Pyrolysis of Methyl Ricinoleate: Distribution and Characteristics of Fast and Slow Pyrolysis Products.

A stable temperature site and the speed of heating the feedstocks play a key role in pyrolysis processes. In this study, the product distribution arising from pyrolysis of methyl ricinoleate (MR) at 550 °C with low and high heating rates was first studied by pyrolysis-gas chromatography/mass spectrometry (Py-GC/MS). The results show that fast pyrolysis of MR favored the production of undecylenic acid methyl ester (UAME) and heptanal (HEP). Density functional theory (DFT) calculations were employed to reveal the UAME and HEP formation process from pyrolysis of MR. The bond dissociation energies (BDEs) of C-C bonds in MR showed that the C11-C12 bond is the weakest. This suggests that UAME and HEP are two major products. The process of slow and fast MR pyrolysis was the dehydration-first and the pyrolysis-first trend, respectively. The calculated activation energies of MR pyrolysis to UAME and HEP and MR dehydration to 9,12-octadecadienoic acid methyl ester were 287.72 and 238.29 kJ/mol, respectively. The much higher product yields obtained in the fast pyrolysis reactors than those from conventional tubular reactors confirmed the proposed process.

Tiaobu Feishen therapy inhibits inflammation induced by cigarette smoke extracts in a human monocyte/macrophage cell line.

OBJECTIVE: To study the mechanistic effects of Tiaobu Feishen therapy (TBFS) on inflammation induced by cigarette smoke extract (CSE) in a human monocyte/macrophage cell line. METHODS: The human monocyte/macrophage cell line THP-1 was stimulated with 10 % CSE in the presence or absence of Bufei Yishen formula (BYF), Bufei Jianpi formula (BJF) and Yiqi Zishen formula (YZF). All formulations contained serum. Pro-inflammatory cytokines were measured in the supernatants using enzyme-linked immunosorbent assay. The activity of STAT3 DNA binding was detected using electrophoretic mobility shift assay and janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway activation was assessed using Western blotting. RESULTS: The results showed that BYF, BJF and YZF treatment strongly decreased the CSE-induced secretion of interleukin (IL)-6, IL-8, tumor necrosis factor-α and matrix metalloproteinase-9 by THP-1 cells. Furthermore, BYF, BJF and YZF treatment attenuated STAT3 DNA binding capacity and JAK2 and STAT3 were shown to be phosphorylated. CONCLUSION: The data revealed that BYF, BJF and YZF effectively inhibited a CSE-induced inflammatory response in THP-1 cells by limiting activation of the JAK2/STAT3 pathway.

Co-infection of Pneumocystis jirovecii pneumonia and pulmonary CMV in a infant with X-linked severe combined immunodeficiency.

We herein report a rare case of co-infection of Pneumocystis jirovecii pneumonia and pulmonary CMV in a 3-month-old infant with X-linked severe combined immunodeficiency, in which diagnostic clues were obtained from the bronchoalveolar lavage fluid. We focus on the value of cytological diagnosis of P. jirovecii pneumonia and pulmonary CMV in the bronchoalveolar lavage fluid. Recognizing morphological characteristics of these pathogenic microorganisms is important to get timely diagnosis and treatment for the patients. Furthermore, repeated severe infections in infants should remind us to screen for immunosuppressed states.

Mechanisms of the lipopolysaccharide-induced inflammatory response in alveolar epithelial cell/macrophage co-culture.

