Deterioration Mechanisms and Advanced Inspection Technologies of Aluminum Windows

Aluminum windows are crucial components of building envelopes since they connect the indoor space to the external environment. Various external causes degrade or harm the functioning of aluminum windows. In this regard, inspecting the performance of aluminum windows is a necessary task to keep buildings healthy. This review illustrates the deterioration mechanisms of aluminum windows under various environmental conditions with an intention to provide comprehensive information for developing damage protection and inspection technologies. The illustrations reveal that moisture and chloride ions have the most detrimental effect on deteriorating aluminum windows in the long run, while mechanical loads can damage aluminum windows in a sudden manner. In addition, multiple advanced inspection techniques potential to benefit assessing aluminum window health state are discussed in order to help tackle the efficiency problem of traditional visual inspection. The comparison among those techniques demonstrates that infrared thermography can help acquire a preliminary defect profile of inspected windows, whereas ultrasonic phased arrays technology demonstrates a high level of competency in analyzing comprehensive defect information. This review also discusses the challenges in the scarcity of nanoscale corrosion information for insightful understandings of aluminum window corrosion and reliable window inspection tools for lifespan prediction. In this regard, molecular dynamics simulation and artificial intelligence technology are recommended as promising tools for better revealing the deterioration mechanisms and advancing inspection techniques, respectively, for future directions. It is envisioned that this paper will help upgrade the aluminum window inspection scheme and contribute to driving the construction of intelligent and safe cities.     

Aloe‐emodin: A review of its pharmacology,toxicity, and pharmacokinetics

Aloe‐emodin is a naturally anthraquinone derivative and an active ingredient of Chinese herbs, such as Cassia occidentalis, Rheum palmatum L., Aloe vera, and Polygonum multiflorum Thunb. Emerging evidence suggests that aloe‐emodin exhibits many pharmacological effects, including anticancer, antivirus, anti‐inflammatory, antibacterial, antiparasitic, neuroprotective, and hepatoprotective activities. These pharmacological properties lay the foundation for the treatment of various diseases, including influenza virus, inflammation, sepsis, Alzheimer's disease, glaucoma, malaria, liver fibrosis, psoriasis, Type 2 diabetes, growth disorders, and several types of cancers. However, an increasing number of published studies have reported adverse effects of aloe‐emodin. The primary toxicity among these reports is hepatotoxicity and nephrotoxicity, which are of wide concern worldwide. Pharmacokinetic studies have demonstrated that aloe‐emodin has a poor intestinal absorption, short elimination half‐life, and low bioavailability. This review aims to provide a comprehensive summary of the pharmacology, toxicity, and pharmacokinetics of aloe‐emodin reported to date with an emphasis on its biological properties and mechanisms of action.     

Z‐ligustilide: A review of its pharmacokinetics and pharmacology

Z‐ligustilide is a natural benzoquinone derivative found in many widely used Chinese herbal medicines such as Angelica sinensis (Oliv.) Diels as well as Ligusticum chuanxiong Hort and so on. It has been used as a part of traditional Chinese medicine and is also present in various Chinese medicine preparations. Pharmacokinetic studies have shown that Z‐ligustilide has poor oral bioavailability in rats due to severe first‐pass metabolic reactions. New evidence suggests that Z‐ligustilide has a wide range of pharmacological properties, including anticancer, antiinflammatory, anti‐oxidant as well as neuroprotective activities and so on. The literature discussed is derived from readily accessible papers spanning the early 1970s to the end of March 2019. Information were collected from journals, books, and online searches (Google Scholar, PubMed, Science Direct, Science Citation Index Finder, Springer link, and CNKI). This review intends to provide a comprehensive overview of the pharmacokinetics and pharmacology of Z‐ligustilide in recent years, with a focus on its biological properties and mechanisms, which is of great significance for Chinese medicine.     

基于网络药理学方法探究补肾活血汤治疗激素性股骨头坏死的作用机制

目的:探讨补肾活血汤治疗激素性股骨头坏死(steroid-induced osteonecrosis of the femoral head,SONFH)的作用机制。方法:通过中医药整合药理学网络计算研究平台(integrative pharmacology-based network computational research platform of Traditional Chinese Medicine,TCMIP)v2.0预测、筛选补肾活血汤组方中14味中药的作用靶标,通过GeneCards、CTD和OMIM数据库查询SONFH的疾病靶点。根据获取的药物靶标和疾病靶点,进一步利用TCMIP v2.0中医药关联网络分析模块构建"药物靶标-疾病靶点"相互作用网络,根据网络拓扑特征值筛选补肾活血汤治疗SONFH的核心作用靶点。利用GO和KEGG数据库,采用富集算法挖掘上述方剂核心作用靶点的生物学功能和通路信息。结果:共获得891个补肾活血汤药物靶标和365个SONFH疾病靶点。经"药物靶标-疾病靶点"相互作用网络分析,最终筛选出31个补肾活血汤治疗SONFH核心靶点,GO功能分析富集出生物过程532条、分子功能29条,KEGG信号通路富集分析出相关通路共12条,主要涉及炎症免疫调节(chemokine signaling pathway,Toll-like receptor signaling pathway,NOD-like receptor signaling pathway,leukocyte transendothelial migration,Complement and coagulation cascades,cytokine-cytokine receptor interaction)、血管新生及血液循环调节(VEGF signaling pathway)、神经系统调节(neuroactive ligand-receptor interaction)和细胞功能调节(apoptosis,regulation of actin cytoskeleton)等方面。结论:结合SONFH的病理机制,排除缺乏特异性的信号通路,我们推测补肾活血汤可能通过调节TLR4/NF-κB和VEGF信号通路发挥补肾壮骨、活血化瘀的功效,这可能是其治疗SONFH的作用机制之一。     

