基于多尺度形态学滤波的CT图像疑似肺结节提取

CT图像中疑似结节病灶区域的分割和提取是肺部CAD系统的关键和难点.研究一种基于肺结节几何特征的多尺度形态学滤波的疑似结节区域提取算法,构造了一组不同尺度的类圆形结构元素进行形态学滤波.经过多尺度处理,不同大小的疑似肺结节区域得到增强和突出,气管、血管等线形解剖组织得到了削弱和抑制,结构元素的几何参数及二值化阈值参数的选取不需要人工设置.实验结果表明,该算法可以较好地实现不同大小疑似结节区域的自动提取.     

An Integrated Mass Spectrometry-Based Glycomics-Driven Glycoproteomics Analytical Platform to Functionally Characterize Glycosylation Inhibitors

Cancer progression is linked to aberrant protein glycosylation due to the overexpression of several glycosylation enzymes. These enzymes are underexploited as potential anticancer drug targets and the development of rapid-screening methods and identification of glycosylation inhibitors are highly sought. An integrated bioinformatics and mass spectrometry-based glycomics-driven glycoproteomics analysis pipeline was performed to identify an N-glycan inhibitor against lung cancer cells. Combined network pharmacology and in silico screening approaches were used to identify a potential inhibitor, pictilisib, against several glycosylation-related proteins, such as Alpha1-6FucT, GlcNAcT-V, and Alpha2,6-ST-I. A glycomics assay of lung cancer cells treated with pictilisib showed a significant reduction in the fucosylation and sialylation of N-glycans, with an increase in high mannose-type glycans. Proteomics analysis and in vitro assays also showed significant upregulation of the proteins involved in apoptosis and cell adhesion, and the downregulation of proteins involved in cell cycle regulation, mRNA processing, and protein translation. Site-specific glycoproteomics analysis further showed that glycoproteins with reduced fucosylation and sialylation were involved in apoptosis, cell adhesion, DNA damage repair, and chemical response processes. To determine how the alterations in N-glycosylation impact glycoprotein dynamics, modeling of changes in glycan interactions of the ITGA5–ITGB1 (Integrin alpha 5-Integrin beta-1) complex revealed specific glycosites at the interface of these proteins that, when highly fucosylated and sialylated, such as in untreated A549 cells, form greater hydrogen bonding interactions compared to the high mannose-types in pictilisib-treated A549 cells. This study highlights the use of mass spectrometry to identify a potential glycosylation inhibitor and assessment of its impact on cell surface glycoprotein abundance and protein–protein interaction.     

高龄原发性肺癌患者的手术治疗（附12例报告）

采用肺叶、支气管袖状肺叶切除等手术方式,对１２例高龄肺癌患者进行手术治疗,手术效果满意。笔者认为：对高龄肺癌患者的手术治疗,只要选择恰当的手术方式,做好围手术期的呼吸道管理,可以降低手术并发症和死亡率,提高术后生活质量。     

小鼠肺腺癌细胞系（LA－795）高、低转移潜能亚系的建立及其形态学比较

利用单细胞克隆化培养技术，对小鼠肺脓癌ＬＡ７９５细胞系进行单细胞克隆化培养，分离出８个亚系，体外培养３５代内生物学特性稳定，反复液氮冻存能复苏。将其中４个亚系细胞在裸鼠体内移植，结果命名为ＬＡ７９５－Ｃ６的细胞亚系较命名为ＬＡ７９５－Ｃ７的细胞亚系具有更大的肺转移能力，表明了母系确实存在转移潜能不同的异质细胞；将高、低转移潜能细胞体外培养，并进行形态学观察，发现高转移潜能细胞比低转移潜能细胞表现为更幼稚，且更具有生长活跃性的特点，说明高转移亚系ＬＡ７９５－Ｃ６和低转移亚系ＬＡ７９５－Ｃ７在体外培养存在着分化程度上的差异，且该肿瘤体内转移能力和体外培养细胞分化程度呈负相关。这提示体外培养的肿瘤细胞其分化程度和体内转移潜能有密切的矢系。     

综合呼吸功能训练对肺癌患者术后康复的影响

目的 观察综合呼吸功能训练对肺癌患者术后康复的促进作用.方法 选择85例择期手术治疗的周围型肺癌患者为研究对象,按护理方式分为对照组和观察组.对照组术后给予常规护理,观察组在常规护理基础上给予围手术期综合呼吸功能训练,比较观察两组患者胸导管留置时间、引流量和术后住院时间;两组患者肺功能恢复情况(指标FEV1、FVC、PEFR);两组患者术后呼吸系统并发症发生率.结果 与对照组比较,观察组患者胸导管留置时间、引流量以及术后住院时间明显减少,组间比较差异具有统计学意义(P<0.01);观察组患者呼吸系统并发症发生率与对照组比较明显降低,组间差异具有统计学意义(P<0.01);观察组患者肺功能恢复情况优于对照组,差异具有统计学意义(P<0.01).结论 围手术期综合呼吸功能训练能够缩短患者住院时间,减少肺癌患者术后并发症发生,促进肺功能恢复,值得临床推广应用.     

