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:Sickness induces coordinated changes in physiology and behavior, including increased sleep, and despite specific circuits responsible for some of them have been recently described, how the brain orchestrates this global state shift remains unclear. Whole-brain-single-cell RNA sequencing in a Drosophila model of sickness revealed that glia, rather than neurons, undergo the most extensive transcriptional remodeling and follow up experiments uncovered a neuron-glia axis that drives sickness sleep behavior. Specifically, the process requires octopaminergic signaling in ensheathing glia (EG) and it is required for a coupled wave of glial and neuronal activation across the brain. EG gap junction functional coupling facilitates brain wide activation, which ultimately promotes sickness behavior through glutamatergic signaling. Altogether, these findings elevate glia from passive supporters to active coordinators of sickness behavior, opening new avenues for understanding the neuromodulatory basis of behavioral state drifts sleep, fatigue, and malaise.
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