382 research outputs found

    Congenitally absent right coronary artery in adult

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    Background: A 44-year-old male patient with atrial fibrillation and cardiac insufficiency (NYHA IV) presented for evaluation for heart transplantation. He was referred for cardiac CT for assessment of potential restrictive cardiomyopathy and evaluation of his right ventricle. Cardiac CT was performed utilizing a dual-source CT scanner. ECG-adapted tube current was used to reduce radiation exposure. No pericardial calcifications were noted. The right atrium and the inferior vena cava were dilated with 82 x 58 mm and 47 mm diameter, respectively. There was no evidence of coronary artery disease

    Radiopyrolysis

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    Statement of responsibility on title-page reads: E.A. Mason, T.H. Timmins, D.T. Morgan, and W.N. Bley"Issued: October 1966.""MIT-334-70 Reactor Technology."Also issued by T.H. Timmins and supervised by E.A. Mason as an Sc. D. thesis , Massachusetts Institute of Technology, Dept. of Nuclear Engineering, 1967Includes bibliographical references (pages A6.1-A6.7)MIT DSR Project no. 79819Work performed for the Savannah River Operations Office, U.S. Atomic Energy Commission under Contract no. AT(38-1)-33

    Friction factor and heat transfer correlation for irradiated organic coolants

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    "September 1965."Series statement handwritten on cover"MIT-334-23 Chemistry."Also written as an M.S. theses written by the first author and advised by the second author, Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 1966Includes bibliographical references (pages 163-165)M.I.T. DSR Project no. 9819Work performed for the Savannah River Operations Office, U.S. Atomic Energy Commission under contract no. AT(38-1)-33

    The oncofetal RNA-binding protein IGF2BP1 is a druggable, post-transcriptional super-enhancer of E2F-driven gene expression in cancer

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    The IGF2 mRNA-binding protein 1 (IGF2BP1) is a non-catalytic post-transcriptional enhancer of tumor growth upregulated and associated with adverse prognosis in solid cancers. However, conserved effector pathway(s) and the feasibility of targeting IGF2BP1 in cancer remained elusive. We reveal that IGF2BP1 is a post-transcriptional enhancer of the E2F-driven hallmark in solid cancers. IGF2BP1 promotes G1/S cell cycle transition by stabilizing mRNAs encoding positive regulators of this checkpoint like E2F1. This IGF2BP1-driven shortening of the G1 cell cycle phase relies on 3′UTR-, miRNA- and m6A-dependent regulation and suggests enhancement of cell cycle progression by m6A-modifications across cancers. In addition to E2F transcription factors, IGF2BP1 also stabilizes E2F-driven transcripts directly indicating post-transcriptional 'super'-enhancer role of the protein in E2F-driven gene expression in cancer. The small molecule BTYNB disrupts this enhancer function by impairing IGF2BP1-RNA association. Consistently, BTYNB interferes with E2F-driven gene expression and tumor growth in experimental mouse tumor models

    Organic moderator-coolant in-pile irradiation loop for the MIT nuclear reactor

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    Includes bibliographical references (leaf 34)Progress report; to July 1, 1961Work performed under contract with Atomics International to November, 1960, and under contract with the Atomic Energy Commission, Idaho Operations Office, after November, 1960Division of Sponsored Research Project no. 8710Atomics International contract no. N9-S-514Atomic Energy Commission contract no. AT(10-1)-106

    A fast ILP-based Heuristic for the robust design of Body Wireless Sensor Networks

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    We consider the problem of optimally designing a body wireless sensor network, while taking into account the uncertainty of data generation of biosensors. Since the related min-max robustness Integer Linear Programming (ILP) problem can be difficult to solve even for state-of-the-art commercial optimization solvers, we propose an original heuristic for its solution. The heuristic combines deterministic and probabilistic variable fixing strategies, guided by the information coming from strengthened linear relaxations of the ILP robust model, and includes a very large neighborhood search for reparation and improvement of generated solutions, formulated as an ILP problem solved exactly. Computational tests on realistic instances show that our heuristic finds solutions of much higher quality than a state-of-the-art solver and than an effective benchmark heuristic.Comment: This is the authors' final version of the paper published in G. Squillero and K. Sim (Eds.): EvoApplications 2017, Part I, LNCS 10199, pp. 1-17, 2017. DOI: 10.1007/978-3-319-55849-3\_16. The final publication is available at Springer via http://dx.doi.org/10.1007/978-3-319-55849-3_1

    Defective removal of ribonucleotides from DNA promotes systemic autoimmunity

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    Genome integrity is continuously challenged by the DNA damage that arises during normal cell metabolism. Biallelic mutations in the genes encoding the genome surveillance enzyme ribonuclease H2 (RNase H2) cause Aicardi-Goutières syndrome (AGS), a pediatric disorder that shares features with the autoimmune disease systemic lupus erythematosus (SLE). Here we determined that heterozygous parents of AGS patients exhibit an intermediate autoimmune phenotype and demonstrated a genetic association between rare RNASEH2 sequence variants and SLE. Evaluation of patient cells revealed that SLE- and AGS-associated mutations impair RNase H2 function and result in accumulation of ribonucleotides in genomic DNA. The ensuing chronic low level of DNA damage triggered a DNA damage response characterized by constitutive p53 phosphorylation and senescence. Patient fibroblasts exhibited constitutive upregulation of IFN-stimulated genes and an enhanced type I IFN response to the immunostimulatory nucleic acid polyinosinic:polycytidylic acid and UV light irradiation, linking RNase H2 deficiency to potentiation of innate immune signaling. Moreover, UV-induced cyclobutane pyrimidine dimer formation was markedly enhanced in ribonucleotide-containing DNA, providing a mechanism for photosensitivity in RNase H2-associated SLE. Collectively, our findings implicate RNase H2 in the pathogenesis of SLE and suggest a role of DNA damage-associated pathways in the initiation of autoimmunity
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