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  • 1
    In: Microbial Pathogenesis, Elsevier BV, Vol. 114 ( 2018-01), p. 409-413
    Type of Medium: Online Resource
    ISSN: 0882-4010
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 1471158-8
    SSG: 12
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  • 2
    In: The Laryngoscope, Wiley, Vol. 124, No. 3 ( 2014-03), p. 616-627
    Abstract: To systematically review the effectiveness and safety of subcutaneous immunotherapy (SCIT) for treatment of allergic rhinoconjunctivitis and asthma, using formulations currently approved in the United States. Study Design We searched the following databases up to May 21, 2012: MEDLINE, Embase, LILACS, and the Cochrane Central Register of Controlled Trials. Methods We included randomized controlled trials published in English comparing SCIT to placebo, pharmacotherapy, or other SCIT regimens that reported clinical outcomes of interest. Studies of adults or mixed age populations were included. Studies were excluded if the diagnosis of allergy and/or asthma was not confirmed with objective testing. Paired reviewers selected articles for inclusion and extracted data. We assessed the risk of bias for each study and graded the strength of evidence for each outcome as high, moderate, or low. Results Sixty‐one studies met our inclusion criteria. Majority of the studies (66%) evaluated single‐allergen immunotherapy regimens. The literature provides high‐grade evidence that SCIT reduces asthma symptoms, asthma medication usage, rhinitis/rhinoconjunctivitis symptoms, conjunctivitis symptoms, and rhinitis/rhinoconjunctivitis disease‐specific quality of life in comparison to placebo or usual care. There is moderate evidence that SCIT decreases rhinitis/rhinoconjunctivitis medication usage. Respiratory reactions were the most common systemic reaction. There were few reports of anaphylaxis; no deaths were reported. Conclusions Generally moderate to strong evidence supports the effectiveness of SCIT for treatment of allergic rhinitis and asthma, particularly with single‐allergen immunotherapy regimens. Adverse reactions to SCIT are common, but no deaths were reported in the included studies. Level of Evidence 1a. Laryngoscope , 124:616–627, 2014
    Type of Medium: Online Resource
    ISSN: 0023-852X , 1531-4995
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 2026089-1
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  • 3
    Online Resource
    Online Resource
    American Medical Association (AMA) ; 2007
    In:  Archives of Otolaryngology–Head & Neck Surgery Vol. 133, No. 7 ( 2007-07-01), p. 725-
    In: Archives of Otolaryngology–Head & Neck Surgery, American Medical Association (AMA), Vol. 133, No. 7 ( 2007-07-01), p. 725-
    Type of Medium: Online Resource
    ISSN: 0886-4470
    Language: English
    Publisher: American Medical Association (AMA)
    Publication Date: 2007
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  • 4
    In: Environmental Health, Springer Science and Business Media LLC, Vol. 22, No. 1 ( 2023-02-23)
    Abstract: Limited data exists suggesting that cumulative exposure to air pollution in the form of fine particulate matter (aerodynamic diameter ≤ 2.5 μm [PM 2.5 ]) may be associated with papillary thyroid carcinoma (PTC), although this relationship has not been widely established. This study aims to evaluate the association between PM 2.5 and PTC and determine the subgroups of patients who are at the highest risk of PTC diagnosis. Methods Under IRB approval, we conducted a case-control study of adult patients (age ≥ 18) newly diagnosed with PTC between 1/2013–12/2016 across a single health care system were identified using electronic medical records. These patients were compared to a control group of patients without any evidence of thyroid disease. Cumulative PM 2.5 exposure was calculated for each patient using a deep learning neural networks model, which incorporated meteorological and satellite-based measurements at the patients’ residential zip code. Adjusted multivariate logistic regression was used to quantify the association between cumulative PM 2.5 exposure and PTC diagnosis. We tested whether this association differed by gender, race, BMI, smoking history, current alcohol use, and median household income. Results A cohort of 1990 patients with PTC and a control group of 6919 patients without thyroid disease were identified. Compared to the control group, patients with PTC were more likely to be older (51.2 vs. 48.8 years), female (75.5% vs 46.8%), White (75.2% vs. 61.6%), and never smokers (71.1% vs. 58.4%) ( p   〈  0.001). After adjusting for age, sex, race, BMI, current alcohol use, median household income, current smoking status, hypertension, diabetes, COPD, and asthma, 3-year cumulative PM 2.5 exposure was associated with a 1.41-fold increased odds of PTC diagnosis (95%CI: 1.23–1.62). This association varied by median household income (p-interaction =0.03). Compared to those with a median annual household income 〈 $50,000, patients with a median annual household income between $50,000 and  〈  $100,000 had a 43% increased risk of PTC diagnosis (aOR = 1.43, 95%CI: 1.19–1.72), and patients with median household income ≥$100,000 had a 77% increased risk of PTC diagnosis (aOR = 1.77, 95%CI: 1.37–2.29). Conclusions Cumulative exposure to PM 2.5 over 3 years was significantly associated with the diagnosis of PTC. This association was most pronounced in those with a high median household income, suggesting a difference in access to care among socioeconomic groups.
