常见植物药对结肠癌的防治作用及其作用机制

植物药对结肠癌具有良好的防治作用。姜黄素、多糖(苹果多糖、香菇多糖)、皂苷(重楼皂苷、人参皂苷)、白藜芦醇、槲皮素等植物药可通过不同信号通路抑制结肠癌细胞的增殖,促进细胞凋亡。此外,植物药还具有抗炎、抗氧化、抗血管生成、减轻化疗药物不良反应、逆转肿瘤细胞耐药等作用。了解植物药对结肠癌的防治作用及其可能的作用机制,能为结肠癌的临床防治提供更多的理论依据及治疗思路。     

Elevated serum levels of Interleukin‐37 are associated with inflammatory cytokines and disease activity in rheumatoid arthritis

Interleukin‐37 (IL‐37) is closely associated with several inflammatory diseases. However, the role of IL‐37 in the pathogenesis of rheumatoid arthritis (RA) remains unclear. The aim of this study was to assess the associations between serum levels of IL‐37 and disease activity, inflammatory cytokines, and bone loss in patients with RA. Serum cytokines levels were examined by Enzyme‐linked immunosorbent assay (ELISA). Radiographic bone erosion was assessed using the van der Heijde‐modified Sharp score and bone mineral density (BMD) was measured using DXA. Serum IL‐37 levels in RA patients were significantly higher than those in HCs (p < 0.001), and were significantly positively correlated with clinical parameters of disease activity and serum levels of IL‐17 and IL‐23. In addition, serum IL‐37 levels were significantly higher in patients with stage IV of radiographic bone erosion than those with stage III and stage I–II, and they were significantly higher in those with osteopenia and osteoporosis than in those with normal BMD. Our results suggest that serum IL‐37 levels were increased in patients with RA and were positively associated with disease activity, IL‐17/IL‐23 and bone loss in RA, suggesting that IL‐37 may play a critical role in the pathogenesis of RA.     

“调任通督”法针刺治疗围绝经期潮热的随机对照研究＊

目的 观察“调任通督法”针刺治疗围绝经期潮热的临床疗效和安全性。方法 将符合纳入标准的72例围绝经期潮热患者，按照1∶1的比例随机分为治疗组（针刺组）和对照组（等待组）。治疗组取穴百会、印堂、神庭、关元、气海、中脘、阴郄、太溪、复溜、三阴交。针刺治疗每次持续30 min，每周2次，连续治疗6周。对照组为等待组，试验期间仅给予同针刺组相同的健康宣教，两组分别于治疗前、治疗第3周、治疗第6周以及第10周随访评估其潮热频率和程度，以及更年期生活质量量表（Menopause-specific quality of life questionnaire，Men-QoL）的变化情况，同时记录针刺不良事件的发生。结果 ①潮热频率及潮热程度：在治疗后及随访时，针刺组较等待组有明显改善，差异具有统计学意义（P < 0.01）。与治疗前相比，针刺组第3周即出现了潮热频率明显下降的趋势（P < 0.01），治疗后以及随访期针刺组潮热频率及潮热程度均较治疗前有明显统计学差异（P < 0.01）。而等待组在各时间点潮热频率及潮热程度均无统计学差异（均P > 0.05）。②围绝经期生活质量量表：治疗后针刺组在Men-QoL总分、血管舒缩功能评分、社会心理、体能状况较等待组比较均有统计学差异（均P < 0.01）。在随访期，针刺组在Men-QoL社会心理以及体能方面明显改善，差异均具有统计学意义（P < 0.01，P < 0.05）。两组Men-QoL性功能在治疗后及随访期均无统计学差异（P > 0.05）。与治疗前相比，在治疗后及随访期，针刺组Men-QoL总分、血管舒缩功能、社会心理、体能状况均有统计学差异（均P < 0.05），在Men-QoL性功能方面无统计学差异（P > 0.05）。等待组在Men-QoL总分及四个域方面均无明显改善，无统计学意义（均P > 0.05）。结论 调任通督法针刺治疗围绝经期潮热安全有效，且对围绝经期生活质量有所改善。     

