1,992 research outputs found

    M. T. Cic. De Officiis Libri Tres

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    M. T. CIC. DE OFFICIIS LIBRI TRES M. T. Cic. De Officiis Libri Tres ( - ) Titelseite ( - ) Liber I. (3) Liber II. (48) Liber III. (75) Cato Maior, Vel de Senectute (109) Laelivs, Vel Del Amicitia (135) Paradoxa Sex, Ad M. Brvtvm (163) Somnivm Scipionis, Ex Lib. VI. Ciceronis de Repvblica (177) Annotationes, et Castigationes (184) In Librvm I. (184) In Librvm II. (189) In Librvm III. (191) In Lib. De Senect. (194) In Lib. De Amicitia. (198) In Paradoxa (201

    Designing and Testing a Quench Heater for a 16 T CIC Dipole

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    The purpose of this project is to create and design a quench heater for the 16 T Cable-in-Conduit (CIC) superconducting magnet. This magnet will be used to create stronger and more cost-effective particle accelerators. The quench heater is a device that is designed to protect the magnet from an unexpected quench. In order to achieve this, the quench heater must be able to produce enough heat to heat the superconducting wires in the CIC cable to approximately 9K over the course of 10 ms. To design a quench heater in this way, it is required to find the dimensions needed using simulations. After finding the required dimensions, a Computer Assisted Design (CAD) file was created so the design could be machined to the exact specifications. Then, using liquid helium and one cable, we tested if the heater would properly heat the cable. Thermocouple wires were integrated into the cable to measure the temperature of the wires during the experiment. This physical experiment has not yet been conducted and thus the results are still unknown. It is expected that the quench heater will be able to properly heat the cable over the 10 ms timeframe. If this experiment is successful, this design for a quench heater will be used for the 16 T CIC cable

    Cancer-Initiating Cells from Colorectal cancer Patients Escape from T Cell-Mediated Immunosurveillance In Vitro through Membrane-Bound IL-4

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    Cancer-initiating cells (CICs) that are responsible for tumor initiation, propagation, and resistance to standard therapies have been isolated from human solid tumors, including colorectal cancer (CRC). The aim of this study was to obtain an immunological profile of CRC-derived CICs and to identify CIC-associated target molecules for T cell immunotherapy. We have isolated cells with CIC properties along with their putative non-CIC autologous counterparts from human primary CRC tissues. These CICs have been shown to display “tumor-initiating/stemness” properties, including the expression of CIC-associated markers (e.g., CD44, CD24, ALDH-1, EpCAM, Lgr5), multipotency, and tumorigenicity following injection in immunodeficient mice. The immune profile of these cells was assessed by phenotype analysis and by in vitro stimulation of PBMCs with CICs as a source of Ags. CICs, compared with non-CIC counterparts, showed weak immunogenicity. This feature correlated with the expression of high levels of immu- nomodulatory molecules, such as IL-4, and with CIC-mediated inhibitory activity for anti-tumor T cell responses. CIC-associated IL-4 was found to be responsible for this negative function, which requires cell-to-cell contact with T lymphocytes and which is impaired by blocking IL-4 signaling. In addition, the CRC-associated Ag COA-1 was found to be expressed by CICs and to represent, in an autologous setting, a target molecule for anti-tumor T cells. Our study provides relevant information that may contribute to designing new immunotherapy protocols to target CICs in CRC patient

    Loss of Capicua alters early T cell development and predisposes mice to T cell lymphoblastic leukemia/lymphoma

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    Capicua (CIC) regulates a transcriptional network downstream of the RAS/MAPK signaling cascade. In Drosophila, CIC is important for many developmental processes, including embryonic patterning and specification of wing veins. In humans, CIC has been implicated in neurological diseases, including spinocerebellar ataxia type 1 (SCA1) and a neurodevelopmental syndrome. Additionally, we and others have reported mutations in CIC in several cancers. However, whether CIC is a tumor suppressor remains to be formally tested. In this study, we found that deletion of Cic in adult mice causes T cell acute lymphoblastic leukemia/lymphoma (T-ALL). Using hematopoietic-specific deletion and bone marrow transplantation studies, we show that loss of Cic from hematopoietic cells is sufficient to drive T-ALL. Cic-null tumors show up-regulation of the KRAS pathway as well as activation of the NOTCH1 and MYC transcriptional programs. In sum, we demonstrate that loss of CIC causes T-ALL, establishing it as a tumor suppressor for lymphoid malignancies. Moreover, we show that mouse models lacking CIC in the hematopoietic system are robust models for studying the role of RAS signaling as well as NOTCH1 and MYC transcriptional programs in T-ALL

    Plut.90 sup.88

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    Plut.90 sup.77/2

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