In asthma, eosinophil roles as main end inflammatory effector cell, but neither the activation process nor the stimuli of that is known clearly, yet. Even though allergic asthma is IgE-mediated type I hypersensitivity disease, it is not clear whether there is FcepsilonRI on the surface of eosinophil like mast cell or basophil which is activated through the FcepsilonRl bridging with sensitized allergens. In this study, we speculate if there's FcepsilonRI on the eosinophil, sensitized allergen activates it like mast cell in allergic asthmatics, and with this result we can find out one of the stimuli of eosinophil in asthma and can suggest the possibility of the existence of FcepsilonRI on the eosinophil. We did direct stimulation of the house dust mite -sensitized astknatics'purified peripheral blood normodense eoisnophils with Dermatophagoides pteronyssiuns. Then we measured the LTC4 and ECP from the supernatant by RIA kit and observed the morphological changes with electron microscopy. There was neither increase in LTC4 and ECP level nor the morphological changes in asthmatics. And there were no significant differences in both LTC4, and ECP level, and morphologic changes between asthmatics and controls. We would summerize that house dust mite dose not dirctly activate eosinophil from house dust mite-sensitized asthmatics and couldn't find out the possibility that there's FcepsilonRI on the surface of eoslnophils. But no exitstence of FcepsilonRI on the eosinophil is the indirect evidence, so from now on we try to find more direct evidence of that by blotting.
Allergens ; Asthma ; Basophils ; Dust* ; Eosinophils* ; Humans* ; Hypersensitivity, Immediate ; Leukotriene C4 ; Mast Cells ; Microscopy, Electron ; Pyroglyphidae*

No abstract available.
Edema* ; Eyelids* ; Lip*

BACKGROUND AND OBJECTIVE: Early in inflammation, adhesion occurs between leukocytes and endothelium where selectins bind to sialyl Lewis x(Sle,) and related oligosaccharides. We tested glycerrhetinic acid(GA), msjor anti-inflammmatory component of licorice, for its ability to inhibit selectin-mediated adhesion of human eosinophils and neutrophils in vitro. MATERIAL AND METHOD: Neutrophils and eosinophils were isolated by density grsdient centrifugation and eosinophils were further purified by immunomagnetic negative selection. Adhesion to unstimulated or IL-1 p-stimulated(5ug/ml, 4-6hr, 37C) umbilical vein endothelial monolayers was tested under static or rotating conditions, where adhesion is E- or L-selectin dependent, respectively. P-selectin-dependent adhesion was tested on immobilized platelets treated with or without TPA(10-7M, 10mins, RT). Stimulus-induced adhesion was always at least four-fold higher than without stimulus, and selectin dependence was confirmed with specific blocking monoclonsl antibody RESULT: All three kinds of selectin-mediated eosinophil and neutrophil adhesion were inhibited by GA and they were reversible without affecting viability. CONCLUSION: The ability of GA to interfere with the selectin mediated adhesion may contribute the one of the mechanism of the anti-inflammatory effects by licorice.
Centrifugation ; Endothelium ; Eosinophils ; Glycyrrhiza* ; Humans ; Inflammation ; Interleukin-1 ; L-Selectin ; Leukocytes ; Neutrophils* ; Oligosaccharides ; Selectins ; Umbilical Veins

The purposes of this study were to evaluate the applicability of pressure ulcer risk assessment tool ; the tool used was that developed by Cubbin and Jackson(1991). The subjects of this study were 253 patients in intensive care units. Data were prospectively collected from Feb 21 to June 10, 1997. Data were analyzed by mean, percentage, chi-square, Mann-Whitney U and stepwise multiple regression. The results of the study are as follows : 1. The factors that will predict pressure ulcer development are general skin condition, incontinence, age and hygiene, and there is a positive relationship between low scoring and pressure ulcer development. 2. The prevalence of the pressure ulcer is 38.3%, and the incidence of the pressure ulcer is 21.7%. 3. The most common pressure ulcer site is the sacrum(64.1%) and the next is the heel(7.69%). 4. Additional pressure ulcer risk factors are hemoglobin level and admission period.
Humans ; Hygiene ; Incidence ; Intensive Care Units ; Pressure Ulcer* ; Prevalence ; Prospective Studies ; Risk Assessment* ; Risk Factors ; Skin

