein LRIF1. Surprisingly, DNA compaction by SMCHD1 does not require ATP and paradoxically, compaction rate is reduced with the addition of ATP. Similarly, SMCHD1 forms clusters with reconstituted nucleosome arrays in the absence of ATP, and the addition of ATP results in a reduction in cluster sizes. Our data provides biophysical and mechanistic insights into the role of SMCHD1 in gene silencing and genome organization.

molecular biology↗

bioRxiv2025

Stage- and tissue-specific gene editing using 4-OHT inducible Cas9 in whole organism

Vertebrate genes usually function in specific tissues at specific stages, and thus their functional studies require conditional knockout or editing. In the zebrafish, spatiotemporally inducible genome editing, especially during early embryonic development, is still challenging. Here, we report inducible Cas9-based gene editing in specific cell types at desired stages in zebrafish. We show that the nCas9ERT2 fusion protein consisting of Cas9 and estrogen receptor flanked by two nuclear localization signals is normally located in the cytoplasm and efficiently translocated into the nucleus upon 4-hydroxytamoxifen (4-OHT) treatment in cultured cells or embryos. As a proof-of-concept, we demonstrate that target genes in primordial germ cells or germ cells of transgenic zebrafish embryos or adults with stable expression of nCas9ERT2 and gene-specific guide RNAs (gRNAs) can be induced to mutate by application of 4-OHT. This inducible nCas9ERT2 system also works in mouse early embryos. Thus, this inducible gene editing approach will be another choice for studying the temporospatial function of genes at the organismal level. Hence, the inducible nCas9ERT2 system expands the tissue- and stage-specific gene editing toolkit.

developmental biology↗

bioRxiv2025

MuSHIN: A multi-way SMILES-based hypergraph inference network for metabolic model reconstruction

Genome-scale metabolic models (GEMs) are indispensable tools for probing cellular metabolism, enabling predictions of metabolic fluxes, guiding strain optimization, and advancing biomedical research. However, their predictive capacity is often compromised by incomplete reaction networks, stemming from gaps in biochemical knowledge, annotation inaccuracies, and insufficient experimental validations. Here we present MuSHIN (Multi-way SMILES-based Hypergraph Interface Network), a novel deep hypergraph learning method that integrates network topology with biochemical domain knowledge to predict missing reactions in GEMs. Evaluated on 926 high- and intermediate-quality GEMs with artificially removed reactions, MuSHIN significantly outperforms state-of-the-art methods, achieving up to a 17% improvement across multiple metrics and maintaining robust recovery even under severe network sparsity. Furthermore, MuSHIN substantially enhances phenotypic predictions in 24 draft GEMs associated with fermentation by resolving critical metabolic gaps, as validated against experimental measurements. Together, these findings highlight MuSHINs potential to advance GEM reconstruction and accelerate discoveries in systems biology, metabolic engineering, and precision medicine.

bioinformatics↗

bioRxiv2025

Multi-omics characterization of the skin microbiota reveals the anti-aging roles of Stenotrophomonas maltophilia

Shifts in the skin microbiome have shown a close link to chronological age. However, the contribution of skin microbiome in skin aging phenotypes remains unclear. To explore this, we performed phenotypic, metabolomic, metagenomic, and functional analyses on a cohort with divergent skin aging phenotypes. Genome-scale metabolic models (GEMs) integrated with metabolomic analysis revealed that Stenotrophomonas maltophilia, enriched in the younger group (categorized by AI-predicted age and skin elasticity), utilizes the glutathione cycle to maintain redox homeostasis. Cellular experiments showed its metabolites enhanced GSH synthesis and alleviated oxidative stress-induced skin aging by upregulating key genes in fibroblasts, including GCLM, PGD, SOD2, and NQO1. Additionally, GEMs highlighted its potential anti-aging roles in regulating host metabolic pathways involving betaine, lysolecithin, and porphyrin. In parallel, Acinetobacter guillouiae was found to influence host melanin metabolism by degrading dopamine (DA) and 3-methoxytyramine (3-MT), offering potential therapeutic strategies for mitigating pigmentation. Our findings highlight the dynamic interplay between skin microbiota and the host in aging, offering new insights for designing targeted anti-aging interventions.

