Physiological genomics最新文献

{"title":"Relationship between Guillain-Barré syndrome and Cardiovascular disease: A bidirectional Mendelian randomization study.","authors":"Tianyi Wang, Na Li, Yong Zeng","doi":"10.1152/physiolgenomics.00048.2024","DOIUrl":"https://doi.org/10.1152/physiolgenomics.00048.2024","url":null,"abstract":"<p><strong>Background and objective: </strong>Guillain-Barré syndrome (GBS) and cardiovascular diseases (CVDs) have been observed to have a potential association, with GBS potentially leading to cardiovascular complications. However, these observational studies may be influenced by confounding factors. This study aimed to assess the causal relationship between GBS and CVDs, including heart failure (HF), atrial fibrillation (AF), and coronary artery disease (CAD), using a two-sample bidirectional Mendelian randomization (MR) analysis.</p><p><strong>Methods: </strong>Datasets for GBS and CVDs were retrieved from the United Kingdom Biobank and analyzed using selected instrumental variables (IVs) related to genetic variations. Sensitivity tests, including heterogeneity and horizontal pleiotropy tests, were conducted to ensure the reliability of the selected IVs. The analysis results were then visualized to illustrate the causal relationships.</p><p><strong>Results: </strong>The study identified genetic variants as IVs for both GBS and CVDs. MR analysis revealed a significant causal effect of GBS on the increased risk of HF (Inverse variance weighted [IVW], <i>p</i><0.05), but no significant causal relationship was found between GBS and AF or CAD. Similarly, no causal effect of CVDs on the occurrence of GBS was observed. Sensitivity analyses indicated no significant heterogeneity or horizontal pleiotropy, supporting the robustness of the results.</p><p><strong>Conclusion: </strong>This bidirectional MR analysis suggests a causal relationship between GBS and an increased risk of HF but not with AF or CAD, nor was a reverse causal effect of CVDs on GBS observed. These findings underscore the importance of considering cardiovascular complications, particularly HF, in the clinical management of patients with GBS in European populations.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MYL9 binding with MYO19 suppresses epithelial-mesenchymal transition in non-small cell lung cancer.","authors":"Meiling Sheng, Qunzhi Wang, Yabo Lou, Yuanchao Xiao, Xiaoming Wu","doi":"10.1152/physiolgenomics.00119.2024","DOIUrl":"https://doi.org/10.1152/physiolgenomics.00119.2024","url":null,"abstract":"<p><strong>Background: </strong>The elusive function of myosin light chain 9 (MYL9) in cancer is an area ripe for further investigation.</p><p><strong>Methods: </strong>Bioinformatics was utilized to compare the expression levels of MYL9 in non-small cell lung cancer (NSCLC) and normal tissues. Gene set enrichment analysis (GSEA) was employed to investigate the pathways associated with MYL9. BioGRID database was utilized to screen for potential targets of MYL9. The expression of MYL9 and myosin 19 (MYO19) mRNA was quantified using quantitative reverse transcriptase PCR. Cell migration was assessed using a scratch wound healing assay. Protein levels of MYL9, MYO19, and epithelial-mesenchymal transition (EMT) biomarkers were examined using western blot (WB). EpCAM expression in different cell groups was profiled using flow cytometry analysis. Co-immunoprecipitation assays were performed to determine the binding affinity between MYL9 and MYO19. Additionally, direct protein interaction between MYL9 and MYO19 was explored using a GST-pull-down assay.</p><p><strong>Results: </strong>In NSCLC patients, MYL9 was significantly downregulated in vivo and in cell cultures, showing high enrichment in the EMT pathway. Scratch assays indicated its inhibitory effect on cell migration. Western blotting revealed that MYL9 suppresses EMT marker protein expression in NSCLC cells. Flow cytometry showed that MYL9 reduced EpCAM levels on the cell surface. MYO19 was identified as a potential target of MYL9 through CoIP and GST-pull-down assays. Rescue experiments demonstrated that MYO19 enhances cell migration, EMT marker expression, and EpCAM levels, but these effects were countered by MYL9 overexpression.</p><p><strong>Conclusion: </strong>MYL9 impedes the migration and EMT in NSCLC cells by binding to MYO19.