低剂量辐射与糖尿病及其合并症的预防和治疗

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Clinicopathological Characteristics and Prognosis of Patients with Adenosquamous Lung Carcinoma

This study was aimed to characterize clinicopathological features and prognosis of patients with adenosquamous lung carcinoma(ASC). Among the 2531 patients with lung cancer who underwent surgery between January 2000 and June 2012 in our hospital, 59 were histologically diagnosed as having ASC. The clinicopathological features and follow-up data of ASC patients were collected and analyzed statistically. Superior lobectomy was accomplished in 40 patients, middle and inferior lobectomy in 3, lobectomy plus partial resection of contralateral lung in 5, partial lung resection in 4, and pneumonectomy in 7. Moreover, 22 cases were found to be adenocarcinoma-predominant, and 18 to be squamous cell carcinoma-predominant. The median survival time was 13.6 months, and the 1-, 3-, and 5-year survival rates were 59.9%, 36.4% and 31.2%, respectively. Of the 52 cases with tissue specimens available, 11 had an EGFR mutation(21.2%) and 2 had a KRAS mutation(3.8%). Multivariate analysis showed that histology subtype, pleural invasion, TNM stage, and postoperative treatment were all independent prognostic factors. The data from the current study demonstrated that SCC-predominant histology represents a better prognosis of ASC. Histology subtype, pleural invasion, TNM stage, and postoperative treatment are independent prognostic factors for ASC and adjuvant therapy may help control the disease.     

低剂量X射线照射对荷人小细胞肺癌(NCI-H446)裸小鼠移植瘤细胞凋亡相关基因mRNA表达的影响

目的 研究低剂量照射（LDR）对荷人小细胞肺癌（NCI-H446）裸小鼠移植瘤细胞凋亡相关基因mRNA表达的影响。方法 对荷人小细胞肺癌裸小鼠进行全身深部X射线照射，采用原位杂交技术检测荷人小细胞肺癌裸小鼠移植瘤组织的p53、Bcl-2、Bax的mRNA表达水平。结果 D1（75mGy）、D2（4Gy）照射后，小细胞肺癌细胞的p53、Bax的mRNA表达呈上升趋势，Bcl-2的mRNA表达呈下降趋势，但与假照组（0 mGy）比较，无明显差异；D1＋D2组的p53、Bax的mRNA表达明显增多，Bcl-2mRNA表达显著下降，与假照组（0mGy）比较有统计学差异（P〈0．05）。结论 LDR在一定程度上可能上调小细胞肺癌细胞的p53、Bax的mRNA表达，下调了Bcl-2mRNA的表达，同时对其后的大剂量照射有协同作用。     

Fli-1在肿瘤发生及发展中的作用

Friend 白血病病毒插入位点1(Fli-1)是属于E26转化特异性因子(ETS)家族的转录因子,在造血干细胞、血管内皮细胞、淋巴细胞和恶性肿瘤细胞中表达,在血管内皮细胞生成和肿瘤细胞增殖过程中具有重要调节作用。血管内皮细胞不仅是正常血管生成的关键因素,而且在肿瘤的生长和转移中均需要新生血管的形成作为肿瘤进展的驱动因素。以Fli-1为治疗靶点,既可抑制肿瘤细胞的增殖,又可阻断肿瘤血管的形成,将成为治疗肿瘤的优秀靶点。因此,详细研究Fli-1结构与功能及其在恶性肿瘤中的表达情况,有助于进一步明确Fli-1在恶性肿瘤发生及发展中的作用。本文作者就Fli-1与肿瘤关系的研究进行综述。     

遗传性蛋白S缺陷症家系基因突变的研究

Objective To identify the clinical phenotypic diagnosis and gene mutation detection of two kindreds with PS deficiency. MethodsPS: A was measured by chromogenic substrate method;TPS:Ag, FPS: Ag levels were measured by ELISA method; PS gene(PROS1 gene)was detected by amplifying 15 exons and flanking intron sequences from the propositus with PCR method. PCR products were purified and directly sequenced. Results For propositus 1,PS: A was 48.6% ,TPS: Ag was 136 mg/L, FPS : Ag was 41 mg/L, PROSI gene exon 2 was in c. Heterozygous base substitutions was detected in C121T locus, which led to Arg-1Cys (R-1C) heterozygous roissense mutation encoded in PS proteins. For propositus 2, PS: A was 29.2%, TPS: Ag was 83 mg/L, FPS: Ag was 26 mg/L, PROSI gene exon 14 was in c. Heterozygous base substitutions was identified in CI687T locus, in which Gln.522Stop heterozygous nonsense mutation was encoded in PS proteins. Conclusions c. C121T is a novel mutation locus detected in PROS1 gene. This heterozygous mutation could lead to type Ⅱ PS hereditary deficiency, while c. C1687T heterozygous mutation could bring about type Ⅰ PS hereditary deficiency.     

