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This study investigated the single-pass performance of a negative corona electrostatic precipitators (ESP) in removing suspended particulates (PM2.5 and PM10), formaldehyde (HCHO), and bioaerosols (bacteria and fungi) and measured the ozone (O3) concentration generated by ESP. The experimental results revealed that if the operational conditions for the ESP were set to high voltage (−10.5 kV) and low air flow rate (2.4 m3/min), ESP had optimal air pollutant removal efficiency. In the laboratory system, its PM2.5 and PM10 removal rates both reached 99% at optimal conditions, and its HCHO removal rate was 55%. In field tests, its PM2.5, PM10, HCHO, bacteria, and fungi removal rates reached 89%, 90%, 46%, 69%, and 85% respectively. The ESP in the laboratory system (−10.5 kV and 2.4 m3/min) generated 7.374 ppm of O3 under optimal conditions. Under the same operational conditions, O3 generated by ESP in the food waste storage room and the meeting room were 1.347 ppm and 1.749 ppm, respectively. The removal of HCHO and bioaerosols was primarily attributed to their destruction in the corona, as well as ozone oxidation, and collection on the dust collection plate.

D-alpha-tocopheryl polyethylene glycol 1000 succinate (TPGS1000) is the most active water-soluble derivative of vitamin E and has been widely used as a carrier of solvents, plasticizers, emulsifiers, absorbent agents and refractory drug delivery systems. However, its anti-hepatocellular carcinoma (HCC) properties have not been explored. HCC cells were treated with different concentrations of TPGS1000. Cell survival was tested by CCK8 assay, and cell migration was tested by wound healing and Transwell assay. EdU staining verified cell proliferation, and signalling pathway was assayed by Western blot analysis. The BALB/c-nu mouse xenograft model was established to test HCC cell growth in vivo. In vitro TPGS1000 significantly inhibited the viability and mobility of HCC cells (HepG2, Hep3B and Huh7) in a dose-dependent manner. Cell cycle analysis indicated that TPGS1000 treatment arrested the HCC cell cycle in the G0/G1 phase, and induction of cell apoptosis was confirmed by TUNEL and Annexin V-7-AAD staining. Further pharmacological analysis indicated that collapse of the transmembrane potential of mitochondria, increased ROS generation, PARP-induced cell apoptosis and FoxM1-p21-mediated cell cycle arresting, were involved in the anti-HCC activity of TPGS1000. Moreover, treatment in vivo with TPGS1000 effectively impaired the growth of HCC xenografts in nude mice.

Endophytic fungi usually establish a symbiotic relationship with the host plant and affect its growth. In order to evaluate the impact of endophytic fungi on the Chinese herbal medicinal plant Houttuynia cordata Thunb., three endophytes isolated from the rhizomes of H. cordata, namely Ilyonectria liriodendra (IL), unidentified fungal sp. (UF), and Penicillium citrinum (PC), were co-cultured individually with H. cordata in sterile soil for 60 days. Analysis of the results showed that the endophytes stimulated the host plant in different ways: IL increased the growth of rhizomes and the accumulation of most of the phenolics and volatiles, UF promoted the accumulation of the medicinal compounds afzelin, decanal, 2-undecanone, and borneol without influencing host plant growth, and PC increased the fresh weight, total leaf area and height of the plants, as well as the growth of the rhizomes, but had only a small effect on the concentration of major secondary metabolites. Our results proved that the endophytic fungi had potential practical value in terms of the production of Chinese herbal medicines, having the ability to improve the yield and accumulation of medicinal metabolites.

Background This study aims to explore the efficacy and safety of prostaglandina E1 (PE1) for the treatment of patients with thrombo-occlusive vasculitis (TOV). Methods Electronic databases (Cochrane Library, PUBMED, EMBASE, Web of Science, Scopus, the Allied and Complementary Medicine Database, Chinese Biomedical Literature Database, and China National Knowledge Infrastructure) will be sought from onset to the March 1, 2020 without language and publication status restrictions. We will include any potential randomized controlled trials that examined the efficacy of PE1 for the treatment of patients with TOV. We will appraise study quality using Cochrane risk of bias tool, and will assess the evidence quality using Grading of Recommendations Assessment Development and Evaluation. We will use RevMan 5.3 Software for statistical analysis. Results A high-quality synthesis of present evidence of PE1 for the treatment of patients with TOV will be provided in this study. Conclusion This study will provide evidence to judge whether PE1 is an effective intervention for TOV. Systematic review registration INPLASY202040081.