No abstract available.
Drug Therapy*

No abstract available.
Acute Kidney Injury* ; Rhabdomyolysis*

PAF itself induces the non-specific bronchial hyperreactivity(NSBH) in asthma. NSBH induced by PAF is nearly as same as that by the sensitized allergen inhalation even though PAF never provokes the late asthmatic response. Usually the amount of allergen for BPT inversely correlated with the severity of asthma, but in PAF, nothing was clarified about that, yet. usually eosinophil is the main effector cell in PAF-induced NSBH. So we want to declare whether PAF inhalation affects the NSBH differently according to the severity of asthma or not in this study and eosinophil is the main effector cell in asthmatics. Single dose PAF(400microgram/microliter) inhalation challenge was done by the Cockcroft' s method but that of methacholine by Chai's method before and after PAF until NSBH returned the basal value. From that, we calculated PC20. Also we checked the eosinophil and platelet count in peripheral blood before and after PAF until those returned the baseline. All these were done in two groups, mild asthmatics and moderate asthmatics classified by the PFT and their PC20. The Bronchoconstriction started at the 3 minutes after PAF inhalation and then relieved completely 30 minutes after inhalation but in mild asthmatics bronchi constricted much more than moderate asthmatics. The fall of NSBH also persisted much longer in mild asthmatics. But the decrease in peripheral eoslnophil counts was nearly same in both groups. None of asthmatics showed the changes in platelet counts in peripheral blood. The degree of bronchoconstriction and decrease in eosinophil counts didn't have any correlation with the persistence of the NSBH. Taken together, PAF inhalation affected the NSBH inversely according to the severity of asthma in this study but eosinophil might not be the only effector cell in PAF-induced NSBH.
Asthma* ; Bronchi ; Bronchial Hyperreactivity* ; Bronchoconstriction ; Eosinophils ; Inhalation* ; Methacholine Chloride ; Platelet Count

PURPOSE: Venous thromboembolism (VTE) is a common life-threatening illness with significant morbidity and mortality rates. In recent years, the incidence of VTE has gradually increased in Korea. In this study, we evaluated the current trends in the management of acute deep vein thrombosis (DVT) in Korea. MATERIALS AND METHODS: A 20-item questionnaire was prepared and sent to 48 members of the Korean Society for Vascular Surgery. Each member worked in a different hospital. Twenty-two members participated in this study. RESULTS: The vascular surgery departments were primarily responsible for managing DVT. Ultrasound and computed tomography (CT) venography were chosen as the most common initial diagnostic tools. Eighty-two percent of participants routinely used the coagulation factor assay. Thrombolysis and inferior vena cava (IVC) filter insertion were performed mainly in the radiology departments. Seventy-seven percent of participants performed thrombolysis only if the thrombus age was less than 21 days. During thrombolysis, IVC filter was routinely inserted by 50% of respondents and removed within 14 days by 64% of respondents. Nearly all participants followed the 2012 American College of Chest Physicians guidelines for anticoagulation therapy. CONCLUSION: The majority of Korean vascular surgeons followed the guidelines. However, CT was frequently used. Thrombolysis and IVC filter insertion were more frequently performed than recommended by the guidelines.
Blood Coagulation Factors ; Surveys and Questionnaires ; Incidence ; Korea ; Mortality ; Phlebography ; Thorax ; Thrombosis ; Ultrasonography ; Veins ; Vena Cava, Inferior ; Venous Thromboembolism ; Venous Thrombosis*

No abstract available.

No abstract available.
Hepatitis*