The Experts below are selected from a list of 27 Experts worldwide ranked by ideXlab platform

Michael M. Paparella - One of the best experts on this subject based on the ideXlab platform.

  • Expression of Mucins in Mucoid Otitis Media
    Journal of the Association for Research in Otolaryngology, 2003
    Co-Authors: Jizhen Lin, Yasuhiro Tsuboi, Hirokazu Kawano, Frank Rimell, George Liu, Katsuhiro Toyama, Michael M. Paparella
    Abstract:

    A hallmark of Mucoid Otitis Media (MOM, i.e., chronic Otitis Media with Mucoid effusion) is mucus accumulation in the middle ear cavity, a condition that impairs transduction of sounds in the ear and causes hearing loss. The mucin identities of mucus and the underlying mechanism for the production of mucins in MOM are poorly understood. In this study, we demonstrated that the MUC5B and MUC4 were major mucins in MOM that formed distinct treelike polymers (mucus strands). The MUC5B and MUC4 mRNAs in the middle ear mucosa with MOM were up regulated 5-fold and 6-fold, compared with the controls. This upregulation was accompanied by the extensive proliferation of the MUC5B- and MUC4-producing cells in the middle ear epithelium. Further study indicated that the mucin hyperproduction was significantly linked to CD4^+ and CD8^+ T cells and/or CD68^+ monocyte macrophages. It suggests that MUC5B and MUC4 expression may be regulated by the products of these cells.

  • induction of mucous cell metaplasia by tumor necrosis factor alpha in rat middle ear the pathological basis for mucin hyperproduction in Mucoid Otitis Media
    Annals of Otology Rhinology and Laryngology, 2002
    Co-Authors: Hirokazu Kawano, Atsushi Haruta, Yasuhiro Tsuboi, Patricia A. Schachern, Michael M. Paparella
    Abstract:

    : Mucoid Otitis Media (MOM), one of the leading causes of acquired hearing loss in children, is characterized by mucous cell hyperplasia in the middle ear cleft associated with mucin accumulation in the middle ear cavity. The factors that stimulate mucous cell metaplasia-hyperplasia and mucin hyperproduction are poorly understood. Recent studies demonstrated that tumor necrosis factor alpha (TNF-alpha), present in human middle ear effusion, stimulated mucin production in vitro and up-regulated mucin gene expression in vivo. These findings suggest that TNF-alpha is important in the development of mucous cell metaplasia-hyperplasia. This study demonstrated that inoculation of TNF-alpha into the middle ear cavity followed by eustachian tube obstruction stimulated mucous cell metaplasia-hyperplasia in the middle ear cleft, accompanied by abundant mucin or mucin-like glycoproteins in the middle ear effusion--a phenotype of MOM in humans. This finding suggests that TNF-alpha plays a key role in the pathogenesis of MOM through induction of mucous cell metaplasia-hyperplasia and mucin production.

  • tympanic membrane and middle ear pathologic correlates in Mucoid Otitis Media
    Otolaryngology-Head and Neck Surgery, 2000
    Co-Authors: Muhammet Tekin, Patricia A. Schachern, Michael M. Paparella, Cemil Mutlu, Vikram J Jaisinghani
    Abstract:

    Abstract Objective: The goal of this study was to correlate tympanic membrane (TM) and middle ear (ME) pathologies in Mucoid Otitis Media (MOM). Methods and Material: Forty ears with MOM and 56 control ears were retrospectively evaluated for TM and ME pathologies. Comparisons of TM thicknesses in MOM versus control ears were correlated with the Student t test; χ 2 analysis was used to correlate pathologic findings of the TM and ME. Results: Thicknesses in all quadrants except the umbo were increased in MOM because of infiltration of inflammatory cells and fibrosis. The most common ME pathologies were granulation tissue and fibrosis. Significant correlations included (1) TM retraction and ME granulation tissue and fibrosis and (2) pars flaccida, posterosuperior, and anteroinferior thickness and ME granulation tissue and fibrosis. Conclusion: TM changes are likely to occur in patients with Otitis Media with effusion (MOM), and their presence is a strong indication of underlying ME pathology. (Otolaryngol Head Neck Surg 2000;123:258–62.)

