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  • SAGE Publications  (4)
  • Lee, Sang Hag  (4)
  • 2010-2014  (4)
Materialart
Verlag/Herausgeber
  • SAGE Publications  (4)
Sprache
Erscheinungszeitraum
  • 2010-2014  (4)
Jahr
Fachgebiete(RVK)
  • 1
    In: Annals of Otology, Rhinology & Laryngology, SAGE Publications, Vol. 122, No. 5 ( 2013-05), p. 339-343
    Kurzfassung: The aims of the present study were twofold. We sought to compare two methods of titrating the level of continuous positive airway pressure (CPAP) — Auto-adjusting titration and titration using a predictive equation — With full-night manual titration used as the benchmark. We also investigated the reliability of the two methods in patients with obstructive sleep apnea syndrome (OSAS). Methods: Twenty consecutive adult patients with OSAS who had successful, full-night manual and auto-adjusting CPAP titration participated in this study. The titration pressure level was calculated with a previously developed predictive equation based on body mass index and apnea-hypopnea index. Results: The mean titration pressure levels obtained with the manual, auto-adjusting, and predictive equation methods were 9.0 ± 3.6, 9.4 ± 3.0, and 8.1 ± 1.6 cm H 2 O, respectively. There was a significant difference in the concordance within the range of ±2 cm H 2 O (p = 0.019) between both the auto-adjusting titration and the titration using the predictive equation compared to the full-night manual titration. However, there was no significant difference in the concordance within the range of ±1 cm H 2 O (p 〉 0.999). Conclusions: When compared to full-night manual titration as the standard method, auto-adjusting titration appears to be more reliable than using a predictive equation for determining the optimal CPAP level in patients with OSAS.
    Materialart: Online-Ressource
    ISSN: 0003-4894 , 1943-572X
    Sprache: Englisch
    Verlag: SAGE Publications
    Publikationsdatum: 2013
    ZDB Id: 2033055-8
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 27, No. 5 ( 2013-09), p. 372-380
    Kurzfassung: Prominent expression of YKL-40 has been associated with pathological conditions characterized by tissue remodeling. We determined the expression level and distribution pattern of YKL-40 in allergic nasal mucosa and evaluated the effect of YKL-40 on the proliferation and migration of fibroblasts, the production of the mediators related to tissue remodeling, and collagen production. Additionally, the cytokine-driven regulation of YKL-40 expression was evaluated in cultured epithelial cells. Methods The expression of YKL-40 in normal, mild, and moderate/severe allergic nasal mucosa was evaluated using real-time polymerase chain reaction (PCR), Western blot, and immunohistochemistry. Fibroblast migration was observed using a scratch wound method, and proliferation was determined by the MTT methods. Expression of proteoglycans, transforming growth factor (TGF) beta1, MMP2, MMP9, TIMP1, TIMP2, and collagen concentration were analyzed in fibroblasts treated with YKL-40. The expression levels of YKL-40 in cultured epithelial cells were examined after stimulation with mediators including Th2 cytokines, interferon (IFN)gamma, and TNF-alpha with real-time PCR and ELISA. Results The expression of YKL-40 was up-regulated in allergic rhinitis and distributed in superficial epithelium, submucosal glands, and vascular endothelium, in addition to infiltrating cells. TGF-beta1, TIMP1, MMP9, and biglycan were up-regulated in fibroblasts on stimulation with YKL-40, accompanying increased proliferation and migration, and collagen production. IL-13, IFN-gamma, and TNF-alpha induced the increased production of YKL-40 in cultured epithelial cells. Conclusion YKL-40 is up-regulated in mild and moderate/severe persistent allergic rhinitis, and its expression can be regulated differentially by different cytokines, possibly contributing to the remodeling of nasal mucosa in allergic rhinitis.