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial Intelligence and Omics in Malignant Gliomas.","authors":"Richa Tambi, Binte Zehra, Aswathy Vijayakumar, Dharana Satsangi, Mohammed Uddin, Bakhrom K Berdiev","doi":"10.1152/physiolgenomics.00011.2024","DOIUrl":"https://doi.org/10.1152/physiolgenomics.00011.2024","url":null,"abstract":"<p><p>The availability of large scale multi-omics data requires development of computational models to infer valuable biological insights for the implementation of precision medicine. Artificial intelligence (AI) refers to a host of computational algorithms that is becoming a major tool capable of integrating large genomic, transcriptomic, proteomic, and metabolomic data. Machine learning (ML) is the most significant AI algorithm in health sciences have exploded, specifically due to the recent progress made by deep learning. Although the use of AI/ML tools in GBM-omics is still at an early stage, a comprehensive discussion of how AI can be used to unravel various aspects of GBM (intratumor heterogeneity, biomarker discovery, survival prediction, and treatment optimization) would be highly relevant to both researchers and clinicians. Here, we aim to review the different AI-based techniques that have been used to study GBM pathogenesis using multi-omics data over the last decade. We first summarize different types of GBM related omics resources that can be used to develop AI models. We then discuss various AI applications for multi-omics data in order to enhance GBM precision medicine. Finally, we discuss the technical and ethical challenges that limit its application and ways to improve its implementation in clinics.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142505924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal-fetal interfaces transcriptome changes associated with placental insufficiency and a novel gene therapy intervention.","authors":"Helen N Jones, Baylea N Davenport, Rebecca L Wilson","doi":"10.1152/physiolgenomics.00131.2024","DOIUrl":"10.1152/physiolgenomics.00131.2024","url":null,"abstract":"<p><p>The etiology of fetal growth restriction (FGR) is multifactorial, although many cases involve placental insufficiency. Placental insufficiency is associated with inadequate trophoblast invasion resulting in high resistance to blood flow, decreased availability of nutrients, and increased hypoxia. We have developed a non-viral, polymer-based nanoparticle that facilitates delivery and transient gene expression of <i>human insulin-like 1 growth factor</i> (<i>hIGF1</i>) in trophoblast for the treatment of placenta insufficiency and FGR. Using the established guinea pig maternal nutrient restriction (MNR) model of placental insufficiency, the aim of the study was to identify novel pathways in the sub-placenta/decidua that provide insight into the underlying mechanism driving placental insufficiency, and may be corrected with <i>hIGF1</i> nanoparticle treatment. Pregnant guinea pigs underwent ultrasound-guided sham or <i>hIGF1</i> nanoparticle treatment at mid-pregnancy, and sub-placenta/decidua tissue was collected 5 days later. Transcriptome analysis was performed using RNA Sequencing on the Illumina platform. The MNR sub-placenta/decidua demonstrated fewer maternal spiral arteries lined by trophoblast, shallower trophoblast invasion and downregulation of genelists involved in the regulation of cell migration. <i>hIGF1</i> nanoparticle treatment resulted in marked changes to transporter activity in the MNR + <i>hIGF1</i> sub-placenta/decidua when compared to sham MNR. Under normal growth conditions however, <i>hIGF1</i> nanoparticle treatment decreased genelists enriched for kinase signaling pathways and increased genelists enriched for proteolysis indicative of homeostasis. Overall, this study identified changes to the sub-placenta/decidua transcriptome that likely result in inadequate trophoblast invasion and increases our understanding of pathways that <i>hIGF1</i> nanoparticle treatment acts on in order to restore or maintain appropriate placenta function.