Differential effects of luminol,nickel, and arsenite on the rejoining of ultraviolet light and alkylation-induced DNA breaks

When Chinese hamster ovary cells were treated with ultraviolet (UV) light or methyl methanesulfonate (MMS), a large number of DNA strand breaks could be detected by alkaline elution. These strand breaks gradually disappeared if the treated cells were allowed to recover in a drug-free medium. The presence of nickel or arsenite during the recovery incubation retarded the disappearance of UV-induced strand breaks, whereas the disappearance of MMS-induced strand breaks was retarded by the presence of arsenite or of luminol, a new inhibitor for poly(ADP-ribose) synthetase. Luminol, however, had no apparent effect on the repair of UV-induced DNA strand breaks, and nickel had no effect on the repair of MMS-induced DNA strand breaks. When UV- or MMS-treated cells were incubated in cytosine arabinofuranoside (AraC) plus hydroxyurea (HU), a large amount of low molecular weight DNA was detected by alkaline sucrose sedimentation. The molecular weight of these DNAs increased if the cells were further incubated in a drug-free medium. This rejoining of breaks in cells pretreated with UV plus AraC and HU was inhibited by nickel and by arsenite, but not by luminol. The rejoining of breaks in cells pretreated with MMS plus AraC and HU was inhibited by luminol and by arsenite, but not by nickel. These results suggest that different enzymes may be used in DNA resynthesis and/or ligation during the repairing of UV- and MMS-induced DNA strand breaks, and that nickel, luminol, and arsenite may have differential inhibitory effects on these enzymes. © 1994 Wiley-Liss, Inc.     

Ag—NOR计数在区分良恶性甲状腺病变中的意义

随机选择经长期随访证实的滤泡性甲状腺癌和腺瘤各10例,正常甲状腺组织5例作为对照。按Ploton的染色方法和Crocker推荐的计数方法分别计算三组每例各50个细胞的Ag-NOR嗜银颗粒平均数,再算出三组各自的AgNOR均数,经统计学检验三者有极显著性差异。可望成为甲状腺滤泡性肿瘤良恶鉴别的一项辅助指标。     

老年2型糖尿病患者胰岛素抵抗相关指标的检测和意义

目的:探讨老年2型糖尿病胰岛素抵抗(IR)及其相关性,为老年2型糖尿病的合理防治提供临床依据。方法:选择120例老年2型糖尿病患者,按胰岛素敏感指数(HOMA)胰岛素抵抗(HOMA-IR)50百分位点将患者分为两组:胰岛素相对敏感组(HOMA-IR<3.56)和胰岛素相对抵抗组(HOMA-IR≥3.56),比较体重指数(BMI)、腰/臀比(WHR)、血压、血生化学检查等指标。用年龄>40岁,<60岁的2型糖尿病患者做对照组。结果:两组老年患者在年龄、性别、舒张压、空腹血糖、胆固醇、高密度脂蛋白、糖化血红蛋白、HOMA胰岛β细胞功能方面无差异;但BMI、WHR、收缩压、甘油三脂、空腹胰岛素、HOMA-IR差异具有显著性。多线性回归分析后,只有腰/臀比、收缩压、甘油三脂、HOMA-IR存在统计学差异。老年患者与对照组相比,IR发生率明显增加,且两者腰/臀比、收缩压、甘油三脂方面也差异显著。结论:IR与老年2型糖尿病密切相关,是临床防治糖尿病的重要靶点。     

Computerized tomography based on DEI refraction information.

Conventional computerized tomography (CT) technique is based on the absorption contrast. In recent years, X-ray phase-contrast CT (PCCT) has been developing rapidly. It uses the phase information to reconstruct the object and provide high contrast and spatial resolution. Diffraction enhanced imaging (DEI) method is one of the three phase-sensitive X-ray imaging techniques. DEI method employs an analyzer crystal to extract the object's refraction information which can be used for CT. However, when DEI refraction CT is combined with the conventional CT algorithm, it should be satisfied that the refraction information of an arbitrary point in the object is invariable at every projection view. In this paper, the invariance condition of refraction information is analyzed and two feasible methods are provided for reconstruction. Using these two methods, two samples of weak absorption are reconstructed with the experimental data obtained at Beijing Synchrotron Radiation Facility (BSRF).     

美托洛尔控释片治疗中青年高血压病的临床观察

高血压病治疗的药物选择是临床医生需要综合考虑的问题，现将我院应用美托洛尔控释片对中青年高血压病进行治疗的观察结果和体会总结如下。     

Horner syndrome

Horner syndrome is an uncommon but important clinical entity, representing interruption of the sympathetic pathway to the eye and face. Horner syndrome is almost always diagnosed clinically, though pharmacological testing can be used to confirm the diagnosis. Imaging modalities such as PET, CT and MRI are important components of work‐up for patients presenting with acquired Horner syndrome. Our patient’s presentation with Horner syndrome unmasked the causative superior sulcus squamous cell carcinoma and a coincidental lower lobe adenocarcinoma. Successful radical treatment of these cancers resulted in complete resolution of the syndrome and disease‐free survival at 18 months. We review the anatomy and pathophysiology underlying this and other causes of Horner syndrome.