  • expression of glycoconjugates in human eustachian tubes with Otitis Media
    Laryngoscope, 1998
    Co-Authors: Michihiko Sone, Patricia A. Schachern, Michael M. Paparella, Noriko Morizono, Jizhen Lin
    Abstract:

    Objectives To characterize glycoconjugate expression in normal human eustachian tubes and study the alterations in glycoconjugate expression found in eustachian tubes with Otitis Media. Study design Using lectin histochemistry, alterations in glycoconjugates were studied in three normal temporal bones, in four temporal bones with Mucoid Otitis Media (MOM), and in five with serous Otitis Media (SOM). Methods Sections of previously processed temporal bones were decelloidinized, and then incubated with seven biotinylated lectins--WGA, SNA, MAA, BPA, PNA, UEA-1, and LcH--that reflect seven carbohydrate residues of glycoconjugates, respectively: GlcNAc/NeuNAc, NeuNAc alpha(2-6)GalNAc, NeuNAc alpha(2-3)GalNAc, Gal beta(1-3) GalNAc, L-fucose, and alpha-mannose residues. Control sections were incubated with inhibitory carbohydrates or without biotinylated lectins. Results In the normal temporal bones, five carbohydrate residues in goblet cells and cilia of the eustachian tube demonstrated moderate to strong activity--NeuNAc alpha(2-6)GalNAc, NeuNAc alpha(2-3)GalNAc, GalNAc, Gal beta(1-3)GalNAc, and L-fucose. Two residues demonstrated weak activity--GlcNAc/NeuNAc and alpha-mannose. Temporal bones with MOM revealed increases in sialic acid and alpha-mannose, and a decrease in L-fucose. Residues of carbohydrates in the cilia of bones with SOM were notably decreased, especially for GalNAc, Gal beta(1-3)GalNAc, and NeuNAc alpha(2-6)GalNAc. Conclusions Glycoconjugates in the normal human eustachian tube are rich in GalNAc, Gal beta(1-3)GalNAc, L-fucose, and NeuNAc alpha(2-3/2-6) GalNAc, but low in alpha-mannose and sialic acid. Eustachian tubes from cases with SOM or MOM demonstrated alterations in glycoconjugate expression in cilia and goblet cells, which may reflect disorder of the carbohydrate metabolism during Otitis Media, especially in SOM.

Jizhen Lin - One of the best experts on this subject based on the ideXlab platform.

  • Expression of Mucins in Mucoid Otitis Media
    Journal of the Association for Research in Otolaryngology, 2003
    Co-Authors: Jizhen Lin, Yasuhiro Tsuboi, Hirokazu Kawano, Frank Rimell, George Liu, Katsuhiro Toyama, Michael M. Paparella
    Abstract:

    A hallmark of Mucoid Otitis Media (MOM, i.e., chronic Otitis Media with Mucoid effusion) is mucus accumulation in the middle ear cavity, a condition that impairs transduction of sounds in the ear and causes hearing loss. The mucin identities of mucus and the underlying mechanism for the production of mucins in MOM are poorly understood. In this study, we demonstrated that the MUC5B and MUC4 were major mucins in MOM that formed distinct treelike polymers (mucus strands). The MUC5B and MUC4 mRNAs in the middle ear mucosa with MOM were up regulated 5-fold and 6-fold, compared with the controls. This upregulation was accompanied by the extensive proliferation of the MUC5B- and MUC4-producing cells in the middle ear epithelium. Further study indicated that the mucin hyperproduction was significantly linked to CD4^+ and CD8^+ T cells and/or CD68^+ monocyte macrophages. It suggests that MUC5B and MUC4 expression may be regulated by the products of these cells.

  • induction of mucin gene expression in middle ear of rats by tumor necrosis factor α potential cause for Mucoid Otitis Media
    The Journal of Infectious Diseases, 2000
    Co-Authors: Jizhen Lin, Atsushi Haruta, Hirokazu Kawano, S K Juhn, George L Adams, Youngki Kim
    Abstract:

    Mucoid Otitis Media (MOM) is characterized by viscous fluid, high in mucin concentration, which accumulates in the middle ear cavity. Recent studies suggest that initial infection in the middle ear cleft may be key to the development of MOM. However, factors of the initial infection attributed to the stimulation of mucin production are not clearly understood. This study demonstrated that tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine in Mucoid effusion, markedly increased Muc2 mucin mRNA expression in middle ear epithelium, in a time- and dose-dependent manner. Parallel to this was a marked increase in mucin glycoprotein in middle ear fluid. Also, TNF-alpha demonstrated an autocrine and/or paracrine effect on the expression of endogenous TNF-alpha gene in the middle ear, which may contribute to the production of mucin in this study. These findings suggest that TNF-alpha plays an important role in the development of MOM by stimulating mucin metabolism.

