MITOCHONDRIAL APOPTOSIS-INDUCED INFLAMMATION
    61.
    发明申请
    MITOCHONDRIAL APOPTOSIS-INDUCED INFLAMMATION 审中-公开
    麻醉诱导诱导的炎症

    公开(公告)号:WO2012016145A2

    公开(公告)日:2012-02-02

    申请号:PCT/US2011045893

    申请日:2011-07-29

    IPC分类号: A61K31/708

    CPC分类号: A61K31/708

    摘要: Various embodiments of the present invention describe a method of treating inflammation, an inflammatory disease, an inflammatory disease condition and/or an autoimmune disease in a subject in need thereof. The method can comprise providing a composition comprising a mitochondrial apoptosis inhibitor or an oxidative nucleotide and administering the composition to the subject to treat the inflammation, the inflammatory disease, the inflammatory disease condition and/or the autoimmune disease. Various embodiments of the present invention is based on the mitochondria acting as a unifying point that integrates diverse NLRP3 stimuli and that mitochondrial dysfunction and apoptosis of macrophages are critical steps in various danger signal-induced NLRP3 inflammasome activation.

    摘要翻译: 本发明的各种实施方案描述了在有需要的受试者中治疗炎症,炎性疾病,炎性疾病状况和/或自身免疫性疾病的方法。 该方法可以包括提供包含线粒体凋亡抑制剂或氧化核苷酸的组合物,并将该组合物施用于受试者以治疗炎症,炎性疾病,炎性疾病状况和/或自身免疫性疾病。 本发明的各种实施方案基于线粒体,其作为整合不同NLRP3刺激的统一点,并且线粒体功能障碍和巨噬细胞的凋亡是各种危险信号诱导的NLRP3炎性体激活的关键步骤。

    BOOSTING IMMUNE DEFENSE BY UPREGULATING CCAAT/ENHANCER BINDING PROTEIN EPSILON
    62.
    发明申请
    BOOSTING IMMUNE DEFENSE BY UPREGULATING CCAAT/ENHANCER BINDING PROTEIN EPSILON 审中-公开
    通过升级CCAAT /增强蛋白结合蛋白EPSILON来增强免疫力

    公开(公告)号:WO2011133692A1

    公开(公告)日:2011-10-27

    申请号:PCT/US2011/033286

    申请日:2011-04-20

    IPC分类号: A61K31/435 A61K47/00

    摘要: The present invention demonstrates the important role of C/EBP ε in innate immune response against pathogens. Specifically, the inventors showed that in the absence of functional C/EBP ε , mice are severely impaired in their ability to clear S. aureus infection. Neutrophils are particularly affected, and susceptibility to S. aureus can be rectified by treatment with interferon-gamma (IFN-γ). Importantly, increased activity of C/EBP ε , either by induced overexpression of C/EBPE or by application of nicotinamide or an analog, derivative or salt thereof, dramatically enhances immune killing of S. aureus and leads to amelioration of infection.

    摘要翻译: 本发明证实了C / EBPe在针对病原体的先天免疫应答中的重要作用。 具体地说,本发明人表明,在没有功能性C / EBPe的情况下,小鼠在清除金黄色葡萄球菌感染的能力方面严重受损。 嗜中性粒细胞特别受影响,通过用干扰素-γ(IFN-γ)治疗可以矫正对金黄色葡萄球菌的易感性。 重要的是,通过C / EBPE的诱导过表达或通过应用烟酰胺或其类似物衍生物或盐来增加C / EBPe的活性,显着地增强了金黄色葡萄球菌的免疫杀伤并导致了感染的改善。

    METHOD AND SYSTEM FOR PLAQUE CHARACTERIZATION
    66.
    发明申请
    METHOD AND SYSTEM FOR PLAQUE CHARACTERIZATION 审中-公开
    方法和系统的PLAQUE特征

    公开(公告)号:WO2011069120A1

    公开(公告)日:2011-06-09

    申请号:PCT/US2010/058979

    申请日:2010-12-03

    IPC分类号: A61B5/05

    摘要: A method of quantifying plaques imaged by cardiac computed tomography angiography ("CCTA") scan data. Calcified and non-calcified component thresholds are determined based at least in part on attenuation values of a pool of blood in the CCTA scan data. An epicardial fat threshold is determined and used to classify epicardial fat in the CCTA scan data. A portion of CCTA scan data positioned between a detected outer boundary of the coronary artery and a portion classified as lumen is classified as arterial wall. NCP and CP seeds are identified in the arterial wall portion. Portions of the CCTA scan data continuous with a NCP seed and having attenuation values greater than an artery wall value and less than the NCP threshold are classified as NCP, and portions of the CCTA scan data continuous with the CP seed and having attenuation values greater than the CP threshold are classified as CP.

