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Plexiform schwannomas representing a rare subset, comprise 5% of all schwannomas. However, their occurrence in the thyroid gland is exceptionally rare. A 32-year-old male presented with an incidentally discovered, asymptomatic thyroid mass. Imaging revealed an approximately 5 cm heterogeneous solid mass on the right thyroid lobe extending to the upper mediastinum and directly invading the upper trachea. Under the suspicion of thyroid malignancy, the patient underwent right thyroidectomy. Histological examination confirmed a plexiform schwannoma with S100-positive spindle cells. Currently, the patient is undergoing outpatient follow-up, with no reported complications. To our knowledge, this is the first documented case of plexiform schwannoma of the thyroid gland within the English literature. This case highlights the diverse and unpredictable clinical manifestations of thyroid masses, emphasizing the importance of a multidisciplinary approach for diagnosing and managing rare entities, such as thyroid gland schwannomas.

Post-acute coronavirus disease (COVID-19) syndrome is defined as persistent symptoms or delayed complications after COVID-19. Several cases of cranial nerve invasion related to COVID-19 have been reported. However, to our knowledge, no cases of solitary unilateral hypoglossal nerve paralysis after mild COVID-19 without intubation have been reported to date. Herein, we report the case of a 64-year-old man with unilateral hypoglossal nerve palsy as a complication of COVID-19. He complained of dysarthria and tongue discomfort 2 weeks after COVID-19 onset. Brain and neck computed tomography, magnetic resonance imaging, ultrasonography, and blood tests ruled out other possible causes. The patient’s nerve palsy was rapidly diagnosed and improved with early rehabilitation. Understanding of the pathology of COVID-19 is still limited. Physicians should focus on patients’ symptoms and their relationship to COVID-19, and investigate complications immediately. This case highlights the importance of early detection and rehabilitation of post-acute COVID-19 syndrome.

Objectives. Obesity, which induces chronic low-grade systemic inflammation in the human body, is a known risk factor for various diseases. Recent studies have shown associations between various otorhinolaryngological diseases and obesity. In particular, inflammatory sinonasal diseases have been found to be strongly associated with obesity-related proinflammatory mediators. Many studies have been conducted to identify therapeutic agents for controlling obesity-related inflammatory airway diseases. Ghrelin, an endogenous peptide from the stomach, has anti-inflammatory and antioxidative effects in a wide range of tissues. However, the effect of ghrelin on the regulation of mucus secretion has not yet been studied in the human nasal mucosa. Therefore, we investigated the effects of ghrelin on lipopolysaccharide (LPS)/leptin-mediated MUC5AC expression and mechanisms involved in human nasal epithelial cells (HNEpCs). Methods. In HNEpCs, the effect and signaling pathways of ghrelin on LPS/leptin-induced MUC5AC expression were examined using reverse transcription polymerase chain reaction, real-time polymerase chain reaction, enzyme immunoassays, Western blotting, and immunofluorescence staining. Results. Growth hormone secretagogue receptor 1a (GHSR1a) was expressed in the HNEpCs. Ghrelin downregulated LPS/leptin-induced MUC5AC expression, which was abolished by D-Lys-3-growth hormone-releasing peptide 6 (D-Lys-3-GHRP-6). Ghrelin significantly inhibited LPS/leptin-activated extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinases (MAPKs). These ghrelin-mediated changes in MAPK activation were abolished by D-Lys-3-GHRP-6. These results showed that ghrelin inhibits LPS/leptin-induced MUC5AC overexpression by modulating the ERK1/2 and p38 MAPK pathways in HNEpCs. Conclusion. These findings suggest that ghrelin is a potential therapeutic agent for treating obesity-related inflammatory sinonasal diseases.

Background: Diesel exhaust particle (DEP) is a harmful kind of particulate matter known to exacerbate pre-existing respiratory diseases. Although their adverse effects on airway pathologies have been widely studied, the mechanistic analysis of signaling pathways and potential targets in reducing DEP-induced mucin secretion and pro-inflammatory cytokine production remain elusive. We, for the first time, investigated the effects of Korean Red Ginseng (KRG) extracts on mucin overproduction and airway inflammation induced by DEP. Methods: The effects of KRG and saponin on DEP-induced expression of MUC5AC and interleukin (IL)-6/8 were examined by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) in human airway epithelial NCI–H292 cells. We conducted Western blotting analysis to analyze the associated signaling pathways. To evaluate the effects of saponin treatment on DEP-induced MUC5AC expression and inflammatory cell infiltrations in ovalbumin (OVA)-sensitized mice, immunohistochemical (IHC) staining and real-time PCR were implemented. Results: The KRG extracts markedly attenuated DEP-induced MUC5AC expression in vitro by inhibiting the TLR4/TRIF/NF-κB pathway. Furthermore, KRG and saponin inhibited DEP-induced pro-inflammatory cytokine IL-6/8 production. The in vivo study revealed that saponin blocked DEP-induced inflammation, mucin production and MUC5AC expression. Conclusion: Our study revealed that KRG extracts have inhibitory effects on DEP-induced expression of MUC5AC and the production of pro-inflammatory cytokines. This finding provides novel insights into the mechanism by which saponin alleviates diesel-susceptible airway inflammation, elucidating its potential as a phytotherapeutic agent for inflammatory pathologies of airway.

