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Ruirui Qi

Researcher at Second Military Medical University

Publications -  19
Citations -  295

Ruirui Qi is an academic researcher from Second Military Medical University. The author has contributed to research in topics: Motion sickness & Mecamylamine. The author has an hindex of 8, co-authored 17 publications receiving 203 citations.

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Journal ArticleDOI

Motion Sickness: Current Knowledge and Recent Advance.

TL;DR: This review summarizes the current knowledge about pathogenesis and pathophysiology, prediction, evaluation, and countermeasures of MS, and indicates that the sensory conflict hypothesis is the most widely accepted theory for MS.
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The hepatocyte-specific HNF4α/miR-122 pathway contributes to iron overload–mediated hepatic inflammation

TL;DR: It is reported that IO induced similar inflammatory responses in human primary hepatocytes and Thp-1-derived macrophages and hepatocyte-specific overexpression of miR-122 rescued IO-mediated hepatic inflammation.
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Evidence for a Role of Orexin/Hypocretin System in Vestibular Lesion-Induced Locomotor Abnormalities in Rats.

TL;DR: The results suggested that the alteration of OXA expression might contribute to locomotor abnormalities after acute vestibular lesion and the orexin receptors might be the potential therapeutic targets for Vestibular disorders.
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CCL2 is Upregulated by Decreased miR-122 Expression in Iron-Overload-Induced Hepatic Inflammation.

TL;DR: A dual-luciferase reporter assay is used to prove that miR-122 regulates CCL2 expression through direct binding to its complementary sequence in the CCL1 mRNA 3’UTR, and propose the roles of miR -122/CCL2 in IO-induced hepatic inflammation.
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Sex and Age Differences in Motion Sickness in Rats: The Correlation with Blood Hormone Responses and Neuronal Activation in the Vestibular and Autonomic Nuclei.

TL;DR: The results suggested that the sex and age differences in motion sickness may not correlate with stress hormone responses and habituation, and the age-dependent decline inmotion sickness susceptibility might be mainly attributed to the neuronal activity changes in vestibulo-autonomic pathways contributing to homeostasis regulation during motion sickness.