    摘要翻译: 定量通过心脏计算机断层摄影(“CCTA”)扫描数据成像的斑块的方法。 钙化和非钙化组分阈值至少部分地基于CCTA扫描数据中血液池的衰减值来确定。 确定心外膜脂肪阈值并用于对CCTA扫描数据中的心外膜进行分类。 位于冠状动脉的检测到的外边界与被分类为管腔的部分之间的CCTA扫描数据的一部分被分类为动脉壁。 在动脉壁部分中鉴定出NCP和CP种子。 具有与NCP种子连续并具有大于动脉壁值且小于NCP阈值的衰减值的CCTA扫描数据的部分被分类为NCP,并且CCTA扫描数据的部分与CP种子连续并且具有大于 CP阈值被分类为CP。

    TOX3 AS A BIOMARKER FOR BREAST CANCER
    67.
    发明申请
    TOX3 AS A BIOMARKER FOR BREAST CANCER 审中-公开
    TOX3作为乳腺癌的生物标志物

    公开(公告)号:WO2011069014A1

    公开(公告)日:2011-06-09

    申请号:PCT/US2010/058795

    申请日:2010-12-02

    发明人: KAYE, Jonathan

    IPC分类号: G01N33/48 G01N33/53

    摘要: The present invention relates to biomarkers useful for the diagnosis, prognosis and treatment of cancer. In an embodiment, the invention relates to the biomarker, TOX3. The inventive compositions and methods are also drawn to the use of anti-TOX3 antibodies and TOX3 nucleic acids and peptides for both detection and modulation of TOX3.

    摘要翻译: 本发明涉及可用于癌症的诊断,预后和治疗的生物标志物。 在一个实施方案中,本发明涉及生物标志物TOX3。 本发明的组合物和方法也被用于使用抗TOX3抗体和TOX3核酸和肽来检测和调节TOX3。

    GENERATION OF INDUCED PLURIPOTENT STEM CELLS WITHOUT THE USE OF VIRAL VECTORS
    68.
    发明申请
    GENERATION OF INDUCED PLURIPOTENT STEM CELLS WITHOUT THE USE OF VIRAL VECTORS 审中-公开
    不使用病毒载体诱导的多功能干细胞的制备

    公开(公告)号:WO2010059806A3

    公开(公告)日:2010-07-15

    申请号:PCT/US2009065117

    申请日:2009-11-19

    IPC分类号: C12N5/07 C12N15/62

    摘要: Presented herein, generally, are methods for generating reprogrammed mammalian cells, e.g., induced pluripotent stem cells, from differentiated mammalian cells without the use of viral or plasmid vectors. In one aspect, the methods involve contacting a differentiated cell with transducible polypeptides comprising a reprogramming factor polypeptide linked to a cell penetration peptide so that a reprogrammed mammalian cell that exhibits at least one characteristic of pluripotency is generated. Also presented herein are methods for cardiac differentiation of a mammalian cell without the use of viral or plasmid vectors. In one aspect, such methods involve contacting a mammalian cell exhibiting at least one characteristic of pluripotency with a transducible polypeptide, so that cardiac differentiation of the cell occurs.

    摘要翻译: 本文一般公开了用于从分化的哺乳动物细胞产生重编程的哺乳动物细胞(例如诱导的多能干细胞)而不使用病毒或质粒载体的方法。 一方面,所述方法包括使分化的细胞与包含与细胞穿透肽连接的重编程因子多肽的转导多肽接触,从而产生表现出多能性的至少一种特征的重编程哺乳动物细胞。 本文还提供了在不使用病毒或质粒载体的情况下用于哺乳动物细胞的心脏分化的方法。 一方面,此类方法涉及使展现出多能性的至少一个特征的哺乳动物细胞与转导多肽接触,从而发生细胞的心脏分化。

    SHORT-FORM HUMAN MD-2 AS A NEGATIVE REGULATOR OF TOLL-LIKE RECEPTOR 4 SIGNALING
    70.
    发明申请
    SHORT-FORM HUMAN MD-2 AS A NEGATIVE REGULATOR OF TOLL-LIKE RECEPTOR 4 SIGNALING 审中-公开
    短型人MD-2作为类似受体4信号的负调节因子

    公开(公告)号:WO2010033294A1

    公开(公告)日:2010-03-25

    申请号:PCT/US2009/050317

    申请日:2009-07-10

    IPC分类号: C07K14/00 A61K38/00

    摘要: The present invention is based on a novel, alternatively spliced human isoform of MD-2 (MD-2s). In various embodiments, the invention relates to methods and kits for preventing, reducing the likelihood of developing and/or treating various conditions using MD-2s. The invention also describes methods of determining the risk of a subject to various conditions.

    摘要翻译: 本发明基于MD-2(MD-2)的新型可变剪接的人同种型。 在各种实施方案中,本发明涉及用于使用MD-2s预防,降低开发和/或治疗各种病症的可能性的方法和试剂盒。 本发明还描述了确定受试者在各种条件下的风险的方法。