Type 2 diabetes mellitus (T2DM)[1] is a type of metabolic disease caused by metabolic disorders in the endocrine system and characterized by hyperglycemia. Insufficient insulin secretion and insulin resistance are the basic pathologic characteristics of T2DM. According to the International Diabetes Federation (IDF),[2] the prevalence of diabetes among adults aged 20–79 in 2017 was 8.8% from a total population of 425 million, which will reach 629 million by 2045. Additionally, it is estimated that approximately half of all adult patients worldwide have not been diagnosed as of 2017. In 2017, approximately 4 million adults died of diabetes, and 46.1% of patients died before reaching the age of 60 years. These data show that the number of patients with diabetes is increasing at an alarming rate and have come to represent a challenge for human health. In addition, T2DM accounts for approximately 95% of the total population of diabetes, which leads to significant losses for human and economic health.[3] T2DM is a chronic disease that can cause a series of complications that can lead to death.[4] Therefore, preventing or delaying the occurrence of complications is the main purpose of treating T2DM, and the key link for those suffering from diabetes is to maintain blood glucose levels within the normal range.[5] At present, the treatment of T2DM mainly depends on lifestyle intervention[6] (such as nutrition therapy and physical activity), oral medication[7] (such as biguanides, sulfonylureas, and α-glucoside inhibitors), injected drugs[8] (such as insulin and glucagon-like peptide-1 [7–36] amide [GLP-1] agonists), surgical treatment,[9] and complementary and alternative treatment.[10] T2DM is known as a major “Xiao-Ke disease” in ancient Chinese books. And Chinese have used herbal medicines to treat the diseases for more than 1500 years. There is a growing body of research showing that herbal medicine can effectively treat T2DM.[11–13] In this study, we reviewed the therapeutic action of herbal medicine in T2DM via anti-inflammatory and anti-oxidation characteristics, regulation of blood lipid metabolism, anti-glucose effects, and other mechanisms [Figures ​[Figures11–5]. Open in a separate window Figure 1 The anti-inflammatory effect of herbal medicine in type 2 diabetes mellitus. TNF-α: tumor necrosis factor-α; TLR4-MyD88: toll-like receptor 4-myeloid differential protein-88; IL-1β: interleukin-1β; NLRP3: NACHT, LRR, and PYD domain-containing protein 3; WMW: Wu-Mei-Wan; NF-κB: nuclear transcription factor kappa B; IκBα: inhibitor of NF-κB; COX2: cyclo-oxgenase 2; IL-8: interleukin-8; IL-6: interleukin-6.

In recent years, eukaryotic microorganisms have been widely applied to offer many solutions for everyday life and have come to play important roles in agriculture, food, health care, and the fine-chemicals industry. However, the complex genetic background and low homologous recombination efficiency have hampered the implementation of large-scale and high-throughput gene editing in many eukaryotic microorganisms. The low efficiency of homologous recombination (HR) not only makes the modification process labor-intensive but also completely precludes the application of many otherwise very useful genome editing techniques. Thus, increasing the efficiency of HR is clearly an enabling technology for basic research and gene editing in eukaryotic microorganisms. In this review, we summarize the current strategies for enhancing the efficiency of HR in eukaryotic microorganisms (particularly yeasts and filamentous fungi), list some small molecules and candidate genes associated with homologous and non-homologous recombination, and briefly discuss the further development prospects of these strategies.