The interaction between alveolar epithelial cells (EpCs) and macrophages (MPs) serves an important role in initiating and maintaining inflammation in chronic pulmonary diseases. The aim of the present study was to investigate the molecular mechanisms of the inflammatory response in co-cultured EpCs and MPs. Briefly, a co-culture system of A549 (EpCs) and THP-1 (monocyte/MPs) cells was established in a filter-separated Transwell plate to evaluate the inflammatory response. Following lipopolysaccharide (LPS) treatment, cytokine levels were measured using ELISAs, NF-κB transcription factor activity was detected using EMSA and protein expression levels were analyzed using Western blot assays subsequently in EpCs and MPs. Co-cultured EpCs/MPs were found to secrete increased levels of interleukin (IL)-6, IL-1ß, IL-8 and tumor necrosis factor (TNF)-α following LPS exposure for 6, 12, 24 and 48 h compared with either EpC or MP monocultures. Concurrently, NF-κB was revealed to be activated in MPs at 6 and 12 h, and in EpCs at 24 h. NF-κB DNA binding, Toll-like receptor 4 expression levels and the p65 phosphorylation status were also increased, which may contribute to the inflammatory response in the EpC/MP co-cultures. Notably, cytokine levels decreased following the inhibition of NF-κB expression with pyrrolidinedithiocarbamate. In conclusion, the present study successfully established an EpC/MP co-culture system using LPS, which may be a useful model for studying chronic inflammation in vitro.

Divergent Roles of miR-3162-3p in Pulmonary Inflammation in Normal and Asthmatic Mice as well as Antagonism of miR-3162-3p in Asthma Treatment.

MicroRNA (miRNA) mimics or antagomirs hold great promise for asthma treatment compared with glucocorticoids as mainstay therapy for asthma. But the role of miRNA in regulating asthmatic inflammation is largely unclear. We previously reported that miR-3162-3p in the peripheral blood of children with asthma was obviously upregulated compared to that in healthy children. This study aimed to elucidate the role of miR-3162-3p in pulmonary inflammation in normal and asthmatic mice as well as preliminarily explore the potential of miR-3162-3p antagomir in asthma treatment. A noninvasive whole-body plethysmograph measured airway responsiveness. Both qRT-PCR and Western blot were used to detect the expression of miRNA, mRNA, or protein. Cells in bronchoalveolar lavage fluid were counted by platelet counting and Wright's staining. Inflammatory infiltration and mucus secretion were identified by hematoxylin and eosin and periodic acid-Schiff  staining, respectively. Cytokines in the lungs were detected by ELISA. The miR-3162-3p mimic intraperitoneally administered to normal mice decreased ß-catenin levels in the lungs without obviously altering the lung histology and cytokine levels. Antagonizing miR-3162-3p in ovalbumin-induced asthmatic mice effectively alleviated the typical features of asthma, such as airway hyper-responsiveness, airway inflammation, and Th1/Th2 cytokine imbalance, and concomitantly rescued the total and active ß-catenin expression. Collectively, we discovered divergent roles of miR-3162-3p in lung inflammation between normal and asthmatic mice. The anti-inflammatory effects of the miR-3162-3p antagomir were comparable to those of glucocorticoid treatment. Our study helped in understanding the contribution of miRNAs to the pathogenesis of asthma.

Adverse impact of ambient PM2.5 on expression and trafficking of surfactant protein A through reactive oxygen species damage to lamellar bodies.

Particulate matter with a diameter of less than 2.5 µm (PM2.5) easily deposits on lung alveoli and degrades human health. Surfactant protein A (SP-A) is the most abundant pulmonary surfactant protein stored in lamellar bodies (LBs) of alveolar epithelial type II cells. The impacts of PM2.5 on SP-A are multifaceted and intractable, and the underlying mechanism remains unclear. In this study, the expression and distribution of SP-A in Balb/c mice and A549 cells under PM2.5 exposure were investigated. The results showed that the low and medium concentration of PM2.5 gradually enhanced SP-A protein and mRNA expression, whereas the high concentration of PM2.5 conspicuously decreased SP-A protein but not its mRNA compared with the control. The trafficking of SP-A to LBs was gradually disturbed, and concomitantly, the lesions of LBs responsible for the transport and storage of SP-A protein were exacerbated with increased PM2.5 concentration. Reactive oxygen species production abundantly increased upon PM2.5 exposure, and it was antagonized by the oxidant inhibitor N-acetylcysteine. Subsequently, the injured LBs and the decrease in SP-A expression under exposure to the high concentration of PM2.5 were well rescued. The present study provides a new perspective to investigate the adverse effects of PM2.5 or diesel exhaust particles on other proteins transported to and stored in LBs.