Wistar大鼠的咬肌放射损伤模型

背景：构建稳定可靠的咬肌放射损伤模型对颌面部肿瘤放疗的相关研究有重要意义。 目的：以放射剂量40 Gy照射后Wistar大鼠咬肌构建大鼠咬肌放射损伤模型。 方法：成年Wistar大鼠20只,随机分成正常对照组和放射损伤组。放射损伤组采用直线加速器照射大鼠咬肌区累积40 Gy制造咬肌放射损伤。在28 d后,在光镜及电镜下观察咬肌放射区病理改变,RT-PCR检测转化生长因子β1的基因表达。 结果与结论：40 Gy照射后28 d大鼠咬肌区出现结构受损、血管密度减低(P < 0.01)等放射损伤表现,同时引起转化生长因子β1的基因表达升高(P < 0.001)等机体被动修复表现。结果证实Wistar大鼠咬肌区直线加速器40 Gy照射可以作为咬肌放射损伤模型。     

不同剂量X射线对雄性大鼠精子顶体酶活性的影响

目的:检测不同剂量X-射线对雄性大鼠精子顶体酶的影响,以探讨体外X-射线对大鼠精子顶体酶活性的影响。方法:将10周龄成熟雄性大鼠40只,随机分为4组:2Gy、4Gy、6Gy照射组和0Gy对照组;每组10只。按不同剂量照射,1h后处死大鼠,以改良的Kennedy法分别测定不同剂量X射线作用下的精子顶体酶活性。结果:2Gy、4Gy、6Gy照射组与0Gy对照组相比顶体酶活性显著降低(P<0.05),照射组酶活性较0Gy对照组有显著降低;4Gy、6Gy照射组与2Gy照射组相比较顶体酶活性显著降低(P<0.05);而4Gy照射组与6Gy照射组相比较则无统计学意义。结论:X-射线对大鼠精子顶体酶有明显的抑制作用。     

咽癌患者调强适形放射治疗期间咽缩肌放射剂量对吞咽功能的影响

目的:观察咽癌患者调强适形放射治疗期间咽缩肌放射剂量与吞咽功能的关系。方法:选取80例咽癌患者作为研究对象,均实施调强适形放射治疗6个月,根据患者治疗需求选取咽缩肌放射剂量,分别于放疗1、3及6个月,记录患者吞咽功能评分,分析咽缩肌放射剂量与吞咽功能评分的相关性。并于放疗结束时,评估患者吞咽功能,将患者分为吞咽功能正常、吞咽障碍轻度、中度及重度障碍,比较无-轻度吞咽障碍组与中-重度吞咽障碍组咽缩肌放射剂量,采用回归分析检验咽缩肌放射剂量对吞咽功能的影响。结果:各时点中,放疗1个月时MDADI总分及各维度评分最高,后由高到低依次为放疗3个月时、放疗6个月时,不同时点MDADI评分比较差异均有统计学意义（P<0.05）;80例咽癌患者咽上缩肌放射剂量为（44.72±5.58） Gy,中咽缩肌放射剂量为（48.94±6.17） Gy,咽下缩肌放射剂量为（38.95±4.74） Gy,咽缩肌放射总剂量为（132.61±28.52） Gy;经一般线性双变量Pearson相关性分析结果显示,不同时点MDADI总分与咽缩肌总放射剂量呈负相关;80例咽癌患者放疗结束时,29例吞咽功能正常,18例轻度吞咽障碍,21例中度吞咽障碍,12例重度吞咽障碍;初步比较中-重度吞咽障碍组与无-轻度吞咽障碍组咽缩肌放射剂量后,经多元Logistic回归分析显示,咽缩肌放射剂量高是患者放疗结束时发生中-重度吞咽障碍的危险因素（OR>1, P<0.05）。结论:咽癌患者调强适形放射治疗期间咽缩肌放射剂量可影响吞咽功能,随剂量增加,患者吞咽功能降低,吞咽障碍发生风险增加。     

