Browsing by Author "Li, Jun"

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    The influence of recent hotel amenities and green practices on guests’ price premium and revisit intention [Summary]
    Kim, Woo Gon; Li, Jun; Kim, Yunkyong; Han, Justin; Soo, Jin (Virginia Tech, 2017)
    This study examines the influence of hotels’ green practices, recent amenities, and traditionally salient attributes on customers’ overall online evaluation, revisit intention and hotel performance. The researchers acquired data from more than one hundred US hotels located across different states with the assistance of an international hotel chain. In order to demonstrate the incremental information content of recently-adopted hotel amenities and levels of green initiatives, the study compared two extended models with the basic model, which incorporates only salient attributes such as cleanliness, location, room, service and value.
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    Phosphorylation of guanosine monophosphate reductase triggers a GTP-dependent switch from pro- to anti-oncogenic function of EPHA4
    Wolff, David W.; Deng, Zhiyong; Bianchi-Smiraglia, Anna; Foley, Colleen E.; Han, Zhannan; Wang, Xingyou; Shen, Shichen; Rosenberg, Masha M.; Moparthy, Sudha; Yun, Dong Hyun; Chen, Jialin; Baker, Brian K.; Roll, Matthew; Magiera, Andrew J.; Li, Jun; Hurley, Edward; Feltri, Maria Laura; Cox, Anderson O.; Lee, Jingyun; Furdui, Cristina M.; Liu, Liang; Bshara, Wiam; LaConte, Leslie E. W.; Kandel, Eugene S.; Pasquale, Elena B.; Qu, Jun; Hedstrom, Lizbeth; Nikiforov, Mikhail A. (Cell Press, 2022-02-10)
    Signal transduction pathways post-translationally regulating nucleotide metabolism remain largely unknown. Guanosine monophosphate reductase (GMPR) is a nucleotide metabolism enzyme that decreases GTP pools by converting GMP to IMP. We observed that phosphorylation of GMPR at Tyr267 is critical for its activity and found that this phosphorylation by ephrin receptor tyrosine kinase EPHA4 decreases GTP pools in cell protrusions and levels of GTP-bound RAC1. EPHs possess oncogenic and tumor-suppressor activities, although the mechanisms underlying switches between these two modes are poorly understood. We demonstrated that GMPR plays a key role in EPHA4-mediated RAC1 suppression. This supersedes GMPR-independent activation of RAC1 by EPHA4, resulting in a negative overall effect on melanoma cell invasion and tumorigenicity. Accordingly, EPHA4 levels increase during melanoma progression and inversely correlate with GMPR levels in individual melanoma tumors. Therefore, phosphorylation of GMPR at Tyr267 is a metabolic signal transduction switch controlling GTP biosynthesis and transformed phenotypes.
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    Photoacoustic microscopy reveals the hemodynamic basis of sphingosine 1-phosphate-induced neuroprotection against ischemic stroke
    Cao, Rui; Li, Jun; Kharel, Yugesh; Zhang, Chenchu; Morris, Emily; Santos, Webster L.; Lynch, Kevin R.; Zuo, Zhiyi; Hu, Song (IvySpring, 2018-11-29)
    Rationale: Emerging evidence has suggested that sphingosine 1-phosphate (S1P), a bioactive metabolite of sphingolipids, may play an important role in the pathophysiological processes of cerebral hypoxia and ischemia. However, the influence of S1P on cerebral hemodynamics and metabolism remains unclear. Material and Methods: Uniquely capable of high-resolution, label-free, and comprehensive imaging of hemodynamics and oxygen metabolism in the mouse brain without the influence of general anesthesia, our newly developed head-restrained multi-parametric photoacoustic microscopy (PAM) is well suited for this mechanistic study. Here, combining the cutting-edge PAM and a selective inhibitor of sphingosine kinase 2 (SphK2) that can increase the blood S1P level, we investigated the role of S1P in cerebral oxygen supply-demand and its neuroprotective effects on global brain hypoxia induced by nitrogen gas inhalation and focal brain ischemia induced by transient middle cerebral artery occlusion (tMCAO). Results: Inhibition of SphK2, which increased the blood S1P, resulted in the elevation of both arterial and venous sO2 in the hypoxic mouse brain, while the cerebral blood flow remained unchanged. As a result, it gradually and significantly reduced the metabolic rate of oxygen. Furthermore, pre-treatment of the mice subject to tMCAO with the SphK2 inhibitor led to decreased infarct volume, improved motor function, and reduced neurological deficit, compared to the control treatment with a less potent R-enantiomer. In contrast, post-treatment with the inhibitor showed no improvement in the stroke outcomes. The failure for the post-treatment to induce neuroprotection was likely due to the relatively slow hemodynamic responses to the SphK2 inhibitor-evoked S1P intervention, which did not take effect before the brain injury was induced. Conclusions: Our results reveal that elevated blood S1P significantly changes cerebral hemodynamics and oxygen metabolism under hypoxia but not normoxia. The improved blood oxygenation and reduced oxygen demand in the hypoxic brain may underlie the neuroprotective effect of S1P against ischemic stroke.