Bing Dai

Association of Dietary Vitamin A and β-Carotene Intake with the Risk of Lung Cancer: A Meta-Analysis of 19 Publications

Whether dietary β-carotene and vitamin A intake protect against lung cancer risk is not clear. Therefore, we performed this meta-analysis to investigate the association between them. The related articles were searched using the databases PubMed and the Web of Knowledge up to May 2015. We used the random-effect model to estimate the relative risk (RR) and their 95% CI. Small-study effect was assessed using Egger’s test. In total, 19 studies comprising 10,261 lung cancer cases met the inclusion criteria. The pooled RR and their 95% CI was 0.855 (0.739–0.989) for higher category of dietary vitamin A intake and lung cancer risk, especially among Asian populations and in the cohort studies. Evidence from 18 studies suggested that higher category of dietary β-carotene intake could reduce lung cancer risk (0.768 (0.675–0.874)).The associations were also significant in American and Asian populations. In conclusions, higher category of dietary β-carotene and vitamin A intakes could reduce the risk of lung cancer. However, the dose-response analysis was not performed due to the limited data in each individual study. Due to this limitation, further studies with detailed dose, cases and person-years for β-carotene and vitamin A of each category are wanted to assess this dose-response association.

Silence of MACC1 expression by RNA interference inhibits proliferation, invasion and metastasis, and promotes apoptosis in U251 human malignant glioma cells

The overexpression of metastasis-associated in colon cancer 1 (MACC1) has been demonstrated not only in colon cancer, but also in various other types of cancer. Gliomas are the most common type of intracranial tumors, and recent studies have reported MACC1 to be involved in human glioma progression. The present study aimed to investigate the effects of MACC1 expression silencing in glioma cells using RNA interference, in order to determine the underlying biological mechanisms of glioma progression, including proliferation, apoptosis, invasion and metastasis. The expression levels of MACC1 were determined in various types of U251 glioma cells using western blot analyses. MACC1-specific short hairpin RNA (shRNA) was used to silence the expression of MACC1 in the U251 cells. The results obtained following MACC1 silencing demonstrated a significant inhibition of cell proliferation, invasion and migration, as well as a marked enhancement of apoptosis. MACC1 shRNA-induced inhibition of cell proliferation was observed by colony forming and MTT assays, and cell apoptosis was measured using flow cytometry and Hoechst staining. In addition, inhibition of cell invasion and migration was assessed using wound healing and transwell assays. Western blotting and fluorescence-activated cell sorting (FACS) revealed a G0/G1 phase cell cycle arrest regulated by cyclins D1 and E; cell apoptosis regulated by caspase-3; and cell invasion and migration regulated by matrix metalloproteinases 2 and 9, respectively. The present study demonstrated that the expression levels of MACC1 were significantly correlated with the biological processes underlying glioma cell proliferation, invasion and metastasis. Therefore, MACC1 may serve as a promising novel therapeutic target in human glioma. Notably, the inhibition of MACC1 expression by shRNA may prove to be an effective genetic therapeutic strategy for glioma treatment.

Melatonin attenuates TGFβ1-induced epithelial-mesenchymal transition in lung alveolar epithelial cells.

Idiopathic pulmonary fibrosis (IPF) is the most common interstitial lung disease. However, the pathogenesis remains to be fully elucidated. Melatonin is secreted by the pineal gland, it has a strong antioxidant effect, and exerts an anti-fibrosis effect. Whether melatonin attenuates pulm -onary fibrosis by inhibiting epithelial‑mesenchymal transition (EMT) requires further research. The present study aimed to investigate whether melatonin prevents transforming growth factor‑β1 (TGF‑β1)‑induced EMT and underlying signaling pathways using reverse transcription‑quantitative polymerase chain reaction, western blot analysis and immunofluorescence. The results demonstrated that melatonin inhibits EMT in A549 cells, and the Wnt/β‑catenin and Smad2/3 signaling pathways are involved in the EMT of the A549 cell line as they were suppressed by melatonin. The present study indicates that melatonin inhibited TGFβ1‑induced epithelial‑mesenchymal transition in the A549 cell line and may potentially be useful in the treatment of IPF.

Oxygen Injection Site Affects FIO2 During Noninvasive Ventilation

BACKGROUND: Most portable bi-level positive airway pressure devices are not equipped with air-oxygen blenders for precisely regulating oxygen concentrations, and supplemental oxygen must be added to increase the FIO2. Very few studies have investigated the factors that affect FIO2, and their conclusions have been inconsistent. We investigated in vitro noninvasive ventilation (NIV) parameters and their effects on FIO2, particularly the effect of the oxygen injection site. METHODS: NIV was simulated with a test lung and manikin setup. FIO2 was measured with 4 oxygen injection sites (mask, in front of the exhalation valve, at the humidifier outlet, and proximal to the ventilator), with 3 exhalation valve types, with 2 oxygen flows, and with 4 combinations of inspiratory and expiratory pressure. RESULTS: Oxygen flow, inspiratory and expiratory pressure, and exhalation valve type all affected FIO2. For a given oxygen flow, the oxygen injection site was the most important factor that affected FIO2. The oxygen injection site that was closest to the patient (on the mask) had the higher FIO2 (P < .001). CONCLUSIONS: The oxygen injection site had the greatest effect on FIO2 during NIV.

