Biology subjects

Ge, Q.

Publications and source records attributed to Ge, Q..

At least 19 recordsLinked to original sources

bioRxiv2026

Eleven deep-sea coral genome assemblies unveil insights into evolution, adaptation, and coral biodiversity

Deep-sea corals are vital in maintaining coral ecosystem biodiversity, yet their genetic characteristics remain largely unexplored. Here, we present 11 deep-sea coral genome assemblies, including four Hexacorallia and seven Octocorallia species, significantly contributing new genomic information across two orders. Our analysis reveals the historical dynamics of coral speciation and the influence of environmental factors on the evolution of coral reef ecosystems.Total of 126 horizontal gene transfer (HGT) events were detected, among which genes from the ancestor of symbiodiniaceae indicate that the ancestors of deep-sea corals may have inhabited shallow-sea environments. Notably, several of these HGTs are involved in phosphorus (PhnX/PhnW) and cholesterol (DHCR7) metabolisms within corals, indicating that HGTs may serve as an adaptive survival strategy for the coral holobionts. Deep-sea corals also rely on symbiotic bacteria to synthesize 10 essential amino acids (such as valine and tyrosine), retaining only partial amino acid synthesis capacity. In addition, we investigated the evolution of key biological rhythm genes and temperature adaptation in corals. The loss of key rhythm genes (e.g., clock and cry) in deep-sea corals and copy number difference of genes related to heat stress (e.g., Cbl-b and Rchy) revealed genetic difference between deep-sea and shallow-sea corals. Our new genome assemblies enhance the understanding of deep-sea coral evolution, biodiversity, and adaptation, providing a genetic foundation for coral conservation.

genomics↗

bioRxiv2026

Beyond Glycogen Storage: AMPKγ2 Regulates Cardiac Hypertrophy and Electrophysiology via Myosin Interaction

IntroductionVariants in PRKAG2 cause hypertrophic cardiomyopathy (HCM) and conduction disturbances. While prior studies associated PRKAG2-related hypertrophy with increased glycogen storage, many HCM phenotypes remain unexplained. We aimed to uncover how PRKAG2 variants induce myocyte hypertrophy and electrical changes during early cardiac development. MethodsWe generated transgenic zebrafish expressing wild-type (TgWT) or pathogenic variant (TgR299Q) Prkag2 cDNA under a myocardium-specific promoter, and examined cardiac electrophysiology, contractile function, and cytoarchitecture during cardiogenesis and in adult hearts. ResultsTgR299Q fish showed hypertrophic cardiomyocytes and progressive contractile abnormalities, recapitulating human HCM phenotypes. Cardiomyocyte glycogen was elevated in adult but not embryonic hearts. Despite the absence of glycogen accumulation at 6-day post-fertilization, TgR299Q hearts showed electrical abnormalities, including reduced conduction velocity and prolonged action potential and Ca2+ transient durations. We observed decreased AMPK phosphorylation in the TgR299Q hearts. However, AMPK activation did not rescue the electrophysiological abnormalities in TgR299Q. Proximity ligation assays and co-immunoprecipitation identified a physical interaction between AMPK{gamma}2 and myosin, enhanced by the R299Q variant and accompanied by increased AMPK{gamma}2 localization to the myofilament. Na/Ca{superscript 2} exchanger (NCX) inhibition increased Ca2+ duration and diastolic Ca2+ in TgWT but not TgR299Q hearts, indicating reduced free cytosolic Ca2+ for NCX-mediated extrusion in TgR299Q. These findings suggest that enhanced AMPK{gamma}2-myosin interaction may promote myofilament Ca{superscript 2} retention, thereby prolonging Ca{superscript 2} transient duration and APD in the mutant. Notably, the myosin inhibitor mavacamten reduced AMPK{gamma}2-myosin interaction in TgR299Q hearts, and both mavacamten and vmhcl knockdown rescued the early electrophysiological abnormalities. ConclusionsThe PRKAG2 variant altered cardiac excitability, contractility, and Ca2+ handling during cardiogenesis, independent of glycogen accumulation. Enhanced interactions between AMPK{gamma}2 and myosin contributed to these early changes. Our study revealed a novel link between cellular energy sensing and contractile machinery, with therapeutic potential for modulating contractile function in cardiomyopathies.