Objectives The emergence of electronic cigarettes (e-cigarettes) has created new perceptions of the tobacco market. Unlike traditional tobacco, the greatest advantage of e-cigarettes is that they have less smell and are convenient and inexpensive. Most e-cigarette smokers believe that e-cigarette smoking is less harmful than traditional smoking. Information on the effects of e-cigarettes on human health is limited, and the issue remains controversial. Methods We studied the effects of e-cigarette vapor on mucin (MUC5AC and MUC5B) and the change of MUC5AC and MUC5B from e-cigarette liquid with or without nicotine in respiratory epithelial cells. The effects of e-cigarette vapor with or without nicotine on mucin, along with the involved signaling pathways, were investigated using reverse transcriptase-polymerase chain reaction (PCR), real-time PCR, enzyme immunoassays, and immunoblot analysis with several specific inhibitors and small interfering RNA. Results E-cigarette vapor with or without nicotine stimulated MUC5AC, but not MUC5B, expression in respiratory epithelial cells. In addition, we showed that e-cigarette vapor with and without nicotine induced MUC5AC expression via activation of the mitogen-activated protein kinase (MAPK; extracellular signal-regulated kinase [ERK] 1/2 and p38) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways in human airway epithelial cells. Conclusion E-cigarette vapor with and with nicotine significantly increased MUC5AC expression in human airway epithelial cells.

Active and prompt scale-up screening tests are essential to efficiently control the coronavirus disease 2019 (COVID-19) outbreak. The goal of this work was to identify shortcomings in the conventional screening system (CSS) implemented in the beginning of the outbreak. To overcome these shortcomings, we then introduced a novel, independently developed system called the Yeungnam University type drive-through (YU-Thru), and distributed it nationwide in Korea. This system is similar to the drive-throughs utilized by fast food restaurants. YU-Thru system has shortened the time taken to test a single person to 2–4 minutes, by completely eliminating the time required to clean and ventilate the specimen collection room. This time requirement was a major drawback of the CSS. YU-Thru system also reduced the risk of subjects and medical staff infecting one another by using a separate and closed examination system. On average, 50 to 60 tests were conducted per day when using the CSS, while now up to 350 tests per day are conducted with the YU-Thru system. We believe that the YU-Thru system has made an important contribution to the rapid detection of COVID-19 in Daegu, South Korea. Here, we will describe the YU-Thru system in detail so that other countries experiencing COVID-19 outbreaks can take advantage of this system.

Background and Objectives Nicotine is oxidized into tobacco-specific nitrosamines (TSNAs; NAB, NAT, NNN, NNAL, NNK) at high temperature and high pressure. TSNAs are associated with airway diseases characterized by mucus hypersecretion as a major pathophysiologic phenomenon. The aim of study is to investigate the effect of TSNAs on mucin overexpression and its molecular mechanism in human airway epithelial cells. Materials and Method The cytotoxicity of TSNAs was evaluated using EX-Cytox and inverted microscopy. The mRNA and protein levels of MUC5AC and MUC5B were measured using real-time PCR and ELISA. Results NAB, NNN, NNAL, and NNK did not affect cell viability. NAT did not affect cell viability up to a concentration of 100 μM in human airway epithelial cells. NAT, NNN, NNAL, and NNK significantly induced MUC5AC expression, but not MUC5B expression. NAB did not affect the expression of MUC5AC and MUC5B. Propranolol (a β-adrenergic receptor antagonist) inhibited NAT, NNN, NNAL, and NNK-induced MUC5AC expression, whereas α-bungarotoxin (an α7-nicotinic acetylcholine receptor antagonist) only inhibited NNN- and NNK-induced MUC5AC expression. Conclusion These results suggested that NAT, NNN, NNAL, and NNK induce MUC5AC expression through β-adrenergic receptor and/or α7-nicotinic acetylcholine receptor in human airway epithelial cells, which may be involved in mucus hypersecretion in inflammatory airway diseases.

Objectives Endoplasmic reticulum (ER) stress is known to be associated with inflammatory airway diseases, and three major transmembrane receptors: double-stranded RNA-activated protein kinase-like ER kinase, inositol requiring enzyme 1, and activating transcription factor 6 (ATF6) play important roles in ER stress-related proinflammatory signaling. However, the effects of ER stress and these three major signaling pathways on the regulation of the production of airway mucins in human nasal airway epithelial cells have not been elucidated. Methods In primary human nasal epithelial cells, the effect of tunicamycin (an ER stress inducer) and 4-phenylbutyric acid (4-PBA, ER stress inhibitor) on the expression of MUC5AC and MUC5B was investigated by reverse transcriptasepolymerase chain reaction, real-time polymerase chain reaction, enzyme immunoassay, and immunoblot analysis. Small interfering RNA (siRNA) transfection was used to identify the mechanisms involved. Results Tunicamycin increased the expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules, including spliced X-box binding protein 1 (XBP-1), transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP), and ATF6. In addition, 4-PBA attenuated the tunicamycin-induced expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules. Furthermore, siRNA knockdowns of XBP-1, CHOP, and ATF6 blocked the tunicamycin-induced mRNA expressions and glycoprotein productions of MUC5AC and MUC5B. Conclusion. These results demonstrate that ER stress plays an important role in the regulation of MUC5AC and MUC5B via the activations of XBP-1, CHOP, and ATF6 in human nasal airway epithelial cells.