  • expression of glycoconjugates in human eustachian tubes with Otitis Media
    Laryngoscope, 1998
    Co-Authors: Michihiko Sone, Patricia A. Schachern, Michael M. Paparella, Noriko Morizono, Jizhen Lin
    Abstract:

    Objectives To characterize glycoconjugate expression in normal human eustachian tubes and study the alterations in glycoconjugate expression found in eustachian tubes with Otitis Media. Study design Using lectin histochemistry, alterations in glycoconjugates were studied in three normal temporal bones, in four temporal bones with Mucoid Otitis Media (MOM), and in five with serous Otitis Media (SOM). Methods Sections of previously processed temporal bones were decelloidinized, and then incubated with seven biotinylated lectins--WGA, SNA, MAA, BPA, PNA, UEA-1, and LcH--that reflect seven carbohydrate residues of glycoconjugates, respectively: GlcNAc/NeuNAc, NeuNAc alpha(2-6)GalNAc, NeuNAc alpha(2-3)GalNAc, Gal beta(1-3) GalNAc, L-fucose, and alpha-mannose residues. Control sections were incubated with inhibitory carbohydrates or without biotinylated lectins. Results In the normal temporal bones, five carbohydrate residues in goblet cells and cilia of the eustachian tube demonstrated moderate to strong activity--NeuNAc alpha(2-6)GalNAc, NeuNAc alpha(2-3)GalNAc, GalNAc, Gal beta(1-3)GalNAc, and L-fucose. Two residues demonstrated weak activity--GlcNAc/NeuNAc and alpha-mannose. Temporal bones with MOM revealed increases in sialic acid and alpha-mannose, and a decrease in L-fucose. Residues of carbohydrates in the cilia of bones with SOM were notably decreased, especially for GalNAc, Gal beta(1-3)GalNAc, and NeuNAc alpha(2-6)GalNAc. Conclusions Glycoconjugates in the normal human eustachian tube are rich in GalNAc, Gal beta(1-3)GalNAc, L-fucose, and NeuNAc alpha(2-3/2-6) GalNAc, but low in alpha-mannose and sialic acid. Eustachian tubes from cases with SOM or MOM demonstrated alterations in glycoconjugate expression in cilia and goblet cells, which may reflect disorder of the carbohydrate metabolism during Otitis Media, especially in SOM.

Youngki Kim - One of the best experts on this subject based on the ideXlab platform.

  • induction of mucin gene expression in middle ear of rats by tumor necrosis factor α potential cause for Mucoid Otitis Media
    The Journal of Infectious Diseases, 2000
    Co-Authors: Jizhen Lin, Atsushi Haruta, Hirokazu Kawano, S K Juhn, George L Adams, Youngki Kim
    Abstract:

    Mucoid Otitis Media (MOM) is characterized by viscous fluid, high in mucin concentration, which accumulates in the middle ear cavity. Recent studies suggest that initial infection in the middle ear cleft may be key to the development of MOM. However, factors of the initial infection attributed to the stimulation of mucin production are not clearly understood. This study demonstrated that tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine in Mucoid effusion, markedly increased Muc2 mucin mRNA expression in middle ear epithelium, in a time- and dose-dependent manner. Parallel to this was a marked increase in mucin glycoprotein in middle ear fluid. Also, TNF-alpha demonstrated an autocrine and/or paracrine effect on the expression of endogenous TNF-alpha gene in the middle ear, which may contribute to the production of mucin in this study. These findings suggest that TNF-alpha plays an important role in the development of MOM by stimulating mucin metabolism.

Hirokazu Kawano - One of the best experts on this subject based on the ideXlab platform.