physiology↗

bioRxiv2025

The biochemical nature of senile plaques: intracellular destabilized-lysosome-enriched neural processes catabolizing extracellular hemorrhagic amyloid materials

The pathological mechanism of senile plaque formation in Alzheimers disease remains a challenging unresolved problem for over one hundred years. In this study, we investigated senile plaque pathogenesis based on immunohistochemistry, fluorescence imaging and quantitative analysis of AD front brain sections with multiple senile plaque related markers such as A{beta}, MAP2, phos-Tau, Cathepsin D, Sortilin 1, Ceruloplasmin and Hemin. Firstly, we confirmed that senile plaque A{beta} deposition mostly happened in MAP2-positive but degenerative neuritic processes. Secondly, we found an interesting dual-component granular or diffusive staining pattern of all of these senile plaque related markers, matching to two states of lysosomes, relatively-stable granule lysosomes and destabilized diffusive lysosomes as shown by lysosome-related marker Cathepsin D or Sortilin 1 staining. Thirdly, dystrophic senile plaque neural processes contain hemorrhage-related markers such as Ceruloplasmin and Hemin. In addition, A{beta} deposition, Tau phosphorylation, lysosome destabilization are all enriched at the sites of microaneurysm formation. Moreover, senile plaques are also characterized by a widespread binary phos-Tau staining pattern with difference in term of staining intensity. We concluded that senile plaques are formed by destabilized-lysosome-enriched neural processes catabolizing extracellular hemorrhagic amyloid materials, with microaneurysm as an important intermediate stage.

cell biology↗

bioRxiv2025

Divergent Neurobehavioral Effects of CFTR Modulators Elexacaftor and Ivacaftor in Mice

Recent advances in cystic fibrosis transmembrane conductance regulator (CFTR) modulator combination therapies have markedly improved survival and quality of life for people with cystic fibrosis (CF). Among these, the elexacaftor-tezacaftor-ivacaftor combination (Trikafta) and its updated formulation, vanzacaftor-tezacaftor-deutivacaftor (Alyftrek), represent major therapeutic milestones. However, emerging reports suggest that Trikafta may contribute to anxiety and depression in some people with CF. In this study, we investigated the neurobehavioral effects of elexacaftor and ivacaftor in mice. Acute administration of elexacaftor elicited anxiety-like behavior, while ivacaftor induced depressive-like behavior. Additionally, we confirmed the presence of Cftr mRNA in the amygdala and hippocampus, brain regions implicated in anxiety and depression. These findings provide preclinical support for the reported mental health side effects experienced by some people with CF and offer new insights into CFTR function within the central nervous system, potentially guiding the development of future CF therapies with improved neuropsychiatric profiles.

physiology↗

bioRxiv2024

Multimodal single-cell analyses reveal molecular markers of neuronal senescence in human drug-resistant epilepsy

The histopathological neurons in the brain tissue of drug-resistant epilepsy exhibit aberrant cytoarchitecture and imbalanced synaptic circuit function. However, the gene expression changes of these neurons remain unknown, making it difficult for the diagnosis or to dissect the mechanism of drug-resistant epilepsy. By integrating whole-cell patch clamp recording and single-cell RNA sequencing approaches, we identified a transcriptionally distinct subset of cortical pyramidal neurons. These neurons highly expressed genes CDKN1A (P21), CCL2 and NFKBIA that associated with mTOR pathway, inflammatory response and cellular senescence. We confirmed the expression of senescent marker genes in a subpopulation of cortical pyramidal neurons with enlarged soma size in the brain tissue of drug-resistant epilepsy. We further revealed the expression of senescent cell markers P21, P53, COX2, {gamma}-H2AX, {beta}-Gal and reduction of nuclear integrity marker Lamin B1 in histopathological neurons in the brain tissue of drug-resistant epilepsy patients with different pathologies, but not in control brain tissue with no history of epilepsy. Additionally, chronic, but not acute, epileptic seizures induced senescent markers expression in cortical neurons in mouse models of drug-resistant epilepsy. These results provide important molecular markers for histopathological neurons and new insights into the pathophysiological mechanisms of drug-resistant epilepsy.