Objectives Clusterin (CLU) is known as apolipoprotein J, and has three isoforms with different biological functions. CLU is associated with various diseases such as Alzheimer disease, atherosclerosis, and some malignancies. Recent studies report an association of CLU with inflammation and immune response in inflammatory airway diseases. However, the effect of CLU on mucin secretion of airway epithelial cells has not yet been understood. Therefore, the effect and brief signaling pathway of CLU on MUC5AC (as a major secreted mucin) expression were investigated in human airway epithelial cells. Methods In the tissues of nasal polyp and normal inferior turbinate, the presence of MUC5AC and CLU was investigated using immunohistochemical stain and Western blot analysis. In mucin-producing human NCI-H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the effect and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway of CLU on MUC5AC expression were investigated using immunohistochemical stain, reverse transcription-polymerase chain reaction, real-time polymerase chain reaction, enzyme immunoassay, and Western blot analysis. Results In the nasal polyps, MUC5AC and CLU were abundantly present in the epithelium on immunohistochemical stain, and nuclear CLU (nCLU) was strongly detected on Western blot analysis. In human NCI-H292 airway epithelial cells or the primary cultures of normal nasal epithelial cells, recombinant nCLU increased MUC5AC expression, and significantly activated phosphorylation of NF-κB. And BAY 11-7085 (a specific NF-κB inhibitor) and knockdown of NF-κB by NF-κB siRNA (small interfering RNA) significantly attenuated recombinant nCLU-induced MUC5AC expression. Conclusion These results suggest that nCLU induces MUC5AC expression via the activation of NF-κB signaling pathway in human airway epithelial cells.

Objectives Excessive production of mucus results in plugging of the airway tract, which can increase morbidity and mortality in affected patients. In patients with diabetes, inflammatory airway disease appears with more frequent relapse and longer duration of symptoms. However, the effects of high glucose (HG) on the secretion of mucin in inflammatory respiratory diseases are not clear. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of HG on MUC5B expression in human airway epithelial cells. Methods The effect and signaling pathway of HG on MUC5B expression were investigated using reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay, and immunoblot analysis with specific inhibitors and small interfering RNA. Results HG increased MUC5B expression and epidermal growth factor receptor (EGFR) expression, and activated the phosphorylation of EGFR and p38 mitogen-activated protein kinase (MAPK). Pretreatment with EGFR inhibitor significantly attenuated the HG-induced phosphorylation of p38 MAPK, and pretreatments with p38 inhibitor or EGFR inhibitor significantly attenuated HG-induced MUC5B expression. In addition, knockdown of p38 MAPK by p38 MAPK siRNA significantly blocked HG-induced MUC5B expression. Conclusion These findings suggest that HG induces MUC5B expression via the sequential activations of the EGFR/p38 MAPK signaling pathway in human airway epithelial cells.

ObjectivesDelphinidin is one of the anthocyanidins. It is believed to have anti-inflammatory property including antioxidant, antiangiogenic, and anti-cancer properties. However, the anti-inflammatory effect of delphinidin in mucin-producing human airway epithelial cells has not been determined. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of delphinidin in lipopolysaccharide (LPS)-induced MUC8 and MUC5B expression in human airway epithelial cells.MethodsIn mucin-producing human NCI-H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay were used for investigating the expressions of MUC8, MUC5, and Toll-like receptor 4 (TLR4), after LPS treatment and delphinidin treatment. And the signaling pathway of delphinidin on LPS-induced MUC8 and MUC5B expression was investigated using the RT-PCR, and immunoblot analysis. To confirm the involvement of TLR4 in LPS-induced MUC8 and MU5B expression, the cells were transfected with TLR4 siRNA.ResultsIn NCI-H292 airway epithelial cells, LPS (100 ng/mL) significantly induced TLR4, MUC8, and MUC5B expression. TLR4 siRNA significantly blocked LPS-induced MUC8 and MUC5B mRNA expression. LPS (100 ng/mL) significantly activated the phosphorylation of extracellular signal related kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK). Delphinidin (50 and 100 µM) inhibited LPS-induced TLR4, MUC8, and MUC5B expression and LPS-induced phosphorylation of ERK1/2 and p38 MAPK. In the primary cultures of normal nasal epithelial cells, delphinidin (50 and 100 µM) significantly inhibited LPS-induced TLR4, MUC8, and MUC5B gene expression.ConclusionThese results suggest that delphinidin attenuates LPS-induced MUC8 and MUC5B expression through the TLR4-mediated ERK1/2 and p38 MAPK signaling pathway in human airway epithelial cells. These findings indicated that delphinidin may be a therapeutic agent for control of inflammatory airway diseases.

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.