顺铂联合放射治疗对大鼠脊髓损伤影响的观察

目的探讨顺铂(c isp latin,DDP)联合放射治疗对大鼠脊髓损伤的影响。方法40只W istar大鼠随机分为5组,即空白组、单纯化疗组、单纯放射组、先化后放组和先放后化组。单化组单次腹腔注射顺铂5 mg/kg。单放组和放化联合组采用瓦里安2300 C/D直线加速器6M eV电子线照射大鼠胸段脊髓,照射野为2 cm×4 cm,5Gy/次,隔日1次,总剂量为40 Gy。联合组顺铂与照射的间隔时间为3天。照射结束后5个月,行活体灌注固定,取材,光镜和电镜观察脊髓的形态学变化。结果光镜下,CT组灰质未见改变,白质内部分有髓神经纤维排列紊乱,部分髓鞘板层结构松解、扭曲。RT组灰质未见改变,白质出现部分水肿坏死,髓鞘板层模糊不清。CT+RT组脊髓灰质、白质改变明显,其中CT+放疗组的灰质内可见到明显的神经元核变成细长形,尼氏体数量减少,白质出现大片坏死。电镜下,CT组髓鞘结构出现轻度变化,表现为部分髓鞘的板层结构松解、扭曲。RT组脊髓损伤表现为板层结构水肿、粘连,模糊不清。CT+RT组的脊髓损伤程度严重,表现为正常髓鞘的板层结构完全消失,轴突及神经纤维裸露,血管增生,部分血管内皮细胞坏死。RT+CT组脊髓损伤表现为正常髓鞘的板层结构部分松解、扭曲、断裂。结论顺铂与放疗联用明显加重脊髓损伤,且放疗前加用顺铂脊髓损伤加重。     

海带多糖对放射性脑损伤小鼠海马细胞的保护作用

目的:探讨海带多糖(LJP)对放射后小鼠认知功能的影响及其影响机制.方法:64只雄性昆明小鼠利用完全随机数字法分为对照组(control)、海带多糖组(LJP)、单纯照射组(IR)、照射+海带多糖组(IR+LJP).放射前7 d连续给药预处理后,采用总剂量30 Gy的钴60(60Co)-γ射线对小鼠脑部进行定位照射以建...     

60Co照射法饲养细胞的制备

目的 :选择合适的60 钴 (60 Co)照射剂量制备饲养细胞。方法 :采用 0Gy、2Gy、5Gy、1 0Gy、2 0Gy、30Gy的60钴 (60 Co)照射人的外周血单个核细胞 (PBMC) ,然后将其继续培养 ,加入CD3 单克隆抗体 (OKT3 )、白细胞介素 - 2(IL - 2 )、植物血球凝集素 (PHA)等 ,观察照射后第 1天、第 7天及第 1 5天细胞的凋亡情况及活细胞的细胞周期分布情况。结果 :γ射线照射剂量的加大会导致PBMC增殖能力的下降、存活细胞 (Annexin -V-/PI-)的减少、凋亡 (Annexin -V /PT-)与死亡 (Annexin -V /PT )的细胞数增加。结论 :采用60 Co照射法制备饲养细胞时 ,1 0Gy的照射剂量可能是最佳照射剂量     

磺胺甲恶唑致大鼠血小板减少模型研究

<正>目的:探讨磺胺甲恶唑致大鼠血小板减少模型的建立。方法:选取5～6周龄SD大鼠(体重约为180～210g,雄雌各半),区组法随机分为阳性对照组(放射照射组)、磺胺50mg/Kg、70mg/Kg组、90mg/Kg组、生理盐水阴性对照组,每组6只。磺胺甲恶唑首次注射大鼠后,1个月内每隔3天取大鼠尾静脉血进行外周血象检查,分别测定白细胞、血红蛋白、血小板计数。当各组外周血血小板计数降低到10×109/L以下时,断椎处死1～2只大鼠进行骨髓切片染色与巨核细胞诱导分化、扩增培养后染色鉴定,验证外周血血小板的检测结果。     