    Materialart: Online-Ressource
    ISSN: 1945-8924 , 1945-8932
    RVK:
    Sprache: Englisch
    Verlag: SAGE Publications
    Publikationsdatum: 2013
    ZDB Id: 2554548-6
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    Online-Ressource
    Online-Ressource
    SAGE Publications ; 2013
    In:  American Journal of Rhinology & Allergy Vol. 27, No. 4 ( 2013-07), p. 278-282
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 27, No. 4 ( 2013-07), p. 278-282
    Kurzfassung: Chronic rhinosinusitis (CRS) is an inflammation of the sinonasal mucosa and many inflammatory cells and cytokines are involved in its pathogenesis. High-mobility group protein B1 (HMGB1) is a DNA-binding protein that has a proinflammatory function when secreted into extracellular space. The purpose of this study was to evaluate the expression of HMGB1 in paranasal sinus mucosa and to determine the difference of HMGB1 expression between CRS patients and normal controls. Methods Paranasal sinus mucosa was obtained from 10 patients with CRS and 10 patients without CRS. Semiquantitative reverse transcriptase–polymerase chain reaction (RT-PCR), real-time PCR and Western blot analysis were performed to detect mRNA and protein. Sections of the mucosa were immunostained for localization of HMGB1 and image analysis was performed. Results RT-PCR and real-time PCR showed that the expression level of HMGB1 mRNA was significantly increased in the tissues of patients with CRS compared with controls. Western blot analysis showed that the expression level of HMGB1 protein was significantly increased in the tissues of CRS. In immunohistochemical staining, the HMGB1 protein was expressed in epithelial cells and inflammatory cells and the expression intensity of HMGB1 protein was stronger in CRS. Conclusion HMGB1 is increased in the paranasal sinus mucosa of patients with CRS. These results suggest a possible contribution of HMGB1 in the pathophysiology of CRS.
    Materialart: Online-Ressource
    ISSN: 1945-8924 , 1945-8932
    RVK:
    Sprache: Englisch
    Verlag: SAGE Publications
    Publikationsdatum: 2013
    ZDB Id: 2554548-6
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Online-Ressource
    Online-Ressource
    SAGE Publications ; 2013
    In:  American Journal of Rhinology & Allergy Vol. 27, No. 1 ( 2013-01), p. 18-23
    In: American Journal of Rhinology & Allergy, SAGE Publications, Vol. 27, No. 1 ( 2013-01), p. 18-23
    Kurzfassung: Nasal polyposis is associated with a chronic inflammatory condition of the sinonasal mucosa and involves myofibroblast differentiation and extracellular matrix (ECM) accumulation. Epigenetic modulation by histone deacetylase (HDAC) inhibitors including trichostatin A (TSA) has been reported to have inhibitory effects on myofibroblast differentiation in lung and renal fibroblasts. The purpose of this study was to investigate the inhibitory effect of TSA on myofibroblast differentiation and ECM production in nasal polyp organ cultures. Methods Nasal polyp tissues from 18 patients were acquired during endoscopic sinus surgery. After organ culture, nasal polyps were stimulated with TGF-beta1 and then treated with TSA. Alpha-smooth muscle actin (α-SMA), fibronectin, and collagen type I expression levels were examined by reverse transcription–polymerase chain reaction (PCR), real-time PCR, Western blot, and immunofluorescent staining. HDAC2, HDAC4, and acetylated H4 expression levels were assayed by Western blot. Cytotoxicity was analyzed by the terminal deoxynucleotidyl transferase biotin–dUTP nick end labeling assay. Results The expression levels of α-SMA, fibronectin, and collagen type 1 were increased in nasal polyp after transforming growth factor (TGF) beta1 treatment. TSA-inhibited TGF-beta1 induced these gene and protein expression levels. Furthermore, TSA suppressed protein expression levels of HDAC2 and HDAC4. However, TSA induced hyperacetylation of histones H4. Treatment with TGF-beta1 with or without TSA did not have cytotoxic effect. Conclusion These findings provide novel insights into the epigenetic regulation in myofibroblast differentiation and ECM production of nasal polyp. TSA could be a candidate of a therapeutic agent for reversing the TGF-beta1–induced ECM synthesis that leads to nasal polyp development.
    Materialart: Online-Ressource
    ISSN: 1945-8924 , 1945-8932
    RVK:
    Sprache: Englisch
    Verlag: SAGE Publications
    Publikationsdatum: 2013
    ZDB Id: 2554548-6
    Standort Signatur Einschränkungen Verfügbarkeit
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