ObjectivesPhorbol 12-myristate 13-acetate (PMA) is widely used as a protein kinase C (PKC) activator, PKC is involved in the secretion of mucins. MUC16, one of the membrane-bound mucins, is produced in human airway epithelial cells. However, the effect and signaling pathway of PMA on MUC16 expression in human airway epithelial cells has not been reported. Therefore, the effect and brief signaling pathway of PMA on MUC16 expression were investigated in human airway epithelial cells in this study.MethodsIn the mucin-producing human NCI-H292 airway epithelial cells and the primary cultures of normal nasal epithelial cells, the effect and signaling pathway of PMA on MUC16 expression were investigated using reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay, and immunoblot analysis with several specific inhibitors and small interfering RNA (siRNA) for p38 mitogen-activated protein kinase (MAPK).ResultsPMA increased MUC16 expression, and activated phosphorylation of p38 MAPK. However, it did not activate phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). SB203580 (p38 MAPK inhibitor) inhibited PMA-induced MUC16 expression, while U0126 (ERK1/2 inhibitor) did not. In addition, the knockdown of p38 MAPK by p38 MAPK siRNA significantly blocked PMA-induced MUC16 mRNA expression. Rottlerin (PKCδ inhibitor) inhibited PMA-induced MUC16 expression, and also inhibited the phosphorylation of activated p38 MAPK by PMA.ConclusionThese results show for the first time that PMA-induced MUC16 expression is regulated by activation of the PKCδ and p38 MAPK signaling pathway in human airway epithelial cells.

ObjectivesDoxycycline is commonly used in medicine for its bacteriostatic antimicrobial properties. Recent studies have reported that doxycycline also has anti-inflammatory effects. Matrix metalloproteinase (MMP)-9 has been found to be involved in the physiological and pathological process of inflammatory airway disease. Phorbol 12-myristate 13-acetate (PMA), a protein kinase C activator, is known to stimulate the expression of MMP and mucin genes in the airway and intestinal epithelial cells. Therefore, the effects and signal pathways of doxycycline on PMA-induced MUC5B expression dependent MMP-9 in human airway epithelial cells were investigated.MethodsIn human NCI-H292 airway epithelial cells, MUC5B and MMP-9 mRNA expression, MUC5B protein expression, and MMP-9 protein activity after the treatment with PMA, MMP-9 or doxycycline were determined by reverse transcriptase-polymerase chain reaction, enzyme immunoassay, gelatin zymography, and Western blot analysis.ResultsPMA increased MMP-9 and MUC5B expression. MMP-9 increased MUC5B expression. Doxycycline inhibited PMA-induced MUC5B expression, and PMA-induced MMP-9 mRNA expression and protein activity. Doxycycline inhibited phosphorylation of p38 induced by PMA and MMP-9.ConclusionThe results of this study suggest that doxycycline inhibited PMA-induced MUC5B mRNA expression and protein production through the MMP-9 and p38 pathways in human NCI-H292 airway epithelial cells.

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.

Background Among a variety of inflammatory mediators, visfatin is a proinflammatory adipocytokine associated with inflammatory reactions in obesity, metabolic syndrome, chronic inflammatory disease, and autoimmune disease. However, the biological role of visfatin in secretion of major mucins in human airway epithelial cells has not been reported. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of visfatin on MUC8 and MUC5B expression in human airway epithelial cells. Results Visfatin significantly induced MUC8 and MUC5B expression. Visfatin significantly activated phosphorylation of p38 MAPK. Treatment with SB203580 (p38 MAPK inhibitor) and knockdown of p38 MAPK by siRNA significantly blocked visfatin-induced MUC8 and MUC5B expression.Visfatin significantly increased ROS formation. Treatment with SB203580 significantly attenuated visfatin-induced ROS formation. Treatment with NAC (ROS scavenger) and DPI (NADPH oxidase inhibitor) significantly attenuated visfatininduced MUC8 and MUC5B expression. However, treatment with NAC and DPI did not attenuate visfatin-activated phosphorylation of p38 MAPK. Visfatin significantly activated the phosphorylation of NF-κB. Treatment with PDTC (NF-κB inhibitor) significantly attenuated visfatin-induced MUC8 and MUC5B expression. Conclusions These results suggest that visfatin induces MUC8 and MUC5B expression through p38 MAPK/ROS/NF-κB signaling pathway in human airway epithelial cells. [ABSTRACT FROM AUTHOR]

Objective: To acquire basic information concerning the function of the membrane-bound mucin MUC16 in nasal mucosa compared with the best-characterized membrane- bound mucin, MUC4. Design: In vitro study using semiquantatitive reverse transcription-polymerase chain reaction analysis and immunoassay. Setting: Yeungnam University College of Medicine. Subjects: We examined the nasal polyps obtained during endoscopic sinus surgery in 10 patients, the normal ethmoid sinus mucosa obtained from 10 patients, and human nasal polyp epithelial (HNPE) cells. Main Outcome Measures: Gene expression of MUC4 and MUC16 in nasal polyps and normal nasal mucosa. In addition, we evaluated the effect of 4 physiologically relevant agents, including retinoic acid, interleukin 1β, phorbol 12-myristate 13-acetate (PMA), and dexamethasone, on the expression of MUC4 and MUC16 in HNPE cells at the gene and protein levels. Results: In nasal polyps, MUC4 was upregulated compared with normal nasal mucosa (P=.009), whereas MUC16 expression did not differ between nasal polyps and normal nasal mucosa. Retinoic acid and interleukin 1β increased MUC4 expression at the gene and protein level in HNPE cells, whereas MUC16 expression was not affected. Unlike retinoic acid and interleukin 1β, PMA and dexamethasone increasedMUC16expression, whereas they had no significant effect on MUC4 expression. Conclusions: Expression of MUC4 and MUC16 are regulated differently in nasal mucosa. Dexamethasone and PMA are potent mediators for the expression of MUC16 in nasal polyps. [ABSTRACT FROM AUTHOR]