Mechanism research of Salvia miltiorrhiza on treating myocardial ischemia reperfusion injury according to network pharmacology combined with molecular docking technique

Myocardial ischemia reperfusion injury (MIRI) is a kind of complicated disease with an increasing incidence all over the world. Danshen was shown to exert therapeutic effect on MIRI. However, its chemical and pharmacological profiles remain to be elucidated. Network pharmacology was applied to characterize the mechanisms of Danshen on MIRI.The active compounds were screened from the online database according to their oral bioavailability and drug-likeness. The potential proteins of Danshen were collected from the TCMSP database, whereas the potential genes of MIRI were obtained from Gene Card database. The function of gene and pathways involved were researched by GO and KEGG enrichment analysis. The compounds-targets and protein–protein interaction networks were constructed by Cytoscape software. The affinity between active components and potential targets was detected by molecular docking simulation.A total of 202 compounds in Danshen were obtained, and 65 were further selected as active components for which conforming to criteria. Combined the network analysis and molecular docking simulation, the results firstly demonstrated that the effect of Danshen on MIRI may be realized through the targeting of vascular endothelial growth factor A, interleukin-6, and AKT1 by its active components tanshinone IIA, cryptotanshinone, and luteolin. The main regulatory pathways involved may include PI3K/ Akt signaling pathway, HIF-1 signaling pathway, and interleukin-17 signaling pathway. The present study firstly researched the mechanism of Danshen on MIRI based on network pharmacology.The results revealed the multicomponents and multi-targets effects of Danshen in the treatment of MIRI. Importantly, the study provides objective basis for further experimental research.     

骨髓基质干细胞向神经细胞诱导分化及其机制的研究进展

骨髓基质干细胞是一种存在于骨髓间质中具备多向分化潜能的成体干细胞,其不仅能分化为中胚层起源的骨、软骨和脂肪细胞,还可以在特定条件下诱导分化为神经外胚层起源的神经细胞。主要对骨髓基质干细胞向神经细胞诱导分化及其机制的研究进展作一综述。     

丙戊酸钠通过激活内源性凋亡途径诱导乳腺癌细胞凋亡的实验研究

目的探讨丙戊酸钠（VPA）诱导乳腺癌细胞凋亡的作用。方法乳腺癌细胞株MCF-7细胞分为0.75～4.0 mmoL/L VPA实验组、对照组（不加VPA）及VPA与caspase抑制剂共同作用组。Annexin V-PI双染法流式细胞术检测细胞凋亡,间接免疫荧光法定量分析及分光光度法检测caspase- 3、caspase-8、caspase-9蛋白丰度和活性,探讨VPA诱导凋亡的机制,同时检测VPA与caspase-3、caspase- 8、caspase-9特异性抑制剂协同作用后细胞凋亡的变化来加以验证。结果各浓度VPA干预MCF-7细胞48 h后,细胞凋亡率显著增加,caspase-3、caspase-9活性升高、蛋白表达明显上调,与对照组相比有显著差异（F=552.1、610.9、312.8、222.8、70.3,均P〈0.001）;而caspase-8活性及蛋白表达未见明显改变;1.5、3.0 mmol/L VPA与caspase-3、caspase-9相应特异性抑制剂共同作用组,细胞凋亡率均较VPA组显著降低（t=109.0、28.7、18.7、32.3,均P〈0.005）;VPA与caspase-8特异性抑制剂共同作用组细胞凋亡率与VPA组比较无明显改变（t=1.03、2.32,均P〉0.05）。结论VPA可通过激活caspase-9介导的内源性凋亡途径,明显诱导乳腺癌细胞凋亡,具有较好的临床应用价值。     

贝莱斯芽孢杆菌Y6杀螺活性及其机制的初步研究

目的 评价芽孢杆菌Y6实验室内杀螺活性,初步探讨其杀螺作用机制.方法 应用形态学、生理生化特性及16S rDNA基因序列同源性分析,对菌株Y6进行生物学鉴定.配制浓度分别为0.005、0.010、0.015 g/mL的芽孢杆菌Y6悬液,采用浸泡法评价其室内杀螺效果.检测芽孢杆菌Y6悬液浸泡后钉螺软体组织内Y6菌体含量和...     

白血病耐药分子机制的研究现状

目前,联合化疗及精准靶向药物的应用在白血病治疗中占据不可替代的地位.但是,相当一部分患者存在化疗及靶向药物治疗耐药,导致白血病难治、复发.有效逆转白血病耐药,是提高和改善白血病患者预后和长期生存的重要途径之一.笔者就近年白血病耐药相关分子机制的研究进展进行阐述,旨在为理解和探索逆转白血病耐药拓宽思路.