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Dive into the research topics where Joel M. Bernstein is active.

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Featured researches published by Joel M. Bernstein.


Acta Oto-laryngologica | 1993

Micro-ecology of the Nasopharyngeal Bacterial Flora in Otitis-prone and Non-otitis-prone Children

Joel M. Bernstein; Howard Faden; Diane Dryja; Jean Wactawski-Wende

The quantitative bacteriology of the adenoid was studied in otitis-prone and non-otitis-prone children. alpha-hemolytic Streptococci (Viridans Streptococci) appeared to be predominant normal flora in the healthy nasopharynx. There was a decrease in alpha-hemolytic Streptococci in the otitis-prone child compared to the non-otitis-prone child. Concomitantly, there appears to be an increase in both nontypable Haemophilus influenzae (NTHI) and S. pneumoniae in the nasopharyngeal flora in the otitis-prone child. The mechanisms responsible for this alteration of the micro-ecology of bacteria of the nasopharynx may be related, in part, to factors that alter mucociliary function. These factors could be viral infection, allergy, local and systemic immunological deficiency and the indiscriminate use of antibiotics. An understanding of the relationship between the normal flora and the potential pathogens may be important in the understanding of both the pathogenesis of otitis media (OM) and possibly the treatment of this disease entity.


Operations Research Letters | 1997

Antibodies against Inner-Ear Proteins in the Sera of Patients with Inner-Ear Diseases

Mikio Suzuki; Marc S. Krug; K.C Cheng; Yoshiro Yazawa; Joel M. Bernstein; T.J. Yoo

Sera from patients with various inner-ear diseases, especially Meniere’s disease, were investigated by Western blot against guinea pig inner-ear proteins. Of 45 patients, 24 (53%) with various inner-e


Laryngoscope | 2009

Genetic polymorphisms in chronic hyperplastic sinusitis with nasal polyposis.

Joel M. Bernstein; Jack B. Anon; Michael Rontal; Jeffrey Conroy; Chong Wang; Lara Sucheston

Although many proinflammatory cytokines have been identified in nasal polyp tissue, the initial trigger that causes this inflammation characterized by edema, lymphocytosis, and eosinophilia, is still unknown. The purpose of the present study is to identify the presence of genetic polymorphisms in proinflammatory, anti‐inflammatory, and chemokine genes that might contribute to genetic susceptibility to chronic hyperplastic sinusitis with nasal polyposis (CHSwNP).


International Journal of Pediatric Otorhinolaryngology | 1999

Waldeyer’s ring and otitis media: The nasopharyngeal tonsil and otitis media

Joel M. Bernstein

This overview of the relationship between the nasopharyngeal tonsil and otitis media will review three important concepts: (1) Adenoid inflammation leads to inflammatory obstruction of the Eustachian tube; (2) early colonization of the adenoid with the three major bacterial pathogens of otitis media is the most important factor in the early pathogenesis of otitis media; (3) the local immune system in the adenoid particularly specific secretory IgA directed against both viruses and bacterial pathogens are probably genetically controlled and represent the immunological factor in protecting the host against invasion of these agents in the Eustachian tube and middle ear. This overview of the relationship between the adenoid and the development of otitis media emphasizes that nasopharyngeal colonization with the three major middle ear pathogens is among the most important risk factors in the pathogenesis of otitis media. Inasmuch as these pathogens normally reside in the nasopharynges of most healthy children, the factors which trigger development of otitis media need to be carefully evaluated. Among these two triggers are viral infections and upper respiratory tract allergy.


Laryngoscope | 2011

Further observations on the role of Staphylococcus aureus exotoxins and IgE in the pathogenesis of nasal polyposis.

