No abstract available.
Bronchitis, Chronic*

No abstract available.
Animals ; Carnitine* ; Heart* ; Myocardium* ; Rats*

BACKGROUND: Th2-like cells are thought to play a crucial role in the recruitment and activation of eosinophil in bronchial asthma. In contrast to Th2 cytokine, Thl cytokine IFN-y decreases eosinophil recruitment. Previous studies have shown that IL-12 promotes differentiation of Th0 into Thl and enhances production of Thl cytokine. IL-12 also prevents differentiation of Th0 into Th2 during primary immune response. Its effect on established Th2 cell, however, is well known. OBJECTIVE: The objective of aur study was focused on whether IL-12 prevents recruitment of eosinophil and expression of Th2 cytokine in murine model for bronchial asthma, and whether its effect differs according to timing of dosage. METHOD: Administration of IL-12 was tested in the 3 different time-frames; 1) allergic sensitization (early dosage) 2) allergic challenge (late doaage) or 3) both. The number of eosinophil in the bronchoalveolar lavage(BAL) fluid and tissue was examined for change of airway inflammation. The effect on cytokine expression was assessed by measuring cytokine in bronchoalveolar lavage fluid (ELISA) and mRNA in peribronchial lymph node (RT-PCR) RESULTS: Early dosage of IL-12, and the combination of early and late dosages, strikingly decreased the numbers of eosinophil in both BAL fluid and tissue(p<0.05). Late dosage of IL-12 decreased tissue eosinophilia, while the number of eosinophil in BAL fluid remained unchanged. IL-12 increased IL-4 and IL-5 levels, and decreased IL-2 and I~FN-r levels. There were no differences in Thl/Th2 cytokine regulation among the three dosage times. Early dosage of IL-12, and the combination of early and late dosages, increased IL-10 level, but late dosage had no effect on IL-10. CONCLUSION: These results demonstrate that depending upon whether IL-12 is administered during sensitization or during subsequent allergen exposure, Thl/Th2 cytokine regulation by IL -12 shows no difference because it seems that difference of inhibition of eosinophil recruitment by IL-12 might be related with the other factors, such as IL-10.
Animals ; Asthma* ; Bronchoalveolar Lavage Fluid ; Eosinophilia ; Eosinophils ; Inflammation* ; Interleukin-10 ; Interleukin-12* ; Interleukin-2 ; Interleukin-4 ; Interleukin-5 ; Lymph Nodes ; Mice* ; RNA, Messenger ; Th2 Cells

BACKGROUND: Infiltration of eosinophils and activated T cells into the airway is a characteristic feature of allergic inflammation such as asthma. IL-4 has been shown to mediate adhesion of eosinophils and T cells to endothelial cells by inducing VCAM-1 expression on endothelial surface. IL-13 shares a number of biologic properties with IL-4. OBJECTIVE: We aimed to investigate the effects of IL-13 on the adhesion of eosinophils to human umbilical vein endothelial cells (HUVEC) and on the expression of VCAM-1 in HUVEC. METHOD: HUVEC was incubated for 24h with IL-13 (10ng/ml), IL-4 (10ng/ml) and TNF-a (10ng/ml). Surface expression of VCAM-1 in HUVEC was detected using irnmuno-cytochemical stain and reverse transcription-polymearse chain reaction (RT-PCR), and the adhesion of eosinophils to HUVEC was quantitated using eosinophil peroxidase (EPO) assay. RESULTS: The VCAM-1 expression on IL-13-treated HUVEC increased more than in the expression on medium-treated HUVEC (p<0.05). The adhesion of eosinophil to IL-13- treated HUVEC also increased more than in the adhesion to medium-treated HUVEC (p<0.05). The VCAM-1 expression was synergistically induced by TNF-a and IL-13 (p<0.05). IL-13 induced VCAM-1 expression and adhesion of eosinophils to HUVEC, similar to IL-4. IL-13 also induced VCAM-1 mRNA expression, with greater expression than with medium and TNF-a(p<0.05). IL-13-induced surface VCAM-1 was associated with expression of mRNA transcripts and adhesion of eosinophils to HUVEC(r=0.89, r=0.93, p<0.05). CONCLUSION: These findings demonstrate that IL-13 stimulates HUVEC to express surface VCAM-1 and has a possible role in promoting VCAM-1/VLA-4 dependent accumulation of eosinophils during allergic and other inflammatory responses.
Asthma ; Endothelial Cells* ; Eosinophil Peroxidase ; Eosinophils* ; Human Umbilical Vein Endothelial Cells ; Inflammation ; Interleukin-13* ; Interleukin-4 ; RNA, Messenger ; T-Lymphocytes ; Vascular Cell Adhesion Molecule-1