  • Expression of Mucins in Mucoid Otitis Media
    Journal of the Association for Research in Otolaryngology, 2003
    Co-Authors: Jizhen Lin, Yasuhiro Tsuboi, Hirokazu Kawano, Frank Rimell, George Liu, Katsuhiro Toyama, Michael M. Paparella
    Abstract:

    A hallmark of Mucoid Otitis Media (MOM, i.e., chronic Otitis Media with Mucoid effusion) is mucus accumulation in the middle ear cavity, a condition that impairs transduction of sounds in the ear and causes hearing loss. The mucin identities of mucus and the underlying mechanism for the production of mucins in MOM are poorly understood. In this study, we demonstrated that the MUC5B and MUC4 were major mucins in MOM that formed distinct treelike polymers (mucus strands). The MUC5B and MUC4 mRNAs in the middle ear mucosa with MOM were up regulated 5-fold and 6-fold, compared with the controls. This upregulation was accompanied by the extensive proliferation of the MUC5B- and MUC4-producing cells in the middle ear epithelium. Further study indicated that the mucin hyperproduction was significantly linked to CD4^+ and CD8^+ T cells and/or CD68^+ monocyte macrophages. It suggests that MUC5B and MUC4 expression may be regulated by the products of these cells.

  • induction of mucous cell metaplasia by tumor necrosis factor alpha in rat middle ear the pathological basis for mucin hyperproduction in Mucoid Otitis Media
    Annals of Otology Rhinology and Laryngology, 2002
    Co-Authors: Hirokazu Kawano, Atsushi Haruta, Yasuhiro Tsuboi, Patricia A. Schachern, Michael M. Paparella
    Abstract:

    : Mucoid Otitis Media (MOM), one of the leading causes of acquired hearing loss in children, is characterized by mucous cell hyperplasia in the middle ear cleft associated with mucin accumulation in the middle ear cavity. The factors that stimulate mucous cell metaplasia-hyperplasia and mucin hyperproduction are poorly understood. Recent studies demonstrated that tumor necrosis factor alpha (TNF-alpha), present in human middle ear effusion, stimulated mucin production in vitro and up-regulated mucin gene expression in vivo. These findings suggest that TNF-alpha is important in the development of mucous cell metaplasia-hyperplasia. This study demonstrated that inoculation of TNF-alpha into the middle ear cavity followed by eustachian tube obstruction stimulated mucous cell metaplasia-hyperplasia in the middle ear cleft, accompanied by abundant mucin or mucin-like glycoproteins in the middle ear effusion--a phenotype of MOM in humans. This finding suggests that TNF-alpha plays a key role in the pathogenesis of MOM through induction of mucous cell metaplasia-hyperplasia and mucin production.

  • induction of mucin gene expression in middle ear of rats by tumor necrosis factor α potential cause for Mucoid Otitis Media
    The Journal of Infectious Diseases, 2000
    Co-Authors: Jizhen Lin, Atsushi Haruta, Hirokazu Kawano, S K Juhn, George L Adams, Youngki Kim
    Abstract:

    Mucoid Otitis Media (MOM) is characterized by viscous fluid, high in mucin concentration, which accumulates in the middle ear cavity. Recent studies suggest that initial infection in the middle ear cleft may be key to the development of MOM. However, factors of the initial infection attributed to the stimulation of mucin production are not clearly understood. This study demonstrated that tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine in Mucoid effusion, markedly increased Muc2 mucin mRNA expression in middle ear epithelium, in a time- and dose-dependent manner. Parallel to this was a marked increase in mucin glycoprotein in middle ear fluid. Also, TNF-alpha demonstrated an autocrine and/or paracrine effect on the expression of endogenous TNF-alpha gene in the middle ear, which may contribute to the production of mucin in this study. These findings suggest that TNF-alpha plays an important role in the development of MOM by stimulating mucin metabolism.

Patricia A. Schachern - One of the best experts on this subject based on the ideXlab platform.

  • induction of mucous cell metaplasia by tumor necrosis factor alpha in rat middle ear the pathological basis for mucin hyperproduction in Mucoid Otitis Media
    Annals of Otology Rhinology and Laryngology, 2002
    Co-Authors: Hirokazu Kawano, Atsushi Haruta, Yasuhiro Tsuboi, Patricia A. Schachern, Michael M. Paparella
    Abstract:

    : Mucoid Otitis Media (MOM), one of the leading causes of acquired hearing loss in children, is characterized by mucous cell hyperplasia in the middle ear cleft associated with mucin accumulation in the middle ear cavity. The factors that stimulate mucous cell metaplasia-hyperplasia and mucin hyperproduction are poorly understood. Recent studies demonstrated that tumor necrosis factor alpha (TNF-alpha), present in human middle ear effusion, stimulated mucin production in vitro and up-regulated mucin gene expression in vivo. These findings suggest that TNF-alpha is important in the development of mucous cell metaplasia-hyperplasia. This study demonstrated that inoculation of TNF-alpha into the middle ear cavity followed by eustachian tube obstruction stimulated mucous cell metaplasia-hyperplasia in the middle ear cleft, accompanied by abundant mucin or mucin-like glycoproteins in the middle ear effusion--a phenotype of MOM in humans. This finding suggests that TNF-alpha plays a key role in the pathogenesis of MOM through induction of mucous cell metaplasia-hyperplasia and mucin production.

  • tympanic membrane and middle ear pathologic correlates in Mucoid Otitis Media
    Otolaryngology-Head and Neck Surgery, 2000
    Co-Authors: Muhammet Tekin, Patricia A. Schachern, Michael M. Paparella, Cemil Mutlu, Vikram J Jaisinghani
    Abstract:

    Abstract Objective: The goal of this study was to correlate tympanic membrane (TM) and middle ear (ME) pathologies in Mucoid Otitis Media (MOM). Methods and Material: Forty ears with MOM and 56 control ears were retrospectively evaluated for TM and ME pathologies. Comparisons of TM thicknesses in MOM versus control ears were correlated with the Student t test; χ 2 analysis was used to correlate pathologic findings of the TM and ME. Results: Thicknesses in all quadrants except the umbo were increased in MOM because of infiltration of inflammatory cells and fibrosis. The most common ME pathologies were granulation tissue and fibrosis. Significant correlations included (1) TM retraction and ME granulation tissue and fibrosis and (2) pars flaccida, posterosuperior, and anteroinferior thickness and ME granulation tissue and fibrosis. Conclusion: TM changes are likely to occur in patients with Otitis Media with effusion (MOM), and their presence is a strong indication of underlying ME pathology. (Otolaryngol Head Neck Surg 2000;123:258–62.)

  • expression of glycoconjugates in human eustachian tubes with Otitis Media
    Laryngoscope, 1998
    Co-Authors: Michihiko Sone, Patricia A. Schachern, Michael M. Paparella, Noriko Morizono, Jizhen Lin
    Abstract:

    Objectives To characterize glycoconjugate expression in normal human eustachian tubes and study the alterations in glycoconjugate expression found in eustachian tubes with Otitis Media. Study design Using lectin histochemistry, alterations in glycoconjugates were studied in three normal temporal bones, in four temporal bones with Mucoid Otitis Media (MOM), and in five with serous Otitis Media (SOM). Methods Sections of previously processed temporal bones were decelloidinized, and then incubated with seven biotinylated lectins--WGA, SNA, MAA, BPA, PNA, UEA-1, and LcH--that reflect seven carbohydrate residues of glycoconjugates, respectively: GlcNAc/NeuNAc, NeuNAc alpha(2-6)GalNAc, NeuNAc alpha(2-3)GalNAc, Gal beta(1-3) GalNAc, L-fucose, and alpha-mannose residues. Control sections were incubated with inhibitory carbohydrates or without biotinylated lectins. Results In the normal temporal bones, five carbohydrate residues in goblet cells and cilia of the eustachian tube demonstrated moderate to strong activity--NeuNAc alpha(2-6)GalNAc, NeuNAc alpha(2-3)GalNAc, GalNAc, Gal beta(1-3)GalNAc, and L-fucose. Two residues demonstrated weak activity--GlcNAc/NeuNAc and alpha-mannose. Temporal bones with MOM revealed increases in sialic acid and alpha-mannose, and a decrease in L-fucose. Residues of carbohydrates in the cilia of bones with SOM were notably decreased, especially for GalNAc, Gal beta(1-3)GalNAc, and NeuNAc alpha(2-6)GalNAc. Conclusions Glycoconjugates in the normal human eustachian tube are rich in GalNAc, Gal beta(1-3)GalNAc, L-fucose, and NeuNAc alpha(2-3/2-6) GalNAc, but low in alpha-mannose and sialic acid. Eustachian tubes from cases with SOM or MOM demonstrated alterations in glycoconjugate expression in cilia and goblet cells, which may reflect disorder of the carbohydrate metabolism during Otitis Media, especially in SOM.