    Type of Medium: Online Resource
    ISSN: 1476-069X
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2092232-2
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  • 5
    Online Resource
    Online Resource
    Elsevier BV ; 2023
    In:  Otolaryngologic Clinics of North America ( 2023-11)
    In: Otolaryngologic Clinics of North America, Elsevier BV, ( 2023-11)
    Type of Medium: Online Resource
    ISSN: 0030-6665
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
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  • 6
    Online Resource
    Online Resource
    Wiley ; 2016
    In:  International Forum of Allergy & Rhinology Vol. 6, No. 2 ( 2016-02), p. 191-200
    In: International Forum of Allergy & Rhinology, Wiley, Vol. 6, No. 2 ( 2016-02), p. 191-200
    Abstract: Bactericidal antibiotics have been shown to stimulate reactive oxygen species (ROS) formation in mammalian cells through mitochondrial dysfunction. This results in oxidative tissue damage that may have negative consequences for long‐term antibiotic use. Antibiotics are widely and heavily used in the treatment of acute and chronic sinusitis; however, the relationship between antibiotics and ROS formation in sinonasal epithelial cells (SNECs) has not yet been demonstrated. Methods Human SNECs were collected from patients during endoscopic sinus surgery and grown in culture at the air‐liquid interface. Differentiated SNECs were stimulated with the bactericidal antibiotics amoxicillin and levofloxacin and the bacteriostatic antibiotic clarithromycin for 24 hours. ROS were quantified via fluorescence. Cell death was quantified by lactate dehydrogenase (LDH) secretion. Expression of inflammatory markers such as tumor necrosis factor α (TNF‐α) and nuclear factor erythroid 2–related factor 2 (Nrf2)‐mediated antioxidant genes were measured by real‐time polymerase chain reaction (RT‐PCR). Results Cultured SNECs treated with the bactericidal antibiotics amoxicillin and levofloxacin resulted in a significant increase in production of ROS ( p 〈 0.05) and secretion of LDH ( p 〈 0.05). The increase in ROS formation correlated with an increase in expression of Nrf2‐mediated antioxidant genes as well as the expression and production of proinflammatory cytokine TNF‐α, and interleukin 1 β (IL‐1β) ( p 〈 0.05). SNECs treated with clarithromycin did not demonstrate statistically significant increases in ROS or proinflammatory cytokine production. Conclusion In this study, we show that treatment of cultured human SNECs with bactericidal antibiotics leads to formation of ROS with an associated increase in inflammatory and antioxidant gene expression and cell death. This suggests that long‐term or inappropriate antibiotic use in the treatment of sinusitis may result in oxidative tissue damage to the sinonasal epithelium. Future studies will explore the clinical implications of such damage to the sinonasal epithelium.
    Type of Medium: Online Resource
    ISSN: 2042-6976 , 2042-6984
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2604059-1
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  • 7
    Online Resource
    Online Resource
    Wiley ; 2016
    In:  International Forum of Allergy & Rhinology Vol. 6, No. 9 ( 2016-09), p. 964-972
    In: International Forum of Allergy & Rhinology, Wiley, Vol. 6, No. 9 ( 2016-09), p. 964-972
    Abstract: Few efficacious topical therapies exist for chronic rhinosinusitis (CRS). The lack of a reproducible mouse model of CRS limits the pilot testing of potential novel anti‐inflammatory therapies. Although the ovalbumin‐induced mouse model of sinonasal inflammation is commonly used, it is difficult to reproduce and can generate variable histologic results. In this study, we explore a variation of this model in different strains of mice and explore various inflammatory cytokines as reproducible molecular markers of inflammation. Methods Allergic sinonasal inflammation was generated in BALB/c and C57BL/6 mice using intraperitoneal high‐dose injections of ovalbumin (Ova; Sigma Chemical Co.) followed by 10 days of high‐dose intranasal sensitization. Real‐time polymerase chain reaction (RT‐PCR) for eotaxin, interleukin 4 (IL‐4), and IL‐13 were measured from sinonasal mucosa. We also pilot tested a known topical budesonide to characterize the anti‐inflammatory response. Histological sections were analyzed for epithelial thickness and eosinophilia. Results Both BALB/c and C57BL/6 mice consistently showed increases in T helper 2 (Th2) cytokines after sensitization with high‐dose Ova ( p 〈 0.0001) when compared to controls. There were also significant increases in epithelial thickening in Ova‐sensitized mice and eosinophilia in both BALB/c and C57BL/6 strains. In addition, topical budesonide significantly reduced anti‐inflammatory cytokines, eosinophilia, and epithelial thickness. Conclusion Our variation of the ovalbumin‐induced mouse model of sinonasal inflammation in both BALB/c and C57BL/6 mice provides an efficacious model for testing potential topical anti‐inflammatory therapies for CRS. The utilization of sinonasal mucosal Th2 cytokines along with histologic markers provides a consistent and quantifiable marker of inflammation in assessing the efficacy of candidate drugs.