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142392477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise to combat cancer: focusing on the ends.","authors":"Josha Denham, Edward S Bliss, Tracy M Bryan, Brendan J O'Brien, Dean Mills","doi":"10.1152/physiolgenomics.00075.2024","DOIUrl":"https://doi.org/10.1152/physiolgenomics.00075.2024","url":null,"abstract":"<p><p>Cancer remains a leading cause of death worldwide and although prognosis and survivorship after therapy has improved significantly, current cancer treatments have long-term health consequences. For decades telomerase-mediated telomere maintenance has been an attractive anti-cancer therapeutic target due to its abundance and role in telomere maintenance, pathogenesis and growth in neoplasms. Telomere maintenance-specific cancer therapies, however, are marred by off target side-effects that must be addressed before they reach clinical practice. Regular exercise training is associated with telomerase-mediated telomere maintenance in healthy cells, which is associated with healthy ageing. A single bout of endurance exercise training dynamically, but temporarily, increases <i>TERT</i> mRNA and telomerase activity, as well as several molecules that control genomic stability and telomere length (i.e., shelterin and TERRA). Considering the epidemiological findings and accumulating research highlighting that exercise significantly reduces the risk of many types of cancers and the anti-carcinogenic effects of exercise on tumour growth <i>in vitro</i>, investigating the governing molecular mechanisms of telomerase control in context with exercise and cancer may provide important new insights to explain these findings. Specifically, the molecular mechanisms controlling telomerase in both healthy cells and tumours after exercise could reveal novel therapeutic targets for tumour-specific telomere maintenance and offer important evidence that could refine current physical activity and exercise guidelines for all stages of cancer care.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142392476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of SNP-SNP interactions of surfactant protein genes with severity of respiratory syncytial virus infection in children.","authors":"Chintan K Gandhi, Lynnlee C Depicolzuane, Chixiang Chen, Catherine M Roberts, Natalie Sicher, Katelyn Johnson Wegerson, Neal J Thomas, Rongling Wu, Joanna Floros","doi":"10.1152/physiolgenomics.00045.2024","DOIUrl":"10.1152/physiolgenomics.00045.2024","url":null,"abstract":"<p><p>The severity of respiratory syncytial virus (RSV) may be linked to host genetic susceptibility. Surfactant protein (SP) genetic variants have been associated with RSV severity, but the impact of single-nucleotide polymorphism (SNP)-SNP interactions remains unexplored. Therefore, we used a novel statistical model to investigate the association of SNP-SNP interactions of <i>SFTP</i> genes with RSV severity in two- and three-interaction models. We analyzed available genotype and clinical data from prospectively enrolled 405 children diagnosed with RSV, categorizing them into moderate or severe RSV groups. Using Wang's statistical model, we studied significant associations of SNP-SNP interactions with RSV severity in a case-control design. We observed, first, association of three interactions with increased risk of severe RSV in a two-SNP model. One intragenic interaction was between SNPs of <i>SFTPA2</i>, and the other two were intergenic, involving SNPs of hydrophilic and hydrophobic SPs alone. We also observed, second, association of 22 interactions with RSV severity in a three-SNP model. Among these, 20 were unique, with 12 and 10 interactions associated with increased or decreased risk of RSV severity, respectively, and included at least one SNP of either <i>SFTPA1</i> or <i>SFTPA2</i>. All interactions were intergenic except one, among SNPs of <i>SFTPA1</i>. The remaining interactions were either among SNPs of hydrophilic SPs alone (<i>n</i> = 8) or among SNPs of both hydrophilic or hydrophobic SPs (<i>n</i> = 11). Our findings indicate that SNPs of all <i>SFTP</i>s may contribute to genetic susceptibility to RSV severity. However, the predominant involvement of <i>SFTPA1</i> and/or <i>SFTPA2</i> SNPs in these interactions underscores their significance in RSV severity.<b>NEW & NOTEWORTHY</b> Although surfactant protein (SP) genetic variants are associated with respiratory syncytial virus (RSV) severity, the impact of single-nucleotide polymorphism (SNP)-SNP interactions of SP genes remained unexplored. Using advanced statistical models, we uncovered 22 SNP-SNP interactions associated with RSV severity, with notable involvement of <i>SFTPA1</i> and <i>SFTPA2</i> SNPs. This highlights the comprehensive role of all SPs in genetic susceptibility to RSV severity, shedding light on potential avenues for targeted interventions.