南京市2015—2019年肺结核流行特征分析

目的 分析南京市肺结核的流行病学特征,为政府制定科学的控制策略提供依据。方法 采用描述性分析、季节指数法以及时空重排扫描法对南京市2015—2019年肺结核登记报告数据进行分析。结果 2015—2019年南京市共登记报告11 761例肺结核病例, 肺结核报告发病率分别为32.47/10万、29.39/10万、24.67/10万、26.30/10万、27.00/10万,总体呈现下降趋势。病例中病原学阳性5 592例（47.55%）。2015—2019年全市2月份确诊病例数较少,4月份、9月份确诊病例的较多。时空重排扫描统计发现1个一类聚集区和5个二类聚集区,主要覆盖高淳区、浦口区、江宁区、六合区、江北新区以及鼓楼区所辖的相关街道。其中,一类聚集区覆盖高淳区全部辖区范围（8个街道）,聚集时间为2015/1/1—2017/6/30 (RR = 2.32,LLR = 181.87 , P＜0.001)。结论 2015—2019年南京市肺结核病例存在明显聚集区域,可以为制定科学、精准的区域性防控策略提供参考。     

山东省潍坊东部地区精神分裂症1号染色体基因扫描研究

目的对精神分裂症患者及正常对照者的1号染色体进行扫描,查找精神分裂症的关联位点。方法在1号染色体上间隔10cM（厘摩）遗传距离,选择了31个微卫星遗传位点,用DNA混合池的方法对119例精神分裂症患者与119名正常对照者的DNA样本分别混合后进行基因组扫描。经卡方检验分析,对比患者组与对照组的等位基因峰型比率的差异。结果在D1S2878遗传位点患者组与对照组的等位基因频率差异有统计学意义,P〈0.01。结论山东省潍坊东部地区精神分裂症患者群体中存在与1号染色体的关联区域。     

Behavioral characteristics of a mouse model of cancer pain

Pain is a major symptom in cancer patients, and most cancer patients with advanced or terminal cancers suffer from chronic pain related to treatment failure and/or tumor progression. In the present study, we examined the development of cancer pain in mice. Murine hepatocarcinoma cells, HCa-1, were inoculated unilaterally into the thigh or the dorsum of the foot of male C3H/HeJ mice. Four weeks after inoculation, behavioral signs were observed for mechanical allodynia, cold allodynia, and hyperalgesia using a von Frey filament, acetone, and radiant heat, respectively. Bone invasion by the tumor commenced from 7 days after inoculation of tumor cells and was evident from 14 days after inoculation. Cold allodynia but neither mechanical allodynia nor hyperalgesia was observed in mice that received an inoculation into the thigh. On the contrary, mechanical allodynia and cold allodynia, but not hyperalgesia, were developed in mice with an inoculation into the foot. Sometimes, mirror-image pain was developed in these animals. These results suggest that carcinoma cells injected into the foot of mice may develop severe chronic pain related to cancer. This animal model of pain would be useful to elucidate the mechanisms of cancer pain in humans.     

人急性白血病淋巴细胞HSP70及 HSP70 mRNA的表达研究

目的：检测急性白血病病人血淋巴细胞热休克蛋白70（HSP70）及其mRNA的表达。方法：ELISA法检测HSP70,RT－PCR法检测HSP70 mRNA。结果：化疗前急性白血病病人淋巴细胞HSP70及mRNA明显低于正常人;而化疗后,急性白血病病人淋巴细胞HSP70及mRNA明显高于正常人（P＜0．01）,结论：HSP70与急性白血病癌细胞关系密切,对癌细胞起保护作用。     

次抑菌浓度喹诺酮类药物体外诱导人型支原体ParE基因突变的研究

目的　探讨体外诱导耐喹诺酮类药物的Mh的ParE基因突变情况。方法　以含氧氟沙星、左旋氧氟沙星、盐酸环丙沙星、司帕沙星的培养基培养Mh标准敏感株 12代后 ,将其ParE基因进行PCR扩增 ,分析其核苷酸序列。结果　氧氟沙星、左旋氧氟沙星诱导Mh发生 70位的G→A的突变 ,导致 4 2 6位的天冬氨酸转变为天冬酰胺。结论　ParE基因中 70位的突变与Mh耐喹诺酮类药物有关。     

