人组织型纤溶酶原激活剂(t-PA)基因在烟草基因组中的整合

为了建立转基因植物生产t-PA的新方法，制备了整合有t-PA基因的转基因烟草植株。通过将t-PA cDNA从质粒pGEM-tPA中切下并插入含有CaMV35S及潮霉素筛选 标记的双元载体pCAMBIA1302中，构建成植物表达载体pCA1302NS-tPA，再将重组载体转入农杆菌GV3101中，通过叶盘法转化烟草。对筛选所得的转化植株进行Southern鉴定显示t-PA基因已整合到烟草基因组中。     

烟毒性弱视的图形视觉诱发电位探讨

目的　研究烟毒性弱视的图形视觉诱发电位的变化。方法　检验对象为 36例 72眼烟毒性弱视患者 ,视力数指～ 0 .8,眼科常规检查无明显病变。检测条件 :视刺激为黑白棋盘格 ,空间频率 1°2 2′视角 ,时间频率 2 .9Hz ,对比度10 0 % .结果　 72眼中 32眼P VEP无波 ,4 0眼P10 0潜伏期延迟。结论　研究说明图形视觉诱发电位是诊断烟毒性弱视特别是早期眼底正常的一种好方法。     

当归注射液对烟酒所致大鼠宫内发育迟缓的拮抗作用及机制

目的 :了解烟酒所致胎儿宫内发育迟缓 (IU GR)时孕鼠胎盘组织抗氧化功能的改变 ,探讨当归注射液的保护作用及机制。方法 :采用烟酒混合因素建立大鼠IUGR模型 ,部分孕鼠给予当归注射液0 .2 5g·kg-1治疗 ,测定胎盘组织中还原型谷胱甘肽(GSH)和丙二醛 (MDA)的含量及超氧化物歧化酶(SOD)、过氧化氢酶 (Cat)和谷胱甘肽过氧化物酶(GSH Px)的活性。结果 :IUGR孕鼠胎盘组织MDA和GSH含量均明显增加 (P <0 .0 1,P <0 .0 5 ) ,SOD、GSH Px和Cat活性显著下降 (P <0 .0 1,P <0 .0 5 )。经当归注射液治疗后 ,胎儿宫内生长发育接近正常 ,上述指标也得到改善。结论 :胎盘氧化损伤可能是IUGR发病的一个重要机制。当归注射液能提高IUGR孕鼠胎盘的抗氧化能力 ,促进胎儿宫内生长发育。     

P2RX7和组蛋白修饰变化在曲古抑菌素A缓解烟草烟雾暴露所致小鼠卵巢损伤中的作用

目的 探索P2RX7和组蛋白修饰变化在曲古抑菌素A（TSA）抑制NLRP3缓解烟草烟雾（CS）暴露所致的 小鼠卵巢损伤过程中的作用。方法 通过CS暴露30 d方法制备小鼠卵巢损伤模型,给予TSA进行治疗;HE染色观 察各组小鼠卵巢组织形态;Western blot技术检测各组小鼠卵巢组织组蛋白去乙酰化酶（HDAC）1、HDAC2、NLR家族 Pyrin域蛋白3（NLRP3）、P2RX7、Zeste同源物增强子2（EZH2）表达以及H3K4me1、H3K4me2、H3K27me3和H3K9ac总 的修饰水平变化。结果 与control组相比,CS组小鼠卵巢总体积减小,卵泡总数减少,卵巢皮质发生萎缩,TSA可有 效抑制CS暴露引起的小鼠卵巢组织形态结构改变。CS组小鼠卵巢组织中HDAC1、HDAC2、NLRP3和P2RX7表达水 平较control 组明显升高,TSA 有效抑制了CS 暴露激活的小鼠卵巢组织HDAC1、HDAC2及焦亡相关蛋白NLRP3和 P2RX7的表达（P＜0.05）。CS暴露后小鼠卵巢组织总H3K4me1、H3K4me2和H3K9ac表达水平明显升高,TSA有效抑 制了CS暴露诱导的小鼠卵巢组织总H3K4me1、H3K4me2和H3K9ac的表达上调（P＜0.05）。结论 P2RX7和组蛋白 修饰变化参与CS暴露所致的卵巢NLRP3炎性小体的激活以及TSA缓解卵巢损伤的过程。     

