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Indigo is an insoluble blue dye, which generates serious pollution in its production process. Increasing focus has come to the biosynthesis of indigo that are more environment-preserved and high-efficient. Hence, this study was designed to explore the specific role of various deep eutectic solvents (DESs) on cytochromeP45-BM-3 catalyzing indole to produce indigo. DESs were synthesized by heating and stirring. The structure of the solvent was analyzed by nuclear magnetic resonance (NMR) and fourier transform infrared spectrum (FT-IR), and the relationship between the viscosity, density and refractive index of the solvent, and the water content of the solvent was examined. Circular dichroism spectrometer was used to detect the tertiary structure of the enzyme protein. The effect of solvent type, concentration, pH, temperature, and water content on the catalytic activity and stability of P450 BM-3 was measured using an ultraviolet spectrophotometer. A new solvent biphasic system was established using DESs and buffers, and indigo was prepared using recombinant E. coli-biocatalyzed indole. DESs were low-melting eutectics formed by molecules interaction of components through hydrogen bonding. The physical properties of DESs such as density, viscosity, and refractive index varied with water content and temperature of the solvent. The pH, water content, and temperature of DESs were positively correlated with the catalytic activity of P450 BM-3. To sum up, DESs can improve the catalytic activity and thermal stability of P450 BM-3. Indigo can be efficiently prepared using the DESs-buffer biphasic system.

Background Myeloid-derived suppressor cells (MDSCs) are known suppressors of antitumor immunity and contribute to immunosuppressive microenvironment during tumor development including lung cancer. Accumulating evidence shows microRNAs (miRNAs) affect tumor-expanded MDSC accumulation and function in tumor microenvironment and favor solid tumor growth. Herein, we aim to characterize the role of miR-21 in regulating the accumulation and activity of MDSCs in lung cancer. Methods The proportions of MDSCs, T helper cells (Th), and cytotoxic T lymphocytes (CTL) were evaluated by flow cytometric analyses of peripheral blood and tumor tissues collected from Lewis lung-cancer-bearing mice. T cell proliferation assay was performed in CD4+ or CD8+ T cells cocultured with MDSCs. MDSC apoptosis was examined by flow cytometric analysis. The levels of IL-10, TGF-β, and GM-CSF in mouse serum were determined by ELISA. miR-21 targeting RUNX1 and RUNX1 interaction with YAP were evaluated by RIP, dual-luciferase reporter gene, and ChIP assays. Results MiR-21 inhibition by its antagomir reduced the proportion of MDSCs, increased the proportion of Th and CTL in peripheral blood and tumor tissues of Lewis lung-cancer-bearing mice, protected Th and CTL from the suppression of MDSCs, increased apoptosis of MDSCs, but reduced IL-10, TGF-β and GM-CSF levels in mouse serum. RUNX1 could transcriptionally inhibit the YAP expression, whereas miR-21 targeting RUNX1 led to elevated YAP expression levels. Mechanistic investigation showed that miR-21 maintained MDSC accumulation in tumor microenvironment and promoted immunosuppressive ability of MDSCs in Lewis lung-cancer-bearing mice by down-regulating RUNX1and up-regulating YAP. Conclusions Taken together, the study provides evidence that targeting miR-21 in MDSCs may be developed as an immunotherapeutic approach to combat lung cancer development.

Background. Overexpression of the MUC5B protein is associated with idiopathic pulmonary fibrosis (IPF), but little information is available regarding the pathogenic effects and regulatory mechanisms of overexpressed MUC5B in IPF. Main Body. The overexpression of MUC5B in terminal bronchi and honeycomb cysts produces mucosal host defensive dysfunction in the distal airway which may play an important role in the development of IPF. This review addresses the possible association of overexpression of MUC5B, with MUC5B promoter polymorphism, MUC5B gene epigenetic changes, effects of some transcriptional factors, and inflammatory mediators in IPF. In addition, the associated signaling pathways which may influence the expression of MUC5B are also discussed. Conclusion. This work has important implications for further exploration of the mechanisms of overexpression of MUC5B in IPF, and future personalized treatment.

Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related death worldwide, while circulatory. Circular RNAs (circRNAs) are found to play important roles in cancer initiation and development. Herein, a novel functional circRNA hsa_circ_0020123 had been identified in NSCLC progression in this study, and elevated hsa_circ_0020123 expression could be observed in cancer tissues compared with that in matched normal lung tissues. Moreover, up-regulation of hsa_circ_0020123 was recognized to be closely associated with a poor differentiation degree, lymph node metastasis, a high TNM stage and dismal prognosis for NSCLC patients. Typically, knockdown of hsa_circ_0020123 could inhibit the NSCLC growth and metastasis both in vitro and in vivo, which could be reversed by the hsa_circ_0020123 overexpression. Importantly, miR-144 was identified as the hsa_circ_0020123-associated miRNA through performing RNA in vivo precipitation (RIP) in NSCLC cells using a biotin-labeled hsa_circ_0020123 probe. Besides, our results suggested that, miR-144 suppression had determined the oncogenic properties mediated by hsa_circ_0020123. In addition, hsa_circ_0020123 could upregulate ZEB1 and EZH2 through competitively binding with miR-144. Finally, the administration of hsa_circ_0020123 siRNA could suppress the growth and metastasis in NSCLC-bearing mice in vivo. In conclusion, the hsa_circ_0020123-miR-144-ZEB1/EZH2 axis is critical for NSCLC progression, which indicates that hsa_circ_0020123 is a potential target for NSCLC treatment.

