No abstract available.
Nasal Mucosa*

There is persuasive epidemiological and experimental evidence that dietary polyphenols have anti-inflammatory activity. Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) have long been used to combat inflammation. Recently, cyclooxygenase (COX) inhibitors have been developed and recommended for treatment of rheumatoid arthritis (RA) and osteoarthritis (OA). However, two COX inhibitors have been withdrawn from the market due to unexpected side effects. Because conventional therapeutic and surgical approaches have not been able to fully control the incidence and outcome of many inflammatory diseases, there is an urgent need to find safer compounds and to develop mechanism-based approaches for the management of these diseases. Polyphenols are found in many dietary plant products, including fruits, vegetables, beverages, herbs, and spices. Several of these compounds have been found to inhibit the inflammation process as well as tumorigenesis in experimental animals; they can also exhibit potent biological properties. In addition, epidemiological studies have indicated that populations who consume foods rich in specific polyphenols have lower incidences of inflammatory disease. This paper provides an overview of the research approaches that can be used to unravel the biology and health effects of polyphenols. Polyphenols have diverse biological effects, however, this review will focus on some of the pivotal molecular targets that directly affect the inflammation process.
Phospholipases A/antagonists & inhibitors ; Phenols/*pharmacology ; Peroxisome Proliferator-Activated Receptors/drug effects/physiology ; NF-kappa B/metabolism ; Lipoxygenase Inhibitors/pharmacology ; Humans ; Flavonoids/*pharmacology ; Cytokines/biosynthesis ; Cyclooxygenase Inhibitors/pharmacology ; Arachidonic Acid/metabolism ; Anti-Inflammatory Agents/*pharmacology ; Animals

Measurement of fractional exhaled nitric oxide (FeNO) is one of the useful markers for airway inflammation. It detects NO in exhaled breath, which is increased along airway inflammation such as asthma. While there are a few tests assessing airway inflammation in noninvasive manners, FeNO has many advantages in that it can be measured easily and repeatedly in very short time with accuracy. In addition it reflects eosinophilic airway inflammation with significant correlation with eosinophilia in bronchial biopsy and sputum. The use of FeNO is useful in screening and diagnosis of asthma, prediction of steroid response, estimation of treatment response, and assessment of asthma control. Furthermore dose of medication can be titrated based on FeNO. The measurement of FeNO can play complementary role in asthma management along with pulmonary function test and airway hyperresponsiveness. In addition to asthma, FeNO maybe used for diagnosis of chronic obstructive pulmonary disease and chronic cough. With advent of new and cheap NO analyzer in near future, the use of FeNO could be introduced in routine practice of asthma.
Asthma ; Biopsy ; Cough ; Eosinophilia ; Eosinophils ; Inflammation ; Mass Screening ; Nitric Oxide ; Pulmonary Disease, Chronic Obstructive ; Respiratory Function Tests ; Sputum

PURPOSE: To evaluate the long-term effectiveness of different surgical procedures according to horizontal eyelid laxity in correcting involutional entropion. METHODS: This retrospective study reviewed 104 eyes of 79 patients with involutional lower eyelid entropion who underwent surgical repair. The 62 eyes with horizontal eyelid laxity were classified as group I. In 17 eyes of group I, we performed the lateral tarsal strip procedure alone (group Ia), while in 45 eyes of group I, we performed the lateral tarsal procedure and Quickert suture (group Ib). The 42 eyes without horizontal eyelid laxity were classified as group II. In 13 eyes of group II, we performed a lower eyelid retractor reinsertion procedure only (group IIa), and in 29 eyes of group II, we performed combined lower eyelid retractor reinsertion and orbicularis resection (group IIb). RESULTS: The recurrence rate in these four surgical subsets (group Ia , group Ib, group IIa, group IIb) was 11.7%, 0%, 15.4%, and 6.9%, respectively, with an average follow-up of 11 months. Six recurrent eyelids and two overcorrected eyelids successfully underwent procedures to correct recurrent entropion and ectropion, respectively. CONCLUSIONS: The lateral tarsal strip procedure is an effective approach for achieving long-lasting correction of involutional entropion with horizontal eyelid laxity, whereas the lower eyelid retractor reinsertion procedure is an effective approach for achieving long-lasting correction for involutional entropion without horizontal eyelid laxity. Use of the Quickert suture reduced the need to repeat the lateral tarsal strip procedure and additional orbicularis resection decreased the need to repeat the lower eyelid retractor reinsertion procedure.
Ectropion ; Entropion ; Eye ; Eyelids ; Follow-Up Studies ; Humans ; Recurrence ; Retrospective Studies ; Sutures