    Type of Medium: Online Resource
    ISSN: 2042-6976 , 2042-6984
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2604059-1
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  • 8
    In: International Forum of Allergy & Rhinology, Wiley, Vol. 11, No. 3 ( 2021-03), p. 213-739
    Abstract: The 5 years since the publication of the first International Consensus Statement on Allergy and Rhinology: Rhinosinusitis (ICAR‐RS) has witnessed foundational progress in our understanding and treatment of rhinologic disease. These advances are reflected within the more than 40 new topics covered within the ICAR‐RS‐2021 as well as updates to the original 140 topics. This executive summary consolidates the evidence‐based findings of the document. Methods ICAR‐RS presents over 180 topics in the forms of evidence‐based reviews with recommendations (EBRRs), evidence‐based reviews, and literature reviews. The highest grade structured recommendations of the EBRR sections are summarized in this executive summary. Results ICAR‐RS‐2021 covers 22 topics regarding the medical management of RS, which are grade A/B and are presented in the executive summary. Additionally, 4 topics regarding the surgical management of RS are grade A/B and are presented in the executive summary. Finally, a comprehensive evidence‐based management algorithm is provided. Conclusion This ICAR‐RS‐2021 executive summary provides a compilation of the evidence‐based recommendations for medical and surgical treatment of the most common forms of RS.
    Type of Medium: Online Resource
    ISSN: 2042-6976 , 2042-6984
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2604059-1
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  • 9
    Online Resource
    Online Resource
    Wiley ; 2022
    In:  International Forum of Allergy & Rhinology Vol. 12, No. 9 ( 2022-09), p. 1200-1203
    In: International Forum of Allergy & Rhinology, Wiley, Vol. 12, No. 9 ( 2022-09), p. 1200-1203
    Type of Medium: Online Resource
    ISSN: 2042-6976 , 2042-6984
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2604059-1
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  • 10
    Online Resource
    Online Resource
    Wiley ; 2016
    In:  International Forum of Allergy & Rhinology Vol. 6, No. 11 ( 2016-11), p. 1145-1150
    In: International Forum of Allergy & Rhinology, Wiley, Vol. 6, No. 11 ( 2016-11), p. 1145-1150
    Abstract: Environmental factors such as inhaled pollutants like cigarette smoke may play a significant role in diseases of the upper airway including chronic rhinosinusitis (CRS). Recent studies have shown that cigarette smoke causes impaired airway epithelial cell barrier function likely through environmental oxidative stress related pathways. The purpose of this study is to explore whether enhancing nuclear factor erythroid 2 [NF‐E2] ‐related factor 2 [Nrf2], the body's master antioxidant system, can ameliorate cigarette smoke–induced sinonasal epithelial cell (SNEC) barrier dysfunction. Methods Human SNECs (HSNECs) were grown from control patients at the air‐liquid interface (ALI). HSNECs were stimulated with cigarette smoke extract (CSE) with and without pharmacologic activation of Nrf2. HSNECs were then stained for the epithelial cell junctional proteins zonula occludens 1 (ZO‐1) and junctional adhesion molecule A (JAM‐A) using confocal microscopy. In addition, transepithelial electrical resistance (TER) was measured in cultures before and after stimulation with CSE. Results CSE stimulation caused a global disruption of the epithelial junctional proteins ZO‐1 and JAM‐A along with an associated decrease in TER levels. Enhancing Nrf2 levels prior to stimulation with CSE was associated with increased localization of ZO‐1 and JAM‐A levels at the cell surface and statistically significant increases in TER levels. Conclusion This is the first study to demonstrate that cigarette smoke induced SNEC barrier dysfunction is reversible by Nrf2 activation. The Nrf2 antioxidant pathway may represent a potential therapeutic target for cigarette smoke–associated sinonasal inflammation.
    Type of Medium: Online Resource
    ISSN: 2042-6976 , 2042-6984
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2604059-1
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