microbiology↗

bioRxiv2025

Neural Timescale of Adolescents Major Depressive Disorder

Adolescent major depressive disorder (MDD) is characterized by heterogeneous symptomatology and complex neurodevelopmental underpinnings. Here, we investigated whether cortical intrinsic neural timescales (INT)--a measure of temporal stability in neural activity--are altered in adolescents with MDD and whether these alterations relate to clinical symptoms, suicidality, early-life adversity, and underlying neurobiological mechanisms. Using resting-state fMRI in adolescents with MDD and healthy controls (HCs), we found widespread reductions in INT in frontal, parietal, and sensorimotor regions, with a notable prolongation in the left temporoparietal junction. Disrupted timescales significantly impaired network modularity and clustering, and SVR-based machine learning revealed that altered INT patterns predicted individual depression and anxiety severity. INT abnormalities were further associated with suicidal ideation and childhood trauma, particularly emotional and physical neglect. Biophysical modeling linked INT variations to local recurrent excitation and external input strength, differing between HCs and MDD. Spatial correlations with PET-derived neurotransmitter receptor maps demonstrated that INT alterations colocalize with serotonergic, dopaminergic, and cholinergic systems. Transcriptomic enrichment analysis revealed associations with genes involved in mitochondrial function, synaptic signaling, and metabolic regulation. Together, these findings identify neural timescale disruption as a core pathophysiological feature of adolescent MDD, bridging macroscale dynamics with microcircuit and molecular architecture. INT may serve as a promising biomarker and mechanistic target for precision psychiatry in youth depression.

neuroscience↗

bioRxiv2025

Interwoven DNA-MOF crystals for multi-millennial data storage

DNA has emerged as a promising medium for high-density and energy-efficient data storage, providing a promising solution to capacity constraints and energy demands resulting from the exponential growth of data. Long-term stable storage of DNA data in ambient conditions is a critical requirement for its practical application. Whereas strategies have been proposed to protect DNA from environmental degradation, they are often at the expense of data storage density. Here, we propose a strategy via interweaving metal-organic framework (MOF) and DNA to synthesize DNA-MOF crystal (DNA-MOF), a high-density and long-lifespan DNA-based information material. The uniform distribution of DNA molecules within the crystalline frameworks enables a high loading capacity of up to 30 wt%, corresponding to a theoretical information density of 106.6 exabytes/g. The crystal structure of MOF-DNA demonstrates efficient resistance to environmental damage such as heat, ultraviolet radiation, DNase, etc., achieving an estimated archival half-life over 24,000 years at 9.4 {degrees}C. The interwoven DNA-MOF crystals establish a material foundation for the reliable operation of DNA storage systems in open-field deployment and provide a new pathway toward sustainable long-term management of massive data.

biochemistry↗

bioRxiv2025

Activation of the impaired NAMPT/SIRT7/SOD2 axis restores alveolar progenitor cell homeostasis in idiopathic pulmonary fibrosis and reverses pulmonary fibrosis in mice

Alveolar type II (AT2) progenitor cell exhaustion and impaired regenerative capacity are key pathogenic hallmarks in idiopathic pulmonary fibrosis (IPF). Nicotinamide adenine dinucleotide (NAD+) functions as a central regulator of cellular energy metabolism. We have reported that downregulation of NAD+-dependent sirtuin signaling contributes to the impaired progenitor function of IPF AT2s. In this study, we identified that a key NAD+ biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT), is significantly downregulated in IPF AT2s. NAMPT deficiency impairs AT2 renewal and enhances lung fibrosis through downregulation of SIRT7 and SOD2, which results in increased oxidative stress, mitochondrial dysfunction, induction of pathological transitional gene expression and impaired regenerative capacity to generate alveolar type I (AT1) cell required for gas exchange. Mice with deletion of Nampt in AT2s showed severely impaired AT2 renewal and increased susceptibility to bleomycin lung injury and spontaneous fibrois. Activation of NAMPT by small molecule activators promoted AT2 renewal, restored homeostasis, and reversed lung fibrosis. NAMPT activation could be a therapeutic strategy for restoring AT2 progenitor function and halting or reversing progressive pulmonary fibrosis.

cell biology↗

bioRxiv2025

Spatio-temporal mass spectrometry in living cells reveals regulators of cuproptosis