Actinidia chinensis Planch. Improves the Indices of Antioxidant and Anti-Inflammation Status of Type 2 Diabetes Mellitus by Activating Keap1 and Nrf2 via the Upregulation of MicroRNA-424

The fruit juice of Actinidia chinensis Planch. has antioxidant and anti-inflammation properties on patients with type 2 diabetes mellitus (T2DM), but the molecular mechanism was unclear. The patients took the juice and the serum level of antioxidant miR-424, Kelch-like ECH-associated protein 1 (Keap1), erythroid-derived 2-like 2 (Nrf2), and biochemical indices were measured. The juice increased the levels of serum microRNA-424, Keap1, and Nrf2 and reduced the levels of interleukin-1 (IL-1) beta and IL-6 in T2DM patients. The levels of SOD and GSH were higher while the levels of ALT and AST were lower in the patients consuming the juice when compared to the patients without taking the juice. The Spearman rank correlation analysis showed that the serum levels of miR-424 were positively related to Keap1 and Nrf2 levels while Keap1 and Nrf2 levels were positively related to the levels of SOD and GSH and negatively related to IL-1 beta and IL-6. Thus, FJACP improves the indices of antioxidant and anti-inflammation status by activating Keap1 and Nrf2 via the upregulation of miR-424 in the patients with T2DM. This trial is registered with ChiCTR-ONC-17011087 on 04/07/2017.

Which Nebulizer Position Should Be Avoided? An Extended Study of Aerosol Delivery and Ventilator Performance during Noninvasive Positive Pressure Ventilation

Background: Research on the effect of nebulizer location on aerosol delivery during noninvasive ventilation has reached inconsistent conclusions. Objective: To investigate the effects of nebulizer position on aerosol delivery efficiency and ventilator performance during noninvasive ventilation. Methods: The Active Servo Lung 5000 respiratory simulation system (ASL5000) was used to simulate a COPD patient. The noninvasive ventilator was set to the spontaneous breathing mode. Six nebulizer positions, 2 exhalation valve types (single-arch exhalation port and whisper swivel), 4 combinations of inspiratory and expiratory pressure, and 2 respiratory rates were used. Results: Significant differences between nebulizer positions existed in aerosol delivery (p < 0.05). Aerosol delivery efficiency was lower for nebulizer locations on either side of the exhalation valve and next to the ventilator outlet. When the nebulizer was located between the exhalation valve and the simulated lung, increased inspiratory pressure increased and increased expiratory pressure decreased delivery efficiency (both p < 0.05). When the nebulization device was located between the exhalation valve and the ventilator, no obvious trend was observed. Compared to baseline, nebulization lowered the air leakage volume displayed on the ventilator. There were no differences in ventilator performance between different nebulizer positions. Conclusions: The closer the nebulizer was to the exhalation valves or ventilator, the lower the aerosol delivery efficiency. Nebulizer position had little clinically significant effect on ventilator performance.

Vitamin D reduces inflammatory response in asthmatic mice through HMGB1/TLR4/NF‑κB signaling pathway

The present study aimed to investigate the effects of vitamin D (VD) on inflammatory responses in asthmatic mice and the underlying mechanism, providing a theoretical basis for clinical application of targeted drug therapy, and the development of novel drugs against asthma. Mouse models of asthma were established. Hematoxylin-eosin staining was performed to observe the pathological changes of the lung tissue. Pulmonary function tests were conducted to determine airway resistance in asthmatic mice. ELISA was performed to measure the serum levels of inflammatory factors. Western blot analysis and reverse transcription-quantitative polymerase chain reaction were performed to determine the changes in apoptosis-inducing factors, and high mobility group box 1 protein (HMGB1)/Toll-like receptor-4 (TLR4)/nuclear factor (NF)-κB signaling pathway-related proteins. VD reduced infiltrated inflammatory factors, attenuated the airway resistance of asthmatic mice, decreased serum levels of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, increased serum levels of IL-10, decreased apoptotic factor Bcl-2-associated X and caspase-3 expression, downregulated HMGB1 and TLR4, NF-κB and phosphorylated-NF-κB p65 expression. When TLR4 expression was inhibited, the anti-inflammatory effects of VD were attenuated, and HMGB1, TLR4, NF-κB and p-NF-κB p65 expression was increased. VD was able reduce the inflammatory response of asthmatic mice and apoptosis in lung tissue through the HMGB1/TLR4/NF-κB signaling pathway.

Eucalyptol Protects Lungs against Bacterial Invasion through Attenuating Ciliated Cell Damage and Suppressing MUC5AC Expression: Effect of Eucalyptol on COPD

This study was conducted to investigate whether eucalyptol plays a role in influencing bacterial growth in cigarette smoke‐exposed lungs. Rats were exposed to air (control) and cigarette smoke (smoking) in the presence and absence of eucalyptol (260 mg/day). Morphological analysis of lung structures and status of airway mucous production were observed under microscope. Pathological changes of ciliated columnar epithelium in airways were examined using transmission electron microscopy. MUC5AC protein and messenger RNA (mRNA) expression in bronchoalveolar lavage fluid (BALF) and lungs were determined. Application of eucalyptol reduced pulmonary bullae formation and airway mucus overproduction in the smoke‐exposed lungs. Treatment with eucalyptol attenuated ciliated cell damage in cigarette smoke‐exposed lungs. Bacterial colonies of lungs were obviously lower in the eucalyptol‐treated rats than that in the smoking rats (p < 0.01). Treatment with eucalyptol reduced the counts of bacterial colonization residing in the challenged lungs (p < 0.01). Application of eucalyptol not only decreased MUC5AC protein expression in BALF and tobacco‐exposed lungs but also suppressed its mRNA expression in the lungs (all p < 0.05). Intervention of eucalyptol benefits elimination of bacterial organisms from tobacco‐exposed lungs through attenuating ciliated cell damage and suppressing MUC5AC expression in the lungs.