Clinical usefulness of breast-specific gamma imaging as an adjunct modality to mammography for diagnosis of breast cancer: a systemic review and meta-analysis

Purpose

The purpose of this study was to assess the diagnostic performance of breast-specific gamma imaging (BSGI) as an adjunct modality to mammography for detecting breast cancer.

Methods

Comprehensive searches of MEDLINE (1984 to August 2012) and EMBASE (1994 to August 2012) were performed. A summary receiver operating characteristic curve (SROC) was constructed to summarize the overall test performance of BSGI. The sensitivities for detecting subcentimetre cancer and ductal carcinoma in situ (DCIS) were pooled. The potential of BSGI to complement mammography was also evaluated by identifying mammography-occult breast cancer.

Results

Analysis of the studies revealed that the overall validity estimates of BSGI in detecting breast cancer were as follows: sensitivity 95 % (95 % CI 93–96 %), specificity 80 % (95 % CI 78–82 %), positive likelihood ratio 4.63 (95 % CI 3.13–6.85), negative likelihood ratio 0.08 (95 % CI 0.05–0.14), and diagnostic odds ratio 56.67 (95 % CI 26.68–120.34). The area under the SROC was 0.9552 and the Q* point was 0.8977. The pooled sensitivities for detecting subcentimetre cancer and DCIS were 84 % (95 % CI 80–88 %) and 88 % (95 % CI 81–92 %), respectively. Among patients with normal mammography, 4 % were diagnosed with breast cancer by BSGI, and among those with mammography suggestive of malignancy or new biopsy-proven breast cancer, 6 % were diagnosed with additional cancers in the breast by BSGI.

Conclusion

BSGI had a high diagnostic performance as an excellent adjunct modality to mammography for detecting breast cancer. The ability to identify subcentimetre cancer and DCIS was also high.     

多时点动态观测原发性痛经寒凝血瘀证患者的脉图参数变化

目的 分析原发性痛经寒凝血瘀证患者脉图参数的动态变化及其与疼痛程度的相关性.方法 以原发性痛经寒凝血瘀证患者为原发性痛经组,健康者为对照组.在痛经典型发作时予以电针治疗,形成4个观测时点(T0:经前7～10 d,T1:经期痛经典型发作时,T2:针刺镇痛治疗30 min结束即刻,T3:针刺镇痛治疗结束后30 min).运...     

冠心病患者白细胞介素-6基因-174G/C的多态性研究

目的　探讨白细胞介素 -6基因多态性是否与冠心病患者有关联。方法　应用聚合酶链反应限制性片断长度多态性技术对湖北地区汉族 112例冠心病患者及 183例正常对照组者白细胞介素 6基因 174G/C位点进行研究。结果　发现冠心病组与正常对照组白细胞介素 6基因 174位点均以GG型为主 ,其频率分别为 0 991和 0 989。 174位点等位基因频率在两组中无显著差异 (P >0 0 5 )。结论　提示白细胞介素 6基因 174G/C位点多态性与中国人冠心病无关联     

Effect of conventional medical treatment plus Qigong exercise on type 2 diabetes mellitus in Chinese patients: A Meta-analysis

OBJECTIVE

To systematically evaluate the effect of conventional medical treatment plus Qigong exercise on type 2 diabetes mellitus (T2DM) in Chinese patients.

康复治疗学专业创新型人才培养的探索与实践

针对新建的康复治疗学专业本科教育,为了培养创新型康复治疗高级人才,首都医科大学康复医学院通过开设一系列科研训练课程、开展毕业设计和学术交流等教学实践活动,构建了创新型人才培养的教学体系,收到了良好的教学效果。     

微生物检验技术课程项目化教学模式的构建与实践

根据教育部在《关于全面提高高等职业教育教学质量的若干意见》文件中的精神,探索微生物检验技术的教学改革方法,构建项目化教学的模式,通过资讯—计划—决策—实施—检查—评估进行实践,有利于提高学生的综合素质,增强就业竞争力。     