Objectives/Hypothesis: Leptin is a pleiotropic hormone that regulates food intake and metabolic and endocrine functions. Serum leptin levels have been reported to be increased in patients with allergic rhinitis and nasal polyposis; however, the explanation for this is unclear. We aimed to demonstrate the differential expression of leptin receptors in normal human nasal mucosa and nasal polyps, and to elucidate the effects of leptin on mucin gene expression in human nasal polyp epithelial cells. Study Design: Case-control and in vitro study. Methods: Normal ethmoid sinus mucosa was obtained from 10 subjects and used as a control; nasal polyps were obtained from 10 patients. Leptin receptor expression was analyzed using reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot analysis. Leptin-induced expression of major respiratory mucins (MUC5AC and MUC5B) in the human nasal polyp epithelial cells was determined using RT-PCR and enzyme-linked immunosorbent assay. Results: The leptin receptor expression was stronger in the nasal polyps than in the normal nasal mucosa. In human nasal polyp epithelial cells, leptin increased the expression of MUC5AC and MUC5B, in a dose- and time-dependent manner, at the gene and protein levels. Leptin-induced mucin expression was inhibited by the leptin receptor antagonist. Conclusions: The increased expression of leptin receptors in nasal polyps implies leptin has a certain role in nasal polyposis. In addition, leptin appears to induce the expression of MUC5AC and MUC5B through leptin receptors in the human nasal polyp epithelial cells. Laryngoscope, 2010 [ABSTRACT FROM AUTHOR]

Background: Glutaredoxins (GRX)-1 is glutathione-dependent oxidoreductase. However, the role of these enzymes remains unknown in airway inflammatory diseases. Therefore, we aimed to establish the expression pattern of GRX-1 in the nasal polyps (NPs) and to assess the regulatory mechanisms associated with GRX-1 expression in interleukin (IL)-1beta-treated airway epithelial cells. Methods: The expression of GRX-1 in NPs and normal nasal mucosa were analyzed by reverse-transcription polymerase chain reaction and immunohistochemical staining. IL-1beta-induced reactive oxygen species (ROS) formation and GRX-1 expression in the airway epithelial cells was determined by flow cytometry and immunoassay. Results: The expression level of GRX-1 in NPs was significantly higher than in the normal nasal mucosa (p < 0.05). GRX-1 was highly expressed in the surface epithelial cells and the submucosal glandular cells in the NPs. IL-1beta increased the intracellular ROS formation and GRX-1 expression in airway epithelial cells. The inhibition of IL-1beta-induced ROS production by N-acetyl-cystein, an ROS scavenger, reduced GRX-1 expression. Diphenyleneiodonium and apocynin, NADPH oxidase inhibitors, did not abolish IL-1beta-induced ROS formation and GRX-1 expression, whereas budesonide attenuated it. Conclusion: High GRX-1 expression in NPs might be a primary defense against chronic inflammatory oxidative stress in nasal mucosa. IL-1beta-induced up-regulation of GRX-1 in airway epithelial cells is probably mediated by ROS. Glucocorticoids can regulate IL-1beta-induced ROS formation and GRX-1 expression. [ABSTRACT FROM AUTHOR]

Objective: To investigate the expression and localization of neutrophil gelatinase--associated lipocalin (NGAL), an antimicrobial peptide, in the normal nasal mucosa and human nasal polyps. Neutrophil gelatinase--associated lipocalin has been identified as a key element in the innate host defense system. However, scant knowledge exists about the expression of NGAL in the human sinonasal tract. Design: Prospective study. Setting: Academic medical center. Patients: Normal inferior turbinate mucosa was obtained from 10 patients who were undergoing augmentation rhinoplasty. The nasal polyps were obtained from 10 patients who were undergoing endoscopic sinus surgery for chronic rhinosinusitis with polyps. Interventions: We performed semiquantitative reverse transcription--polymerase chain reaction, immunohistochemical staining, and Western blot analysis. Main Outcome Measures: We analyzed the expression of the NGAL messenger RNA (mRNA) and localization of the NGAL protein. Results: The NGAL mRNA and NGAL protein were highly expressed in the nasal polyps. The ratio of NGAL mRNA to glyceraldehyde-3-phosphate dehydrogenase mRNA in the nasal polyps was greater compared with that in the normal turbinate mucosa (P=.002). The NGAL protein was observed in the epithelium, the infiltrating inflammatory cells, and the submucosal gland of the nasal polyps, but it was very rarely detected in the normal nasal mucosa. Conclusion: Expression of NGAL is upregulated in nasal polyps, and additional work is needed to reveal the possible role of NGAL in the defense systems of the nasal mucosa and the process of polyp formation. [ABSTRACT FROM AUTHOR]

The article describes the case of a 64-year-old male patient who was diagnosed with basal cell adenoma (BCA) in the inferior turbinate of the left nasal cavity. It notes that the tumor of the patient was mistaken for a hemangioma preoperatively owing to his symptoms and the findings on the magnetic resonance imaging (MRI). It cites that the complete surgical excision of the mass with surrounding normal tissue is considered as the optimal treatment for BCA of the nasal cavity to prevent postoperative recurrence.