neuroscience↗

bioRxiv2024

A unified central thalamus mechanism underlying diverse recoveries in disorders of consciousness

Disorders of consciousness (DoC) encompass a range of states characterized by prolonged altered awareness due to heterogeneous brain damage and are associated with highly diverse prognoses. However, the neural mechanisms underlying such diverse recoveries in DoC remain unclear. To address this issue, we analysed neuronal spiking activities recorded from the central thalamus (CT), a key hub in arousal regulation, in a cohort of 23 DoC patients receiving deep brain stimulation treatment. Using machine learning techniques, we identified a core set of electrophysiological features of the CT, particularly the theta rhythm, that could account for individual recovery outcomes across highly varied etiologies (trauma, brainstem hemorrhage, and anoxia), clinical baselines and patient ages. These features also correctly identified one subgroup of patients who exhibited poor initial clinical manifestations but recovered unexpectedly. Simulating a conductance-based model further revealed the neurodynamics of the theta rhythm in the CT during different stages of consciousness recovery. Taken together, these findings uncover a previously unknown, unified CT mechanism that governs the recoveries in DoC.

neuroscience↗

bioRxiv2024

Pathological axonal enlargement in connection with amyloidosis, lysosome destabilization and hemorrhage is a major defect in the Alzheimer's disease

AbstractAlzheimers disease (AD) is a multi-amyloidosis disease with A{beta} deposits in the cerebral blood vessels, microaneurysms and senile plaques. How A{beta} amyloidosis affects axon pathology is not well-examined. We studied A{beta}-related axonal phenotypes with histochemistry, immunohistochemistry and fluorescence imaging methods. Widespread axonal amyloidosis with distinctive axonal enlargement was observed in AD. A{beta}-positive axon diameters in AD brains were 1.72 times of control brain axons by average. Axonal amyloidosis also associated with MAP2 reduction, Tau phosphorylation, lysosome destabilization and hemorrhagic markers such as ApoE, HBA, HbA1C and Hemin. Lysosome destabilization in AD was also clearly identified in the neural soma, associating with the co-expression of A{beta} and Cathepsin D, HBA, ACTA2 and ColIV, implicating exogeneous hemorrhagic protein intake might influence neural lysosome stability. The data showed that A{beta}-containing lysosomes were 2.23 times as large as the control lysosomes. Furthermore, under rare conditions, axon breakages were observed, which likely resulted in Wallerian degeneration. In summary, axonal enlargement associated with amyloidosis, chronic microhemorrhage and lysosome destabilization is a major defect in Alzheimers disease.

cell biology↗

bioRxiv2024

Different Emotional States Engage Distinct Descending Pathways from the Prefrontal Cortex

Effective emotional processing, crucial for adaptive behavior, is mediated by the medial prefrontal cortex (mPFC) via connections to the basolateral amygdala (BLA) and nucleus accumbens (NAc), traditionally considered functionally similar in modulating reward and aversion responses. However, the functional specialization of the mPFC[->]BLA and mPFC[->]NAc pathways in representing affective states remains unclear. We found that while overall firing patterns appeared consistent across emotional states, deeper analysis revealed distinct variabilities. Specifically, mPFC[->]BLA neurons, especially "center-ON" neurons, exhibited heightened activity during behaviors classically associated with anxiety-like states, suggesting their involvement in aversive behavioral regulation. Conversely, mPFC[->]NAc neurons were more active during exploratory and approach-related behaviors, implicating them in the processing of positively valenced behavioral states. Notably, mPFC[->]NAc neurons showed significant pattern decorrelation during social interactions, suggesting a pivotal role in processing social preference. Additionally, repeated win/loss outcomes in the tube test produced distinct hierarchy-dependent behavioral changes and elevated corticosterone levels in loser mice, supporting the biological relevance of these behaviorally defined states. Together, these findings reveal pathway-specific representations of affect-related behavioral states in mPFC circuits and provide a framework for understanding how prefrontal outputs organize adaptive behavior across environmental contexts.

