眼镜蛇毒细胞毒素缓释微球瘤内注射对裸鼠人肝癌皮下移植瘤的影响

目的：评价眼镜蛇毒细胞毒素（cytotoxin,CTX）-聚乳酸-羟基乙酸（polylactic-co-glycolic acid,PLGA）微球经皮瘤内注射治疗裸鼠肝癌的安全性和有效性。 方法：采用甲基噻唑基四唑法检测分离纯化得到的眼镜蛇毒CTX体外细胞毒活性,复乳-溶剂挥发法制备眼镜蛇毒CTX-PLGA缓释微球。40只BALB/c裸小鼠皮下接种人肝癌细胞系BEL-7404细胞建立裸鼠皮下移植瘤肝癌模型,分为生理盐水组、空白微球组、游离CTX组和CTX-PLGA微球组。瘤内注射相应药物,治疗后每周用高频超声观察肿瘤内部回声和血流情况;治疗后第26天,剥离肿瘤称取质量并计算抑瘤率;取肿瘤组织和心、肝、肾等重要脏器,观察其病理学改变。 结果： 眼镜蛇毒CTX对体外培养的人肝癌BEL-7404细胞具有较强的毒性作用。眼镜蛇毒CTX-PLGA缓释微球粒径约（34.45±9.85）μm,具有较高的包封率和较好的缓释效果。瘤体内一次性注射眼镜蛇毒CTX-PLGA微球后,肿瘤体积增长缓慢,抑瘤率达52.36%;光学显微镜观察显示肿瘤组织大部分坏死,但心、肝、肾等重要脏器在形态学上无明显改变。 结论：眼镜蛇毒CTX-PLGA微球瘤内注射可抑制裸鼠肝癌的生长,且具有较高的安全性。     

胸腺素α1凝胶剂的制备与质量控制

目的制备胸腺素α1凝胶剂并建立质量控制方法。方法以卡波姆940为基质制备胸腺素α1凝胶剂,采用高效液相色谱法测定凝胶剂中胸腺素α1的含量。结果胸腺素α1在0.001～0.04mg/ml浓度范围内线性关系良好(r=0.9999),平均回收率100.13%,RSD=1.20%(n=3)。结论胸腺素α1凝胶剂制备方法可行,含量测定方法简便,准确。     

复方聚乙二醇电解质散与番泻叶在结肠镜检查前肠道准备中的应用

为观察复方聚乙二醇电解质散与番泻叶联合应用在结肠镜检查前肠道准备的临床效果,将复方聚乙二醇电解质散与番泻叶联合应用为观察组和单用复方聚乙二醇电解质散为对照组,观察术前的排便次数和粪便性状、术中的肠道清洁满意度。结果显示．观察组排便结束时间明显短于对照组（P〈0．05）。肠道清洁满意度观察组为80．6％（162／201）,对照组为69．6％（133／191）（P〈0．05）。结果表明,复方聚乙二醇电解质散与番泻叶联合应用在结肠镜检查前肠道准备的效果比单用复方聚乙二醇电解质散效果好。     

吸入麻醉药预处理对心肌缺血“第二保护窗”的作用机制

吸入麻醉药预处理对心肌缺血侑罐注损伤具有急性期和“第二保护窗”两个时间段的保护作用。“第二保护窗”起效缓慢而持久,临床上有充分的时间在手术前给予,能更方便有效地预防围术期心肌缺血的并发症。它可诱导一些触发因子如腺苷、一氧化氮的产生,通过信号转导通路蛋白激酶C、核因子-κB等,作用于ATP敏感性钾通道及活性氧族等终末效应离子通道或保护蛋白而发挥迟发性心肌保护。现就近年来关于吸入麻醉药预处理对心肌“第二保护窗”的作用机制作一综述。     

医学检验专业第二课堂活动的实践与思考

本文结合广东医学院医学检验专业第二课堂活动的实践,从设计原则、组织形式、探索和思考几方面阐述了第二课堂教育的模式,探讨了第二课堂活动在医学检验专业学生综合素质培养中的作用,旨在促进医学检验专业教学改革,提高学生的社会适应能力。     

放射性视网膜病变大鼠视网膜内皮细胞改变的实验研究

目的 通过放射线60Co照射SD大鼠,观察大鼠视网膜毛细血管内皮细胞的改变,以探讨放射性视网膜病变发病机制.方法 45只雄性SD大鼠随机分成正常对照组、10Gy组、30Gy组(每组15只),60Co照射大鼠制备实验模型.之后分别于照射之后1个月、3个月、6个月处死10Gy、30Gy、正常对照组各1组动物(每组5只).做大鼠视网膜铺片,光镜观察毛细血管内皮细胞数量.结果正常对照组大鼠随时间的延长,视网膜毛细血管内皮细胞数量无显著差异(P>0.05).而模型组与对照组比较:检测毛细血管内皮细胞数量:[1]1个月,10Gy、 30Gy与对照组比较无显著差异;[2]3个月:30Gy组与对照组有显著差异(P<0.05);[3]6个月:30Gy组与对照组有极显著差异(P<0.01);[4]对照组间随时间改变比较无显著差异;[5]6个月:10Gy组与对照组比较有显著差异(P<0.05).结论放射线60Co照射SD大鼠后,大鼠视网膜毛细血管受损,毛细血管内皮细胞数量减少,并随着实验时间延长和剂量的增加愈加严重.这就为探讨放射性视网膜病变发病机制提供实验依据.     