Introduction: Eotaxin-2 and -3 of the C-C chemokine subfamily function as potent chemoattractant factors for eosinophil recruitment and various immune responses in allergic and inflammatory airway diseases. Mucin 5AC (MUC5AC), a major gel-forming secretory mucin, is overexpressed in airway inflammation. However, the association between mucin secretion and eotaxin-2/3 expression in the upper and lower airway epithelial cells has not been fully elucidated. Therefore, in this study, we investigated the effects of eotaxin-2/3 on MUC5AC expression and its potential signaling mediators. Methods: We analyzed the effects of eotaxin-2 and -3 on NCI-H292 human airway epithelial cells and primary human nasal epithelial cells (HNEpCs) via reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, and western blotting. Along with immunoblot analyses with specific inhibitors and small interfering RNA (siRNA), we explored the signaling pathway involved in MUC5AC expression following eotaxin-2/3 treatment. Results: In HCI-H292 cells, eotaxin-2/3 activated the mRNA expression and protein production of MUC5AC. A specific inhibitor of C-C motif chemokine receptor 3 (CCR3), SB328437, suppressed eotaxin-2/3-induced MUC5AC expression at both the mRNA and protein levels. Eotaxin-2/3 induced the phosphorylation of extracellular signal-regulated kinase (ERK)-1/2 and p38, whereas pretreatment with a CCR3 inhibitor significantly attenuated this effect. Induction of MUC5AC expression with eotaxin-2/3 was decreased by U0126 and SB203580, specific inhibitors of ERK1/2 and p38 mitogen-activated protein kinase (MAPK), respectively. In addition, cell transfection with ERK1/2 and p38 siRNAs inhibited eotaxin-2/3-induced MUC5AC expression. Moreover, specific inhibitors (SB328437, U0126, and SB203580) attenuated eotaxin-2/3-induced MUC5AC expression in HNEpCs. Conclusion: Our results imply that CCR3-mediated ERK1/2 and p38 MAPK are involved in the signal transduction of eotaxin-2/3-induced MUC5AC overexpression. [ABSTRACT FROM AUTHOR]

Background: Diced cartilage glue (DG) grafts have been widely used in dorsal augmentation but can induce dorsal irregularities. The authors evaluated the postoperative feasibility of a crushed septal cartilage-covered diced cartilage glue (CCDG) graft. Methods: The medical records of 38 patients who underwent dorsal augmentation rhinoplasty with an open approach were retrospectively reviewed. DG graft was used in 18 patients (47.4%), and CCDG graft was used in 20 patients (52.6%). Surgical outcomes were assessed by comparing anthropometric data on facial photographs and satisfaction questionnaires on aesthetic outcomes and palpable irregularities on nasal dorsum before and after surgery. Results: Both groups showed successful aesthetic outcomes. Dorsal height, radix height, and tip projection were all increased postoperatively in both groups. Tip rotation did not significantly increase (p > 0.05). Both groups showed similar outcomes in terms of aesthetic satisfaction but a significant difference in palpable irregularity. CCDG graft group showed significantly better (p = 0.04) satisfaction with dorsal irregularities (4.15 ± 0.75) than the DG graft group (3.56 ± 0.92). CCDG graft group also showed significantly better mean values (p = 0.048) in the degree of irregularity by two surgeons (3.85 ± 0.65) than the DG graft group (3.25 ± 0.97). No patient had significant complaints about irregular dorsum, and none of them underwent a revision rhinoplasty. Conclusion: CCDG graft can be a complementary option for avoiding postoperative irregular dorsum complications. Level of evidence IV: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266. [ABSTRACT FROM AUTHOR]

Background. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a novel infectious respiratory disease called COVID-19, which is threatening public health worldwide. SARS-CoV-2 spike proteins connect to the angiotensin converting enzyme 2 (ACE2) receptor through the receptor binding domain and are then activated by the transmembrane protease serine subtype 2 (TMPRSS2). The ACE2 receptor is highly expressed in human nasal epithelial cells. Nasal ciliated cells are primary targets for SARS-CoV-2 replication. However, the effect of SARS-CoV-2 on the upper respiratory tract remains unknown, thus leading to the purpose of our study. We investigate the effects of SARS-CoV-2 on cytokines and mucin expression in human nasal epithelial cells. Methods. We investigated the effects of the SARS-CoV-2 spike protein receptor binding domain (RBD) on cytokines (IL-1β, IL-6, and IL-8) and MUC5AC/5B expression via real-time PCR, ELISA, periodic acid-Schiff (PAS) staining, and immunofluorescence staining in cultured human nasal epithelial cells. Results. The mRNA expression and protein production of cytokines (IL-1β, IL-6, and IL-8) and MUC5AC/5B were increased by SARS-CoV-2 spike protein RBD. ACE2 receptor inhibitor suppressed the expression of cytokines (IL-1β, IL-6, and IL-8) and MUC5AC/5B induced by SARS-CoV-2 spike protein RBD. Conclusions. SARS-CoV-2 induced cytokines (IL-1β, IL-6, and IL-8) and MUC5AC/5B expression through the ACE 2 receptor in human nasal epithelial cells. Therefore, ACE2 receptor inhibitors can be an effective therapeutic option for SARS-CoV-2 infection. [ABSTRACT FROM AUTHOR]