neuroscience↗

bioRxiv2023

SARS-CoV-2 neurotropism-induced anxiety and depression-like behaviors require Microglia activation

The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been associated with a wide range of "long COVID" neurological symptoms. However, the mechanisms governing SARS-CoV-2 neurotropism and its effects on long-term behavioral changes remain poorly understood. Using a highly virulent mouse-adapted SARS-CoV-2 strain, denoted as SARS2-N501YMA30, we demonstrated that intranasal inoculation of SARS2-N501YMA30 results in viral dissemination to multiple brain regions, including the amygdala and hippocampus. Behavioral assays indicated a marked elevation in anxiety- and depression-like behaviors post infection. A comparative analysis of RNA expression profiles disclosed alterations in the post-infected brains. Additionally, we observed dendritic spine remodeling on neurons within the amygdala after infection. Infection with SARS2-N501YMA30 was associated with microglial activation and a subsequent increase in microglia-dependent neuronal activity in the amygdala. Pharmacological inhibition of microglial activity subsequent to viral spike inoculation mitigates microglia-dependent neuronal hyperactivity. Transcriptomic analysis of infected brains revealed the upregulation of inflammatory and cytokine-related pathways, implicating microglia-driven neuroinflammation in the pathogenesis of neuronal hyperactivity and behavioral abnormality. Overall, these data provide critical insights into the neurological consequences of SARS-CoV-2 infection and underscore microglia as a potential therapeutic target for ameliorating virus-induced neurobehavioral abnormalities.

neuroscience↗

bioRxiv2023

Neuronal acid-sensing ion channel 1a regulates neuron-to-glioma synapses

Neuronal activity promotes high-grade glioma progression via secreted proteins and neuron-to-glioma synapses, and glioma cells boost neuronal activity to further reinforce the malignant cycle. Whereas strong evidence supports that the activity of neuron-to-glioma synapses accelerates tumor progression, the molecular mechanisms that modulate the formation and function of neuron-to-glioma synapses remain largely unknown. Our recent findings suggest that a proton (H+) signaling pathway actively mediates neuron-to-glioma synaptic communications by activating neuronal acid-sensing ion channel 1a (Asic1a), a predominant H+ receptor in the central nervous system (CNS). Supporting this idea, our preliminary data revealed that local acid puff on neurons in high-grade glioma-bearing brain slices induces postsynaptic currents of glioma cells. Stimulating Asic1a knockout (Asic1a-/-) neurons results in lower AMPA receptor-dependent excitatory postsynaptic currents (EPSCs) in glioma cells than stimulating wild-type (WT) neurons. Moreover, glioma-bearing Asic1a-/- mice exhibited reduced tumor size and survived longer than the glioma-bearing WT mice. Finally, pharmacologically targeting brain Asic1a inhibited high-grade glioma progression. In conclusion, our findings suggest that the neuronal H+-Asic1a axis plays a key role in regulating the neuron-glioma synapse. The outcomes of this study will greatly expand our understanding of how this deadly tumor integrates into the neuronal microenvironment.

neuroscience↗

bioRxiv2023

The type of DNA damage response after Decitabine treatment depends on the level of DNMT activity

