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Yalai Bai

Researcher at Yale University

Publications -  43
Citations -  1184

Yalai Bai is an academic researcher from Yale University. The author has contributed to research in topics: Breast cancer & Medicine. The author has an hindex of 15, co-authored 28 publications receiving 835 citations. Previous affiliations of Yalai Bai include Icahn School of Medicine at Mount Sinai.

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Early and multiple origins of metastatic lineages within primary tumors.

TL;DR: T tumor phylogenetics is performed using molecular evolutionary models, reconstructed ancestral states of somatic mutations, and inferred cancer chronograms to yield three conclusions, one of which is that in contrast to a linear model of cancer progression, metastases can originate from divergent lineages within primary tumors.
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Interferon-γ Induces Human Vascular Smooth Muscle Cell Proliferation and Intimal Expansion by Phosphatidylinositol 3-Kinase–Dependent Mammalian Target of Rapamycin Raptor Complex 1 Activation

TL;DR: This work establishes an immunologic stimulus for mTORC1 signaling in vascular smooth muscle cells, emphasizes that m TORC1 activation is critical in immune-mediated vascular remodeling, and provides further mechanistic insight into the successful clinical application of rapamycin therapy for atherosclerosis and graft arteriosclerosis.
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Ki67 reproducibility using digital image analysis: an inter-platform and inter-operator study.

TL;DR: The reproducibility of Ki67 measurement between three image analysis platforms with supervised classifiers performed by the same operator, by multiple operators, and finally in prognostic potential is investigated to justify multi-institutional DIA studies to assess clinical utility.
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Recruitment of CXCR3+ and CCR5+ T cells and production of interferon-γ-inducible chemokines in rejecting human arteries

TL;DR: Recruitment of allogeneic T cells to different vascular compartments correlated with the expression of chemokines and their receptors are investigated, and the suggestion that the arterial media may be a site of immunological privilege is reinforced.