慕课在我国高等医学教育中应用的文献计量分析

目的　探讨慕课在我国高等医学教育领域的应用现状和发展趋势，为本领域今后的研究提供参考。方法　检索中国知网、万方数据服务平台、维普数据库、中国生物医学文献数据库建库以来至2020年3月1日收录的相关文献，运用文献计量学方法对年发文量、期刊分布、基金支持、著者分布、被引频次、文献类型和高频关键词进行统计分析。将导出的资料用Excel 2010建立数据库，借助频数分析法进行描述性统计。结果　纳入文献754篇，分别收录于262种期刊；以医学教育类期刊为主；基金资助率达50%；黄坪、张欣、李鑫辉等7人为核心作者；以人体解剖学为代表的基础医学类课程应用研究最多；慕课应用研究以理论课程为主；课程评价包括终末性评价、形成性评价、平台考核、综合能力和自主学习能力５大方面；研究热点为基于慕课的混合式教学模式及其在护理教育、中医教育及继续医学教育中的应用。结论　近5年，慕课在我国高等医学教育中发展迅速，核心作者已形成，但缺乏深度合作。未来应增加实验（训）类课程的应用研究，同时应进一步完善实验性研究的设计及课程评价体系。     

miR-147对胶质瘤U87细胞增殖、凋亡和侵袭的影响

目的:比较胶质瘤患者胶质瘤组织和瘤旁组织中miR-147表达水平的差异性，进一步分析miR-147与胶质瘤细胞生物学活性的相关性。方法:通过实时荧光定量PCR检测65例胶质瘤患者瘤组织和瘤旁组织中miR-147的表达水平；采用Lipofectamine 2000转染法转染胶质瘤细胞，分为miR-147 mimics组和NC组，检测两组转染效率；进一步通过CCK-8实验、流式细胞实验和Transwell实验比较两组细胞生物活性。结果:胶质瘤组织中miR-147表达水平显著低于瘤旁组织；与NC组比较，miR-147 mimics组细胞不论是增殖能力还是侵袭能力都明显降低，但是，miR-147 mimics组的细胞凋亡率升高。结论:胶质瘤组织中存在miR-147低表达的现象。miR-147在胶质瘤细胞中表达升高能够抑制细胞的增殖能力、降低其侵袭能力，并促使更多的细胞发生晚期凋亡。miR-147可能在胶质瘤中扮演着抑癌基因的重要角色。     

针刺调控α7nAchR激活胆碱能抗炎通路的研究现状

胆碱能抗炎通路是一条神经免疫通路,主要依靠乙酰胆碱与巨噬细胞及其他细胞表面上的α7nAchR相结合抑制促炎因子的合成与释放,从而防止组织损伤。α7nAchR是胆碱能递质的主要受体,在胆碱能抗炎通路中起关键作用。针刺治疗有明确的抗炎作用,其作用机制可能与调控α7nAchR激活胆碱能抗炎通路有关。近年来虽然国内外学者对针刺抗炎机制进行了大量研究,然而针刺抗炎的作用机制目前仍不明确。该文从胆碱能抗炎通路概述、α7nAchR结构及功能、α7nAchR的分布、α7nAchR在胆碱能抗炎通路的作用、针刺调控α7nAchR激活胆碱能抗炎通路的机制等方面对针刺调控α7nAchR激活胆碱能抗炎通路进行分析总结,为今后探究针刺抗炎作用机制提供借鉴思路和科学依据。     

MicroRNA‐375‐3p enhances chemosensitivity to 5‐fluorouracil by targeting thymidylate synthase in colorectal cancer

Resistance to chemotherapy is a major challenge for the treatment of patients with colorectal cancer (CRC). Previous studies have found that microRNAs (miRNAs) play key roles in drug resistance; however, the role of miRNA‐373‐3p (miR‐375‐3p) in CRC remains unclear. The current study aimed to explore the potential function of miR‐375‐3p in 5‐fluorouracil (5‐FU) resistance. MicroRNA‐375‐3p was found to be widely downregulated in human CRC cell lines and tissues and to promote the sensitivity of CRC cells to 5‐FU by inducing colon cancer cell apoptosis and cycle arrest and by inhibiting cell growth, migration, and invasion in vitro. Thymidylate synthase (TYMS) was found to be a direct target of miR‐375‐3p, and TYMS knockdown exerted similar effects as miR‐375‐3p overexpression on the CRC cellular response to 5‐FU. Lipid‐coated calcium carbonate nanoparticles (NPs) were designed to cotransport 5‐FU and miR‐375‐3p into cells efficiently and rapidly and to release the drugs in a weakly acidic tumor microenvironment. The therapeutic effect of combined miR‐375 + 5‐FU/NPs was significantly higher than that of the individual treatments in mouse s.c. xenografts derived from HCT116 cells. Our results suggest that restoring miR‐375‐3p levels could be a future novel therapeutic strategy to enhance chemosensitivity to 5‐FU.     

