Project description:Sixteen severly RAO (Recurrent Airway Obstruction) affected horses were studied. All RAO affected male horses were hybridized with GSM1332974 (Thoroughbred male 1, male reference), and the female horses were with GSM1332975 (Thoroughbred female 2, female reference). Finally results are compared with GSE55266 and two other control horses (SPA-H1-3 and SPA-H1-5) and relatively novel RAO CNVs were reported.
Project description:The purpose of this experiment was to further our understanding of gene expression in the central nervous system (thalamus and cerebrum) after exposure to West Nile virus. To that end, three different analyses were performed. The first examined differences in gene expression between horses not vaccinated and exposed to WNV and normal control horses (exposure). The second examined differences in gene expression between horses not vaccinated and exposed to WNV and horses vaccinated and exposed to WNV (survival). And the third examined differences between the nonvaccinated cerebrum and nonvaccinated thalamus of horses exposed to WNV (location). Six conditions- Gene expression in the thalamus and cerebrum of three different groups of horses (Non-vaccinated horses exposed to West Nile virus, Vaccinated horses exposed to West Nile virus, normal horses not exposed to West Nile virus). Biological replicates- 6 normal cerebrums, 6 normal thalamus, 6 vaccinated and exposed cerebrums, 6 vaccinated and exposed thalamus, 6 non-vaccinated and exposed cerebrum, 6 non-vaccinated and exposed thalamus.
Project description:38 horses from 16 diverse breeds and Przewalski's Horse were used to generate a composite CNV map of equine genome. This map was used to detect novel copy number variation in six horses affected with disorder of sexual development (DSD).
Project description:The purpose of this experiment was to further our understanding of gene expression in the central nervous system (thalamus and cerebrum) after exposure to West Nile virus. To that end, three different analyses were performed. The first examined differences in gene expression between horses not vaccinated and exposed to WNV and normal control horses (exposure). The second examined differences in gene expression between horses not vaccinated and exposed to WNV and horses vaccinated and exposed to WNV (survival). And the third examined differences between the nonvaccinated cerebrum and nonvaccinated thalamus of horses exposed to WNV (location).
Project description:Investigating genome-wide characteristics of CNVs in 6 horses representing 6 distinct breeds by using the aCGH method and performed GO and KEGG analysis for the CNVs genes.This result is an important complement to the mapping of horse whole-genome CNVs and helpful to study plateau horses’ adaption to the plateau’s environment.
Project description:We undertook gene expression microarray experiments to identify genes that are differentially expressed in heaves-affected horses versus matched controls. Mediastinal (pulmonary-draining) lymph nodes were sterilely obtained from affected and control horses, dissected, and frozen at -80oC. RNA was extracted from these tissues for downstream applications. These experiments utilized a commercially available Agilent horse array that featured >43,000 probes on a 4x44k array format. Mediastinal lymph node RNA from seven heaves-affected horses was compared to matching RNA from healthy, normal control horses.
Project description:Equine Papillomavirus Type 2 (EcPV2) appears to be a causal factor for the development of genital especially penile squamous cell carcinomas (SCC) and as such have an important clinical impact on horses. However, the pathomechanisms associated with this cancer transformation are not known, yet. To analyze the host’s and viral transcriptome in EcPV2 affected horses, tissue samples were collected from horses with EcPV2-positive genital lesions as well as from healthy EcPV2-negative horses. Expression levels of host and viral genes were evaluated by RNA-Seq.
Project description:Objective: The objective of this study was to characterize extracellular vesicles (EVs) in plasma and synovial fluid obtained from horses with and without naturally occurring post-traumatic osteoarthritis (PTOA). Animals (Samples): EVs were isolated from plasma and synovial fluid from horses with (n = 6) and without (n = 6) PTOA. Methods: Plasma and synovial fluid EVs were characterized with respect to quantity, size, and surface markers. Small RNA sequencing was performed and differentially expressed miRNAs underwent bioinformatic analysis to identify putative targets and to explore potential associations with specific biological processes. Results: Plasma and synovial fluid samples from horses with PTOA had a significantly higher proportion of exosomes and a lower proportion of microvesicles compared to horses without PTOA. Small RNA sequencing revealed several differentially expressed miRNAs including miR-144, miR-219-3p, and miR-199a-3p in plasma and miR-199a-3p, miR-214, and miR-9094 in synovial fluid EVs. Bioinformatics analysis of the differentially expressed miRNAs highlighted their potential role in fibrosis, differentiation of chondrocytes, apoptosis, and inflammation pathways in PTOA. Clinical Relevance: We have identified dynamic molecular changes in small non-coding signatures of plasma and synovial fluid EVs in horses with naturally occurring PTOA. These findings could serve to identify promising biomarkers in the pathogenesis of PTOA, to facilitate the development of targeted therapies, and to aid in establishing appropriate translational models of PTOA.
Project description:Horses receiving antimicrobials may develop diarrhea due to changes in the gastrointestinal microbiome and metabolome. This matched, case-controlled study compared the fecal microbiome and metabolome in hospitalized horses on antibiotics that developed diarrhea (AAD), hospitalized horses on antibiotics that did not develop diarrhea (ABX) and a healthy, non-hospitalized control population (CON). Naturally-voided fecal samples were collected from AAD horses (n=17) the day that diarrhea developed and matched to ABX (n=15) and CON (n=31) horses for diet, antimicrobial agent and duration of antimicrobial therapy (< 5 days or > 5 days). Illumina sequencing of 16S rRNA genes on fecal DNA was performed. Alpha and beta diversity metrics were generated using QIIME 2.0. A Kruskal-Wallis with Dunn’s post-test and ANOSIM testing was used for statistical analysis. Microbiome composition in AAD was significantly different from CON (ANOSIM, R= 0.568, p=0.001) and ABX (ANOSIM, R=0.121, p=0.0012). Fecal samples were lyophilized and extracted using a solvent-based method. Untargeted metabolomics using gas chromatography-mass spectrometry platforms was performed. Metabolomic data was analyzed using Metaboanalyst 4.0 and Graphpad Prism v 7. Principal component analysis plots (PCA) were used to visualize the distribution of metabolites between groups. Heat maps were used to identify the relative concentrations amongst the most abundant 25 metabolites. A one-way ANOVA was used to compare differences in metabolites amongst the three groups of horses. Only named metabolites were included in the analysis. The microbiome of AAD and ABX horses had significantly decreased richness and evenness than CON horses (p<0.05). Actinobacteria (q=0.0192) and Bacteroidetes (q=0.0005) were different between AAD and CON. Verrucomicrobia was markedly decreased in AAD compared to ABX and CON horses (q=0.0005). Horses with AAD have a dysbiosis compared to CON horses, and show minor differences in bacterial community composition to ABX horses. Metabolite profiles of horses with AAD clustered separately from those with AAD or CON. Ten metabolites were found to be significantly different between groups (P<0.05) and are listed according to their metabolic pathway: amino acid metabolism (R-equol, L-tyrosine, kynurenic acid, xanthurenic acid, 5-hydroxyindole-3-acetic acid ) lipid metabolism (docosahexaenoic acid ethyl ester), biosynthesis of secondary metabolites (daidzein, isoquinoline) and two metabolites with unidentified pathways (1,3-divinyl-2-imidazolidinone, N-acetyltyramine).