Search

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]

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. [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]

Background and Objectives: Insulin is a peptide hormone that regulates the metabolism of carbohydrates and fats by promoting the absorption of glucose from the blood to skeletal muscles. Insulin has been reported to be closely related to cardiovascular, respiratory, and endocrine disease. However, the effect of insulin on production of major mucins in human airway epithelial cells has not been reported. Therefore, this study investigated the relationship between high levels of insulin and mucin in human airway epithelial cells. Materials and Methods: This study analyzed the effect of high level of insulin on MUC4, MUC5AC, and MUC5B expression using reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay in human airway epithelial cells. Results: In human NCI-H292 airway epithelial cells, high level of insulin significant increased MUC4, MUC5AC, and MUC5B mRNA expression and glycoprotein production. In the primary cultures of normal nasal epithelial cells, high level of insulin also increased MUC4, MUC5AC, and MUC5B expression. Conclusion: These results suggest that insulin plays a role in control of mucus hypersecretion in human airway epithelial cells. [ABSTRACT FROM AUTHOR]

Background: MUC5AC, a major secreted mucin, is increased in chronic inflammatory airway disease. Spleen tyrosine kinase (SYK) is a mediator, which acts as an important regulator of intracellular signal transduction in the inflammatory response. SYK was originally identified in hematopoietic cells, and its expression in some nonhematopoietic cells, including respiratory epithelial cells, was recently demonstrated. However, the effects of SYK on mucin secretion in human airway epithelial cells have not been studied. The objective of this study was to investigate the effect and brief signaling pathways of SYK on MUC5AC expression in human airway epithelial cells. Methods: In mucin-producing human NCI-H292 cells and primary cultures of human nasal epithelial cells, the effects and signaling pathways of SYK on MUC5AC expression were investigated by reverse transcriptase-polymerase chain reaction, real-time polymerase chain reaction, enzyme immunoassay, and immunoblot analysis with several specific inhibitors and small interfering RNA (siRNA). Results: SYK induced MUC5AC expression. SYK activated significant phosphorylation of extracellular signal-related kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) signaling pathways. SYK-induced MUC5AC expression was significantly attenuated by pretreatment with U0126 (ERK1/2 MAPK inhibitor) and SB203580 (p38 MAPK inhibitor). In addition, the knockdown of ERK2 and p38 MAPK by ERK2 and p38 MAPK siRNA significantly blocked SYK-induced MUC5AC expression. Conclusion: These results indicated that SYK increased MUC5AC expression via ERK2 and p38 MAPK signaling pathways in human airway epithelial cells. [ABSTRACT FROM AUTHOR]

The article presents abstracts of articles related to oral oncology including "The Impact of Primary Tumor and Node Characteristics on the Time to Radiotherapy," by Hugo Fontan Köhler and Luiz Paulo Kowalski, "Ewing's Sarcoma in Mandible," by Paulo C. Rozental Fernandes and colleagues, and "The Influence of Surgical Margins on Local Recurrence in T1/T2 OSCC," by Richard Shaw and Conor Barry.

Background: Asian sand dust (ASD) is a natural phenomenon and originates from the deserts of China and is known to contain various chemical and biomolecular components that enhance airway inflammation. The overproduction of airway mucins is an important pathologic finding in inflammatory airway diseases. However, the mechanism of ASD on mucin production of airway epithelial cells has not been elucidated. Objective: To investigate the effect and signaling pathway of ASD on mucin expressions in human airway epithelial cells. Methods: In the NCI-H292 cells and the primary cultures of human nasal epithelial cells, the effect and signaling pathway of ASD on MUC8 and MUC5B expressions 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: ASD increased MUC8 and MUC5B expressions and activated the phosphorylations of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK). U0126 (ERK1/2 MAPK inhibitor) and SB203580 (p38 MAPK inhibitor) inhibited ASD-induced MUC8 and MUC5B expressions. In addition, knockdowns of ERK2 and p38 MAPK by siRNA blocked ASD-induced MUC8 and MUC5B mRNA expressions. Toll-like receptor 4 (TLR4) mRNA expression was increased after treatment with ASD. Knockdown of TLR4 by siRNA blocked ASD-induced MUC8 and MUC5B mRNA expressions. Furthermore, the phosphorylations of ERK1/2 and p38 MAPK were blocked by knockdown of TLR4. Conclusions: These results show that ASD induces MUC8 and MUC5B expressions via TLR4-dependent ERK2 and p38 MAPK signaling pathway in human airway epithelial cells. [ABSTRACT FROM AUTHOR]

