医用直线加速器矩形野散射因子的简便计算方法

 目的　建立一种适合于临床应用的加速器散射因子 Sc.p的简便计算方法。方法　 ( 1 )通过测量方野的散射因子 ,建立方野散射因子与射野边长的拟合公式 ;( 2 )利用 Kim的经验公式 ,计算矩形野的等效方边长 ;( 3)应用已拟合的方野散射因子公式计算矩形野的散射因子 ,并与矩形野的测量结果进行比较。结果　采用该方法计算医用加速器散射因子的最大误差在 0 .5%以下 ,而采用面积 -周长比原理确定的等效方边长 ,最大误差达到 3%左右。结论　该方法可用于简便快速地确定方野和矩形野的散射因子 ,精确度高 ,完全可应用于临床.     

电子束不对称照射野输出因子的实验研究

目的 探讨电子束不对称照射野输出因子的变化规律.方法 用电离室法对不同大小限光筒不同能量下3个特定照射野按照偏离中心轴不同距离实测其输出因子,计算不对称照射野输出因子与对称照射野输出因子的偏差.结果 不对称照射野的输出因子随着偏轴距离的变化规律与所对应限光筒标准方野离轴比的变化基本上是一致的,提示不对称照射野的输出因子与标准方野的离轴比相关.限光筒和铅挡野大小对输出因子偏差值的影响不明显.结论 电子束不对称照射野输出因子的变化主要与标准方野的离轴比有关,是否修正可根据标准方野离轴比的变化情况决定.     

外挂式多叶准直器对准直器散射因子的影响

目的　用电离室测量外挂式多叶准直器 (MLC)对准直器散射因子 (Sc)的影响 ,并用双源模型对结果进行分析。方法　测量MLC形成的 2个不规则射野序列 ,并与等效方野的测量值进行了比较 ,应用双源模型得出MLC对Sc产生影响时叶片所处的位置公式。结果　当MLC叶片位置离中心足够近时 ,叶片将对准直器散射因子产生影响 ;产生影响时叶片位置计算值与测量结果相符。结论　基于双源模型的MLC位置公式较好地描述了当外挂式准直器 (MLC或铅块 )形成的射野小于公式给出值时 ,准直器散射因子将受其影响。     

直线加速器小照野物理数据的测量和比较

背景与目的：对于精确的肿瘤放射治疗特别是立体定向和调强放射治疗,为了建立可靠的治疗计划系统剂量计算模型,提供准确的小照射物理数据尤其重要。本研究通过测量不同能量下小照野的物理数据,分析和比较不同方法和不同电离室之间相应的测量误差。方法：在直线加速器4、6、8MV光子线下,采用0．65、0．13、0．01cm^3的三种指形电离室,在30cm×30cm×30cm的固体水体模中测量了1cm×1cm～10cm×10cm照射野的总散射因子（total scatter factor,Scp）、准直器散射因子（collimator scatter factor,Sc）和组织最大剂量比（tissue-maximum ratio,TMR）等物理数据。对相应的测量结果进行了分析和比较。结果：照射野〉3cm×3cm时,不同电离室的Scp和Sc测量结果偏差在0．8％以内：3cm×3cm以下的照射野的测量结果差别较大（最大64％）;在4、6、8MV光子线1cm×1cm和2cm×2cm照射野的Sc测量中。0．13cm^3电离室拉长源皮距（〉150cm）比标准源皮距处（100cm）的测量结果分别大25．4％、6．9％、24．6％和1．4％、1．4％、2．2％;两种电离室0．01cm^3和0．13cm^3拉长距离测量的Sc对≥2cm×2cm照射野没有明显的偏差．对1cm×1cm照射野0．13cm^3比0．01cm^3测量值小0．2％、8．5％、3．4％。在1cm×1cm照射野的TMR测量中,0．01cm,和0．13cm^3电离室在15cm以下区域的测量偏差较大,约为4％左右。对于2cm×2cm及以上照射野TMR的测量结果偏差较小（〈1％）。〉3cm×3cm的照射野中,TMR测量的结果与百分深度剂量（percentage depth dose,PDD）转换得到的TMR数据在深度15cm之前一致性较好。15cm深度之后有明显的偏差（〉2％）。结论：测量小照射野物理数据时。由于侧向电子散射不够,需要谨慎选择测量探头。不同的测量探头对小照野物理数据的准确性可能存在较大的影响。当侧向电子平衡不能建立时,测量?     

