桦木酸对大鼠肺纤维化模型肺组织的影响＊

目的 探讨桦木酸对大鼠肺纤维化模型肺组织中NF-κB、β-arrestin2表达的影响。方法 15只SPF级雄性SD大鼠分为对照组、模型组、桦木酸组，每组5只。对照组予以单次气管内注射1 mL·kg^-1 0.9%生理盐水，模型组和桦木酸组予单次气管内快速注射5 mg·kg^-1博来霉素建立大鼠肺纤维化模型。造模1天后，对照组及模型组给予10 mL·kg^-1 1%可溶性淀粉溶液，桦木酸组给予50 mg·kg^-1的桦木酸悬浮液，持续21天。HE、Masson染色方法观察肺组织病理改变。酶联免疫吸附法（ELISA）检测肺组织匀浆IL-6的水平。免疫组化法检测肺组织中NF-κB、β-arrestin2、IκBα的表达。结果 与对照组相比，模型组肺组织匀浆中IL-6水平升高，NF-κB、β-arrestin2、IκBα蛋白表达均上调（P<0.05）。与模型组相比，桦木酸组肺组织匀浆中IL-6水平降低，肺组织中NF-κB、β-arrestin2、IκBα蛋白表达均下调（P<0.05）。结论 桦木酸可减轻肺部炎症、减慢肺纤维化的发生发展，可能与下调肺组织中NF-κB、β-arrestin2有关。     

基于CiteSpace可视化分析代谢组学在中医药领域的研究现状及趋势＊

目的 应用可视化方法分析代谢组学在中医药领域的现状及趋势。方法 检索中国知网数据库（CNKI）和Web of Science 核心合集数据库2021年3月15日之前收录的中医药领域代谢组学研究的相关文献，应用CiteSpace软件对纳入的文献进行关键词、作者、研究机构等内容进行可视化分析。结果 共纳入中文文献247篇，英文文献350篇。文献数量在波动中迅速上升。中、英文文献作者合作网络显示，张爱华是中医药领域代谢组学研究发文量最多的作者，并形成了核心研究团队。发文机构显示，中国医学科学院是该领域的重要研究机构，机构间合作紧密。中、英文文献关键词分析显示，研究内容主要集中在核磁共振、代谢标记物、冠心病、质谱技术、代谢通路等相关领域。结论 中医药领域代谢组学研究的热点主要为中医药治疗代谢性疾病的机制研究。研究趋势为卵泡代谢组学研究及中药有效成分的研究。     

北京市三级甲等医院结直肠癌患者就医流向规律分析

目的 分析不同特征的结直肠癌患者就医行为选择在中医院（含中西医结合医院）、西医院及肿瘤专科医院间的差异，为合理引导结直肠癌患者适宜就医及制订相关政策提供依据。方法 收集北京地区2018年1月-2019年12月17家三级甲等医院21894例首诊结直肠癌成年住院患者的病案首页数据，采用EmpowerStats 2.0对数据进行描述性分析。结果 21894例结直肠癌患者中就诊于中医院的有862例（3.93%），西医院的有8723例（39.85%），肿瘤专科医院的有12309例（56.22%）。对于不同医疗机构，男性占比均大于女性，58-68岁患者占比最大。且结直肠癌患者年龄、医疗付款方式及肿瘤分期在不同医疗机构间的分布存在差异（P<0.001）。西医院及肿瘤专科医院结直肠癌Ⅲ期患者占比最大，而就诊于中医院患者中结直肠癌Ⅳ期最多。从地域分布来看，异地就诊比例（57.32%）大于本地，且就诊于肿瘤专科医院的患者中73.66%来自外地。患者来源前三名分别是北京市、河北省及内蒙古自治区。而在北京市内，西医院患者主要来源于朝阳区、海淀区及西城区，中医院患者主要来源于海淀区、朝阳区及丰台区，肿瘤专科医院则主要来源于朝阳区、海淀区及丰台区。结论 应大力倡导年轻以及早期结直肠癌患者向中医院分流，充分施展中医药在结直肠癌患者中的治疗优势；发挥三级医院带动作用，建立对口帮扶医院，减少不必要的跨省流动及提倡结直肠癌的早筛早治，以降低结直肠癌死亡率。     

Worry as a mechanism of the relationship between perceived new knowledge and discouragement to smoke elicited from graphic cigarette warnings

Journal of Behavioral Medicine - Evidence supports the use of graphic warnings to educate the public about the health harms of smoking and suggests warnings eliciting negative emotional responses...     

Quantification of myocardial fibrosis using noninvasive T2-mapping magnetic resonance imaging: Preclinical models of aging and pressure overload

Noninvasive imaging of cardiac fibrosis is important for early diagnosis and intervention in chronic heart diseases. Here, we investigated whether noninvasive, contrast agent-free MRI T₂-mapping can quantify myocardial fibrosis in preclinical models of aging and pressure overload. Myocardial fibrosis and remodeling were analyzed in two animal models: (i) aging (15-month-old male CF-1 mice vs. young 6- to 8-week-old mice), and (ii) pressure overload (PO; by transverse aortic constriction in 4- to 5-month-old male C57BL/6 mice vs. sham-operated for 14 days). In vivo T₂-mapping was performed by acquiring data during the isovolumic and early diastolic phases, with a modified respiratory and ECG-triggered multiecho TurboRARE sequence on a 7-T MRI. Cine MRI provided cardiac morphology and function. A quantitative segmentation method was developed to analyze the in vivo T₂-maps of hearts at midventricle, apex, and basal regions. The cardiac fibrosis area was analyzed ex vivo by picro sirius red (PSR) staining. Both aged and pressure-overloaded hearts developed significant myocardial contractile dysfunction, cardiac hypertrophy, and interstitial fibrosis. The aged mice had two phenotypes, fibrotic and mild-fibrotic. Notably, the aged fibrotic subgroup and the PO mice showed a marked decrease in T₂ relaxation times (25.3 ± 0.6 in aged vs. 29.9 ± 0.7 ms in young mice, p = 0.002; and 24.3 ± 1.7 in PO vs. 28.7 ± 0.7 ms in shams, p = 0.05). However, no significant difference in T₂ was detected between the aged mild-fibrotic subgroup and the young mice. Accordingly, an inverse correlation between myocardial fibrosis percentage (FP) and T₂ relaxation time was derived (R² = 0.98): T₂ (ms) = 30.45 – 1.05 × FP. Thus, these results demonstrate a statistical agreement between T₂-map–quantified fibrosis and PSR staining in two different clinically relevant animal models. In conclusion, T₂-mapping MRI is a promising noninvasive contrast agent-free quantitative technique to characterize myocardial fibrosis.