肺癌患者血清P53抗体及肺癌组织P53表达对肺癌诊断价值的研究

目的探讨肺癌患者血清P53抗体水平及肺癌组织P53表达对肺癌诊断的价值.方法采用ELISA法检测肺癌患者血清P53抗体水平,并采用免疫组化法检测肺癌组织P53表达情况.结果肺癌患者血清P53抗体（17.84±8.73）ng/L水平比正常对照组（5.43±1.90）ng/L显著升高（P〈0.001）,肺癌患者血清P53抗体水平与肿瘤大小、淋巴转移、远端转移、TNM分期有关.肺癌患者癌组织P53表达的阳性率为61.5%（168/273）,肺癌患者癌组织P53阳性表达率与肿瘤大小、淋巴转移、远端转移、TNM分期、分化程度、病理类型有关.结论血清P53抗体水平与癌组织中的表达有着良好的平行关系,测定血清P53抗体水平或检查肺癌患者癌组织P53的表达可对肺癌的诊断、分期、治疗和预后提供重要依据.     

四生散对肺癌细胞增殖的抑制作用及毒性研究

主要探讨中药制剂四生散对人肺癌A5 4 9细胞株的增殖抑制作用以及其急性毒性.应用改进的MTT法测定四生散对肺癌细胞增殖的影响;采用琼脂糖凝胶电泳测定四生散对诱导肿瘤细胞凋亡的影响;再用分剂量组灌胃小鼠的方法,鉴定四生散的急性毒性.实验结果表明,四生散对人肺癌A5 4 9细胞株的增殖有较强的抑制作用,并具有明显的量效和时效相关性;经四生散处理后的A5 4 9细胞呈现凋亡特征性电泳条带;在3 2倍于人的剂量时,小鼠饮食和体重均在正常水平,并无异常,证实口服四生散无急性毒性.     

改进的YOLOv4肺结节检测算法

针对目标检测YOLOv4算法在肺结节检测中存在的小目标漏检和肺结节位置失真等问题,设计了一种改进的YOLOv4肺结节检测算法.在原始YOLOv4网络的基础上,将特征融合网络的上采样过程替换为双线性插值法,并采用张量堆叠的方法使顶层的语义信息与底层的位置信息形成更高通道的特征张量.实验结果表明,与原始的YOLOv4算法相比,改进的YOLOv4算法在公开数据集LUAN16上的平均精确度与预测速度分别提高了4.54%和28.1%,可视化结节位置表达更精准.     

Chemical Constituents from the Flowers of Carthamus tinctorius L. and Their Lung Protective Activity

A new flavonoid, saffloflavanside (1), a new sesquiterpene, safflomegastigside (2), and a new amide, saffloamide (3), together with twenty-two known compounds (4–25), were isolated from the flowers of Carthamus tinctorius L. Their structures were determined based on interpretation of their spectroscopic data and comparison with those reported in the literature. The protective effects against lipopolysaccharide (LPS)-stimulated damage on human normal lung epithelial (BEAS-2B) cells of the compounds were evaluated using MTT assay and cellular immunofluorescence assay. The results showed that compounds 2–3, 8–11, and 15–19 exhibited protective effects against LPS-induced damage to BEAS-2B cells. Moreover, compounds 2–3, 8–11, and 15–19 can significantly downregulate the level of nuclear translocation of NF-κB p-p65. In summary, this study revealed chemical constituents with lung protective activity from C. tinctorius, which may be developed as a drug for the treatment of lung injury.     

Structure-Based Discovery and Biological Assays of a Novel PRMT5 Inhibitor for Non-Small Cell Lung Cancer

Protein arginine methyltransferase 5 (PRMT5) is a popular anticancer target that regulates histone or nonhistone methylation and is linked to the development and poor prognosis of non-small cell lung cancer. PRMT5 inhibitors have shown great promise in clinical trials as a cancer therapy. However, most inhibitors reported recently act in a SAM-competitive mode and lack structural diversity. In this paper, a novel non-SAM inhibitor, 3039-0164, was discovered by the structure-based virtual screening method. The binding mechanism of 3039-0164 to PRMT5 was revealed via molecular docking and molecular dynamics simulations. 3039-0164 inhibited PRMT5 enzymatic activity, downregulated the expression of PRMT5 downstream target genes (FGFR3 and eIF4E), and blocked the activation of the PI3K/AKT/mTOR and ERK signaling pathways. The discovery of 3039-0164 provides precise and creative hit compounds for the design optimization of PRMT5 lead compounds in non-small cell lung cancer.