The application of SFDI and LSI system to evaluate the blood perfusion in skin flap mouse model.

The aim of this study is to evaluate whether the blood perfusion to tissues for detecting ischemic necrosis can be quantitatively monitored by spatial frequency domain imaging (SFDI) and laser speckle imaging (LSI) in a skin flap mouse model. Skin flaps were made on Institute of Cancer Research (ICR) mice. Using SFDI and LSI, the following parameters were estimated: oxyhemoglobin (HbO2), deoxyhemoglobin (Hb), total hemoglobin (THb), tissue oxygen saturation (StO2), and speckle flow index (SFI). Histologically, epithelium thickness, collagen deposition, and blood vessel count of skin flap tissues were analyzed. Then, the correlation of SFDI and histological results was assessed by application of Spearman rank correlation method. As the result, the number of blood vessels and the percentage of collagen areas showed significant difference between the necrotic tissue group and the non-necrotic one. Especially, the necrotic tissue had a complete epithelial loss and loses its normal structure. We identified that SFDI/LSI parameters were significantly different between non-necrotic and necrotic tissue groups. Especially, all SFDI and LSI parameters measured on the 1st day after surgery showed significant difference between necrotic tissue and non-necrotic tissue. In addition, the number of blood vessel and percentage of collagen area were positively correlated with HbO2 and StO2 among SFDI/LSI parameters. Meanwhile, the number of blood vessel and percentage of collagen area showed the negative correlation with Hb. By applying SFDI and LSI simultaneously to the skin flap, we could quantitatively monitor the blood perfusion and the tissue condition which can help us to detect ischemic necrosis objectively in early stage.

Effects of Low-Level Laser Irradiation in a Mouse Model of Allergic Rhinitis.

BACKGROUND AND OBJECTIVES: To evaluate the antiallergic effect of low-level laser irradiation (LLLI) at 650 nm in a mouse model of allergic rhinitis (AR), and to examine the underlying mechanisms. STUDY DESIGN/MATERIALS AND METHODS: BALB/c mice were sensitized with ovalbumin (OVA) and alum and challenged intranasally with OVA. Straight- and diffusion-type LLLI were applied directly into the intranasal cavity of the mice once daily for 10 days (650 nm, 5 mW, 15 min/day) and multiple allergic parameters were evaluated. RESULTS: LLLI reduced allergic symptoms, such as rubbing and sneezing, and suppressed the serum total immunoglobulin E (IgE), OVA-specific IgE, and OVA-specific IgG1 levels. Diffusion-type LLLI significantly reduced eosinophil infiltration of nasal mucosa and lymph nodes (LNs). LLLI reduced the expression of interleukin-4 (IL-4) and IL-17 in cervical LN and splenocyte culture supernatant, as well as their messenger RNA levels in nasal mucosa. However, the expression of interferonγ (IFN-γ) and IL-6 was unaffected by LLLI. The levels of reactive oxygen species (ROS) and nitric oxide (NO) in LN cells and the nasal mucosa, which were increased in the AR group, were reduced by LLLI, suggesting involvement of ROS and NO within their mechanism. CONCLUSIONS: LLLI exerted an antiallergic effect by decreasing local and systemic IL-4, IL-17, and IgE levels, as well as eosinophilic infiltration into the nasal mucosa, in a mouse model of AR by modulating ROS and NO levels. Diffusion-type LLLI exhibited greater efficacy against AR than straight-type LLLI. Lasers Surg. Med. © 2019 Wiley Periodicals, Inc.

Cigarette smoke promotes eosinophilic inflammation, airway remodeling, and nasal polyps in a murine polyp model.

BACKGROUND: Exposure to cigarette smoking (CS) is a major risk factor for airway inflammation. However, little is known about the effects of CS exposure on eosinophilic rhinosinusitis with nasal polyps (ERSwNPs). Histopathological and molecular studies were performed to investigate its effects using a murine model of ERSwNPs. METHODS: Mice were assigned to one of the following four groups (n = 8 for each group): control group, CS exposure (CS group), ERSwNP (ERS group), and ERSwNPs exposed to CS (ERS + CS group). Histopathological changes were investigated using various stains, including hematoxylin and eosin for inflammation and polyp-like lesions, Sirius red for eosinophils, toluidine blue for mast cells, Alcian blue for goblet cells, and Masson's trichrome stain for collagen fibers. mRNA expression of cytokines from nasal mucosae was measured. Serum IgE and systemic cytokine levels were measured by enzyme-linked immunosorbent assays. The expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF) 1-alpha was evaluated by immunohistochemical staining. RESULTS: The ERS + CS group showed more severe symptoms, increased the number of polyp-like lesions, infiltration of eosinophils, goblet cell hyperplasia, and subepithelial fibrosis, compared with the ERS group. Additionally, mRNA expressions of IL-4 and IL-17A were up-regulated in ERS + CS group and higher levels of IL-4, IL-6, IL-17A, and interferon gamma from splenocytes were observed significantly in the ERS + CS group compared with the ERS group. In the ERSwNP murine model, exposure to CS enhanced the expression of VEGF and HIF-1-alpha in nasal epithelial cells. CONCLUSION: Chronic exposure to CS aggravated eosinophilic inflammation and promoted airway remodeling and nasal polyp formation in a murine model of ERSwNPs. The underlying mechanism might involve up-regulated expression of VEGF and HIF-1-alpha.