Serum microRNA expression prior to motion sickness stimulus
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ABSTRACT:
PROVIDER: PRJNA852603 | ENA |
REPOSITORIES: ENA
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2015-01-08 | E-MTAB-3213 | biostudies-arrayexpress
Project description:Motion sickness (MS) is defined as a disorder with cardinal manifestations including nausea-related syndrome (i.e. epigastric discomfort, pallor, cold sweating, hypersalivation nausea and vomit) and sopite-related symptoms (i.e. drowsiness, lethargy, headache and dizziness) induced by passive physical movements 1-4. Precise characterization of molecular profile associated with MS susceptibility is critical for objective MS prediction and diagnosis and help to clarify molecular basis underlying MS symptoms. As varieties of environmental aspects (motion pattern, temperature and smells) and individual characters (gender, age, race, personality and genetic background) affect individual differences in MS susceptibility 5-8, it is still a great challenge for objective discriminating susceptible (SUS) and non-susceptible (nonSUS) subjects among normal populations. Identification of circulation biomarkers receive great concerns due to the successful application of high-throughput multi-omics technology in discovering
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2018-06-18 | E-MTAB-5614 | biostudies-arrayexpress
Project description:Background: We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy and promotes physiological hypertrophy in an aortic banding model. To identify transcriptional pathways regulated by CHF1/Hey2 in hypertrophy, we cultured primary neonatal mouse cardiac myocytes from wild type and transgenic mice overexpressing CHF1/Hey2 and treated them with serum, a potent hypertrophic stimulus. We determined transcriptional profiles by hybridization to Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays. We identified important biological processes regulated by CHF1/Hey2 by Gene Set Analysis using Biological Process Gene Sets from the Gene Ontology Consortium. Results: We found that overexpression of CHF1/Hey2 suppresses gene sets involved in water transport, regulation of adenylate cyclase activity, embryonic eye morphogenesis, gut development and fluid transport after serum stimulation. Genes involved in protein dephosphorylation, in contrast, demonstrate increased expression in myocytes overexpressing CHF1/Hey2, and this increase is independent of serum treatment. Genes overexpressed prior to serum treatment are involved in regulation of transcription factor activity, protein export from the nucleus, and steroid hormone receptor signaling. Genes overexpressed after serum treatment are involved in autophagy, apoptosis and mitochondrial biogenesis. Conclusions: CHF1/Hey2 suppresses fluid transport, activation of adenylate cyclase activity, promotes phosphatase activity, autophagy and regulates other important biological processes likely relevant to hypertrophy. Transgenic Mice and Neonatal Mouse Myocyte Culture: WT no serum, 5; WT with serum, 7; TG no serum, 6; TG with serum, 7.
2010-04-08 | E-GEOD-14288 | biostudies-arrayexpress
Project description:During neurogenesis, expression of the basic Helix-Loop-Helix NeuroD6/Nex1/MATH-2 transcription factor parallels neuronal differentiation, while maintaining the differentiated state in the mature nervous system. To further dissect NeuroD6 differentiation properties, we previously generated a NeuroD6-overexpressing stable PC12 cell line, PC12-ND6, which displays a neuronal phenotype characterized by spontaneous neuritogenesis, accelerated NGF-induced differentiation, and increased regenerative capacity. Furthermore, we reported that NeuroD6 promotes long-term neuronal survival upon oxidative stress triggered by serum deprivation. In this study, we identified the NeuroD6-mediated transcriptional regulatory pathways linking neuronal differentiation to survival, by conducting a genome-wide microarray analysis using PC12-ND6 cells and serum deprivation as a stress paradigm. Through a series of filtering steps and a gene-ontology analysis, we found that NeuroD6 promotes distinct but overlapping gene networks, consistent with the differentiation, regeneration, and survival properties of PC12-ND6 cells. Using a gene set enrichment analysis, we provide the first evidence of a compelling link between NeuroD6 and a set of heat shock proteins in the absence of stress, which may be instrumental to confer stress tolerance to PC12-ND6 cells. Immunocytochemistry results showed that HSP27 and HSP70 interact with cytoskeletal elements, consistent with their roles in neuritogenesis and preserving cellular integrity. HSP70 also colocalizes with mitochondria located in the soma, growing neurites and growth cones of PC12-ND6 cells prior to and upon stress stimulus, consistent with its neuroprotective functions. Collectively, our findings support the notion that NeuroD6 links neuronal differentiation to survival via the network of molecular chaperones and endows the cells with increased stress tolerance. Experiment Overall Design: The experimental design involved six replicates of serum-grown PC12 cells (control), serum-grown PC12-ND6 cells (t=0), and serum-deprived PC12-ND6 cells (t=48 hrs).
2009-05-11 | E-GEOD-15942 | biostudies-arrayexpress
Project description:Explore the effect of grass sickness on the equine faecal microbiome.
| PRJEB11642 | ENA
Project description:Previous literature suggests a relationship between individual characteristics of motion perception and the peak frequency of motion sickness sensitivity. Here, we used well-established paradigms to relate motion perception and motion sickness on an individual level. We recruited 23 participants to complete a two-part experiment. In the first part, we determined individual velocity storage time constants from perceived rotation in response to Earth Vertical Axis Rotation (EVAR) and subjective vertical time constants from perceived tilt in response to centrifugation. The cross-over frequency for resolution of the gravito-inertial ambiguity was derived from our data using the Multi Sensory Observer Model (MSOM). In the second part of the experiment, we determined individual motion sickness frequency responses. Participants were exposed to 30-minute sinusoidal fore-aft motions at frequencies of 0.15, 0.2, 0.3, 0.4 and 0.5 Hz, with a peak amplitude of 2 m/s2 in five separate sessions, approximately 1 week apart. Sickness responses were recorded using both the MIsery SCale (MISC) with 30 s intervals, and the Motion Sickness Assessment Questionnaire (MSAQ) at the end of the motion exposure. The average velocity storage and subjective vertical time constants were 17.2 s (STD = 6.8 s) and 9.2 s (STD = 7.17 s). The average cross-over frequency was 0.21 Hz (STD = 0.10 Hz). At the group level, there was no significant effect of frequency on motion sickness. However, considerable individual variability was observed in frequency sensitivities, with some participants being particularly sensitive to the lowest frequencies, whereas others were most sensitive to intermediate or higher frequencies. The frequency of peak sensitivity did not correlate with the velocity storage time constant (r = 0.32, p = 0.26) or the subjective vertical time constant (r = - 0.37, p = 0.29). Our prediction of a significant correlation between cross-over frequency and frequency sensitivity was not confirmed (r = 0.26, p = 0.44). However, we did observe a strong positive correlation between the subjective vertical time constant and general motion sickness sensitivity (r = 0.74, p = 0.0006). We conclude that frequency sensitivity is best considered a property unique to the individual. This has important consequences for existing models of motion sickness, which were fitted to group averaged sensitivities. The correlation between the subjective vertical time constant and motion sickness sensitivity supports the importance of verticality perception during exposure to translational sickness stimuli.
| S-EPMC8006642 | biostudies-literature