Ontology highlight
ABSTRACT:
PROVIDER: PRJNA612483 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11304628_1.fastq.gz | Fastqsanger.gz | |||
| SRR11304628_2.fastq.gz | Fastqsanger.gz | |||
| SRR11304629_1.fastq.gz | Fastqsanger.gz | |||
| SRR11304629_2.fastq.gz | Fastqsanger.gz | |||
| SRR11304630_1.fastq.gz | Fastqsanger.gz |
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Project description:This study included four dog groups (group A: 10 healthy dogs, group B: 9 dogs with idiopathic epilepsy receiving antiepileptic medication-AEM, group C: 8 dogs with idiopathic epilepsy without AEM administration and group D: 7 dogs with seizures due to structural brain abnormalities). The epileptic dogs were allocated into these 3 groups after a diagnostic investigation that included laboratory testing, thoracic radiographic and abdominal ultrasonographic examination, brain imaging, CSF routine and proteomic analysis. The purpose of the current study was to investigate and compare the proteomic profile among the four groups of dogs.
2020-10-19 | PXD018893 | Pride
Project description:This study included four groups of dogs (group A: healthy controls, group B: idiopathic epilepsy receiving antiepileptic medication (AEM), group C: idiopathic epilepsy without AEM administration, group D: structural epilepsy), for which comparative proteomic analysis of serum samples was performed.
2023-10-30 | PXD041129 | Pride
Project description:Introduction: The relationship between epilepsy and cognitive dysfunction has been investigated in canines, and memory impairment was prevalent in dogs with epilepsy. There is some evidence that canines with epilepsy have greater amyloid-β (Aβ) accumulation and neuronal degeneration than healthy controls. The present study investigated plasma Aβ42 levels and performed proteomic profiling in dogs with refractory epilepsy and healthy dogs. Methods: In total, eight dogs, including four healthy dogs and four dogs with epilepsy, were included in the study. Blood samples were collected to analyze Aβ42 levels and perform proteomic profiling. Changes in the plasma proteomic profiles of dogs were determined by nano LC-MS/MS. Results and discussion: The plasma Aβ42 level was significantly higher in dogs with epilepsy (99 pg/mL) than in healthy dogs (5.9 pg/mL). In total, 155 proteins were identified, and of these, the expression of 40 proteins was altered in epilepsy. Among these proteins, which are linked to neurodegenerative diseases, 10 (25%) were downregulated in dogs with epilepsy, whereas 12 (30%) were upregulated. The expression of the acute phase proteins haptoglobin and α2-macroglobulin significantly differed between the groups. Complement factor H and ceruloplasmin were only detected in epilepsy dogs, suggesting that neuroinflammation plays a role in epileptic seizures. Gelsolin, which is involved in cellular processes and cytoskeletal organization, was only detected in healthy dogs. Gene Ontology annotation revealed that epilepsy can potentially interfere with biological processes, including cellular processes, localization, and responses to stimuli. Seizures compromised key molecular functions, including catalytic activity, molecular function regulation, and binding. Defense/immunity proteins were most significantly modified during the development of epilepsy. In Kyoto Encyclopedia of Genes and Genomes pathway analysis, complement and coagulation cascades were the most relevant signaling pathways affected by seizures. The findings suggested that haptoglobin, ceruloplasmin, α2-macroglobulin, complement factor H, and gelsolin play roles in canine epilepsy and Aβ levels based on proteomic profiling. These proteins could represent diagnostic biomarkers that, after clinical validation, could be used in veterinary practice as well as proteins relevant to disease response pathways. To determine the precise mechanisms underlying these relationships and their implications in canine epilepsy, additional research is required.
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Project description:Morphine causes microbial dysbiosis. In this study we focused on restoration of native microbiota in morphine treated mice and looked at the extent of restoration and immunological consequences of this restoration. Fecal transplant has been successfully used clinically, especially for treating C. difficile infection2528. With our expanding knowledge of the central role of microbiome in maintenance of host immune homeostasis17, fecal transplant is gaining importance as a therapy for indications resulting from microbial dysbiosis. There is a major difference between fecal transplant being used for the treatment of C. difficile infection and the conditions described in our studies. The former strategy is based on the argument that microbial dysbiosis caused by disproportionate overgrowth of a pathobiont can be out-competed by re-introducing the missing flora by way of a normal microbiome transplant. This strategy is independent of host factors and systemic effects on the microbial composition. Here, we show that microbial dysbiosis caused due to morphine can be reversed by transplantation of microbiota from the placebo-treated animals.
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2023-10-16 | MSV000093123 | MassIVE
Project description:Objective: To identify genes involved in idiopathic absence epilepsies by analysing gene expression using a monozygotic (MZ) twin design. Methods: Genome-wide gene expression in lymphoblastoid cell lines was determined using microarrays derived from five discordant and four concordant MZ twin pairs with idiopathic absence epilepsies and five unaffected MZ twin pairs. Gene expression was analysed using three strategies: discordant MZ twins were compared as matched pairs, MZ twins concordant for epilepsy were compared to control MZ twins, and a singleton design of affected versus unaffected MZ twin individuals was used irrespective of twin pairing. An overlapping gene list was generated from these analyses. Dysregulation of genes recognised from the microarray experiment were validated using quantitative real time PCR (qRT-PCR) in the twin sample and in an independent sample of 18 sporadic absence cases and 24 healthy controls. Results: Sixty-five probe sets were identified from the microarray analysis strategies. Sixteen genes were chosen for validation and nine of these genes confirmed by qRT-PCR in the twin sample. Differential expression of the immediate early gene EGR1 and RCN2, coding for the calcium-binding protein Reticulocalbin 2, was re-confirmed by qRT-PCR in the independent sample. Interpretation: Using a unique sample of discordant MZ twins, our study identified genes with altered expression, which suggest novel mechanisms in idiopathic absence epilepsy. Dysregulation of EGR1 and RCN2 might represent common transcriptional alterations in idiopathic absence epilepsy. Keywords: Childhood Absence Epilepsy, Juvenile Absence Epilepsy, Idiopathic Generalised Epilepsy, gene expression, twin study, monozygotic twins
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