慢性粒细胞白血病Ph1染色体和bcr/abl融合基因检测的意义

目的：探讨Ph¹染色体和bcr/abl融合基因检测在慢性粒细胞白血病诊断中的意义。 方法：选择95例慢性粒细胞白血病患者和20例缺铁性贫血患者作为研究对象,采用骨髓细胞短期培养法制备染色体、采用RT-PCR法分析bcr/abl融合基因。 结果：95例慢性粒细胞白血病患者中,Ph¹染色体阳性者83例（87.4%）,bcr/abl阳性阳性者90例（94.7%）,Ph¹和bcr/abl均阳性83例（94.7%）,Ph¹阴性、bcr/abl阳性7例（7.4%）,Ph¹和bcr/abl均阴性5例（5.3%）。20例缺铁性贫血患者Ph¹和bcr/abl均阴性。 结论：Ph¹染色体、bcr/abl融合基因的检测有助于慢性粒细胞白血病的诊断和鉴别诊断。     

G-CSF动员的外周血与骨髓CD34+细胞黏附分子的表达

目的：研究黏附分子在外周血干细胞动员机制中的作用。 方法：应用流式细胞仪检测粒细胞集落刺激因子G-CSF动员的外周血细胞与骨髓CD34⁺细胞表达的黏附分子非常延迟抗原4(VLA-4)、淋巴细胞功能相关抗原1(LFA-1)和L-选择素(CD62L)。 结果：G-CSF动员后的外周血CD34⁺细胞表达的VLA-4、LFA-1与骨髓CD34⁺细胞相比明显减少,CD62L无明显改变。 结论：黏附分子VLA-4及LFA-1降低可能是G-CSF动员造血干细胞进入外周血过程中的一个重要环节。     

恶性血液病Flt3基因内部串联重复突变分析

目的：研究Flt₃-ITD在恶性血液病中的突变及分布情况。 方法：采用PCR法检测103例恶性血液病患者基因组DNA Flt₃-ITD突变。结果：44例初治急性髓细胞白血病（AML）患者中8例发生Flt₃-ITD突变,突变率为18.2%,以M1型最高;急性淋巴细胞白血病（ALL）、骨髓增生异常综合征（MDS）、多发性骨髓瘤（MM）、非何杰淋巴瘤（NHL）及慢性髓细胞白血病（CML）均未检出Flt₃-ITD突变。 结论：Flt₃-ITD可作为AML重要分子标志。     

苯丁酸钠联合吉非替尼增强抑制NB4细胞的PKC信号传导途径

目的：探讨联合应用苯丁酸钠(SPB)与吉非替尼对NB4细胞的抑制效果。方法：将NB4细胞随机分为对照组、PKC激动剂PMA组、PKC抑制剂H-7组、SPB组、SPB+PMA组、吉非替尼组、吉非替尼+PMA组及SPB+吉非替尼组。应用MTT法检测药物对细胞的抑制率,流式细胞仪检测细胞的凋亡情况, Western blotting 法检测蛋白激酶C（PKC）、周期素依赖性激酶4（CDK₄）及野生型P53蛋白的表达。结果：SPB+吉非替尼联合用药物组肿瘤细胞受到明显抑制,生长抑制率和增殖指数分别为92.80%和5.96%;与SPB组（生长抑制率和增殖指数分别为45.1%和29.6%）以及吉非替尼组（生长抑制率和增殖指数分别为61.0%和35.9%）相比,差异均有显著性（P<0.05）;SPB+吉非替尼组P53表达增加,CDK₄和磷酸化的PKC表达下降,与单纯用药组比较,差异均具有显著性（P<0.05)。结论：SPB与吉非替尼联合用药比单一用药明显提高肿瘤细胞的抑制率和促凋亡率,其机制是通过联合抑制PKC的信号传导通路从而阻滞肿瘤细胞的增殖周期。     

老年抑郁症住院患者的支持性心理干预研究

目的探讨支持性心理干预对老年抑郁症住院患者的效果。方法采用临床对照研究,选择20例确诊的住院患者作为对照组,给予抗抑郁药物治疗和一般精神科护理。另外选择同期住院的与之相匹配的20例患者作为研究组,在对照组的基础上,给予支持性心理干预4周。用Montgomery＆Asberg（MADS）抑郁量表评定效果。结果2组干预前后MADS总分均显著下降（p〈0．01）,但从第3周开始研究组MADS分低于对照组（p〈0．05）,且2组MADS各因子分比较显示,研究组的内心紧张、睡眠减少等七项因子分均低于对照组,差别有统计学意义（P〈0．05）。研究组住院天数少于对照组（p〈0．05）。结论对于临床住院老年抑郁患者,支持性心理干预联合药物治疗有利于其更快更好的恢复,有利于其症状的改善。