Brain arteriovenous malformations are type of intracranial high-flow vascular malformation that can present with incidental finding in asymptomatic patients, seizures, headache, ischemic events due to vascular steal from normal brain, hemorrhage. Pulsatile tinnitus is the result of blood flow related sounds transmitted to the inner ear and coincides with heartbeat. AVMs are a rare cause of pulsatile tinnitus which contributes to less than 1% of published cases in the literature. We report a case of morbid tinnitus due to brain AVM which was resolved completely by endovascular embolization of the lesion. [ABSTRACT FROM AUTHOR]

Clinical data provided by the patient are not always reliable or could be difficult to collect. In this case, a difficult history collection resulted in a diagnostic delay. Major complications were avoided performing an urgent surgical intervention. [ABSTRACT FROM AUTHOR]

Background: Glyoxal (GO), and methylglyoxal (MGO) are among the most toxic compounds emitted by electronic cigarette (E-cig) and regular tobacco cigarette smoke. Airway diseases presented mucus over production as their major pathophysiologic feature. However, the effects of GO and MGO on pro-inflammatory cytokines and mucin expression in human nasal epithelial cells, as well as the underlying signaling pathway, have not yet been studied. Objective: This study is to determine whether GO and MGO induce pro-inflammatory cytokines, and MUC5AC/5B expression via mitogen-activated protein kinase (MAPK)s and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways. Methods: The effect of GO, and MGO on pro-inflammatory cytokines, mucins expression and the signalling pathway of GO and MGO were investigated using water-soluble tetrazolium salt-1, enzyme immunoassays, and immunoblot analysis with specific inhibitors and small interfering RNA. Results: GO and MGO did not affect cell viability up to 2 mM in human nasal epithelial cells. GO and MGO increased production of pro-inflammatory such as interleukin (IL)-1β and IL-6) and MUC5AC/5B. Additionally, GO and MGO significantly activated extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAPK, and NF-κB. Whether ERK1/2, p38 MAPK, and NF-κB signaling pathway were involved in GO and MGO-induced production of pro-inflammatory cytokines (IL-1β and IL-6) and MUC5AC/5B, we used specific inhibitors and siRNA transfection. These significantly repressed GO- and MGO-induced expression of pro-inflammatory cytokines (IL-1β and IL-6) and MUC5AC/5B. Conclusions: GO and MGO induced pro-inflammatory cytokines and MUC5AC/5B expression via ERK1/2, p38 MAPK, and NF-κB in human nasal epithelial cells. These results suggested that GO and MGO may be involved in mucus hypersecretion-related airway diseases. [ABSTRACT FROM AUTHOR]

The article describes the case of primary small cell neuroendocrine carcinoma in the sublingual gland of a 94-year-old female patient. The patient was presented with slow-growing mass on the mouth floor mass. She was also diagnosed with colorectal adenocarcinoma after undergoing laparoscopic right hemicolectomy. The patient opted to refuse adjuvant radiation therapy due to old age and her general condition.

An introduction is presented in which the editor discusses articles in the issue on topics including methods for the analysis of transcriptome dynamics; toxicity of combined exposure of zinc oxide nanoparticles; and toxicity effects of bisphenol S exposure to Caenorhabditis elegans.

Mucus plays an important role in protecting the respiratory tract from irritants. However, mucus hypersecretion is a major indicator of airway diseases. 1,2-Benzisothiazolin-3-one (BIT), as a microbicide, induces asthmatic inflammation. Therefore, we focused on the effects of BIT-related mucin secretion in airway epithelial cells. Our in vivo study showed increased mucus and MUC5AC expressions in the bronchioles of mice that inhaled BIT. For investigating the signaling pathways, we performed experiments in human airway epithelial cells. BIT induced the MUC5AC expression and significantly increased the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), p38, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). The specific inhibitors of ERK1/2, p38, and NF-κB blocked the BIT-induced MUC5AC expression. Therefore, these results suggest that BIT induces the MUC5AC expression via the ERK1/2, p38, and NF-κB pathways in human airway epithelial cells, which may be involved in mucus hypersecretion associated with airway inflammatory diseases. [ABSTRACT FROM AUTHOR]

The article describes the case of a 50-year-old man who presented with a neck injury caused by a blade of a grass cutter that suddenly dislodged on impact and penetrated his neck. Topics covered include the findings of the soft tissue X-ray and computed tomography (CT) imaging to clarify the existence of a foreign body, the location of the foreign body as revealed by the CT image, and the neck exploration under general anesthesia that was conducted to safely remove the foreign body.