Rationale: Respiratory syncytial virus (RSV) is a single-stranded negative-sense RNA virus that belongs to the family of paramyxoviruses. RSV is the most common pathogen that causes acute lower respiratory tract infection in infants and young children. However, its incidence in immunocompromised adults remains unclear. In the present study, we report an adult patient with chronic nephropathy, who received long-term immunosuppressants and died of rapid respiratory failure due to RSV infection. Patient concerns: A 54-year-old male patient with chronic nephropathy, who received long-term immunosuppressants, was admitted to the Department of Respiratory Medicine due to the symptoms of fever, cough, expectoration, and dyspnea. Diagnoses: Pulmonary radiology revealed multiple bilateral ground-glass opacity. Laboratory tests revealed elevated inflammation indicators, implying infection with bacteria, viruses, and/or fungi. Furthermore, the patient was positive for RSV antibodies, without positive results for other pathogens. Moreover, the patient was immunocompromised due to the long-term use of corticosteroids and immunosuppressants, as evidenced by decreased total IgG levels and reduced CD4 and CD8 T-lymphocyte counts. Interventions and outcome: Despite the intensive anti-infection treatment and respiratory support, the patient developed rapid progression, and subsequently died of respiratory failure. Lessons: RSV infection should be fully considered in adults who are immunocompromised or have underlying diseases, such as nephropathy patients receiving long-term immunosuppressants, especially in the presence of respiratory symptoms and computed tomography (CT) chest findings of diffuse ground-glass opacities.

Rationale Respiratory syncytial virus (RSV) is a single-stranded negative-sense RNA virus that belongs to the family of paramyxoviruses. RSV is the most common pathogen that causes acute lower respiratory tract infection in infants and young children. However, its incidence in immunocompromised adults remains unclear. In the present study, we report an adult patient with chronic nephropathy, who received long-term immunosuppressants and died of rapid respiratory failure due to RSV infection. Patient concerns A 54-year-old male patient with chronic nephropathy, who received long-term immunosuppressants, was admitted to the Department of Respiratory Medicine due to the symptoms of fever, cough, expectoration, and dyspnea. Diagnoses Pulmonary radiology revealed multiple bilateral ground-glass opacity. Laboratory tests revealed elevated inflammation indicators, implying infection with bacteria, viruses, and/or fungi. Furthermore, the patient was positive for RSV antibodies, without positive results for other pathogens. Moreover, the patient was immunocompromised due to the long-term use of corticosteroids and immunosuppressants, as evidenced by decreased total IgG levels and reduced CD4 and CD8 T-lymphocyte counts. Interventions and outcome Despite the intensive anti-infection treatment and respiratory support, the patient developed rapid progression, and subsequently died of respiratory failure. Lessons RSV infection should be fully considered in adults who are immunocompromised or have underlying diseases, such as nephropathy patients receiving long-term immunosuppressants, especially in the presence of respiratory symptoms and computed tomography (CT) chest findings of diffuse ground-glass opacities.

Salidroside is a active constituent of traditional herbal medicine Rhodiola rosea, responsible for the neuroprotective, antidepressant, anxiolytic and anti-tumor actions. However, the mechanism of its anticancer effect is unclear as there have little molecular studies regardingcell migration, invasion, cell cycle, induction of apoptosis in healthy and cancerous cells. Hypoxia-inducible factor-1α (HIF-α) plays an important role in tumor growth, angiogenesis and lymph node metastasis of non-small cell lung cancer (NSCLC). Thus, the present study aims to investigate changes from hypoxia-inducible factor-1α (HIF-α) of NSCLC A549 cell after using salidroside treatment by quantitative polymerase chain reaction (QPCR) and western-bolt on mRNA level and protein level, respectively. The results demonstrated that HIF-α was significantly down-regulated in salidroside treatment group in comparison to the A549 groupon mRNA level (P < 0.05), on protein level, HIF-α was also highly decreased in salidrosidetreatment group in comparison to control group. The present study provides improvement in understanding the molecular pathogenic mechanism of lung cancer and development salidroside as effective anticancer drugs. Key words: Salidroside, A549, HIF-α, QPCR, NSCLC, Western-bolt.