Joel M. Bernstein; Cheryl Allen; Gary Rich; Diane Dryja; Paul Bina; Raoul Reiser; Mark Ballow; Gregory E. Wilding

Recent studies have suggested that Staphylococcus aureus secrete exotoxins that may act as superantigens and upregulate the variable beta region of lymphocytes in chronic hyperplasticsinusitis with nasal polyposis (CHSwNP). The aim of this study was to add further information for correlating the presence of staphylococcal species and the upregulation of the Vβ region of both nasal polyp lymphocytes and peripheral blood lymphocytes. Furthermore, IgE‐mediated hypersensitivity directed against these exotoxins produces an additional independent immunologic mechanism in upregulating the inflammatory response in the lateral wall of the nose in nasal polyposis.


Archive | 2010

The Inflammatory Process in Nasal Polyposis: Genetics, Molecular Biology, and Electrophysiology

Joel M. Bernstein

Nasal polyposis is the ultimate manifestation of chronic inflammation in the lateral wall of the nose. At least two factors that may lead to the development of inflammation in the lateral wall of the nose are (1) genetic polymorphism of inflammatory genes, particular the A allele at position −308 in the promotor region of the TNF-α gene and (2) the production of exotoxins by Staphylococcus aureus and their ability to upregulate the variable β (Vβ) region of the TCR of lymphocytes. Cytokines in nasal polyps drive the inflammatory response. TNF-α can upregulate VCAM-1 (vascular cell adhesion molecule-1), which is a major counterreceptor for the integrins on the surface of both lymphocytes and eosinophils. TNF-α can also be released by eosinophils, resulting in an autocrine upregulation of eosinophils into the nasal polyp. Eosinophils release major basic protein, a granular protein that is capable of increasing net sodium flux across the apical surface of the nasal polyp epithelium, resulting in increased water absorption and the ultimate development of edema, a major histopathological feature of polyposis. The increased number of open sodium channels, known to exist in both CF epithelium and non-CF polyp epithelium, can be abrogated by the use of topical diuretics such as amiloride and furosemide.


International Congress Series | 2003

Antibodies against inner ear proteins in the sera of patients with inner ear diseases

Mikio Suzuki; Marc S. Krug; K.C Cheng; Yoshiro Yazawa; Joel M. Bernstein; S.S Kwon; Renzo Mora; T.J. Yoo

Sera from patients with various inner-ear diseases, especially Ménières disease, were investigated by Western blot against guinea pig inner-ear proteins. Of 45 patients, 24 (53%) with various inner-ear diseases had antibodies against inner-ear proteins, compared with 0 of 10 (0%) in control subjects without inner-ear diseases. Of the 10 proteins that showed a positive reaction with patient sera, the 28-kD band was unique in that it appeared only in the membranous fraction of the inner ear and was highly positive (28%) in reaction with Ménières disease patient sera. The results in the present study with proteins extracted from guinea pig inner ear were consistent with our previous study using proteins from human inner ear, suggesting that the 28-kD protein may be a candidate for detecting autoimmune inner-ear disease.


Laryngoscope | 1966

Metastatic tumors to the maxilla, nose, and paranasal sinuses.†

Joel M. Bernstein; William W. Montgomer; Károly Balogh


Otolaryngologic Clinics of North America | 2005

Update on the Molecular Biology of Nasal Polyposis

Joel M. Bernstein


Journal of Heterocyclic Chemistry | 1983

BIMANES. 19. CHARACTERISTICS OF THE MOLECULAR STRUCTURES OF 1,5-DIAZABICYCLO(3.3.0)OCTADIENEDIONES (9,10-DIOXABIMANES) DETERMINED BY X-RAY CRYSTALLOGRAPHY

Israel Goldberg; Joel M. Bernstein; Edward M. Kosower; Ehud Goldstein; Barak Pazhenchevsky

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Mikio Suzuki

Shiga University of Medical Science

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Yoshiro Yazawa

Shiga University of Medical Science

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K.C Cheng

University of Tennessee Health Science Center

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Marc S. Krug

University of Tennessee Health Science Center

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T.J. Yoo

University of Tennessee Health Science Center

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Barak Pazhenchevsky

State University of New York System

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Edward M. Kosower

State University of New York System

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