1,325 research outputs found

    Benign Pleomorphic Adenoma of the Soft Palate Metastasizing to the Sphenoid Sinus

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    A benign pleomorphic adenoma is the most common tumor of the salivary glands. This tumor has the potential to metastasize to bone, the head and neck region, visceral organs and skin. Although there a few reports about a benign pleomorphic adenoma metastasizing to the maxillary sinus in the paranasal sinuses, there are no reports about a metastatic benign pleomorphic adenoma in the sphenoid sinus. We report here on a case of a benign pleomorphic adenoma of the soft palate that metastasized to the sphenoid sinus, and we briefly review the relevant clinical literature

    Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells

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    <p>Abstract</p> <p>Background</p> <p>Many studies have found that smoking reduces lung function, but the relationship between cigarette smoke and allergic asthma has not been clearly elucidated, particularly the role of mast cells. This study aimed to investigate the effects of smoke exposure on allergic asthma and its association with mast cells.</p> <p>Methods</p> <p>BALB/c mice were sensitized and challenged by OVA to induce asthma, and bone marrow-derived mast cells (BMMCs) were stimulated with antigen/antibody reaction. Mice or BMMCs were exposed to cigarette smoke or CSE solution for 1 mo or 6 h, respectively. The recruitment of inflammatory cells into BAL fluid or lung tissues was determined by Diff-Quik or H&E staining, collagen deposition by Sircol assay, penh values by a whole-body plethysmography, co-localization of tryptase and Smad3 by immunohistochemistry, IgE and TGF-Ī² level by ELISA, expressions of Smads proteins, activities of signaling molecules, or TGF-Ī² mRNA by immunoblotting and RT-PCR.</p> <p>Results</p> <p>Cigarette smoke enhanced OVA-specific IgE levels, penh values, recruitment of inflammatory cells including mast cells, expressions of smad family, TGF-Ī² mRNA and proteins, and cytokines, phosphorylations of Smad2 and 3, and MAP kinases, co-localization of tryptase and Smad3, and collagen deposition more than those of BAL cells and lung tissues of OVA-induced allergic mice. CSE solution pretreatment enhanced expressions of TGF-Ī², Smad3, activities of MAP kinases, NF-ĪŗB/AP-1 or PAI-1 more than those of activated-BMMCs.</p> <p>Conclusions</p> <p>The data suggest that smoke exposure enhances antigen-induced mast cell activation via TGF-Ī²/Smad signaling pathways in mouse allergic asthma, and that it exacerbates airway inflammation and remodeling.</p

    Effect of Epigallocatechin-3-Gallate on PMA-Induced MUC5B Expression in Human Airway Epithelial Cells

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    ObjectivesAmong the inflammatory mediators, phorbol 12-myristate 13-acetate (PMA) is associated with the regulation of MUC5B expression in the airway epithelial cells. Epigallocatechin-3-gallate (EGCG) is the major component of green tea extract. The biological activity of EGCG includes reduction of cholesterol and antioxidant activity, as well as anti-inflammatory effect. However, the precise action mechanism of anti-inflammatory effect of EGCG in the airway epithelial cells has not been fully defined. This study investigates the effect and the brief signaling pathway of EGCG on PMA-induced MUC5B expression in the airway epithelial cells.MethodsIn NCI-H292 airway epithelial cells, the effect and signaling pathway of EGCG on MUC5B expression were investigated using real-time polymerase chain reaction analysis, enzyme immunoassay, immunohistochemical analysis, gelatin zymography assay, and immunoblot analysis.ResultsIn NCI-H292 airway epithelial cells, PMA induced MUC5B expression, phosphorylation of p38 mitogen-activated protein kinase (MAPK), and matrix metalloproteinase-9 (MMP-9) expression and protein activity. EGCG significantly decreased PMA-induced MUC5B expression, phosphorylation of p38 MAPK, and MMP-9 expression and protein activity. SB203580 (p38 MAPK inhibitor) significantly decreased PMA-induced MMP-9 expression. In addition, SB203580 and MMP-9 I (MMP-9 inhibitor) significantly decreased PMA-induced MUC5B expression.ConclusionThese results suggest that EGCG down-regulates PMA-induced MUC5B expression through the p38 MAPK dependent MMP-9 signaling pathway in human airway epithelial cells

    Does acellular dermal matrix expand in response to tissue expander inflation?

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    Background Acellular dermal matrices (ADMs) have recently become widely used in breast reconstruction, but the correlation between the final expander volume and the surface area of the ADM is not well understood. In this study, the expansion of the surface area of ADM and the expander volume was studied retrospectively in cases of acellular dermisā€“assisted tissue expander breast reconstruction. Methods Twenty cases of immediate breast reconstruction using an ADMā€“assisted tissue expander from January 2015 to December 2015 were evaluated. In all 20 cases, CGCryoDerm was used as the matrix, with a thickness of 1ā€“3 mm. No slit incisions were made. Finally, the proportional increase in the area of the fully expanded ADM was compared to that of the tissue expander volume. Results The proportional increase in the ADM surface area was calculated to be from 1.1 to 2.46, with a mean value of 1.7. Additionally, under the assumption that the expander had a spherical shape, the increase in its radius (the cube root of its volume) was assessed. The range of the proportional increase in the expander radius was 1.1 to 2.24, with a mean value of 1.66. The proportional increase in the radius of the expanded ADM surface area ranged from 1.04 to 1.34, with a mean ratio of 1.28. Conclusions The results of this study confirmed that the ADM expanded when the tissue expander was inflated. However, the ADM expanded to a lesser extent than the tissue expander, indicating that the muscle and other tissues expanded more than the ADM when the tissue expander was inflated

    Detection of swine hepatitis E virus in the porcine hepatic lesion in Jeju Island