Cuproptosis is a unique form of regulated cell death triggered by excessive copper accumulation in mitochondria. To decipher the mechanisms of cuproptosis, we develop Spatio-Temporal Mass Spectrometry (STMS) technique to characterize dynamic subcellular proteomic changes during its early stage. STMS analysis reveals distinct subcellular proteome alterations and unique trafficking patterns over time. Through a genetic functional screen, we discover that copper stress reduces OXA1L in mitochondria, disrupting MRPL20 import and impairing oxidative phosphorylation complex I synthesis. This mitochondrial dysfunction promotes MRPL20 nuclear translocation, triggering the mitochondrial unfolded protein response as an adaptive mechanism to restore mitochondrial proteostasis during early cuproptosis. Meanwhile, AMPK phosphorylates ISCU at serine 29, stabilizing ISCU protein, and increasing the abundance of Fe-S cluster-containing proteins, which, in turn, enhances cells susceptible to cuproptosis. Building on this mechanistic insight, we develop AMPK-SPARK, a phase separation-based EGFP reporter for real-time visualization of endogenous AMPK activity in living cells during cuproptosis. Additionally, we identify COMMD4 as a cuproptosis sensor and establish a GFP-tagged COMMD4 cell model for high-content drug screening. Using this platform, we identify three FDA-approved drugs including Plerixafor, Dithranol, and Bleomycin as potential cuproptosis inhibitors. Overall, our work advances the understanding of cuproptosis regulation and provides valuable molecular tools and data resource for future research in this area.

cell biology↗

bioRxiv2025

PCNA is a Nucleotide Exchange Factor for the Clamp Loader ATPase Complex

All life requires loading ring-shaped sliding clamp protein complexes onto DNA. The sliding clamp loader is a conserved AAA+ ATPase that binds the sliding clamp, opens the ring, and places it onto DNA. While recent structural work on both the canonical and alternative clamp loaders has shed light into how these machines perform their task once, it remains unclear how clamp loaders are recycled to load multiple sliding clamps. Here, we present structures of the Saccharomyces cerevisiae clamp loader Replication Factor C (RFC) in absence of sliding clamp or supplemented nucleotide. Our structures indicate that RFC holds onto ADP tightly in at least two of its four ATPase active sites, suggesting that nucleotide exchange is regulated. Our molecular dynamics simulations and biochemical data indicate that binding of the sliding clamp PCNA causes rapid exchange of tightly bound ADP. Our data suggests that PCNA acts as a nucleotide exchange factor by prying apart adjacent subunits, providing a pathway for ADP release. We propose that, by using its own substrate as a nucleotide exchange factor, RFC excludes off-pathway states that would arise from binding DNA prior to PCNA.

biochemistry↗

bioRxiv2025

Structure and iron-transporting mechanism of brain organic cation transporter 1

Brain organic cation transporter 1 (BOCT1), also known as the solute carrier family 22 member 17 (SLC22A17) or the receptor for lipocalin-2 (LCN2), plays critical roles in health and disease. Its deficiency in mice results in early postnatal mortality and severe neurogenesis impairments. Despite its importance in physiology and pathophysiology, BOCT1s structure and transport mechanism remain elusive. Here, we integrate cryo-electron microscopy (cryo-EM), functional assays, biochemical experiments, and molecular dynamics simulations to elucidate the structure, substrate recognition, and transport mechanism of mouse BOCT1 (mBOCT1). The high-resolution cryo-EM structure reveals a distinctive N-terminal domain with a unique folding pattern dominated by a transmembrane loop atop TM6 (TML6), diverging from both known structures of SLC22 transporters and AlphaFold predictions. Notably, mBOCT1 functions as a high-capacity, low-affinity iron transporter independent of LCN2 binding. Iron transport is facilitated by a substrate gating mechanism involving TML6. These findings establish a structural basis for BOCT1s role as an independent iron transporter, enhancing our understanding of the transport mechanisms within major facilitator superfamily (MFS) transporters and providing new insights into brain iron homeostasis.

biophysics↗

bioRxiv2025

Molecular mechanisms of 10-Butyl Ether Minocycline (BEM), a novel non-antibiotic tetracycline, as a potential treatment for inflammatory and neuroimmune-related disorders.