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11495184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gill ionocyte remodeling mediates blood pH regulation in rockfish (<i>Sebastes diploproa</i>) exposed to environmentally relevant hypercapnia.","authors":"Garfield T Kwan, Alexander M Clifford, Kaelan J Prime, Till S Harter, Martin Tresguerres","doi":"10.1152/physiolgenomics.00057.2024","DOIUrl":"10.1152/physiolgenomics.00057.2024","url":null,"abstract":"<p><p>Marine fishes excrete excess H⁺ using basolateral Na⁺-K⁺-ATPase (NKA) and apical Na⁺/H⁺ exchanger 3 (NHE3) in gill ionocytes. However, the mechanisms that regulate H⁺ excretion during exposure to environmentally relevant hypercapnia (ERH) remain poorly understood. Here, we explored transcriptomic, proteomic, and cellular responses in gills of juvenile splitnose rockfish (<i>Sebastes diploproa</i>) exposed to 3 days of ERH conditions (pH ∼7.5, ∼1,600 μatm Pco₂). Blood pH was fully regulated at ∼7.75 despite a lack of significant changes in gill <i>1</i>) mRNAs coding for proteins involved in blood acid-base regulation, <i>2</i>) total NKA and NHE3 protein abundance, and <i>3</i>) ionocyte density. However, ERH-exposed rockfish demonstrated increased NKA and NHE3 abundance on the ionocyte plasma membrane coupled with wider apical membranes and greater extension of apical microvilli. The observed gill ionocyte remodeling is consistent with enhanced H⁺ excretion that maintains blood pH homeostasis during exposure to ERH and does not necessitate changes at the expression or translation levels. These mechanisms of phenotypic plasticity may allow fishes to regulate blood pH during environmentally relevant acid-base challenges and thus have important implications for both understanding how organisms respond to climate change and for selecting appropriate metrics to evaluate its impact on marine ecosystems.<b>NEW & NOTEWORTHY</b> Splitnose rockfish exposed to environmentally relevant hypercapnia utilize existing proteins (rather than generate additional machinery) to maintain homeostasis.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Podocyte cell-specific <i>Npr1</i> is required for blood pressure and renal homeostasis in male and female mice: role of sex-specific differences.","authors":"Chandramohan Ramasamy, Kandasamy Neelamegam, Samivel Ramachandran, Huijing Xia, Daniel R Kapusta, Farhad R Danesh, Kailash N Pandey","doi":"10.1152/physiolgenomics.00137.2023","DOIUrl":"10.1152/physiolgenomics.00137.2023","url":null,"abstract":"<p><p>Atrial and brain natriuretic peptides (ANP and BNP) bind to guanylyl cyclase A/natriuretic peptide receptor A (GC-A/NPRA), stimulating natriuresis and diuresis and reducing blood pressure (BP), but the role of ANP/NPRA signaling in podocytes (highly specialized epithelial cells covering the outer surfaces of renal glomerular capillaries) remains unclear. This study aimed to determine the effect of conditional deletion of podocyte-specific <i>Npr1</i> (encoding NPRA) gene knockout (KO) in male and female mice. Tamoxifen-treated wild-type control (PD <i>Npr1</i> f/f; WT), heterozygous (PD-Cre-<i>Npr1</i> f/+; HT), and KO (PD-Cre-<i>Npr1</i> f/-) mice were fed a normal-, low-, or high-salt diet for 4 wk. Podocytes isolated from HT and KO male and female mice showed complete absence of <i>Npr1</i> mRNA and NPRA protein compared with WT mice. BP, plasma creatinine, plasma sodium, urinary protein, and albumin/creatinine ratio were significantly increased, whereas plasma total protein, albumin, creatinine clearance, and urinary sodium levels were significantly reduced in the HT and KO male and female mice compared with WT mice. These changes were significantly greater in males than in females. On a normal-salt diet, glomerular filtration rate was significantly decreased in PD <i>Npr1</i> HT and KO male and female mice compared with WT mice. Immunofluorescence of podocin and synaptopodin was also significantly reduced in HT and KO mice compared with WT mice. These observations suggest that in podocytes, ANP/NPRA signaling may be crucial in the maintenance and regulation of glomerular filtration and BP and serve as a biomarker of renal function in a sex-dependent manner.