Decitabine and Azacytidine are considered as epigenetic drugs that induce DNA- methyltransferase (DNMT)-DNA crosslinks, resulting in DNA-hypomethylation and -damage. Although they are applied against myeloid cancers, important aspects of their mode of action remain unknown, which highly limits their clinical potential. Using a combinatorial approach, we reveal that the efficacy profile of both compounds primarily depends on the level of induced DNA-damage. Under low DNMT-activity, only Decitabine has a substantial impact. Conversely, when DNMT-activity is high, toxicity and cellular response to both compounds are dramatically increased, but do not primarily depend on DNA-hypomethylation or RNA-associated processes, contradicting an RNA-dependent effect of Azacytidine. By applying spatial proteomics, we show that Decitabine induces a strictly DNMT-dependent multifaceted DNA- damage response based on chromatin-recruitment of various repair-associated proteins. The choice of DNA-repair pathway herby depends on the severity of Decitabine-induced DNA- lesions. While mismatch (MMR) and base-excision DNA repair (BER) as well as RAD50- dependent DNA double-strand break repair are always activated in response to Decitabine, Fanconi anemia-dependent DNA-repair combined with homologous recombination is only activated when DNMT-activity is moderate. In contrast, high DNMT-activity and therefore immense replication stress, induce DNA repair by non-homologous and alternative end-joining.

biochemistry↗

bioRxiv2023

Acid-sensing ion channel 1a contributes to the prefrontal cortex ischemia-enhanced neuronal activities in the amygdala

Following a stroke, the emergence of amygdala-related disorders poses a significant challenge, with severe implications for post-stroke mental health, including conditions such as anxiety and depression. These disorders not only hinder post-stroke recovery but also elevate mortality rates. Despite their profound impact, the precise origins of aberrant amygdala function after stroke remain elusive. As a target of reduced brain pH in ischemia, acid-sensing ion channels (ASICs) have been implicated in synaptic transmission after ischemia, hinting at their potential role in reshaping neural circuits following a stroke. This study delves into the intriguing relationship between post-stroke alterations and ASICs, specifically focusing on postsynaptic ASIC1a enhancement in the amygdala following prefrontal cortex (PFC) ischemia induced by endothelin-1 (ET-1) injection. Our findings intriguingly illustrate that mPFC ischemia not only accentuates the PFC to amygdala circuit but also implicates ASIC1a in fostering augmented synaptic plasticity after ischemia. In contrast, the absence of ASIC1a impairs the heightened induction of long-term potentiation (LTP) in the amygdala induced by ischemia. This pivotal research introduces a novel concept with the potential to inaugurate an entirely new avenue of inquiry, thereby significantly enhancing our comprehension of the intricate mechanisms underlying post-stroke neural circuit reconfiguration. Importantly, these revelations hold the promise of paving the way for groundbreaking therapeutic interventions.

neuroscience↗

bioRxiv2023

Aβ-aggregation-generated blue autofluorescence illuminates senile plaques, complex blood and vascular pathologies in the Alzheimer's disease

Senile plaque blue autofluorescence in the Alzheimers disease (AD) was discovered around 40 years ago, however, its impact on AD pathology is not fully examined. We analyzed senile plaques with immunohistochemistry and fluorescence imaging on AD brain pathological sections and also the A{beta} aggregation process in vitro in test tubes. In DAPI or Hoechst staining experiments, the data showed that the nuclear blue fluorescence could only be correctly assigned after subtracting the blue autofluorescence background. The plaque cores have very strong blue autofluorescence which is roughly 2.09 times of average DAPI nuclear staining and roughly 1.78 times of average Hoechst nuclear staining. The composite flower-like structures formed by Cathepsin D lysosomal staining wrapping dense core blue fluorescence should not be considered as central-nucleated neurons filled with defective lysosomes since there was no nuclear staining in the plaque core when the blue autofluorescence was subtracted. Furthermore, the dense cores were shown to be completely lack of nuclear signals by PI staining. The A{beta} aggregation assay indicated that both A{beta} self-oligomers and A{beta}/Hemoglobin (Hb) heterocomplexes had significant blue autofluorescence. However, the blue autofluorescence intensity was not always proportional to the intensity of A{beta} immunostaining. The majority of aggregates in the A{beta}/Hb incubations were sensitive to Proteinase K (PK) digestion while the rest were PK resistant. The blue autofluorescence of A{beta} aggregates not only labels senile plaques but also illustrates red blood cell aggregation, hemolysis, CAA, vascular amyloid plaques, vascular adhesion and microaneurysm. In summary, we conclude that A{beta}-aggregation-generated blue autofluorescence is an excellent amyloid pathology marker in the senile plaques, blood and vascular pathologies in the Alzheimers disease.

