20 research outputs found

    The Journal of the Friends' Historical Society vol. 3 No. 3

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    1. Notices. 2. Notes and Queries. 3. Letter from William Penn. 4. David Lloyd II. 5. Friends on the Atlantic. 6. King's Briefs the Forerunners of Mutual Insurance Societies. 7. Whitefield's Estimate of Quakerism. 8. Earlham College Library, Richmond, Ind. 9. Editors' Notes. 10. Large Gatherings of Friends. 11. Meeting Records I. 12. Friends in Current Literature. 13. A Quotation in the London Y.M. Epistle. 14. List of Officers for 1906-7. 15. Accounts and Balance Sheet for 1905

    A Context-Specific Role for Retinoblastoma Protein-Dependent Negative Growth Control in Suppressing Mammary Tumorigenesis

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    The ability to respond to anti-growth signals is critical to maintain tissue homeostasis and loss of this negative growth control safeguard is considered a hallmark of cancer. Negative growth regulation generally occurs during the G0/G1 phase of the cell cycle, yet the redundancy and complexity among components of this regulatory network has made it difficult to discern how negative growth cues protect cells from aberrant proliferation.The retinoblastoma protein (pRB) acts as the final barrier to prevent cells from entering into the cell cycle. By introducing subtle changes in the endogenous mouse Rb1 gene (Rb1(ΔL)), we have previously shown that interactions at the LXCXE binding cleft are necessary for the proper response to anti-growth signals such as DNA damage and TGF-ÎČ, with minimal effects on overall development. This disrupts the balance of pro- and anti-growth signals in mammary epithelium of Rb1(ΔL/ΔL) mice. Here we show that Rb1(ΔL/ΔL) mice are more prone to mammary tumors in the Wap-p53(R172H) transgenic background indicating that negative growth regulation is important for tumor suppression in these mice. In contrast, the same defect in anti-growth control has no impact on Neu-induced mammary tumorigenesis.Our work demonstrates that negative growth control by pRB acts as a crucial barrier against oncogenic transformation. Strikingly, our data also reveals that this tumor suppressive effect is context-dependent

    Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

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    Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

    Inaugural Address of Isaac Sharpless, May 19, 1887

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    Isaac Sharpless served as President of Haverford College from 1887-1917

    The story of a small college,

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    "This book, partly historical, partly autobiographical, is an account of the development of the ideals and policy of Haverford College."--Pref.Mode of access: Internet

    The American college

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    Includes bibliographical references.Mode of access: Internet

    Political leaders of provincial Pennsylvania,

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    Introduction.--William Penn.--Thomas Lloyd.--David Lloyd.--James Logan.--John Kinsey.--Isaac Norris.--James Pemberton.--John Dickinson.Mode of access: Internet

    Astronomy for schools and general readers.

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    Mode of access: Internet
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