<b>NEW & NOTEWORTHY</b> Our results demonstrate that the podocyte-specific deletion of <i>Npr1</i> showed increased blood pressure (BP) and altered biomarkers of renal functions, with greater magnitudes in animals fed a high-salt diet in a sex-dependent manner. The results suggest a direct and sex-dependent effect of <i>Npr1</i> ablation in podocytes on the regulation of BP and renal function and reveal that podocytes may be considered an important target for the ANP-BNP/NPRA/cGMP signaling cascade.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11495182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141889913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A matter of food and substrain: obesogenic diets induce differential severity of cardiac remodeling in C57Bl/6J and C57Bl/6N substrains.","authors":"Lorena Cascarano, Hrag Esfahani, Pierre Michel, Caroline Bouzin, Chantal Dessy, Jean-Luc Balligand, Lauriane Y M Michel","doi":"10.1152/physiolgenomics.00044.2024","DOIUrl":"10.1152/physiolgenomics.00044.2024","url":null,"abstract":"<p><p>The prevalence of metabolic syndrome in cardiac diseases such as heart failure with preserved ejection fraction (HFpEF) prompts the scientific community to investigate its adverse effects on cardiac function and remodeling. However, the selection of a preclinical model of obesity-induced cardiac remodeling has proven more challenging with inconsistencies often found in very similar mouse models. Here, we investigated the implication of genetic background as well as diet composition to identify a suitable model of diet-induced cardiac alterations. C57Bl/6J and C57Bl/6N male mice were subjected to distinct obesogenic diets consisting of high-fat and moderate sucrose content (HF-S) or high-sucrose and moderate lipid content (F-HS) versus matching control diets. Five-month dietary intervention with obesogenic diets induced weight gain, adipocyte hypertrophy, and increased visceral and subcutaneous fat mass in both substrains. Obese mice showed similar impairment of glucose disposition and insulin tolerance, with both strains developing insulin resistance within 2 mo. However, echocardiographic follow-up and histological analysis confirmed that the HF-S diet increased cardiac hypertrophy, interstitial fibrosis, and left atrial area in the C57Bl/6J strain only. In contrast, the C57Bl/6N strain exhibited cardiac eccentric remodeling under control diets, possibly owing to a genetic mutation in the myosin light chain kinase 3 (<i>Mylk3</i>) gene, specific to this substrain, which was not further enhanced under obesogenic diets. Altogether, the present results highlight the importance of carefully selecting the suitable mouse strain and diets to model diet-induced cardiac remodeling. In this regard, C57Bl/6J mice develop significant cardiac remodeling in response to HF-S and seem to be a suitable model for cardiometabolic disease.<b>NEW & NOTEWORTHY</b> Metabolic syndrome is highly prevalent in cardiac pathologies. Underlying mechanisms have not been thoroughly investigated, owing to the lack of reliable preclinical model of diet-induced cardiac remodeling. Our work demonstrates that genetic variants in inbred strains influence the response to metabolic stress and identifies C57Bl/6J mice as a suitable model for cardiometabolic disease in response to high-fat diet. These findings reinforce the need to carefully select the mouse strain in relation to the imposed pathophysiologic stress.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141617031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of the anti-inflammatory drug budesonide on the gut microbiota and cytokine production of 13-lined ground squirrels during pre-hibernation fattening","authors":"Kirsten Grond, Jewel Zur Tulod, Courtney C. Kurtz, Khrystyne N Duddleston","doi":"10.1152/physiolgenomics.00034.2024","DOIUrl":"https://doi.org/10.1152/physiolgenomics.00034.2024","url":null,"abstract":"Physiological Genomics, Ahead of Print. <br/>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":null,"pages":null},"PeriodicalIF":4.6,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142200692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}