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University of North Carolina at Chapel Hill | Chapel Hill, North Carolina | United States | 28 days ago
of NEC, microfluidic gut-on-a-chip platform, and patient samples to study the intestinal mucosal immune response and understand the signaling pathways that are involved in the pro-inflammatory response
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Research Associate FLSA Exempt CAMPUS SPECIFIC INFORMATION The Graduate Center (GC) is the focal point for advanced teaching and research at the City University of New York (CUNY), the nation's largest urban
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strategies that are best for different subgroups, and to implement evidence at the point of care to guide clinical decisions. The BIO5 Institute at the University of Arizona brings together world-class
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patch-clamp electrophysiology, and mouse tissue processing to investigate how neural circuits, synaptic physiology, and neuroinflammatory pathways contribute to pain modulation. Candidates should hold a
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. Preferred Qualifications: Strong background in ultrasound imaging Experience in photoacoustic imaging Strong hands-on skills in medical device development or strong computational skills including signal
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will also be considered. Experience with electronic health records, physiological signal processing, or predictive analytics in healthcare. Certifications/Licenses Required Knowledge, Skills, and
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with a team in an interdisciplinary environment. Good: - Experience with optics, spectroscopy, and optically active point defects in quantum materials - Experience with device synthesis and integration
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the analysis of massive datasets. Extensive experience in signal processing and advanced statistical inference (e.g., Bayesian statistics, Fourier analysis) for extracting robust patterns from noisy, high
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of maladaptive innate immune pathways in neuronal stress and death, and (2) examine how mito-nuclear retrograde signaling contributes to microglial dysfunction and senescence in Alzheimerâ™s disease and related
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of maladaptive innate immune pathways in neuronal stress and death, and (2) examine how mito-nuclear retrograde signaling contributes to microglial dysfunction and senescence in Alzheimer’s disease and related