LPS and IFN-r induce nitric oxide synthase in macrophages and the resultant NO causes apoptotic cell death in the activated macrophages. NO production and apoptosis were inhibited by N-monomethyl L-arginine (NMMA), a competitive inhibitor of NO synthase. To study the role of BCL-X proteins, RAW 264.7 cells were transfected with the expression vectors with human bcl-Xl or bcl-Xs cDNAs, respectively. Stable transfectants were selected and confirmed by RT-PCR. NO production in response to LPS and IFN-r caused apoptosis in RAW 264.7 cells and vector transfected control cells within 24 hr. Both NO production and apoptosis were inhibited by N(G)-monomethyl L-arginine (NMMA). In contrast, bcl-Xs transfectant appeared slightly susceptible and bcl-X(L)< transfectant appeared slightly resistant, although NO production was similar to control cells. These results suggest that bcl-X proteins play roles in both positive and negative regulation of apoptosis induced by NO.
Apoptosis* ; Arginine ; bcl-X Protein* ; Cell Death ; DNA, Complementary ; Humans ; Macrophages* ; Nitric Oxide ; Nitric Oxide Synthase

BACKGROUND AND OBJECTIVES: In cystic fibrosis, chronic bronchitis, and asthma, the mucociliary mechanism is impaired when mucin is produced excessively. The mRNA encoding MUC8 has been shown to be the major up-regulated mucin under inflammatory condition and is likely to contribute to the airway mucus plugging characteristic of these diseases. The aim of this study is to determine the intracellular signaling pathway directly involved in the MUC8 regulation following inflammatory mediator treatments. MATERIALS AND METHOD: Passage-2 normal human airway epithelial cells were used in all experiments. Inflammatory signal-induced MAP kinase activity was measured by Western blot analysis using phosphospecific anti-active MAP kinase antibodies. Inflammatory signal-induced MUC8 expression was measured in the absence or presence of SB203580 by the semi-quantative RT-PCR. RESULTS: Inflammatory stimuli such as LPS, TNF-alpha, and IL-lbeta activated the p38 MAP kinase and subsequently up-regulated the MUC8 expression. Interestingly, the TNF-alpha or IL-lbeta-inducibility of the MUC8 gene expression was greatly enhanced by specific inhibition of the p38 MAP kinase by using SB 203580 CONCLUSION: These results suggest that the intracellular p38 MAP kinase activity is a negative regulator for the MUC8 up-regulation in human nasal epithelial cells following infiammatory stimuli.
Antibodies ; Asthma ; Blotting, Western ; Bronchitis, Chronic ; Cystic Fibrosis ; Epithelial Cells* ; Gene Expression* ; Humans* ; Mucins ; Mucus ; p38 Mitogen-Activated Protein Kinases* ; Phosphotransferases ; RNA, Messenger ; Signal Transduction* ; Tumor Necrosis Factor-alpha ; Up-Regulation

No abstract available.

No abstract available.
Cerebrospinal Fluid Rhinorrhea* ; Cerebrospinal Fluid*

No abstract available.
Mucous Membrane* ; Muramidase* ; Turbinates*

No abstract available.
Blood Grouping and Crossmatching* ; Humans* ; Nasal Mucosa*