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下肢长短不等之疗法

中华医学杂志 1933年第4期19卷 642-643页

作者： E. W. hey-groves, med. ann.al, p. 264, 1932 齐大医学院编译部齐大医学院编译部

下肢长短不等之原因,大抵有四:(一)因骨折后之连接不良而致者,例如二折骨块重叠,致较常为短。(二)因髋关节强硬不正而致者,此在关节染脓毒后见之。(三)因婴儿瘫痪而致者。(四)因先天性髋关节脱骱而致者。对于此数疾患,用预防法自然优于

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骨盆折之要点

中华医学杂志 1932年第6期18卷 1081-1082页

作者： med. ann. 1921. p. 197 齐大编译部齐大编译部

Wakeley氏注意髂骨有一最厚而坚之块,起於髋臼,继斜向上後内至骶髂关节,以支持脊柱之重量。髂骨折多在此块之前或後,而不累及此块。挽言之,折断线多在骶骨之旁块或闭孔周围之骨。

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坐骨直肠窝脓肿

中华医学杂志 1932年第6期18卷 1080-1081页

作者： J. P. Lockhart Mummery, med. ann., 1931, p. 249 齐大编译部齐大编译部

此脓肿之要点在常发生直肠瘘。其原因为细菌,该菌或由直肠之淋巴管至坐骨直肠窝上部之腺,使之生脓。其因直肠直接受损伤者较少,因结核病者不及18%。常见之细菌为大肠桿菌,链球菌,粪链球菌等,亦有受混合传染者。

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膀胱外翻

中华医学杂志 1933年第4期19卷 643-643页

作者： J. Fraser, med. ann. p. 66 1932 齐大医学院编译部齐大医学院编译部

膀胱外翻之畸形,系膀胱缺乏前壁,而腹下部之中央处亦有缺,故在耻骨联合上可见有膀胱后壁之粘膜,且可见二输尿管之口并见尿由之向下流出。而不入于尿道。英美二派外科医师对于治疗此病之意见相同。其法:即开腹将左右二输尿管移于

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Leptin-induced Notch and IL-1 signaling crosstalk in endometrial adenocarcinoma is associated with invasiveness and chemoresistance

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World Journal of Clinical Oncology 2019年第6期10卷 222-233页

作者： Danielle Daley-Brown Adriana Harbuzariu ann.Anu Kurian Gabriela Oprea-Ilies Ruben Rene Gonzalez-Perez Department of Microbiology Biochemistry and Immunology Morehouse School of Medicine Atlanta GA 30310 United States Department of Pathology and Laboratory med.cine Emory University Atlanta GA 30322 United States

BACKGROUND Obesity is a recognized risk factor for endometrial cancer (EmCa) and other cancer types. Leptin levels are significantly increased in obese individuals. Leptin-induced signaling crosstalk [Notch, Interleukin-1 (IL-1) and leptin outcome, NILCO] has been associated with breast cancer progression. This complex signaling crosstalk affects cancer cell proliferation, migration, invasion, angiogenesis, apoptosis and chemoresistance. NILCO expression was previously detected in human EmCa. However, it is unknown whether leptin regulates NILCO and alters EmCa’s response to chemotherapeutics. It is hypothesized that leptin induces NILCO and increases aggressiveness and chemoresistance in EmCa cells. AIM To determine whether leptin induces NILCO molecules in EmCa affecting cell proliferation, aggressiveness and chemoresistance. METHODS Leptin’s effects on the expression of NILCO molecules [mRNAs and proteins for Notch receptors (Notch1-4), ligands (JAG1 and DLL4) and downstream effectors (survivin, hey2), and leptin (OB-R) and IL-1 (IL-1R tI) receptors] was examined in EmCa cells (type I: Ishikawa, and HEC-1A, and type II: An3Ca and KLE) using Real-time PCR and Western blot analysis, respectively. In addition, the effects of leptin on cell cycle, proliferation and cell invasion were determined using cytometric analysis (Cellometer Vision CBA system), MTT cell proliferation and Matrigel-based invasion assays, respectively. Inhibitors of leptin (nanoparticlebound leptin peptide receptor antagonist-2, IONP-LPrA2), IL-1 (anti-IL-1R tI antibody) and Notch (siRNA interference RNA) were used to investigate NILCO’s effects on cell proliferation and invasion. Leptin’s effects on Paclitaxel cytotoxicity in EmCa cells was determined by the CCK8 and Cellometer-based ann.xin V assays. RESULTS For the first time it was shown that leptin is an inducer of Notch in EmCa. Experimental data suggest that leptin induced the expression of NILCO molecules, promoted proliferation and S- ph

关键词： Endometrial cancer Leptin Notch Interleukin-1 Notch, IL-1 and Leptin crosstalk outcome Chemoresistance