紫草素对卵巢癌细胞株SKOV3放疗敏感性的影响及相关机制研究

目的:研究紫草素对人卵巢癌细胞株SKOV-3的放射增敏作用,并探讨其可能的作用机制。方法:MTT法检测不同浓度(0、5、10、20、40、80和120 mg/L)紫草素对SKOV-3细胞活力的影响;克隆形成实验检测8 mg/L紫草素联合不同剂量(0、2、4、6和8 Gy)X射线照射对SKOV-3细胞增殖能力的影响。将SKOV-3细胞分为4组:对照组、紫草素组(8 mg/L紫草素处理)、8 Gy组(8 Gy X射线照射处理)和紫草素+8 Gy组(给予8 mg/L紫草素处理48 h后,再进行8 Gy X射线照射处理)。PI染色及流式细胞术检测各组SKOV-3细胞周期的变化;Western blot检测各组SKOV-3细胞p-PI3K和p-AKT的蛋白表达水平。结果:在0～80 mg/L浓度范围内,紫草素浓度依赖性抑制SKOV-3细胞活力(P0.05),IC_(50)为(38.54±0.57) mg/L;紫草素联合放疗处理后的SKOV-3细胞的存活曲线较单独放疗左移,放射增敏比为1.45±0.05。与8 Gy组相比,紫草素+8 Gy组G_2/M期细胞所占比例下降(P0.05),p-PI3K和p-AKT蛋白水平均显著降低(P0.05)。结论:紫草素具有提高人卵巢癌细胞株SKOV-3放射敏感性的作用,其作用机制可能与紫草素缓解X射线引起的G_2/M期阻滞及抑制PI3K/AKT信号通路有关。     

不同预处理方案对异基因骨髓移植物抗宿主病的影响

目的　建立大鼠异基因骨髓移植模型 ,应用不同的预处理方案 ,研究它们对移植物抗宿主病 (GVHD)严重程度的影响。方法　Wistar大鼠为供鼠 ,SD大鼠为受鼠 ,受鼠分 4组 ,分别予以不同的预处理方案 ,A、B组受鼠自移植前 4～ 1d ,腹腔注射氟达拉宾 (Fludarabine ,Flu) 1mg kg ,移植当天分别接受 2、6Gy的全身照射 ;C、D组受鼠在移植当天分别接受 2、6Gy的全身照射。制备供鼠骨髓细胞。照光 4h后 ,经尾静脉输注供鼠骨髓细胞 3.6× 10 7。观察各受鼠GVHD反应。结果　GVHD程度依次为 :Flu +2Gy组 <2Gy组 相似文献   

白术多糖对肺癌模型大鼠免疫功能的调节作用及机制研究

目的研究白术多糖对肺癌模型大鼠免疫相关因子及癌细胞增殖凋亡的影响,探讨其肿瘤抑制机制。方法观察记录不同给药剂量20、50、80mg/(kg·d)白术多糖对肺癌模型大鼠肺指数、脾脏指数、胸腺指数的影响。全自动血细胞分析仪检测大鼠外周血中白细胞和溶菌酶含量。ELISA法检测大鼠血清中IgG、IgA、Ig M水平。流式细胞仪分析T淋巴细胞亚群CD3~+、CD4~+、CD8~+比例。MTT法和Annexin V-FITC/PI双染法分别检测癌细胞增殖和凋亡。结果与模型组相比,白术多糖各剂量组大鼠肺指数均下降(P 0.01),脾脏和胸腺指数上升(P 0.01),大鼠外周血中白细胞和溶菌酶含量升高(P 0.01),且均呈剂量依赖性。ELISA法和流式细胞仪分析结果显示,白术多糖给药组大鼠血清免疫球蛋白IgG、IgA、Ig M水平和T淋巴细胞亚群CD3~+、CD4~+、CD4~+/CD8~+水平呈剂量依赖性升高(P 0.01)。MTT法和AnnexinV-FITC/PI双染法检测结果表明,对比模型组,白术多糖各剂量组肺癌模型大鼠癌细胞增殖率降低(P 0.01),细胞凋亡率增大(P 0.01)。结论白术多糖能够增强肺癌模型大鼠机体免疫功能,抑制癌细胞增殖并诱导凋亡。     

Low dose radiation overcomes diabetes-induced suppression of hippocampal neuronal cell proliferation in rats