Histopathologic Spectrum of Intraoral Irritant and Contact Hypersensitivity Reactions: A Series of 12 cases

BackgroundIrritant contact stomatitis (ICS) and contact hypersensitivity stomatitis (CHS) are often caused by alcohol, flavoring agents and additives in dentifrices and foods, and contactants with high or low pH. A well-recognized contactant for ICS is Listerine™ mouthwash, while that for CHS is cinnamic aldehyde. However, many other flavoring agents and even smokeless tobacco are contactants that cause mucosal lesions that are entirely reversible. The objective of this study is to 1) present cases of ICS and CHS with a clear history of a contactant at the site and the histopathologic features of the resulting lesion and 2) define the histopathologic features that characterize such lesions.Methods12 cases of ICS and CHS with known contactants that exhibited distinct histopathologic patterns were identified.ResultsICS are characterized by three patterns in increasing order of severity namely: 1) superficial desquamation, 2) superficial keratinocyte edema, and 3) keratinocyte coagulative necrosis with/out spongiosis and microabscesses. CHS is characterized by two patterns namely plasma cell stomatitis with an intense plasma cell infiltrate and a lymphohistiocytic infiltrate with or without non-necrotizing granulomatous inflammation. Three patterns of the latter are recognized: (1) lymphohistiocytic infiltrate at the interface with well-formed or loosely aggregated non-necrotizing granulomas; (2) lymphohistiocytic infiltrate at the interface with peri- and para-vascular lymphohistiocytic nodules; and (3) lymphohistiocytic infiltrate at the interface with peri- and para-vascular lymphohistiocytic nodules containing non-necrotizing granulomas. The same contactant may elicit ICS and CHS, while one histopathologic pattern may be brought on by various contactants.ConclusionICS and CHS have distinct histologic patterns. Recognizing that these patterns are caused by contactants would help clinicians manage such mucosal lesions.     

Increased cancer risk among relatives of nonsmoking lung cancer cases

Lung cancer has been shown to aggregate in families of nonsmoking lung cancer cases with an earlier age at onset. The current study evaluates whether relatives of nonsmoking lung cancer cases are at increased risk of cancers at sites other than lung. Families were identified through 257 population‐based, nonsmoking lung cancer cases and 277 population‐based, nonsmoking controls residing in metropolitan Detroit. Data were collected for 2,252 relatives of cases and 2,408 relatives of controls. First‐degree relatives of nonsmoking lung cancer cases were at 1.52‐fold (95% CI, 1.02–2.27) increased risk of cancer of the digestive system after adjustment for each relative's age, race, sex, and smoking status. Relative risk estimates also were elevated, but not significantly, for tobacco‐related cancers (RR = 1.39) and breast cancer (RR = 1.72). Among first‐degree relatives of younger probands (age 40–59), risk was non‐significantly increased 72% (95% CI 0.95–3.10) for all cancers combined and 3.14‐fold for cancers of the digestive system (95% CI 0.76–12.9). Nonsmoking relatives of cases were at increased risk of all cancer sites combined (RR = 1.32; 95% CI 1.003–1.73), cancers other than lung (RR = 1.37; 95% CI 1.03–1.82), and digestive system cancers (RR = 2.01; 95% CI 1.20–3.37). These findings of moderate familial aggregation for cancers of the lung, digestive system, breast, and tobacco‐related sites suggest that common susceptibility genes may act to increase risk for a variety of cancers in families. Genet. Epidemiol. 17:1–15, 1999. © 1999 Wiley‐Liss, Inc.