Long-term survival and risk of second cancers after radiotherapy for cervical cancer

PURPOSE: To evaluate the risk of second cancers after cervical cancer treated with radiotherapy for Asian populations. METHODS AND MATERIALS: We reviewed 2,167 patients with cervical cancer undergoing radiotherapy between 1961 and 1986. Intracavitary brachytherapy was performed with high-dose rate source (82%) or low-dose rate source (12%). Relative risk (RR), absolute excess risk (AR), and cumulative risk of second cancer were calculated using the Japanese disease expectancy table. For 1,031 patients, the impact of smoking habit on the increasing risk of second cancer was also evaluated. RESULTS: The total number of person-years of follow-up was 25,771, with 60 patients being lost to follow-up. Among the 2,167 patients, 1,063 (49%) survived more than 10 years. Second cancers were observed in 210 patients, representing a significant 1.2-fold risk (95% confidence interval [CI], 1.1-1.4) of developing second cancer compared with the general population, 1.6% excess risk per person per decade of follow-up, and elevating cumulative risk up to 23.8% (95% CI, 20.3-27.3) at 30 years after radiotherapy. The RR of second cancer was 1.6-fold for patients with the smoking habit and 1.4-fold for those without. CONCLUSIONS: Small but significant increased risk of second cancer was observed among Japanese women with cervical cancer mainly treated with high-dose rate brachytherapy. Considering the fact that about half of the patients survived more than 10 years, the benefit of radiotherapy outweighs the risk of developing second cancer.     

Risk of second malignancies after adjuvant radiotherapy for breast cancer: a large-scale, single-institution review

PURPOSE: The aim of this study was to estimate the risk of second malignancies (SM) after radiation therapy (RT) for breast cancer (BC) in a large, institutional, homogeneous cohort of patients. METHODS AND MATERIALS: We retrospectively studied 16,705 patients with nonmetastatic BC treated at the Institut Curie in Paris between 1981 and 1997. Adjuvant RT was given to 13,472 of these patients, and no RT was given to 3,233. The SM included all first nonBCs occurring during follow-up. Cumulative risks for each group were calculated using Kaplan-Meier estimates, censoring for contralateral cancer or death. RESULTS: Median patient age at diagnosis of BC was 55 years for the whole population, and 53 and 60 years for patients who had and had not undergone irradiation, respectively. At the 10.5-year median follow-up, 709 patients were diagnosed with SM (113 in the non-RT and 596 in the RT group). There was a significant increase in the rate of sarcomas and lung cancers in the RT group compared with non-RT group (p 0.02). Treatment with RT was not found to increase the risk of other types of cancers such as thyroid cancer, malignant melanoma, gastrointestinal or genitourinary, and hematologic SM. CONCLUSIONS: This study suggests that adjuvant RT increased the rate of sarcomas and lung cancers, whereas it did not increase the rate of other malignancies.     

Characterization of the P373L E-cadherin germline missense mutation and implication for clinical management

Aim

Hereditary diffuse gastric cancer (HDGC) is a cancer susceptibility syndrome caused by E-cadherin germline mutations. One-third of these mutations are of the missense type, representing a burden in genetic counselling. A new germline missense mutation (P373L) was recently identified in a HDGC Italian family. The present work aimed at addressing the disease-causative nature of the P373L mutant.

Methods

Assessment of the P373L mutation effect was based on cell aggregation and invasion assays. LOH analysis at the E-cadherin locus, search for somatic E-cadherin mutations and for promoter hypermethylation were performed to identify the mechanism of inactivation of the E-cadherin wild-type allele in the tumour.

Results

In vitro the P373L germline mutation impaired the E-cadherin functions. E-cadherin promoter hypermethylation was observed in the tumour of the P373L mutation carrier.

Conclusion

We conclude that the combination of clinical, in vitro and molecular genetic data is helpful for establishing an accurate analysis of HDGC-associated CDH1 germline missense mutations and subsequently for appropriate clinical management of asymptomatic mutation carriers.     

A population-based study of survival in patients with secondary myelodysplastic syndromes (MDS): impact of type and treatment of primary cancers

Objective Myelodysplastic syndromes (MDS) following treatment with chemotherapy or irradiation are termed ‘secondary’ MDS. Clinical observations suggest a worse prognosis for secondary than for primary MDS, but differences in survival have not been studied in a general population sample. Methods We analyzed data from the Surveillance, Epidemiology, and End Results (SEER) program to describe survival in MDS patients according to previous cancer diagnosis. Our study included 3,938 MDS cases diagnosed in 2001–2004 and reported by registries which have participated in SEER since the 1970s. Results A previous cancer diagnosis (26% of MDS cases) was associated with 13% increased risk of death from any cause among MDS cases (hazard ratio [HR]=1.13, 95% confidence interval [CI]: 1.02–1.25). Radiation treatment for a previous cancer was associated with 52% increased risk of death (95% CI: 1.15–2.02). Shortened survival was most pronounced if the latency between the previous cancer and MDS was less than five years, including lung cancer diagnosed in the year preceding MDS (HR = 3.43, 95% CI: 1.93–6.10) and lymphohematopoietic cancer 1–5 years before MDS (HR = 2.11; 95% CI: 1.33–3.36). Conclusions Our results confirm a more severe prognosis for secondary MDS than for primary MDS, associated with certain types and treatments of previous cancer. Financial support: Dr. De Roos’ and Dr. Davis’ work was supported by a grant from the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute (NO1-PC-55020-20), and Dr. Deeg’s work was supported by grants from the National Heart, Lung, and Blood Institute of the National Institutes of Health (HL36444 and HL082941).