肺癌合并慢性阻塞性肺疾病外科治疗的肺功能评价

目的评价慢性阻塞性肺疾病(COPD)患者合并肺癌行肺叶切除的手术风险和手术对肺功能的影响.方法回顾分析1998年1月至2005年1月我院收治的中度COPD合并周围型非小细胞肺癌32例患者的临床资料.其中,男29例,女3例;平均年龄(65.0±5.4)岁.病理分型:鳞癌2l例,腺癌11例;病理分期:Ⅰ期2例,Ⅱ期5例,Ⅲa期24例,Ⅲb期l例.所有患者均接受肺叶切除术.结果术前患者肺功能第1秒用力呼吸容积(FEV1)和动脉氧分压平均值分别为(64±9)%和(85±12)mmHg,术后分别为(62±10)%和(87±11)mmHg,虽然FEV1略有下降,但均无显著性差异(P＞0.05).本组无围手术期死亡者.结论中度COPD患者仍有一定的肺功能储备,可耐受肺叶切除手术.     

Diethylstilbestrol impaired oogenesis of yellow catfish juveniles through disrupting hypothalamic–pituitary–gonadal axis and germ cell development

Diethylstilbestrol (DES), a non‐steroidal estrogen, has been found to cause altered germ cell development and disordered ovarian development in fish females. However, the mechanisms that might be involved are poorly understood. In this study, female juveniles of yellow catfish (Pelteobagrus fulvidraco) (120 days post‐hatching) were exposed to two doses (10 and 100 ng l^?1) of DES for 28 days. After the endpoint of exposure, decreased ovary weight and gonadosomatic index, as well as various ovarian impairments were observed in response to DES. Besides, DES elevated the mRNA levels of vitellogenin 1 (vtg 1) and estrogen receptor 1 (esr 1) in liver and decreased 17β‐estradiol level in plasma. Correspondingly, suppressed mRNA levels of the key genes in the hypothalamic–pituitary–gonadal axis (such as cyp19a1b, gnrh‐II, fshβ and lhβ in brain and fshr, lhr and cyp19a1a in ovary) after DES exposure were also observed. The declined level of plasma 17β‐estradiol and altered gene expressions of genes in the hypothalamic–pituitary–gonadal axis were thus supposed to be closely related to the disrupted oogenesis in DES‐treated fish. Analyses further demonstrated that, higher concentration of DES elevated the expression ratio of bax/bcl‐2, indicating the enhanced apoptosis occurred in ovary. Moreover, DES upregulated the expressions of genes involved in proliferation (cyclin d1 and pcna), meiotic entry (cyp26a1 and scp3) and meiotic maintenance (dmc1), resulting in arrested oogenesis in catfish. The present study greatly extended our understanding on the mechanisms underlying of reproductive toxicity of DES on fish oogenesis.