Project description:Motion Sickness increases risk of performance deficits and safety of flight concerns. The etiology of motion sickness is poorly understood. Here, we attempted to quantify the physiological effects of motion sickness on static balance and determine the genetic predictors associated with these effects.
Project description:Motion sickness susceptible (MSS) and insusceptible (inMSS) rats were identified by quantifying rotation-induced MS symptoms: defecation and spontaneous locomotion activity. Microarray analysis was used to screen differentially expressed genes in the caudal vestibular nucleus (CVN) after rotation.
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
Project description:Trypanosoma brucei gambiense is the causative agent of the fatal human disease African sleeping sickness. Using Digital Gene Expression we have compared the transcriptome of two isogenic T.b.gambiense lines that are either sensitive or resistant to human serum.
Project description:Trained immunity (a form of innate immune memory), defined in part by heightened responses to pathogen restimulation, can be generated by many different stimuli. However, both the quantitative differences in trained states generated by different stimuli and the downstream consequences of those differences remain unclear. Here, we used primary human monocyte-derived macrophages to demonstrate phenotypic and molecular stimulus specificity of trained immunity six days after initial exposure. Quantification of cytokine production with single-molecule RNA imaging demonstrated stimulus-specific patterns of response to restimulation, with trained cells showed stronger responses to secondary stimuli more similar to their initial stimulation. Differential licensing of inflammatory transcription factors was associated with encoding of specificities in chromatin six days after training, while memory of some, but not all, training stimuli is lost by eleven days post-training in vitro. Overall, our findings demonstrate that different training stimuli can impart specific memories which generate distinct training phenotypes.
Project description:Shotgun sequencing of sleeping sickness patient blood. WARNING: these results cannot be compared with those from trypanosome poly(A)+ mRNA, because the poly(A) selection introduces substantial bias, including loss of long mRNAs. Details will appear in the publication. These are additional sequencing runs that match some from E-MTAB-5293
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.