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Clare Bao

Researcher at Johns Hopkins University School of Medicine

Publications -  24
Citations -  4900

Clare Bao is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Nitric oxide synthase & Nitric oxide. The author has an hindex of 21, co-authored 24 publications receiving 4695 citations. Previous affiliations of Clare Bao include Johns Hopkins University.

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Leptin regulates proinflammatory immune responses

TL;DR: An important and novel function for leptin is identified: up-regulation of inflammatory immune responses, which may provide a common pathogenetic mechanism that contributes to several of the major complications of obesity.
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Hyaluronan (HA) fragments induce chemokine gene expression in alveolar macrophages. The role of HA size and CD44.

TL;DR: The hypothesis that HA fragments generated during inflammation induce the expression of macrophage genes which are important in the development and maintenance of the inflammatory response is supported.
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Nitric Oxide Regulates Exocytosis by S-Nitrosylation of N-ethylmaleimide-Sensitive Factor

TL;DR: It is shown that NO inhibits exocytosis of Weibel-Palade bodies, endothelial granules that mediate vascular inflammation and thrombosis, by regulating the activity of N-ethylmaleimide-sensitive factor (NSF).
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P53-induced microRNA-107 inhibits HIF-1 and tumor angiogenesis

TL;DR: It is shown that p53 regulates hypoxic signaling through the transcriptional regulation of microRNA-107, a microRNA expressed by human colon cancer specimens and regulated by p53, and that miR-107 can mediate p53 regulation of Hypoxic signaling and tumor angiogenesis.
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Hyaluronan Fragments Induce Nitric-oxide Synthase in Murine Macrophages through a Nuclear Factor κB-dependent Mechanism *

TL;DR: Examination of the effect of low molecular weight fragments of the extracellular matrix glycosaminoglycan hyaluronan (HA) on the induction of nitric-oxide synthase (iNOS) in macrophages supports the hypothesis that HA may be an important regulator of macrophage activation at sites of chronic tissue inflammation.