电子线矩形野与方野输出因子的换算

目的　选择一种能准确适用于临床应用的电子线矩形野与方野输出因子的换算方法。方法　使用 6、12、15MeV电子线 ,国产TL30 0 0C剂量仪 ,0 .6cm3 电离室探头 ;采用源皮距 (SSD)方法测量。比较 3个不同输出因子转换理论公式的计算值与实际测量值的符合程度。结果　理论公式OUF(X ,Y) =[OUF(X ,X) ·OUF(Y ,Y) ]1/ 2 计算值与实际测量值符合较好 ,较大野时理论计算值与实际值更符合。结论　对于边长大于射程的矩形野 ,其输出因子可以由理论公式较精确地计算 ,它是适合于临床应用的计算方法。     

60Co机准直器散射因子(Sc)的性质

目的测量６０Ｃｏ机准直器散射因子（Ｓｃ）的性质，为临床使用提供依据。材料与方法在两种类型６０Ｃｏ机上，用指形电离室测量Ｓｃ随各种因素的变化规律。测量时，电离室的轴线与照射野的射线束轴重合。结果获得了Ｓｃ与源皮距的关系数据。分析了不同矩形野Ｓｃ的变化，挡块对Ｓｃ影响等。结论在一般照射野大小，Ｓｃ与源皮距无关，并可用二次函数来拟合Ｓｃ随照射野大小的变化。挡块及有机玻璃托盘对Ｓｃ影响可忽略。但在大野时Ｓｃ略有不同。根据测量的数据提出了矩形照射野的Ｓｃ等效方野的计算公式     

用加铅挡块的方法直接测定体模散射因子Sp的探讨

目的：按Ｓｐ的定义，直接测量体模散射因子Ｓｐ。方法：在准直器开口不变的情况下，用加挡块的方法改变各射野在模体中的散射面积。分别测定各射野在模体中参考点处的吸收剂量率和加挡块和同一点的吸收剂量率，再根据Ｓｐ的定义、计算出Ｓｐ因子。结果：通过测量，直接得到各射野的体模散射因子Ｓｐ和总散射校正因子Ｓｃｐ，然后求出各射野的准直器散射修正因子Ｓｃ。结论：用本文加挡块的方法测定Ｓｐ因子，可以降低制作高能Ｘ线的     

鼻咽癌放疗面颈联合颈后电子束野铅模制作问题的研究

目的探讨鼻咽癌放疗面颈联合颈后电子束野铅模制作问题。方法对5例不同等中心点深度的鼻咽癌面颈联合野放疗患者,按照分野前后的灯光野投影,在患者固定面罩上画出颈后电子束照射野。应用几何关系计算出所给定源片距的校正源片距,分别按照实际源片距和校正后源片距制作电子束铅模,到加速器下治疗摆位,测量源片距校正前后铅挡野与体表野的符合性。结果应用几何关系计算出所给定源片距的校正源片距,均大于给定源片距。源片距校正前的铅挡野与体表野偏差明显较大,最大偏差达1.25 cm;源片距校正后铅挡野与体表野偏差较小,最大偏差为0.22 cm。结论鼻咽癌面颈联合野后程分野颈后电子束野铅模制作时,应用首程等中心照射影像资料制作出来的铅模,偏差较大,通过源片距校正方法,铅挡野与体表照射野符合性较好。     

电子束矩形野输出因子等效转换方法的对比实验研究

目的：比较方根式、一维式和面积周长比3种方法计算的电子束矩形照射野输出因子的精确性和可行性。方法：用电离室法对不同大小限光简不同能量下8个特定矩形照射野输出因子实测和用3种方法计算，比较此3种方法与实测值偏差。结果：（1）同一能量下，面积周长比法偏差较大，一维式和方根式偏差较小；（2）电子束限光筒大小、射线能量和矩形照射野大小对3种方法计算的矩形照射野输出因子有一定影响。结论：面积周长比法计算矩形照射野输出因子偏差较大，建议不予采用。一维式和方根式法精度较高，一维式法优于方根式法，而方根式法更适合于临床。     