Objectives: Staphylococcus aureus enterotoxins are known to induce an inflammatory response of the airways, increase sensitization to inhaled allergens, and decrease T‐cell sensitivity to steroids. However, the effects of Staphylococcus enterotoxin A (SEA) on mucin secretion of airway epithelial cells have not yet been reported. Therefore, in this study, the effect and brief signaling pathway of SEA on MUC5B expression were investigated in human airway epithelial cells. Methods: In the mucin‐producing human NCI‐H292 airway epithelial cells and the primary cultures of normal nasal epithelial cells, the effect and signaling pathway of SEA on MUC5B 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: SEA increased MUC5B mRNA and protein expression. Toll‐like receptor 2 (TLR2) mRNA expression was significantly increased after treatment with SEA. Knockdown of TLR2 by siRNA significantly blocked SEA‐induced MUC5B mRNA expression. SEA significantly activated phosphorylation of extracellular signal‐regulated kinase 1/2 (ERK1/2) and p38 mitogen‐activated protein kinase (MAPK). U0126 (ERK1/2 MAPK inhibitor) and SB203580 (p38 MAPK inhibitor) significantly inhibited SEA‐induced MUC5B mRNA expression. In addition, knockdown of ERK1/2 and p38 MAPK by siRNA significantly blocked SEA‐induced MUC5B mRNA expression. Furthermore, the phosphorylation of ERK1/2 and p38 MAPK was significantly blocked by knockdown of TLR2 by siRNA. Conclusions: These results show for the first time that SEA induces MUC5B expression via TLR2, ERK1/2, and p38 MAPK signaling pathway in human airway epithelial cells. [ABSTRACT FROM AUTHOR]

Background: Staphylococcus aureus enterotoxins are known to induce an inflammatory response of the airways, increase sensitization to inhaled allergens, and decrease T-cell sensitivity to steroids. However, the effects of Staphylococcus enterotoxin A (SEA) on mucin secretion of airway epithelial cells still have not been reported. Therefore, in this study, the effect and brief signaling pathway of SEA on MUC5B expression were investigated in human airway epithelial cells. Methods: In the mucin-producing human NCI-H292 airway epithelial cells and the primary cultures of normal nasal epithelial cells, the effect and signaling pathway of SEA on MUC5B expression were investigated using reverse transcriptase-polymerase chain reaction (PCR), real-time PCR, enzyme immunoassay, and immunoblot analysis with several specific inhibitors and small interfering RNA (siRNA). Results: SEA increased MUC5B mRNA and protein expression. Toll-like receptor 2 (TLR2) mRNA expression was significantly increased after treatment with SEA. Knockdown of TLR2 by siRNA significantly blocked SEA-induced MUC5B mRNA expression. SEA significantly activated phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK). U0126 (ERK1/2 MAPK inhibitor) and SB203580 (p38 MAPK inhibitor) significantly inhibited SEA-induced MUC5B mRNA expression. In addition, knockdown of ERK1/2 and p38 MAPK by siRNA significantly blocked SEA-induced MUC5B mRNA expression. Furthermore, the phosphorylation of ERK1/2 and p38 MAPK was significantly blocked by knockdown of TLR2 by siRNA. Conclusion: These results show for the first time that SEA induces MUC5B expression via TLR2, ERK1/2, and p38 MAPK signaling pathway in human airway epithelial cells. [ABSTRACT FROM AUTHOR]

The article lists people who contributed to the reviewing of articles for the 2013 issue of the periodical "The Laryngoscope" including Mona Abaza, Jean Abitbol and Oliver Adunka.