cell biology↗

bioRxiv2023

Transcriptomic profiling of nuclei from PFA-fixed and FFPE brain tissues

Formalin-fixed and paraffin-embedded (FFPE) tissue archives are the largest repository of clinically annotated specimens, and FFPE-compatible single cell gene expression workflow had been developed and applied recently. However, for tissues where cells are hard to dissociate or brains with complex neuronal cells, nuclear transcriptomic profiling are desirable. Moreover, the effects of standard pathological practice on the transcriptome of samples obtained from such archived specimens was also largely anecdotal. Here, we performed RNA-seq of nuclei from hippocampal of mice that underwent freezing, paraformaldehyde (PFA) fixation, and paraffin embedding. Then, we comprehensively evaluated the parameters affecting mRNA quality, transcription patterns, functional level and cell states of nuclei, including PFA fixation time and storage time of FFPE tissues. The results showed that the transcriptome signatures of nuclei isolated from fresh PFA-fixed and fresh FFPE tissues were more similar to matched frozen samples. By contrast, the brain fixed for more than 3 days had prominent impacts on the sequencing data, such as the numbers and biotypes of gene, GC content and ratio of reads interval. Commensurately, prolonged fixation time will result in more differentially expressed genes, especially those enriched in spliceosome and synaptic related pathways, affecting the analysis of gene splicing and neuron cells. MuSiC deconvolution results revealed that PFA infiltrating brains for 3 days will destroy the real cell states, and the proportion of neuron, endothelial and oligodendrocytes diminished while that of microglia was reversed. Yet the effect of storage time on cell composition was more neglectable for FFPE samples. In addition, oligodendrocyte precursor cells were most affected in all fixed samples, and their destruction was independent of fixation time and preservation time. The comprehensive results highlighted that fixation time had much more influences on the nuclear transcriptomic profiles than FFPE retention time, and the cliff-like effects appeared to occur over a fixed period of 1-3 days, with no more differences from additional fixation durations.

molecular biology↗

bioRxiv2023

Re-evaluating the nuclear staining on pathological sections in Alzheimer's disease

A paper recently published on Nature Neuroscience, asserting that lysosome leakage induces neuronal cell death and the formation of senile plaques in Alzheimers disease. The study believed that flower-like perikaryal rosettes formed by packed autophagic vacuoles around central nuclei, termed "PANTHOS" neurons, are responsible for the senile plaque formation. However, all of the nuclei staining in this paper based on images in the blue fluorescence channel. We did detailed studies on the senile plaque blue autofluorescence and found that senile plaque blue autofluorescence could be easily mistaken as nuclear staining. The blue "nuclear" staining in this paper is probably inaccurate since it was not verified in red or green fluorescence channels and their "nuclei"-related data might be mis-interpreted.

neuroscience↗

bioRxiv2021

A database and comprehensive analysis of the algae genomes

Algae characterize their high diversity, taxonomy and morphology for wide-used studying the plant origins and terrestrialization, as well as multicellular evolution. Due to the genome assembly challenge of algae caused by symbionts with microbiome, the published algae genomes are relatively less than the terrestrial plants. Here we comprehensively collected and re-annotated 191 available algae genomes distributed in nine major lineages. We systemically investigated the genome features including genome size, assembly continuity and integrity, GC content, abundance of repetitive sequences and protein-coding gene number. We construct the phylogenetic trees using 193 algae genomes, which is consistent with the well-known evolution path that Glaucophyte is the most ancient, going through eight lineages, and finally evolved to terrestrial plants. We also examined the Horizontal Gene Transfer (HGT) genes distribution in algae genomes and provides a substantial genomic resource for functional gene origins and plant evolution.