The pleiotropy of minocycline (MINO), including anti-inflammatory, antioxidant, anti-migratory, anti-MMP, and neuroprotective effects, has been extensively reported. A novel non-antibiotic minocycline derivative, 10-butyl ether minocycline (BEM), was synthesized to retain the pleiotropy of minocycline while minimizing side effects such as antibiotic resistance and gut dysbiosis. Previously, we showed that BEM reduced alcohol consumption in dependent murine and porcine models of Alcohol Use Disorder (AUD). In this study, we investigated the molecular mechanisms of BEM to determine its potential as a therapeutic agent for neuroimmune and inflammatory conditions such as AUD. Here, we report that BEM showed a nearly complete loss of antimicrobial activity against E. coli, S. typhi, and C. albicans. BEM showed a dose-dependent reduction in cell viability as measured by the MTT assay, similarly to MINO. BEM also suppressed LPS-induced microglial activation as shown by reduced Iba1 expression in immunohistochemistry and western blot analyses. Inhibition of MMP-9 by BEM (IC50 = 42.2 {micro}M) was improved compared to MINO (IC50 = 60.3 {micro}M) while MMP-8 inhibition was moderate (IC50: BEM = 69.4 {micro}M; MINO = 45.4 {micro}M). BEM was found to be effective in inhibiting VEGF-induced endothelial cell migration and L-glutamine-induced ROS levels. Limited inhibition of 15-LOX activity was observed (IC50: BEM = 92.6 {micro}M; MINO = 65.6 {micro}M). BEM was not toxic to mitochondria, even at high concentrations (200 {micro}M). By eliminating antimicrobial properties while preserving therapeutic pleiotropy, BEM presents an advancement in the development of a promising candidate with multimodal mechanisms to treat neuroimmune-inflammatory pathologies. ImpactOur current approach to correlate non-antibacterial actions of BEM to MINOs established mechanistic effects will enable the informed use of BEM for several medical indications including for inflammation and neuroimmune conditions. The focus on BEMs multimodal actions and long-term safety during drug discovery represents a paradigm shift toward complex therapeutic drug development and repositioning, improving upon traditional singular high-affinity target-based approaches. Such new drug discovery attempts could potentially enhance treatment relevance in complex disorders with multiple targets and theoretically guide the creation of second-generation analogs. Significance statementWe report mechanisms of action for BEM, a minocycline analog under evaluation for the treatment of Alcohol Use Disorder, which may also show efficacy for other complex disease processes that involve inflammatory or neuroimmune components. We show that BEM had a nearly complete loss of antimicrobial action, yet retained the pleiotropy of MINO, likely making it a better multimodal therapeutic for long-term treatment of complex diseases with neuroimmune-related components. Visual abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=120 SRC="FIGDIR/small/661183v3_ufig1.gif" ALT="Figure 1"> View larger version (54K): org.highwire.dtl.DTLVardef@1ade11corg.highwire.dtl.DTLVardef@961d1borg.highwire.dtl.DTLVardef@15101f8org.highwire.dtl.DTLVardef@158810e_HPS_FORMAT_FIGEXP M_FIG C_FIG

pharmacology and toxicology↗

bioRxiv2025

Simulation and experimental study on the strategy of soil auxiliary heating in a solar greenhouse in northeast China

When solar greenhouses in north eastern China experience extreme weather, the internal soil requires varying auxiliary heating to ensure the normal growth of crops. In this study, considering the effects of four kinds of extreme weather on solar greenhouses, four different types of heating requirements were obtained through experiences in a Liaoshen-type solar greenhouse. Four distinct heating strategies were simulated using a soil temperature prediction model. The initial temperatures for these strategies were 13{degrees}C, 11{degrees}C, 13{degrees}C, and 14{degrees}C, respectively, while the target temperature was uniformly set at 15{degrees}C. The heating durations for the respective strategies were 432,000 seconds, 432,000 seconds, 864,000 seconds, and 1,728,000 seconds. To ensure a minimum soil temperature of 15{degrees}C within the solar greenhouse, the temperature of the heating layer located 400 mm underground needed to be maintained at or above 20{degrees}C, 28{degrees}C, 18{degrees}C, and 19{degrees}C, respectively. The simulation results were validated through experimental verification, with maximum and minimum errors of 3.1% and 0.5%, respectively. Several targeted promotional suggestions were also proposed. The model exhibited high accuracy and is capable of developing optimal and precise soil heating strategies for various types of solar greenhouses in north eastern China.

plant biology↗