No abstract

BackgroundBjerkandera adusta (B. adusta) is one of the most important etiological fungi associated with chronic cough. However, precise details of the inflammatory response to exposure are not well understood yet. B. adusta was recently identified in Asian sand dust (ASD) aerosol. Therefore, in the present study the exacerbating effects of ASD on B. adusta-induced lung inflammation and B. adusta + ASD on ovalbumin (OVA)-induced murine lung eosinophilia were investigated using experimental mice.MethodsIn order to prepare testing samples, B. adusta obtained from ASD aerosol was inactivated by formalin and ASD collected from the atmosphere was heated to remove toxic organic substances (H-ASD). CD-1 mice were instilled intratracheally with 12 different samples prepared with various combinations of B. adusta, H-ASD, and OVA in a normal saline solution. The lung pathology, cytological profiles in bronchoalveolar lavage fluid (BALF), and the levels of inflammatory cytokines/chemokines in BALF were investigated.ResultsH-ASD aggravated the lung eosinophilia induced by B. adusta alone, which also aggravated the lung eosinophilia induced by OVA. The mixture of OVA, H-ASD, and B. adusta caused serious fibrous thickening of the subepithelial layer, eosinophil infiltration, and proliferation of goblet cells in the airways along with remarkable increases of IL-13, eotaxin, IL-5, and MCP-3 in BALF.ConclusionsThe results of the present study demonstrated that B. adusta isolated from ASD aerosol induces allergic lung diseases. H-ASD enhanced allergic reactions caused by OVA or B. adusta. A mixture of B. adusta, H-ASD, and OVA caused the most remarkable exacerbation to the allergic airway inflammation via remarkable increases of pro-inflammatory mediators.

No abstract

No abstract

Bjerkandera adusta (B. adusta) causes fungus-associated chronic cough. However, the inflammatory response is not yet fully understood. Recently, B. adusta was identified in Asian sand dust (ASD) aerosol. This study investigated the enhancing effects of ASD on B. adusta-induced lung inflammation. B. adusta was inactivated by formalin. ASD was heated to remove toxic organic substances. ICR mice were intratracheally instilled with saline, B. adusta 0.2 µg, or B. adusta 0.8 µg with or without heated ASD 0.1 mg (H-ASD), four times at 2-week intervals. Two in vitro experiments were conducted to investigate any enhancing effects using bone marrow-derived macrophages (BMDM) from Toll-like receptor (TLR) knockout mice and ICR mice. Co-exposure to H-ASD and B. adusta, especially at high doses, caused eosinophil infiltration, proliferation of goblet cells in the airway, and fibrous thickening of the subepithelial layer, and remarkable increases in expression of Th2 cytokines and eosinophil-related cytokine and chemokine expression in bronchoalveolar lavage fluid. In the in vitro study using BMDM from wild-type, TLR2-/-, and TLR4-/- mice, the TLR-signaling pathway for cytokine production caused by B. adusta was predominantly TLR2 rather than TLR4. H-ASD increased the expression of NF-κB and cytokine production by B. adusta in BMDM from ICR mice. The results suggest that co-exposure to H-ASD and B. adusta caused aggravated lung eosinophilia via remarkable increases of pro-inflammatory mediators. The aggravation of inflammation may be related, at least in part, to the activation of the TLR2-NF-κB signaling pathway in antigen presenting cells by H-ASD.

No abstract

Background Recurrence of colorectal polyps is common and impacted by various factors. This study was performed to explore the association between lipid profiles and recurrence of colorectal polyps. Methods This study retrospectively analyzed the lipid profiles of 435 patients who underwent colonoscopy with removal of colorectal polyps and assessed recurrence of polyps by follow-up colonoscopy. Multivariate regression logistic analysis was used to evaluate the association between lipid profiles and polyp recurrence. Results During the 1.5-year follow-up, recurrence of colorectal polyps was observed in 135 of 435 patients (30.34%). Patients with recurrent polyps showed a higher level of triglycerides (P = 0.006) and lower levels of high-density lipoprotein cholesterol (P = 0.008) and apolipoprotein A1 (P = 0.033). The multivariate regression logistic model suggested that an elevated triglyceride level was an independent risk factor for polyp recurrence (odds ratio, 1.55; 95% confidence interval, 1.02–2.35; P = 0.039) in patients with advanced adenoma. Conclusions Lipid profiles are associated with recurrence of colorectal polyps. An elevated triglyceride level is an independent risk predictor of polyp recurrence in patients with advanced adenoma.

Edge-preserving image smoothing is one of the fundamental tasks in the field of computer graphics and computer vision. Recently, L0 gradient minimization (LGM) has been proposed for this purpose. In contrast to the total variation (TV) model which employs the L1 norm of the image gradient, the LGM model adopts the L0 norm and yields much better results for the piecewise constant image. However, as an improvement of the total variation (TV) model, the LGM model also suffers, even more seriously, from the staircasing effect and is not robust to noise. In order to overcome these drawbacks, in this paper, we propose an improvement of the LGM model by prefiltering the image gradient and employing the L1 fidelity. The proposed improved LGM (ILGM) behaves robustly to noise and overcomes the staircasing artifact effectively. Experimental results show that the ILGM is promising as compared with the existing methods.