X线立体定向治疗系统的剂量测量—小野剂量分布测量方法

目的 :本文叙述我院利用半导体探头测量X射线立体定向治疗的剂量学参数 ,并对其结果给予评价 ,说明小野剂量分布的特点。材料与方法 :由于半导体探头具有体积小 ,灵敏度高等优点 ,我们选择P型半导体探头 ,以测量准直器 5m～ 5 0mm直径照射野的百分深度剂量 (PDD) ,离轴比 (OAR)及射野输出因子 (Sc ,p) ,所得结果与其他测量方法诸如电离室 ,胶片等 ,以及有关文献报导进行比较。结果 : 1 0和 3 0准直器的PDD值 ,在 5cm～ 2 0cm深度范围内 ,测量值与文献 7报道值的差别在± 0 .6以内。将PDD转换为TMR(组织最大剂量比 ) ,外推法计算 6MV -X线零野的有效线性衰减系数为 0 .0 5 1 0cm- 1。测量射野输出因子 ,在常规用照射野范围 ,半导体探头与NE2 5 71电离室所得数值 ,偏差为± 0 .4%以内 ,但当射野直径小于电离室直径的 2倍时 ,偏差增大。而用半导体测量准直器直径在 1 2 .5～ 2 7.5所得值 ,与报导用MonteCarlo方法计算值基本相吻合。对于射野离轴比 ,半导体和我们自行设计的胶片法组出的结果 ,差别在 1mm以内 ;半导体所测得的照射野半影区宽度 (90 %～ 1 0 % )与报导值极其接近。结论 :对于小野 ,由于照射野边缘剂量梯度过大和缺少侧向电平衡 ,选用探头的大小和测量位置 ,是影响精确测量极为重要的因素。     

Lung cancer risk in never-smokers: An overview of environmental and genetic factors

Lung cancer is the leading cause of cancer-related mortality globally, accounting for 1.8 million deaths in 2020. While the vast majority are caused by tobacco smoking, 15%−25% of all lung cancer cases occur in lifelong never-smokers. The International Agency for Research on Cancer (IARC) has classified multiple agents with sufficient evidence for lung carcinogenesis in humans, which include tobacco smoking, as well as several environmental exposures such as radon, second-hand tobacco smoke, outdoor air pollution, household combustion of coal and several occupational hazards. However, the IARC evaluation had not been stratified based on smoking status, and notably lung cancer in never-smokers (LCINS) has different epidemiological, clinicopathologic and molecular characteristics from lung cancer in ever-smokers. Among several risk factors proposed for the development of LCINS, environmental factors have the most available evidence for their association with LCINS and their roles cannot be overemphasized. Additionally, while initial genetic studies largely focused on lung cancer as a whole, recent studies have also identified genetic risk factors for LCINS. This article presents an overview of several environmental factors associated with LCINS, and some of the emerging evidence for genetic factors associated with LCINS. An increased understanding of the risk factors associated with LCINS not only helps to evaluate a never-smoker’s personal risk for lung cancer, but also has important public health implications for the prevention and early detection of the disease. Conclusive evidence on causal associations could inform longer-term policy reform in a range of areas including occupational health and safety, urban design, energy use and particle emissions, and the importance of considering the impacts of second-hand smoke in tobacco control policy.     

Crosstalk between TF/FVIIa and EGFR signaling in colorectal cancer cells

TF/FVIIa (Tissue Factor/Active Coagulation factor VII) and EGFR (Epidermal Growth Factor Receptor) signaling both promote malignant progression of colorectal cancer. However, the crosstalk of these two signaling pathways in human colorectal cancer cells remains unclear. Here we detected the changes of mRNA profile in human colorectal cancer cell SW620 exposed to FVIIa. Microarray showed that mRNA levels of EGFR ligands were significantly upregulated. Western blot analysis confirmed the upregulation of EGFR ligands and the phosphorylation of EGFR at tyrosine-845 in colorectal cancer cells exposed to FVIIa. However, knockdown of TF by RNAi could block the upregulation of EGFR ligands induced by FVIIa stimulation. On the other hand, the expression of components of TF/FVIIa signaling was significantly upregulated in LoVo cells stimulated by EGF. However, the crosstalk between the two signaling pathways could not be detected in HT-29 colon cancer cells bearing wild-type KRAS. Taken together, our study suggest that the crosstalk between TF/FVIIa and EGFR signaling pathways in colon cancer cells depends on KRAS mutation.     

The role of tumour necrosis factor-alpha (TNF-alpha) and platelet-activating factor (PAF) interaction on murine candidosis

