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Xi Chen

Researcher at University of California, Davis

Publications -  629
Citations -  28889

Xi Chen is an academic researcher from University of California, Davis. The author has contributed to research in topics: Sialic acid & Medicine. The author has an hindex of 71, co-authored 548 publications receiving 22541 citations. Previous affiliations of Xi Chen include University of California, Riverside & Cleveland Clinic.

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MicroRNA-31 initiates lung tumorigenesis and promotes mutant KRAS-driven lung cancer

TL;DR: It is determined that miR-31 is overexpressed in human lung adenocarcinoma and this overexpression independently correlates with decreased patient survival and is distinguished as a driver of lung tumorigenesis that promotes mutant KRAS-mediated oncogenesis and reveals that mi R-31 directly targets and reduces expression of negative regulators of RAS/MAPK signaling.
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Loss of claudin-3 expression induces IL6/gp130/Stat3 signaling to promote colon cancer malignancy by hyperactivating Wnt/β-catenin signaling

TL;DR: A novel and tissue-specific role of claudin-3, a tight junction integral protein, in inhibiting colon cancer progression by serving as the common rheostat of Stat-3 and Wnt-signaling activation is discovered.
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Predictors of Hemodynamic Instability During Surgery for Pheochromocytoma

TL;DR: Tumor size, open adrenalectomy, and type of α blockade were associated with intraoperative HDI during pheochromocytoma resection and Selective blockade was associated with significantly more episodes of intraoperative hypertension but no perioperative adverse outcomes.
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Cloning and expression of rat lung acidic Ca2+-independent PLA2 and its organ distribution

TL;DR: A clone for a rat acidic Ca2+-independent phospholipase A2(aiPLA2) was isolated from a cDNA library prepared from rat granular pneumocytes with a probe based on the human aiPLA2 sequence and results show marked enrichment of a iPLA2 in the lung compared with the other organs and suggest translational control of ai PLA2 expression.
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Progranulin Does Not Bind Tumor Necrosis Factor (TNF) Receptors and Is Not a Direct Regulator of TNF-Dependent Signaling or Bioactivity in Immune or Neuronal Cells

TL;DR: The neuroinflammatory phenotype associated with PGRN deficiency in the CNS is not a direct consequence of the loss of TNF antagonism, but may be a secondary response by glia to disrupted interactions between P GRN and Sortilin and/or other binding partners yet to be identified.