We investigated the effect of low dose radiation on diabetes induced suppression of neurogenesis in the hippocampal dentate gyrus of rat. After 0.01 Gy, 0.1 Gy, 1 Gy and 10 Gy radiation was delivered, the dentate gyrus of hippocampus of streptozotocin (STZ)-induced diabetic rats were evaluated using immunohistochemistry for 5-bromo-2-deoxyuridine (BrdU), caspase-3, and terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) staining. The number of BrdU positive cells in the non-diabetic rats, diabetic rats without radiation, diabetic rats with 0.01 Gy radiation, diabetic rats with 0.1 Gy radiation, diabetic rats with 1 Gy radiation and diabetic rats with 10 Gy radiation were 55.4+/-8.5/mm2, 33.3+/-6.4/mm2, 67.7+/-10.5/mm2, 66.6+/-10.0/mm2, 23.5+/-6.3/mm2 and 14.3+/-7.2/mm2, respectively. The number of caspase-3 positive cells was 132.6+/-37.4/mm2, 378.6+/-99.1/mm2, 15.0+/-2.8/mm2, 57.1+/-16.9/mm2, 191.8+/-44.8/mm2 and 450.4+/-58.3/mm2, respectively. The number of TUNEL-positive cells was 24.5+/-2.0/mm2, 21.7+/-4.0/mm2, 20.4+/-2.0/mm2, 18.96+/-2.1/mm2, 58.3+/-7.9/mm2, and 106.0+/-9.8/mm2, respectively. These results suggest low doses of radiation paradoxically improved diabetes induced neuronal cell suppression in the hippocampal dentate gyrus of rat.     

Acute and late radiation injury in rhesus monkey parotid glands. Evidence of interphase cell death.

Acute and chronic salivary gland dysfunction are common sequelae of radiotherapy for head and neck cancer; but the associated morphologic changes, especially of the acute damage, have received relatively little study. For investigation of the morphologic characteristics of acute radiation injury to parotid glands, rhesus monkeys were studied 1-72 hours after parotid irradiation with single doses of 2.5-15.0 Gy. The acute damage from all doses was clearly expressed by 24 hours. Histologically, parotid glands irradiated with 2.5 or 5.0 Gy had random degeneration and necrosis of the serous acinar cells. Doses of 7.5-15.0 Gy produced widespread degeneration along with necrosis of whole acini. Serous cell damage was accompanied by neutrophilic inflammation that subsided after 24 hours to become replaced by plasma cell and lymphocytic infiltrates. Parotid glands receiving 7.5-15.0 Gy were atrophic at 16-22 weeks after irradiation and showed no recovery by 40 weeks. Although parotid acinar cells are well-differentiated nondividing cells, these observations show that they express lethal radiation injury in interphase within hours of receiving a radiation dose as low as 2.5 Gy. This is unlike most mammalian cells that express radiation injury during mitosis. Chronic atrophy is a consequence of this direct, irreversible, and early injury, rather than the result of radiation-induced changes in the vasculature.     

椎体转移瘤的立体定向适形放射治疗

目的 报告立体定向适形放射治疗椎体转移瘤的结果，并作临床分析。方法 1997年7月至2000年5月我院采用立体定向适形放射治疗8例椎体转移瘤，并进行了随访。肿瘤的临床靶体积（CTV）为7．5－60．5cm^3（平均为28．6cm^3），计划靶体积最小照射量为每次4．96－8．00Gy（平均为5．74Gy），计划靶体积最大照射量为6．25－10．08Gy（平均为7．29Gy），分次进行照射。结果 治疗过程中无一例死亡。患者一般计分标准（KPS），治疗前10－80分（平均50分），治疗后20－100分（平均78分）。在治疗后1－12个月随记期间，观察到87．65％受照射椎体转移瘤得到控制，疼痛得以明显缓解。结论 立体定向放射治疗对椎体转移瘤能有效且有良好的止痛效果。     

Risk of leukemia after chemotherapy and radiation treatment for breast cancer.

BACKGROUND. Few studies have evaluated the late effects of adjuvant chemotherapy for breast cancer. Moreover, the relation between the risk of leukemia and the amount of drug given and the interaction of chemotherapy with radiotherapy have not been described in detail. METHODS. We conducted a case-control study in a cohort of 82,700 women given a diagnosis of breast cancer from 1973 to 1985 in five areas of the United States. Detailed information about therapy was obtained for 90 patients with leukemia and 264 matched controls. The dose of radiation to the active marrow was estimated from individual radiotherapy records (mean dose, 7.5 Gy). RESULTS. The risk of acute nonlymphocytic leukemia was significantly increased after regional radiotherapy alone (relative risk, 2.4), alkylating agents alone (relative risk, 10.0), and combined radiation and drug therapy (relative risk, 17.4). Dose-dependent risks were observed after radiotherapy and treatment with melphalan and cyclophosphamide. Melphalan was 10 times more leukemogenic than cyclophosphamide (relative risk, 31.4 vs. 3.1). There was little increase in the risk associated with total cyclophosphamide doses of less than 20,000 mg. CONCLUSIONS. Although leukemia occurs in few patients with breast cancer, significantly elevated risks were linked to treatments with regional radiation and alkylating agents. Melphalan is a more potent leukemogen than cyclophosphamide or radiotherapy. Low risks were associated with the levels of cyclophosphamide in common use today. Systemic drug therapy combined with radiotherapy that delivers high doses to the marrow appears to enhance the risk of leukemia.     