BACKGROUND: Primary stenting as a direct reperfusion procedure after acute myocardial infarction might reduce recurrent myocardial infarction and target vessel revascularization. However, result of long or multiple stenting in the long or tandem lesions were not known. METHOD: From Jan. 1996 to Dec. 1998, patients with acute myocardial infarction including cardiogenic shock were undergone primary stenting using long or multiple stent. The clinical end points were death, recurrent infarction, subsequent bypass surgery, or repeat angioplasty of the infarct-related vessel. The results were compared with age, sex, lesion, and risk matched standard stenting group. RESULT: Baseline characteristics were similar for the 20 patients who underwent standard length stenting and the 13 patients who underwent long or multiple stenting. Stent diameter was similar in two group (3.4+/-0.3 mm vs. 3.5+/-0.4 mm, p=0.65), but total stent length was longer in long or multiple stenting group (15.5+/-1.8 mm vs. 40.18.4 mm, p=0.01). Average numbers of stent using in multiple stenting were 1.5+/-0.7. Stenting in the infarct-related artery was successful in all patients randomized to stent treatment. At 6 months, the incidence of the primary end point was 25% (5/20) in the standard stent group and 31%(4/13) in the long or multiple stent group (p=0.5). CONCLUSION: Outcomes of long or multiple stenting including mortality, recurrent myocardial infarction and target vessel revascularization was similar to standard stenting. Long or multiple stenting after acute myocardial infarction may possible procedure in some selective cases having long or tandem lesion.
Angioplasty* ; Arteries ; Humans ; Incidence ; Infarction ; Mortality ; Myocardial Infarction ; Reperfusion ; Shock, Cardiogenic ; Stents*

BACKGROUND: N-acetylcysteine(ACE) is used both orally and intravenously in a variety of experimental pathologies resembling human disease states which exhibit endothelial toxicity as a result of oxidative stress, including acute pulmonary oxygen toxicity, septicemia and endotoxin shock. Despite these observations in vivo, it is not certain how this thiol drug produces its protective effects. ACE is a cysteine derivative which is able to directly react with oxygen radicals and may also act as a cysteine and glutathione(GSH) precursor following deacetylation. In this paper, we tried to know whether the therapeutic doses of ACE can modify the inflammatory function of the neutrophils and can increase the glutathione level of plasma in chronic obstructive pulmonary disease(COPD) patients. In addition, the effect of ACE to the purified neutrophil in terms of superoxide release and glutathione synthesis were observed. METHOD: Firstly, we gave 600mg of ACE for seven days and compare the release of superoxide, luminol-enhanced chemiluminescence from the neutrophils, neutrophil chemotaxis, and plasma GSH levels before and after ACE treatment in COPD patients. Secondly, we observed the dose dependent effect of ACE to the purified neutrophil's superoxide release and GSH levels in vitro. RESULTS: 1) Usual oral therapeutic doses(600mg per day) of ACE for seven days did affect neither on the neutrophils superoxide release, chemiluminescence, chemotaxis, nor on the plasma GSH concentration in the COPD patients. 2) ACE decreases the purified neutrophil's superoxide release and increase the GSH production in dose dependent fashion in vitro. CONCLUSION: Despite the fact that oral ACE treatment did not affect on the neutrophil's inflammatory function and plasma GSH concentration in COPD patients in usual therapeutic doses, it decreases the superoxide release and increases the GSH production from the isolated neutrophils in high molar concentrations. These findings suggest that to obtain an antioxidative effects of ACE, it might be needed to increase the daily dosage of ACE or therapeutic duration or change the route of adminisration in COPD patients.
Acetylcysteine* ; Chemotaxis* ; Cysteine ; Glutathione* ; Humans ; Luminescence ; Molar ; Neutrophils* ; Oxidative Stress ; Oxygen ; Pathology ; Plasma* ; Pulmonary Disease, Chronic Obstructive ; Reactive Oxygen Species ; Sepsis ; Shock ; Superoxides*

No abstract available.
Diagnosis* ; Tuberculosis, Pulmonary*

No abstract available.
Sarcoidosis*

We report a case of sarcoidosis which developed in the skin, lung and eyes in a 50-year-old woman. The skin lesions showed two types of cutaneous manifestations which were subcutaneous nodules on her back and erytrematous papules on the face for several months. Our patient's seurm angiotensin converting enzyme (ACE) level was elevated at 33.5 IU/L(reference range, 8.3-21.4 IU/L) and the purified protein derivative(PPD) skin test had a negative result. On her roentgenographic examinations, we could find multiple nodular densities with hazziness on both her lungs and radionuclides(Gallium 67) uptakes in right lower lung field. The ratio of helper to suppressor T cells was 9 in bronchial lavage. Diagnosis of sarcoidosis was made on the basis of histologic findings of non-caseating granulomas from skin and lung tissue. Treatment was initiated with oral alternate-day prednisone 40mg. The cutaneous lesions and dyspnea improved in 2 and 4 weeks respectively, and serum ACE level returned to normal in 2 months.
Bronchoalveolar Lavage ; Diagnosis ; Dyspnea ; Female ; Granuloma ; Humans ; Lung ; Middle Aged ; Peptidyl-Dipeptidase A ; Prednisone ; Sarcoidosis* ; Skin ; Skin Tests ; T-Lymphocytes

Chronic obstructive pulmonary disease (COPD) generally follows decades of heavy cigarette smoking; although other risk factors may be present, burning of biomass fuels in developing countries is of particular concern. Most of the patients with COPD complain of dyspnea owing to obstructive airway disease, hyperinflation, and respiratory failure. Pulmonary hypertension, corpulmonale, and other smoking-related diseases such as cardiovascular disease and lung cancer may also be prominent in COPD patients. COPD patients are also prone to develop pneumothorax and chronic pulmonary thromboembolic disease. In this review, I briefly summarize the complications and accompanying disorders in association with COPD.
Biomass ; Burns ; Cardiovascular Diseases ; Developing Countries ; Dyspnea ; Humans ; Hypertension, Pulmonary ; Lung Neoplasms ; Pneumothorax ; Pulmonary Disease, Chronic Obstructive* ; Respiratory Insufficiency ; Risk Factors ; Smoking