Background: Chitin is an essential structural component of the wall of fungal cells and is present in the exoskeleton of arthropods. It has been generally assumed that mammals lack the ability to produce chitinase proteins, the enzymes responsible for chitin degradation. However, recent studies have indicated that mammals produce chitinases and chitinase-like proteins, and chitinase plays a potential role in human asthma and allergic inflammation. In this study, the effect and brief signaling pathway of chitinase on MUC5B expression were investigated in human airway epithelial cells. Methods: In the mucin-producing human NCI-H292 airway epithelial cells and the primary cultures of normal nasal epithelial cells, the effect and signaling pathway of chitinase on MUC5B expression were investigated using the 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: In the mucin-producing human NCI-H292 airway epithelial cells, chitinase increased MUC5B expression. Chitinase significantly activated the phosphorylation ofp38 mitogen-activated protein kinase (MAPK) but not the phosphorylation of extracellular signa-l-related kinase (ERK) 2/2. The SB203580 (p38 MAPK inhibitor) significantly attenuated chitinase-induced MUC5B mRNA expression, but U0126 (ERK1/2 inhibitor) did not. Knockdown of p38 MAPK by p38 MAPK siRNA significantly blocked chitinase-induced MUC5B expression. In the primary cultures of normal nasal epithelial cells, chitinase significantly increased MUC5B gene expression and this was significantly attenuated after pretreatment with SB203580. Conclusion: These results suggest that chitinase induces MUC5B expression by activation of the p38 MAPK signaling pathway in human airway epithelial cells. [ABSTRACT FROM AUTHOR]

Mucoepidermoid carcinoma (MEC) of the salivary glands are rarely found in childhood we report the case of a 6-year old boy presenting with 2-month history of a submandibular swelling. In oral examination, a non-tender, firm mass was detected in the submandibular region involving the left cheek and left angle of the mandible. It was firm in consistency with obvious areas of multiple nodularity along the inferior border of the mass. Clinically there were no palpable lymph nodes. Radiographs revealed a radiolucent lesion in the left body of the mandible. The tumor showed sheets and nests of predominantly epidermoid cells along with occasional large pale mucous-like cells and frosted-glass appearance infiltrating the fibro-connective tissue. The lesion was diagnosed as mucoepidermoid carcinoma, high grade type. [ABSTRACT FROM AUTHOR]

Leptin, an adipocyte-secreted hormone that regulates food intake and metabolic response, has been recently reported to increase in the serum during inflammatory airway disease associated with mucus-hypersecretion. We investigated the effects of leptin on mucin expression in human airway epithelial cells and the signaling pathways. The expression of the leptin receptor was evaluated in human nasal mucosa and NCI-H292 cells. Leptin-induced expression of major respiratory mucins in NCI-H292 cells was analyzed. Mutant leptin, which acts as a receptor antagonist, and specific inhibitors of extracellular signal-regulated kinase (ERK1/2), p38 and Janus kinase-2 (JAK2)/signal transducer and activator of transcription-3 (STAT3) were used. Leptin receptors were expressed in the nasal mucosa and NCI-H292 cells. Treatment with leptin significantly increased the expression of MUC5AC and MUC5B in NCI-H292 cells; these effects were blocked by mutant leptin. The cells activated by leptin showed increased ERK1/2, p38, and STAT3 phosphorylation. Leptin-induced MUC5B expression was blocked by the ERK1/2 and p38 pathway inhibitors, but not by the JAK2/STAT3 pathway inhibitor. Leptin might significantly contribute to the production of major gel-forming mucins by direct stimulation of airway epithelial cells and the activation of leptin receptors coupled with the activation of ERK1/2 or p38, but not the JAK2/STAT3 pathway. [ABSTRACT FROM AUTHOR]

The article presents a list of reviewers who reviewed articles for the 2009 issue of the journal which includes Mona Abaza, Utku Aydil, and Jiang Cao.

Conclusion. Neutrophil gelatinase-associated lipocalin (NGAL) and Ki-67 expression were up-regulated in cholesteatoma and the expression pattern of NGAL in the epithelial layer was inversely related to the expression of Ki-67. Therefore, NGAL may be related to dysregulated differentiation in the keratinocytes during the development of a cholesteatoma. Objectives. We investigated the differential expression and localization of NGAL in middle ear cholesteatoma and compared the results to normal external auditory canal (EAC) skin. We also compared the expression and localization of NGAL with the expression and localization of Ki-67 in middle ear cholesteatoma. Subjects and methods. Tissue samples from middle ear cholesteatomas and normal EAC skin were obtained from 20 patients undergoing middle ear surgery. NGAL mRNA expression was determined by the reverse transcriptase-polymerase chain reaction (RT-PCR). The expression of NGAL protein was analyzed by Western blot. NGAL and Ki-67 were localized by immunohistochemical staining. Results. A significantly greater expression of the NGAL mRNA was observed in cholesteatoma epithelium than in normal EAC skin (p < 0.05). NGAL was detected in the granular layer of cholesteatoma. However, NGAL was scarcely expressed in normal EAC skin. Ki-67 was detected predominantly in the basal and parabasal layers of cholesteatoma epithelium. [ABSTRACT FROM AUTHOR]