Endogenous glucocorticoids modulate neutrophil migration and synovial P-selectin but not neutrophil phagocytic or oxidative function in experimental arthritis

Pharmacologic glucocorticoids are powerful inhibitors of the inflammatory response at many levels, including leucocyte trafficking and function. The adhesion molecule P-selectin is a key participant in polymorphonuclear neutrophil (PMN) migration to sites of inflammation. The extent to which endogenous glucocorticoids influence PMN migration and activation is not clear. We used the glucocorticoid receptor antagonist RU486 to examine the effect of endogenous glucocorticoid blockade on PMN migration and function in carrageenan monoarthritis in the rat. Arthritis was induced by intra-articular injection of carrageenan and disease severity measured by PMN count in synovial lavage fluid. Decalcified frozen sections of injected joints were analysed for expression of P-selectin by immunohistochemistry. Adrenal glucocorticoid action was blocked in vivo with RU486 20 mg/kg. PMN phagocytosis and reactive oxygen species synthesis were measured by flow cytometry. Carrageenan injection was associated with severe arthritis (synovial lavage PMN 5.9 ± 0.7 × 10⁶, P < 0.01 versus control) which was dose-dependent. P-selectin was not detected in normal joints but was abundant in joints injected with 500 μg carrageenan. RU486 resulted in exacerbation of carrageenan arthritis (9.7 ± 0.8 × 10⁶, P < 0.05). RU486 also altered the threshold for disease induction, in that most RU486-treated animals were susceptible to arthritis at a dose of carrageenan (2.5 μg) which did not induce arthritis in most control-treated animals (P < 0.05), denoting an altered threshold for arthritis induction. RU486 treatment was associated with increased synovial P-selectin expression. Activation status as measured by PMN phagocytic and oxidative function were not influenced by endogenous glucocorticoid blockade. These findings suggest that endogenous glucocorticoids selectively influence PMN migration to inflamed joints via P-selectin expression, but have no effect on PMN activation status.     

Radiation dose estimate in small animal SPECT and PET

Calculations of radiation dose are important in assessing the medical and biological implications of ionizing radiation in medical imaging techniques such as SPECT and PET. In contrast, radiation dose estimates of SPECT and PET imaging of small animals are not very well established. For that reason we have estimated the whole-body radiation dose to mice and rats for isotopes such as 18F, 99mTc, 201Tl, (111)In, 123I, and 125I that are used commonly for small animal imaging. We have approximated mouse and rat bodies with uniform soft tissue equivalent ellipsoids. The mouse and rat sized ellipsoids had a mass of 30 g and 300 g, respectively, and a ratio of the principal axes of 1:1:4 and 0.7:1:4. The absorbed fractions for various photon energies have been calculated using the Monte Carlo software package MCNP. Using these values, we then calculated MIRD S-values for two geometries that model the distribution of activity in the animal body: (a) a central point source and (b) a homogeneously distributed source, and compared these values against S-value calculations for small ellipsoids tabulated in MIRD Pamphlet 8 to validate our results. Finally we calculated the radiation dose taking into account the biological half-life of the radiopharmaceuticals and the amount of activity administered. Our calculations produced S-values between 1.06 x 10(-13) Gy/Bq s and 2.77 x 10(-13) Gy/Bq s for SPECT agents, and 15.0 x 10(-13) Gy/Bq s for the PET agent 18F, assuming mouse sized ellipsoids with uniform source distribution. The S-values for a central point source in an ellipsoid are about 10% higher than the values obtained for the uniform source distribution. Furthermore, the S-values for mouse sized ellipsoids are approximately 10 times higher than for the rat sized ellipsoids reflecting the difference in mass. We reviewed published data to obtain administered radioactivity and residence times for small animal imaging. From these values and our computed S-values we estimated that the whole body dose in small animals ranges between 6 cGy and 90 cGy for mice and between about 1 cGy and 27 cGy for rats. The whole body dose in small animal imaging can be very high in comparison to the lethal dose to mice (LD50/30 approximately 7 Gy). For this reason the dose in small animal imaging should be monitored carefully and the administered activity should be kept to a minimum. These results also underscore the need of further development of instrumentation that improves detection efficiency and reduces radiation dose in small animal imaging.     

