Solid‐type poorly differentiated adenocarcinoma of the stomach: Deficiency of mismatch repair and SWI/SNF complex

ARID1A, one of the subunits in SWI/SNF chromatin remodeling complex, is frequently mutated in gastric cancers with microsatellite instability (MSI). The most frequent MSI in solid‐type poorly differentiated adenocarcinoma (PDA) has been reported, but the SWI/SNF complex status in solid‐type PDA is still largely unknown. We retrospectively analyzed 54 cases of solid‐type PDA for the expressions of mismatch repair (MMR) proteins (MLH1, PMS2, MSH2, and MSH6), SWI/SNF complex subunits (ARID1A, INI1, BRG1, BRM, BAF155, and BAF170) and EBER, and mutations in KRAS and BRAF. We analyzed 40 cases of another histological type of gastric cancer as a control group. The solid‐type PDAs showed coexisting glandular components (76%), MMR deficiency (39%), and complete/partial loss of ARID1A (31%/7%), INI1 (4%/4%), BRG1 (48%/30%), BRM (33%/33%), BAF155 (13%/41%), and BAF170 (6%/2%), EBER positivity (4%), KRAS mutation (2%), and BRAF mutation (2%). Compared to the control group, MMR deficiency and losses of ARID1A, BRG1, BRM, and BAF155 were significantly frequent in solid‐type PDAs. Mismatch repair deficiency was associated with the losses of ARID1A, BRG1, and BAF155 in solid‐type PDAs. In the MMR‐deficient group, solid components showed significantly more frequent losses of ARID1A, BRG1, BRM, and BAF155 compared to glandular components (P = .0268, P = .0181, P = .0224, and P = .0071, respectively). In the MMR‐proficient group, solid components showed significantly more frequent loss of BRG1 compared to glandular components (P = .012). In conclusion, solid‐type PDAs showed frequent losses of MMR proteins and the SWI/SNF complex. We suggest that loss of the SWI/SNF complex could induce a morphological shift from differentiated‐type adenocarcinoma to solid‐type PDA.     

Transarterial Chemoembolization vs Radioembolization for Neuroendocrine Liver Metastases: A Multi-Institutional Analysis

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不同氢溴酸右美沙芬口服固体制剂的溶出度考察

目的：对6个厂家不同氢溴酸右美沙芬口服固体制剂进行体外溶出度考察，比较体外溶出情况，为临床用药提供参考。方法：采用转篮法，转速100 r·min^-1，用高效液相色谱法测定氢溴酸右美沙芬口服固体制剂在0.1 mol·L^-1盐酸溶液中的溶出曲线；以威布尔方程拟合溶出参数T₅₀、T_d、m，并对参数进行方差分析。结果：氢溴酸右美沙普通片、分散片、胶囊以及软胶囊的平均累积溶出度分别为94.3%、101.3%、105.2%、93.4%。溶出参数T₅₀、T_d差异较大，其中T₅₀最大的是最小的13.4倍。结论：氢溴酸右美沙片、分散片、胶囊以及软胶囊体外溶出行为差别大，产品质量存在较大差异。     

葫芦素B固体分散体的制备

目的制备葫芦素B固体分散体。方法溶剂法制备固体分散体后,以溶出度为评价指标筛选药物-载体(PVP K30)比例。扫描电子显微镜(SEM)、傅里叶变换红外光谱(FTIR)、差示扫描量热(DSC)、X射线衍射(XRD)进行表征。结果药载比为1∶11时,60 min内溶出度为62.01%。葫芦素B可能以无定形状态分散于载体中。结论该方法简便可行,葫芦素B制成固体分散体后体外溶出度明显提高。     

Ex vivo identification of atherosclerotic plaque calcification by a 31P solid-state magnetic resonance imaging technique.

Calcified tissue is a common component of atherosclerotic plaques, and occurs most often in mature plaques. The process of calcification is a poorly understood risk factor that may contribute to a plaque's vulnerability to sudden rupture. In this study a solid-state imaging sequence, termed single-point imaging (SPI), was used to observe calcification directly in ex vivo atherosclerotic plaques. Standards were used to validate the ability of (31)P SPI to detect and differentiate calcification from crystalline cholesterol, phospholipids, and other plaque components. After suitable experimental parameters were found, human carotid specimens obtained by endarterectomy were imaged ex vivo by (31)P solid-state imaging and standard (1)H methods. In contrast to (1)H imaging methods, (31)P imaging detected only the calcification in the plaque.     

多巴酚丁胺负荷实验对家猪急性冬眠心肌模型QT离散度影响的实验研究

目的 观察多巴酚丁胺负荷期间QT离散度(QTd)的变化情况,探讨其临床意义.方法 对13只小型中国家猪采用闭胸介入法制备急性冬眠心肌模型(右冠状动脉为靶血管),利用多巴酚丁胺超声负荷实验(DSE,0～40 μg·Kg-1·min-1)检出冬眠心肌,之后成功复灌,处死动物,对心脏行TTC大体染色及光镜检查.分别于模型制备前后、DSE期间及复灌后观察QTd的变化情况.结果 ①10只动物(76.92%)成功制备成模型,病理检查未示心肌坏死改变.②模型制备成功后QTd较正常状态明显增加[(68.75±5.33)ms和(25.00±1.77)ms,P＜0.05];复灌后明显降低[(35.62±3.47)ms和(68.75±5.33)ms,P＜0.05],与正常状态差异无统计学意义[(35.62±3.47)ms和(25.00±1.77)ms,P＞0.05].③DSE期间QTd呈现先降低后增加的双相反应的变化趋势.④模型制备成功后的QTd与DSE检出的急性冬眠心肌节段数呈中等程度的负相关(r=-0.64,P＜0.05).结论 ①.急性冬眠心肌动物模型的QTd明显增加,早期有效复灌可降低QTd.②DSE期间急性冬眠心肌模型的QTd呈现双相反应趋势.③急性冬眠心肌模型的QTd是反映冬眠心肌数量的指标之一.     

沙利度胺治疗肝癌的实验研究

目的研究沙利度胺对肝癌的治疗作用。方法采用小鼠肝癌移植性模型。观察沙利度胺对实体型和腹水型肿瘤的治疗作用。结果沙利度胺按每日200mg／kg连续给药10d，能明显抑制肝癌实体型肿瘤的生长，不降低小鼠血细胞数及淋巴细胞增殖；对腹水型肿瘤小鼠虽无明显生命延长作用，但沙利度胺与阿霉素联合用药对肝癌实体型及腹水型均有协调抗肿瘤作用，且可阻止阿霉素造成的小鼠血细胞减少、免疫功能降低。沙利度胺日剂量200mg／kg能明显增加肿瘤组织坏死，促进肿瘤组织边缘淋巴细胞侵润。结论沙利度胺对小鼠肝癌有确切治疗作用，与阿霉素联合用药效果更好。