丙戊酸钠慢性作用及停药后对C6神经胶质瘤细胞GAT-3及GABA-TmRNA表达的影响

目的通过研究丙戊酸钠(VPA)慢性作用及停药后对C6神经胶质瘤细胞γ-氨基丁酸转运体-3(GAT-3)和γ-氨基丁酸转氨酶(GABA-T) mRNA表达水平的影响,从星形胶质细胞的角度来探讨VPA的停药反跳机制。方法用含50 mg/L VPA的DMEM培养基将C6细胞培养2周后制成VPA慢性作用模型,采用半定量RT-PCR方法检测VPA慢性作用及停药后对C6神经胶质瘤细胞GAT-3和GABA-T mRNA表达水平的变化。结果(1)在VPA慢性作用下,相对灰度值(RV值,即GAT-3、GABA-T电泳条带与相应的β-actin灰度积分的百分比)为(39.1±0.5)%,低于正常对照组的(46±1.3)%;各停药组的RV值均低于VPA慢性作用组,其中停药24 h组的最低,为(11.7±1.6)%,停药30 min组的最高,为(38.9±0.6)%;而停药48 h组又升高到(33.5±1.1)%。(2)VPA慢性作用组[RV值为(71.31±6.91)%]与对照组[RV值为(34.77±3.26)%]相比,GABA-T mRNA表达明显上调;各停药组与VPA慢性作用组相比GABA-T mRNA的表达明显下调,其中停药12 h组[RV值为(25.36±7.68)%]降至最低。结论VPA慢性作用可使GAT-3 mRNA的表达下调,使GABA-T mRNA表达上调。VPA慢性作用后停药造成的GAT-3和GABA-T mRNA表达水平的波动可能与VPA停药反跳有关。     

Discovery of Cobimetinib as a novel A-FABP inhibitor using machine learning and molecular docking-based virtual screening

Adipocyte fatty acid-binding protein (A-FABP, also called FABP4, aP2) is an adipokine identified as a critical regulator of metabolic function due to its dual functions of fatty acid transport and pro-inflammation. Because of the high therapeutic potential of A-FABP inhibition for the treatment of metabolic diseases and related vascular complications, numerous inhibitors have been developed against A-FABP. However, none of these inhibitors have been approved for use in patients due to severe side effects. Here, we used a virtual screening (VS) strategy to identify potential inhibitors of A-FABP in the latest FDA-approved drug library (∼2600 compounds), aiming to explore the existing drugs with proven safety profiles. We firstly combined ligand-based machine learning and structure-based molecular docking to develop a screening pipeline for identifying A-FABP inhibitors. The screening of FDA-approved drugs identified four compounds (Cobimetinib, Larotrectinib, Pantoprazole, and Vildagliptin) with the highest scores, whose inhibitory effects on A-FABP were further assessed in cellular assays. Among the selected compounds, Cobimetinib significantly inhibited the activation of the JNK/c-Jun signaling pathway by A-FABP in mouse macrophages without causing obvious cytotoxicity. In summary, we present an integrated VS pipeline for A-FABP inhibitor screening, and identified Cobimetinib as a novel A-FABP inhibitor that may be repurposed for the treatment of metabolic diseases and associated vascular complications.

The integrated virtual screening pipeline was constructed to identify potential inhibitors of A-FABP in the latest FDA-approved drug library, aiming to explore the existing drugs with proven safety profiles.     

A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage

AimsWhite matter (WM) injury is a critical factor associated with worse outcomes following subarachnoid hemorrhage (SAH). However, the detailed pathological changes are not completely understood. This study investigates temporal changes in the corpus callosum (CC), including WM edema and oligodendrocyte death after SAH, and the role of lipocalin‐2 (LCN2) in those changes.MethodsSubarachnoid hemorrhage was induced in adult wild‐type or LCN2 knockout mice via endovascular perforation. Magnetic resonance imaging was performed 4 hours, 1 day, and 8 days after SAH, and T2 hyperintensity changes within the CC were quantified to represent WM edema. Immunofluorescence staining was performed to evaluate oligodendrocyte death and proliferation.ResultsSubarachnoid hemorrhage induced significant CC T2 hyperintensity at 4 hours and 1 day that diminished significantly by 8 days post‐procedure. Comparing changes between the 4 hours and 1 day, each individual mouse had an increase in CC T2 hyperintensity volume. Oligodendrocyte death was observed at 4 hours, 1 day, and 8 days after SAH induction, and there was progressive loss of mature oligodendrocytes, while immature oligodendrocytes/oligodendrocyte precursor cells (OPCs) proliferated back to baseline by Day 8 after SAH. Moreover, LCN2 knockout attenuated WM edema and oligodendrocyte death at 24 hours after SAH.ConclusionsSubarachnoid hemorrhage leads to T2 hyperintensity change within the CC, which indicates WM edema. Oligodendrocyte death was observed in the CC within 1 day of SAH, with a partial recovery by Day 8. SAH‐induced WM injury was alleviated in an LCN2 knockout mouse model.