A rat model for radiation-induced proctitis

Radiation proctitis is a frequent acute complication encountered with pelvic irradiation. This study was aimed at establishing the optimal radiation dose for radiation-induced proctitis in rats. Female Wistar rats were used. The rectal specimens were examined morphologically at 5th and 10th day following 10-30 Gy irradiation in single fraction. With increasing dose, mucosal damage became worse, and there was a prominent reaction after > or =15 Gy. We selected 17.5 Gy as an optimal dose for radiation proctitis and examined specimens at day 1-14 and at week 4, 6, 8, and 12 after 17.5 Gy. The rectal mucosa revealed characteristic histological changes with time. An edema in lamina propria started as early as 1-2 days after irradiation and progressed into acute inflammation. On day 7 and 8, regeneration was observed with or without ulcer. Four weeks later, all regeneration processes have been completed with end result of either fibrosis or normal appearing mucosa. This study showed that the radiation injury of the rectum in rat develops in dose-dependent manner as it has reported in previous studies and suggested that 17.5 Gy in single fraction is the optimum dose to evaluate the protective effect of various medications for radiation proctitis in face of the clinical situation.     

The analysis of prognostic factors affecting post-radiation acute reaction after conformal radiotherapy for non-small cell lung cancer

Introduction

The aim was to evaluate the risk of acute side effects in the lung after 3-dimensional conformal radiotherapy (3D-CRT) in patients treated for non-small cell lung cancer (NSCLC). An attempt was made to single out clinical factors and factors related to treatment technique which may induce acute post-radiation pneumonitis.

Material and methods

The analysis concerned 34 consecutive patients who underwent radical radiation therapy for NSCLC. Intensity of early toxicity was evaluated using modified RTOG/EORTC toxicity score. The endpoint for this analysis was the occurrence of radiation pneumonitis of grade 2 or higher. Factors related to treatment techniques were included in the statistical analysis.

Results

Fifty-three percent of patients included in the study suffered from acute post-radiation pneumonitis. The results of the study revealed the existence of lung tissue sensitivity to low doses of ionizing radiation. The multivariate analysis showed that total lung volume receiving a low dose of 10 Gy increased the risk of post-radiation pneumonitis (p = 0.01).

Conclusions

Acute post-radiation pneumonitis was a relevant clinical problem in patients who underwent radical radiotherapy for non-small cell lung cancer. The lung volume receiving a dose of 10 Gy was the most important dosimetric factor which influenced the post-radiation acute pneumonitis.     

不同分割剂量同步推量调强放疗治疗肺癌脑转移瘤的安全性分析

目的:分析不同分割剂量同步推量调强放疗治疗肺癌脑转移瘤的安全性及生存情况。方法:选取肺癌脑转移瘤患者75例,随机分为3组,均实施同步推量调强放疗,其中A组放疗方案为全脑40 Gy/20f（2.0 Gy/f）+瘤区同步推量46 Gy/20f（2.3 Gy/f）,B组方案为全脑40 Gy/20f（2.0 Gy/f）+瘤区同步推量52 Gy/20f（2.6 Gy/f）,C组方案为全脑40 Gy/20f（2.0 Gy/f）+瘤区同步推量58 Gy/20f（2.9 Gy/f）。放疗开始后,对3组患者危及器官（眼球、晶体、视神经、脑干）平均剂量及最大剂量和3组患者放疗相关不良反应进行比较。治疗结束后定期复查颅脑MRI评价疗效,观察3组患者1年生存率。结果:A、B、C组危及器官平均剂量及最大剂量差异不显著（P>0.05）;A、B、C组急性放疗不良反应发生率差异不显著（P>0.05）,晚期神经系统不良反应发生率亦差异不显著（P>0.05）,3级放疗不良反应低于5%,无4级放疗不良反应发生。随访1年,C组生存率高于A、B组（P<0.05）。结论:同步推量调强放疗治疗肺癌脑转移瘤是一种安全有效的方法,随着放疗剂量增加,疗效有增加趋势。