Tumour necrosis factor-alpha (TNF-alpha) is related to some other factors in addition to being the essential cytokine of the sepsis which results from Candida infections. In our study, we investigated serum TNF-alpha levels, measured by enzyme-linked immunosorbent assay (ELISA), and platelet-activating factor (PAF)-like activity, measured by high-pressure liquid chromatography (HPLC) of the mice infected with Candida species. The PAF antagonist, ginkgolide BN 52021 was used to evaluate the possible interaction between TNF-alpha and PAF. The average TNF-alpha levels were found to be 396, 489, 699 and 803 pg ml(-1) on the 4th, 5th, 6th and 19th days of Candida albicans infection, respectively (P<0.05). There was no statistically significant difference between the serum TNF-alpha levels of the groups infected with other Candida species, such as C. kefyr, C. krusei and C. tropicalis (P>0.05). Serum TNF-alpha levels were found to be more significantly different in mice with C. albicans infection that were injected with PAF antagonists on the 6th day (23 pg ml(-1)). It was therefore thought that PAF antagonists have an inhibitory effect on TNF-alpha production. No significant difference was found between PAF levels in the three groups: healthy control mice, C. albicans-infected mice and C. albicans-infected mice given PAF antagonists (466 milli-absorbance unit (mAU), 475 mAU and 329 mAU, respectively). It was noticed that the positive interaction between PAF and TNF-alpha was not important after the first 4 days of the infection had passed.     

Reversal of Tumor Necrosis Factor Resistance in Tumor Cells by Adriamycin via Suppression of Intracellular Resistance Factors

Tumor necrosis factor (TNF) and various chemotherapeutic drugs show synergistic antitumor effects in vitro and in vivo , though the mechanism is not clear. Based on our previous finding that endogenous TNF (enTNF) acts as an intracellular resistance factor against exogenous TNF by scavenging oxygen free radicals (OFR) with induced manganous superoxide dismutase (MnSOD), we examined the suppression of these resistance factors by chemotherapeutic drugs and the resulting increase in TNF cytotoxicity. Pretreatment of HeLa cells, which produce an appreciable amount of enTNF and show apparent TNF resistance, with TNF followed by adriamycin (ADM) resulted in an additive effect, whereas pretreatment with ADM followed by TNF resulted in a synergistic effect. After treatment of HeLa cells with ADM, the expression of enTNF was remarkably suppressed and MnSOD activity was decreased by one-half. These results indicate that suppression of the intracellular resistance factors, i.e., enTNF and MnSOD, by ADM plays an important role in the mechanism of the synergistic antitumor effect of TNF in combination with ADM.     

Combination therapy of imatinib mesylate and interferon-alpha demonstrates minimal activity and significant toxicity in metastatic renal cell carcinoma: results of a single- institution phase II trial

Background

Renal cell carcinoma (RCC) is characterized by increased expression of vascular endothelial growth factor and platelet-derived growth factor (PDGF)-β, both of which contribute to its angiogenic phenotype. Interferon-α (IFN-α) improves survival in patients with metastatic RCC, perhaps partly because of its antiangiogenic properties. Imatinib mesylate inhibits PDGF-mediated signal transduction and might thus have antiangiogenic activity as well.

Patients and Methods

Patients with metastatic RCC were treated with IFN-α (9 × 10⁶ IU subcutaneously 3 times weekly) and oral imatinib mesylate (600 mg daily starting on day 8). Therapy was continuous, and response was evaluated at 8-week intervals using the Response Evaluation Criteria in Solid Tumors. Baseline plasma PDGF-AA, PDGF-AB, and PDGF-BB levels were obtained.

Results

Between January 2003 and January 2005, 17 patients were treated. One patient (6%) had a partial response, 4 (24%) had stable disease, 7 (41%) had progressive disease, and 5 (29%) were unevaluable because of early withdrawal secondary to toxicity. Median time to progression (TTP) using the Kaplan-Meier method was 8 weeks, and median overall survival was 17.8 months. Six patients (35%) withdrew from therapy because of toxicity, and 9 patients (53%) experienced ≥ 1 grade 3/4 toxicity. Platelet-derived growth factor AA, AB, and BB plasma levels did not correlate with TTP or overall survival.

Conclusion

Based on a response rate of only 6%, a median TTP of 2 months, and significant toxicities, further study of IFN-α in combination with imatinib mesylate is not recommended in patients with metastatic RCC.     

前列腺癌与凝血和纤溶因子研究进展

前列腺癌病人中血液高凝状态常见，近年越来越多研究显示凝血和纤溶因子异常与前列腺癌进展间有密切联系，本文回顾近年国内外关于前列腺癌病人中各种凝血和纤溶途径成分异常的临床和基础研究，并就前列腺癌与凝血和纤溶因子研究进展进行综述.     

Citation indexes do not reflect methodological quality in lung cancer randomised trials.