Apatinib Monotherapy or Combination Therapy for Non-Small Cell Lung Cancer Patients With Brain Metastases

Apatinib, an oral small molecular receptor tyrosine kinase inhibitor (TKI) developed first in China, exerts antiangiogenic and antineoplastic function through selectively binding and inhibiting vascular endothelial growth factor receptor 2 (VEGFR-2). In this study, we aimed to explore the efficacy and safety profile of apatinib monotherapy, or combined with chemotherapy or endothelial growth factor receptor (EGFR)-TKI in heavily pretreated non-small cell lung cancer (NSCLC) patients with brain metastases. We performed a retrospective analysis for relapsed NSCLC patients with brain metastases from our institute, who received apatinib (250 mg or 500 mg p.o. qd) monotherapy, or combination with EGFR-TKI or chemotherapy as second or more line systemic therapy until disease progression or unacceptable toxicity occurred. The objective response rate (ORR), disease control rate (DCR), median progression-free survival (mPFS), median overall survival (mOS), and safety were analyzed. A total of 26 eligible patients were included: 24 patients diagnosed with adenocarcinoma, 2 with squamous carcinoma, and 14 patients harboring EGFR sensitizing mutations. The mPFS and mOS were 4.93 (range, 0.27−32.91; 95% CI 3.64−6.22) and 14.70 (range, 0.27−32.91; 95% CI 0.27−43.60) months for the whole group. The ORR and DCR were 7.7% (2/26) and 69.2% (18/26) for the entire lesions, and 7.7% (2/26) and 79.6% (20/26) for brain metastases, respectively. Compared with patients who received apatinib monotherapy, patients who received apatinib combination treatment had more favorable mPFS (11.77 vs. 2.27 months, p<0.05) and mOS (24.03 vs. 6.07 months, p<0.05). Treatment-related toxicities were tolerable including grade 1/2 hypertension, hand-and-foot syndrome, fatigue, nausea, liver dysfunction, myelosuppression, skin rash, and palpitation. In conclusion, apatinib exhibited high activity and good tolerance for NSCLC patients with brain metastasis, and it might become a potential choice for metastatic brain tumors in NSCLC patients.     

miR-122 Inhibits Hepatocarcinoma Cell Progression by Targeting LMNB2

In the present study, we investigated the role of miR-122 in hepatocarcinoma progression and explored the mechanism. In hepatocarcinoma tissues and cells, we used qRT-PCR to validate the miR-122 expression level. Next, we used colony formation by crystal violet staining assay to compare cell proliferation ability, and we used scratch test or Transwell assay to compare cell migration or invasion ability. We then conducted bioinformatics or luciferase reporter gene assay to prove the regulation effect of miR-122 on lamin B2 (LMNB2), and the biological function of LMNB2 was analyzed. We used nude mouse tumorigenicity assay to test the inhibition effect of miR-122 ASO therapy against hepatocarcinoma. miR-122 was reduced in hepatocarcinoma tissues compared to the paracarcinoma tissues, which was relatively low or high in hepatocarcinoma cell line SMMC7721 or Hep3B, and overexpressed miR-122 inhibited proliferation, migration, and invasion in hepatocarcinoma cells. Additionally, some reports showed that LMNB2 was regulated by miR-122, which inhibited the expression of LMNB2. Moreover, LMNB2 functioned to promote cell proliferation, migration, and invasion. We could achieve the inhibition of hepatocarcinoma using miR-122 therapy through decreasing LMNB2 expression in vivo. Our data indicated that miR-122 could inhibit hepatocellular carcinoma cell progression by targeting LMNB2 and as a therapeutic target for hepatocarcinoma treatment.