Background Insulin is involved in a glucose homeostatic regulation and a cellular metabolism via phosphorylation of phosphoinositide 3 kinase (PI3K) pathway and mitogen-activated protein kinase (MAPK) pathway. Hyperinsulinemia reduces insulin sensitivity and is an obvious potential factor affecting airway inflammation in chronic airway diseases. MUC5AC is a major secreted mucin, which plays a critical role in inflammatory response in the respiratory tract. However, the relationship between insulin and MUC5AC expression has not been studied. Objective This study investigated the effect and the brief signaling pathway of high concentration of insulin (HI) on MUC5AC expression in human airway epithelial cell. Methods In NCI-H292 cells and primary cultures of normal nasal epithelial cells, the effect and signaling pathway of HI on MUC5AC expression were investigated using reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay, and immunoblot analysis with several specific inhibitors and small interfering RNA (siRNA). Results HI significantly increased MUC5AC expression and activated PI3K/AKT, extracellular signal-related kinase 1/2 (ERK1/2) and p38 MAPKs. The specific PI3K and AKT inhibitor as well as knockdown of AKT1 and AKT2 by the respective siRNAs significantly blocked HI-mediated expression of MUC5AC. Meanwhile, the specific ERK1/2 MAPK and p38 MAPK inhibitor as well as knockdown of ERK1, ERK2, and p38 MAPK by the respective siRNAs also attenuated HI-induced expression of MUC5AC. Conclusion The results of this study suggest that HI induces MUC5AC expression via PI3K/AKT and MAPK signaling pathways in human airway epithelial cells. [ABSTRACT FROM AUTHOR]

Background: Mucin 5AC, oligomeric mucus/gel-forming (MUC5AC) expression is significantly increased in allergic and inflammatory airway diseases. Interleukin (IL) 36 gamma is predominantly expressed in airway epithelial cells and plays an important role in innate and adaptive immune responses. IL-36 gamma is induced by many inflammatory mediators, including cytokines and bacterial and viral infections. However, the association between IL-36 gamma and mucin secretion in human airway epithelial cells has not yet been fully investigated. Objective: The objective of this study was to determine whether IL-36 gamma might play a role in the regulation of mucin secretion in airway epithelial cells. We investigated the effect and brief signaling pathway of IL-36 gamma on MUC5AC expression in human airway epithelial cells. Methods: Enzyme immunoassay, immunoblot analysis, immunofluorescence staining, reverse transcriptase–polymerase chain reaction (PCR), and real-time PCR were performed in mucin-producing human airway epithelial NCI-H292 cells and in human nasal epithelial cells after pretreatment with IL-36 gamma, several specific inhibitors, or small interfering RNAs (siRNA). Results: IL-36 gamma induced MUC5AC expression and activated the phosphorylation of extracellular signal regulated kinase (ERK) 1 and 2, p38, and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF–kappa B). IL-36 receptor antagonist significantly attenuated these effects. The specific inhibitor and siRNA of ERK1, ERK2, p38, and NF–kappa B significantly attenuated IL-36 gamma induced MUC5AC expression. Conclusion: These results indicated that IL-36 gamma induced MUC5AC expression via the IL-36 receptor–mediated ERK1/2 and p38/NF–kappa B pathway in human airway epithelial cells. [ABSTRACT FROM AUTHOR]

Objective:Titanium dioxide nanoparticles (TiO2NPs) are utilized with growing frequency for a wide variety of industrial applications. Recently, acute and chronic exposures to TiO2NPs have been found to induce inflammatory response in the human respiratory tract. However, the effect and mechanism underlying the induction of major airway mucins by TiO2NPs have not been elucidated. This study was conducted to characterize the effect of TiO2NPs, and the mechanism involved, on the expressions of airway mucins in human airway epithelial cells. Materials and methods:In NCI-H292 cells and primary cultures of normal nasal epithelial cells, the effects of TiO2NPs and signaling pathway for airway mucin genes were investigated by reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassays and immunoblot analysis using several specific inhibitors and small interfering RNAs (siRNAs). Results:TiO2NPs increased MUC5B expression and activated the phosphorylations of extracellular signal-related kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK). U0126 (an ERK1/2 MAPK inhibitor) and SB203580 (a p38 MAPK inhibitor) inhibited TiO2NPs-induced MUC5B expression. And knockdown of ERK1, ERK2 and p38 MAPK using siRNAs significantly blocked TiO2NPs-induced MUC5B mRNA expression. Furthermore, Toll-like receptor 4 (TLR4) mRNA expression was increased by TiO2NPs, and knockdown by TLR4 siRNA significantly attenuated TiO2NPs-induced MUC5B mRNA expression and the TiO2NPs-induced phosphorylations of ERK1/2 and p38 MAPK. Discussion and conclusions:These results demonstrate for the first time that TiO2NPs induce MUC5B expressionviaTLR4-dependent ERK1/2 and p38 MAPK signaling pathways in respiratory epithelium. [ABSTRACT FROM PUBLISHER]

ABSTRACT Background The Korean Society of Thyroid Head and Neck Surgery established a nationwide multicenter registry of anaplastic thyroid carcinoma (ATC) and evaluated the prognostic factors and treatment outcomes of ATC. Methods The present study enrolled 329 patients who were diagnosed with ATC between January 2000 and December 2012 at 19 medical centers in Korea. Survival outcomes were evaluated according to various clinical factors and treatments. Results Multivariate analysis identified age ≥70 years old, the presence of initial clinical symptoms, distant metastasis, and treatment modality as significant risk factors ( p <.05). The patients who underwent curative resection and adjuvant radiotherapy (RT) or concurrent chemoradiotherapy (CRT) showed the best survival on multivariate analysis ( p < 0.05). Conclusion Although ATC is a lethal neoplasm, long-term survival may be acquired in cases in which the aggressive management, including curative resection or RT/concurrent CRT, is possible for therapeutic intent. © 2016 Wiley Periodicals, Inc. Head Neck 39: 133-139, 2017 [ABSTRACT FROM AUTHOR]