BACKGROUND: Citation factors are applied to assess scientific work despite the fact that they were developed commercially in order to compare competing journals. The aim of the present study was to determine whether there is a relationship between citation factors and a trial's methodological quality using published randomised trials in lung cancer clinical research. Material and methods All of the randomised trials included in nine systematic reviews performed by the European Lung Cancer Working Party (ELCWP) were assessed using two quality scales (Chalmers and ELCWP). RESULTS: One hundred and eighty-one articles were eligible. The median overall ELCWP and Chalmers quality scores were 61.8% and 49.0%, respectively, with a correlation coefficient (r(s)) of 0.74 (P <0.001). A weak association was observed between citation factors and quality scores with the respective correlation coefficients ranging from 0.18 to 0.40 (ELCWP scale) and from 0.21 to 0.38 (Chalmers scale). American authors published trials significantly more often in journals with high citation factors than European or non-American authors (P <0.0001), despite no better methodological quality. Positive trials, which were significantly more likely to be published in journals with higher citation factors, were of no better quality than negative ones. CONCLUSION: Journals with higher citation factors do not appear to publish clinical trials with higher levels of methodological quality, at least for trials in the field of lung cancer research.     

Tumor suppressor function of a dominant negative retinoic acid receptor mutant

Mutations in receptors for the vitamin A metabolite retinoic acid (RAR) that repress retinoic acid (RA)-responsive gene expression have been identified and characterized. We previously reported an absence of target gene response to RA in all but one of a series of transformed human epithelial cell lines. To elucidate the mechanisms of this unresponsiveness, we created stable transfectants that expressed an RARα mutant (RARα403) previously shown to have dominant negative activity due to a C-terminal truncation. All clones exhibited repressed RA-responsive gene expression. These cells grew slowly and demonstrated greater growth inhibition by RA. Pretreatment of both control and experimental groups with RA enhanced epidermal growth factor–induced proliferation despite RA-dependent downregulation of epidermal growth factor receptor expression. In addition, clones expressing the mutant RARα were 60% less invasive in an in vitro assay. This reduced invasiveness correlated with decreased gelatinase activity in these cells. We showed for the first time that a dominant negative mutation in RARα can function as a tumor suppressor in transformed epithelial cells. Mol. Carcinog. 22:26–33, 1998. © 1998 Wiley-Liss, Inc.     

Spontaneous regression of lung metastasis in the absence of tumor necrosis factor receptor p55

In order to clarify the roles of tumor necrosis factor (TNF)-alpha in lung metastasis, we injected Renca cells intravenously into TNF receptor p55-deficient (TNF-Rp55 KO) and wild-type (WT) mice. Microscopic and macroscopic metastasis foci appeared in lungs at 7 and 14 days after the tumor injection, respectively. Moreover, metastasis foci expanded at similar rates in both WT and TNF-Rp55 KO mice until 21 days, and lungs were occupied with metastasis foci. However, later than 21 days after the injection, metastasis foci spontaneously regressed in TNF-Rp55 KO mice, whereas WT mice exhibited a progressive growth of metastasis foci. Moreover, metastasis foci remained reduced sizes in TNF-Rp55 KO mice even at 26 days, when all WT mice died with lungs filled with metastasis foci. Later than 21 days after the tumor injection, the number of apoptotic tumor cells was increased in TNF-Rp55 KO mice. In contrast, neovascularization was less evident in TNF-Rp55 KO than WT mice, with depressed hepatocyte growth factor (HGF) gene in TNF-Rp55 KO mice at 21 days after the tumor injection. Thus, TNF-Rp55-mediated signals can maintain tumor neovascularization at least partly by inducing HGF expression, and eventually support lung metastasis process.     

表皮生长因子及其受体在胃癌患者中的表达

采用放射免疫法测定２６例胃癌病人血清、尿液ＥＧＦ水平，同时采用免疫组化ＳＡＢＣ法检测胃粘膜组织切片中ＥＧＦＲ染色的阳性率，并与正常对照进行比较分析。结果表明：胃癌患者血清和尿ＥＧＦ水平均显著高于正常对照（３．７２±１．８３μｇ／Ｌ与１．７７±０．６０μｇ／Ｌ，Ｐ＜０．０１；１８．４４±１７．８８ｎｇ／ｍｇ与５．１９±６．３７ｎｇ／ｍｇ，Ｐ＜０．０１），胃粘膜组织切片ＥＧＦＲ染色阳性率也明显高于正常对照（７３％与１１％，Ｐ＜０．０１）。胃癌病人中，ＥＧＦＲ染色阳性者血清ＥＧＦ水平显著高于ＥＧＦＲ阴性者（Ｐ＜０．０５），但两者尿ＥＧＦ水平无显著性差异。胃癌患者血清、尿ＥＧＦ水平与胃癌大小、分化程度及淋巴结转移无显著性相关。