genomics↗

bioRxiv2021

Integrated Multi-Omics Data Reveals the Molecular Subtypes of Prostate Cancer

Prostate cancer (PCa), the second most common male malignancy, is the fifth leading cause of cancer-related death and places notable burdens on medical resources. Most of the previous subtypes only focused on one or fewer types of data or ignored the genomic heterogeneity among PCa patients with diverse genetic backgrounds. Therefore, it is essential to precisely identify the specific molecular features and judge potential clinical outcomes based on multi-omics data. In the current study, we first identified the PCa multi-omics classification (PMOC) system based on the multi-omics, including mRNA, miRNA, lncRNA, DNA methylation, and gene mutation, using a total of ten state-of-the-art clustering algorithms. The PMOC1 subtype, also called the inflammatory subtype, contains the highest expression levels of immune checkpoint proteins, moderate activated immune-associated pathways. The PMOC2 tumor-activated subtype demonstrated the worst prognosis, which might be impacted by the activated cell cycle and DNA repair pathways, and also characterized by the most genetic alterations of mutant TP53, mutant APC and copy number alteration of 8q24.21 region. The PMOC3 subtype is likely to be a balance subtype, with the activated oncogenic signaling pathways, including hypoxia, angiogenesis, epithelial mesenchymal transition, and PI3K/AKT pathways. As well as with the activated proinflammatory pathways, including IL6/JAK/STAT3, IL2/STAT5, Notch and TNF- signaling. Additionally, PMOC3 subtype also linked with the activation of the androgen response and the high response rate of ARSI treatment. Taken together, we defined the PMOC system for PCa patients via multi-omics data and consensus results of ten algorithms, this multi-omics consensus PCa molecular classification can further assist in the precise clinical treatment and development of targeted therapy.

cancer biology↗

bioRxiv2020

An Experimental Validation of the Computer Fluid Dynamics of Normal Human Nasal Airflow Using a Precise 3-D Printing Model

Computer Fluid Dynamics (CFD) is a popular method for studying airflow of nasal cavities. However, the data of CFD studies has rarely been validated through experiments. To test the accuracy of CFD computation, we studied the consistency of the air pressure of nasal cavities in the CFD and the experiment. A proportional resin model of a normal human subjects nasal cavities was created by a 3-d printer with a precision value of 0.1mm. The pressure of 63 check points in the nasal cavities in different breathing states was measured. The experimental data was compared with the data obtained by CFD simulation. At the flow rates of 180 ml s-1 and 560 ml s-1, the pressure in all check points remained highly consistent with the CFD data. At 1100 ml s-1 flow rate, there was a significant deviation in the posterior segment of the nasal cavity during exhalation. The method used in this study to measure the pressure in the nasal cavities can be used in experimental validation of CFD data. The computational methods and the boundary conditions used in this study resulted in a high agreement between the results of the CFD simulation and the experiment. Author SummaryIn the contemporary era, Computer fluid dynamics (CFD) is the mainstream method for studying air flow. Due to the complex anatomical structure of the nasal cavity, the CFD results of the nasal flow have rarely been experimentally verified. This study provides a method to verify the methods and results of nasal CFD. We printed an accurate model of a normal persons nasal cavity with a high-precision 3D printer. In this nasal cavity model, we set 63 small holes to detect the air pressure of the places we concerned. Three different nasal flow quantity are used to represent different breathing conditions: high (1100 ml s-1), medium (560 ml s-1), and low (180 ml s-1). In medium and low nasal flow quantities, our CFD results are in good agreement with the experimental pressure values. On this basis, we analyzed the characteristics of nasal airflow in normal people. The method used in this study to measure the pressure in the nasal cavities can be used in experimental measurements of the partial resistance of the nasal cavity. With proper modification, it can be applied to the clinical practice for nasal resistance, giving more help for the design of the operation plan.

biophysics↗