俄歇电子发射体67Ga-EDTMP 对骨肉瘤细胞株辐射效应的形态学变化

目的　研究俄歇电子发射体67Ga-EDTMP对人骨肉瘤细胞株 (HOS - 86 0 3)的辐射效应 ,探讨67Ga作为原发肿瘤和骨转移癌内照射治疗核素的可能性。方法　用成集落实验和透射电镜研究受照细胞的形态变化。结果　发现67Ga-EDTMP对肿瘤细胞有明显的杀伤和抑制增殖作用 ,并随剂量的加大 ,抑制效率增加 ;倒置显微镜下细胞集落数量减少 ,集落偏小 ,细胞稀疏。电镜下胞浆中空泡形成 ,细胞溶解、坏死 ,细胞核固缩 ,出现典型的细胞凋亡改变 ,形成凋亡小体。结论　67Ga可能是一种有前途的骨肉瘤和骨转移癌的放射性治疗核素     

牙周治疗对根除胃内幽门螺杆菌感染的影响

目的探讨控制口腔牙菌斑对根除胃内幽门螺杆菌再复发的作用.方法对80例确诊为幽门螺杆菌感染的胃、十二指肠疾病患者进行口腔卫生指数调查,并随机分成4组进行治疗观察,在治疗停药后1个月、6个月分别进行胃镜复查,观察胃内幽门螺杆菌感染的根除疗效.结果 80例幽门螺杆菌感染的患者口腔卫生状况较差,多属中、重度牙周炎.铋三联疗法配以周密牙周治疗组与单纯三联疗法组,近期胃内幽门螺杆菌根除效果无显著性差异(P>0.05),但在治疗停药半年后,铋三联配以牙周治疗组幽门螺杆菌感染复发率明显低于单纯铋三联治疗组(P<0.05).结论铋三联疗法配以周密牙周治疗,治疗胃、十二指肠疾病中幽门螺杆菌感染,是防止胃内幽门螺杆菌再复发的重要手段.     

胃癌细胞肿瘤坏死因子受体的研究

目的　探讨人胃癌细胞肿瘤坏死因子受体 ( TNFR)的数目与胃癌细胞分化程度以及与肿瘤坏死因子突变体 ( TNF- m)细胞毒效应之间的关系。方法　以12 5I- TNF- m为配体 ,用放射配体结合分析法 ,检测了高、中、低不同分化程度的体外培养胃癌细胞 ( MKN2 8、SGC790 1、MKN4 5)的 TNFR,同时用 MTT比色法研究了 TNF- m对三株胃癌细胞的细胞毒效应。结果　三株胃癌细胞 TNFR数目分别为每细胞 9.8× 10 -12 nmol、5.6× 10 -12 nmol、3.2× 10 -12 nmol,三者之间比较 ,TNFR数目差异有显著性 ( P<0 .0 5)。解离常数基本一致 ,同一温度时三株胃癌细胞 TNF- m的内化率几乎相等 ,且呈温度依赖关系。TNFR的半衰期大约为 90分钟 ,胞膜与胞浆 TNFR数目之比约为 1∶ 2 ,TNF- m对三株胃癌细胞的最大杀伤率分别为 86%、60 %、34 % ,差异有显著性 ( P<0 .0 5) ,且 39℃时的杀伤率高于37℃时的杀伤率。结论　胃癌细胞表面 TNFR数目与胃癌分化程度相关。 TNF- m的细胞毒效应与TNF数目及 TNF- m的内化量有关。     

The tumorigenic phenotype of a mutated form of Fc gamma RIIB1, lacking the ability to generate soluble receptor and allowing a low-level of ligand binding

Non immunohematopoietic murine tumor cells ectopically expressing Fc gamma RIIB1 (B1) were recently shown to express a higher tumorigenicity phenotype than cells not expressing this receptor. Utilizing a genetic approach we studied the possible contribution of a soluble form of B1 to tumor enhancement. A mutated form of the B1, lacking the cleavage site responsible for the generation of soluble B1 was produced using gene splicing by overlap extension PCR. A deletion confirmed by sequence analysis from 172 to 178 residues was generated. Stable transfectants expressed the B1 deleted form (B1 Delta) both as specific RNA and as a membrane protein receptor allowing a low level of ligand binding. The soluble form of B1 was undetectable in tissue culture supernatants of Bib transfected cells while it was present in supernatants of wild type B1-transfectants. Stable B1 Delta transfectants were significantly more tumorigenic than negative control transfectants. Tumor incidence was almost as high as that of intact B1 and lagged in the latency period before the appearance of palpable tumors. It is suggested that the soluble B1 has a minimal contribution to tumor enhancement.