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    Swine hepatitis E virus (HEV) is an emerging zoonotic pathogen due to its close genomic similarity to human HEV. The prevalence of swine HEV in the hepatic lesion of pigs from the Jeju Island was investigated by reverse transcriptase polymerase chain reaction (RT-PCR). In total, 40 pigs with hepatitis lesions were selected from 19 different farms, based on examination by microscopy. RTPCR findings revealed swine HEV in 22 cases (55%), including 18 suckling pigs and 4 growing pigs. Several histopathological lesions, including multifocal lymphoplasmacytic hepatitis, portal inflammation, and focal hepatocellular necrosis, were observed in liver sections of swine HEV PCR-positive pigs. The present study suggests that the prevalence of swine HEV is very high in the pig population in Jeju Island, and that pigs are infected at early stages of growth (under 2 months of age). The high prevalence of swine HEV in pigs in Jeju Island and the ability of this virus to infect across species puts people with swine-associated occupations at possible risk of zoonotic infection.This work was supported by the Research Project on the Production of Bio-organs (No. 200503010403), Ministry of Agriculture and Forestry, Korea

    Mechanisms of Acquired Resistance to AZD9291 A Mutation-Selective, Irreversible EGFR Inhibitor

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    IntroductionAZD9291, a third-generation and mutation-selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is active against patients with EGFRT790M-mutant nonā€“small-cell lung cancer (NSCLC) who failed prior treatment with EGFR TKIs. However, acquired resistance to AZD9291 is inevitable. In this study, we identified the mechanisms of acquired resistance to AZD9291 in EGFRT790M-mutant NSCLC.MethodsFour NSCLC patients with both an EGFR exon 19 deletion and the EGFRT790M mutation after developing acquired resistance to first-generation EGFR TKIs received AZD9291 at doses of 20 to 80 mg/day in a phase I trial (NCT01802632). Paired tumor samples before and after treatment were obtained to evaluate EGFR modifications, alternative pathway activation, and histologic transformation. Genetic alterations were analyzed using Sanger sequencing, fluorescence in situ hybridization, real-time polymerase chain reaction, and targeted exome sequencing.ResultsAll four patients achieved a partial response (median duration of response, 9 months [range, 9ā€“11 months]) and subsequently showed resistance to AZD9291. EGFRT790M-mutant clones depopulated AZD9291-resistant tumors to below 1% (baseline, 14%ā€“36%) in three patients with progression: one with the loss of EGFRLREAT747del/T790M-double mutant clones and two accompanied by transformation to small-cell carcinoma and focal fibroblast growth factor receptor 1 (FGFR1) amplification, respectively. EGFRT790M-mutant clones remained and the EGFR ligand was overexpressed in one patient with focal progression to AZD9291.ConclusionAcquired resistance mechanisms of AZD9291 in patients with EGFRT790M-mutant NSCLC who failed treatment with first-generation EGFR TKIs include the loss of EGFRT790M-mutant clones plus alternative pathway activation or histologic transformation and EGFR ligandā€“dependent activation

    Primary Osteosarcoma in Patients Older than 40 Years of Age

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    Among the 665 patients who registered at our hospital, we reviewed 39 cases of high grade primary osteosarcoma in patients who were older than 40 yr of age. The aim of this study was to determine if a primary osteosarcoma in older patients has different clinical features, and a poorer prognosis than in younger patients. Two evaluations were performed. In the first, an attempt was made to determine the possible prognostic factors such as gender, location, size, alkaline phosphatase, radiological findings, chemotherapy intensity, chemotherapy-induced tumor necrosis, and surgical margin. The second evaluation involved assessment of whether there were any significant clinical differences between older patients and adolescents. According to the results, a primary osteosarcoma in older patients did not reveal any significant prognostic variables. A primary osteosarcoma in older patients showed a poorer prognosis due to relatively unusual locations, common abnormal radiological findings, and a poor response to chemotherapy. Therefore, careful attention should be paid to making an accurate diagnosis and new strategies for more effective treatment, including chemotherapy, must to be developed in order to achieve long term survival in older patients with osteosarcoma

    Influence of sarcopenia on postoperative complications in patients undergoing autologous microsurgical breast reconstruction: an inverse probability of treatment weighting analysis

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    BackgroundSarcopenia is characterized by the loss of skeletal muscle mass and power. Preoperative sarcopenia may be associated with an increased risk of postoperative complications after autologous free-flap breast reconstruction surgery; however, this relationship is controversial.ObjectivesThis study aimed to determine whether preoperative sarcopenia is associated with a high complication rate in patients undergoing autologous free-flap breast reconstruction.MethodsPatients who underwent autologous free-flap breast reconstruction at our hospital between 2019 and 2021 were included in the study. Data on significant complications requiring surgical intervention were retrospectively collected from the medical records. Sarcopenia was defined as having a skeletal muscle index value &lt;41 cm2/m2. The skeletal muscle index was calculated by dividing the sum of the psoas and iliopsoas muscle areas at the level of the third lumbar vertebra by the patientā€™s height in meters squared. The relationship between preoperative sarcopenia and postoperative complications was investigated using an inverse probability of treatment weighting (IPTW) analysis.ResultsAmong the 203 participants, 90 (44.33%) had preoperative sarcopenia. The general patient characteristics were similar between the sarcopenia and non-sarcopenia groups after IPTW adjustment. Sarcopenia did not significantly increase the risk of flap failure or emergency surgery related to breast reconstruction before IPTW adjustment. However, after IPTW adjustment, the rates of recipient site infection and hematoma were significantly higher in participants with sarcopenia than in those without sarcopenia (p &lt; 0.001 and p = 0.014, respectively).ConclusionPreoperative sarcopenia may influence certain complications of autologous free-flap breast reconstruction surgery
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