Objective: To report clinical characteristics and treatment outcomes of actinomycosis of the paranasal sinus. Study Design: Retrospective review. Subjects and Methods: The medical records of six patients with actinomycosis of the paranasal sinus between 1998 and 2006 were analyzed. Results: There were no immunocompromised patients and all lesions were unilateral. Only one patient had a history of an oroantral fistula due to facial trauma. On CT scan, all patients had unilateral opacification of the maxillary sinus with focal calcified densities. All cases underwent endoscopic sinus surgery followed by relatively short-term antibiotic administration, and there was no recurrence. Conclusions: Chronic unilateral maxillary sinusitis, a calcified density in the involved sinus on radiological studies, and unresponsiveness to antibiotics are characteristics of actinomycotic sinusitis. Surgical removal of the involved tissues and the restoration of sinus ventilation seem to be important factors for treating the disease. [Copyright &y& Elsevier]

Objective: Management of maxillary odontogenic cysts consists of transoral resection or curettage. Large lesions require extensive dissection, leading to perioperative morbidity and need for extensive reconstruction. 1) Describe the use of transnasal endoscopic marsupialization for the management of maxillary odontogenic cysts. 2) Understanding this approach can minimize morbidity with effective treatment. Method: Case series. Endoscopic sinus surgical techniques were used to treat large benign maxillary odontogenic cysts in five patients between June 2008 and October 2011. Results: Patients underwent endoscopic marsupialization after creation of a wide maxillary antrostomy. Molars associated with the cystic lesions were displaced into portions of the maxillary sinus in 2 cases. The molars were dissected and removed through the transnasal dissection in each of these cases. Histological and radiological findings were consistent with 1 odontogenic keratocyst, 3 dentigerous cysts, and 1 radicular cyst. The lesions were able to be marsupialized endoscopically with relief of the patient's initial symptoms and no recurrence. Follow‐up has shown an excellent functional outcome in all cases. Conclusion: Benign maxillary odontogenic cysts can be effectively treated using transnasal endoscopic approaches. The techniques are less invasive and can reduce morbidity compared to transoral techniques. [ABSTRACT FROM AUTHOR]

Objective: Tumor necrosis factor (TNF) is an important mediator of inflammation and is produced by macrophages in response to stimuli such as bacterial lipopolysaccharide (LPS) and viruses. This study examined the effects of a TNF‐α antagonist on the LPS‐induced inflammatory response in the nasal cavity and sinus of rats. Method: Experimental groups received an instillation of lipopolysaccharide (LPS) plus an intramuscular injection of amoxicillin/clavulanate (antibiotic group), an instillation of sTNFRI (sTNFRI group), an instillation of sTNFRI and an injection of amoxicillin/clavulanate (sTNFRI/antibiotic group), or no additional treatment (LPS group). Histopathological changes were determined using hematoxylin‐eosin and periodic acid‐Schiff (PAS) staining. Leakage of exudate was determined using fluorescence microscopy. Vascular permeability was measured using the Evans blue dye technique. Expression of MUC5AC was measured using reverse transcriptase PCR. Results: The sTNFRI, antibiotic, and sTNFRI/antibiotic groups had significantly less capillary permeability, mucosal edema, PAS staining, and expression of MUC5AC than the LPS group. There were no differences in capillary permeability, mucosal edema, PAS staining, and MUC5AC expression between the sTNFRI and sTNFRI/antibiotic groups. The antibiotic group had PAS staining similar to that of the sTNFRI and sTNFRI/antibiotic groups but had a greater increase in capillary permeability, mucosal edema, and MUC5AC expression. Conclusion: Intranasal administration of sTNFRI reduces inflammatory activity, including elevated microvascular permeability and tissue edema, and mucus hypersecretion, including production of mucosubstance and expression of MUC5AC, in LPS‐induced rhinosinusitis in rats. Results demonstrate that intranasal administration of sTNFRI reduces inflammatory activity and mucus hypersecretion in LPS‐induced rhinosinusitis in rats. [ABSTRACT FROM AUTHOR]