// Yue-Lun Zhang 1, 2 , Jin-Qiu Yuan 1, 2 , Kai-Feng Wang 3 , Xiao-Hong Fu 1, 2 , Xiao-Ran Han 1, 2 , Diane Threapleton 1 , Zu-Yao Yang 1, 2 , Chen Mao 1, 2 , Jin-Ling Tang 1, 2 1 Division of Epidemiology, The Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong, China 2 Shenzhen Municipal Key Laboratory for Health Risk Analysis, Shenzhen Research Institute of The Chinese University of Hong Kong, Shenzhen, Guangdong Province, China 3 Division of Epidemiology, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou, Guangdong Province, China Correspondence to: Chen Mao, email: maochen@cuhk.edu.hk Jin-Ling Tang, email: jltang@cuhk.edu.hk Keywords: non-small cell lung cancer, epidermal growth factor receptor, prevalence, systematic review, meta-analysis Received: May 17, 2016 Accepted: September 25, 2016 Published: October 12, 2016 ABSTRACT Objectives: Estimate the epidermal growth factor receptor ( EGFR ) mutation prevalence in all non-small cell lung cancer (NSCLC) patients and patient subgroups. Results: A total of 456 studies were included, reporting 30,466 patients with EGFR mutation among 115,815 NSCLC patients. The overall pooled prevalence for EGFR mutations was 32.3% (95% CI 30.9% to 33.7%), ranging from 38.4% (95% CI: 36.5% to 40.3%) in China to 14.1% (95% CI: 12.7% to 15.5%) in Europe. The pooled prevalence of EGFR mutation was higher in females (females vs. males: 43.7% vs. 24.0%; OR: 2.7, 95% CI: 2.5 to 2.9), non-smokers (non-smokers vs. past or current smokers: 49.3% vs. 21.5%; OR: 3.7, 95% CI: 3.4 to 4.0), and patients with adenocarcinoma (adenocarcinoma vs. non-adenocarcinoma: 38.0% vs. 11.7%; OR: 4.1, 95% CI: 3.6 to 4.8). Materials and Methods: PubMed, EMBASE, and the Cochrane Library were searched to June 2013. Eligible studies reported EGFR mutation prevalence and the association with at least one of the following factors: gender, smoking status and histology. Random-effects models were used to pool EGFR mutation prevalence data. Conclusion: This study provides the exact prevalence of EGFR mutations in different countries and NSCLC patient subgroups.

To investigate the relation between the changes of dendritic cell (DC) function and down-regulation of beta-centractin in hepatocellular carcinoma.DC derived from peripheral blood were cultured and then pulsed by lysates from hepatocarcinoma cells (HCC) with high, low, or none metastatic potential of the lines HCCLM6, MHCC97L, and Hep3B, and from normal human liver cell of the line Chang liver. DC not pulsed were used as control group. Three days later scanning electron microscopy and inverted microscopy were used to observe the morphology of the DC. Flow cytometry was used to observe the phenotype. The protein expression of beta-centractin was detected by Western blotting and immunocytochemistry.Scanning electron microscopy and inverted microscopy showed no change in the morphology of the DC pulsed by different antigens. The expression levels of HLA-DR, CD80, CD83, and CD86 of the 4 pulsed groups were all significantly higher than that of the un-pulsed group (all P0.05). The expression of CD86 of the DC + LM6 group was significantly lower than those of the DC + Chang, DC + Hep3B, and DC + 97L groups (all P0.05). The mixed lymphocyte reaction (MLR) levels of the 4 pulsed groups were all significantly higher than that of the control group (all P0.05). The MLR level of the DC + LM6 group was significantly lower than those of the DC + Chang, DC + Hep3B, and DC + 97L groups (all P0.05). Western blotting showed that beta-centractin was not expressed in the control DC and was expressed in the 3 pulsed DC groups, and the beta-centractin expression levels of the DC + Chang, DC + Hep3B, and DC + 97L groups were all higher than that of the DC + LM6 group. The results of immunocytochemistry were similar to that of Western blotting.The down-regulation of beta-centractin in the DC pulsed with high metastatic potential HVV cell lysates is associated DC dysfunction and may be one of the mechanisms of HCC immune escape.