No abstract available.
Inflammation*

Adenosis tumor is a ra re tumor of the breast and primarily consists of adenosis. Authors report a case of surgically proved adenosis tumor in a 31-year-old woman. Mammogram showed a Iobulated, well-circumscribed mass with several surrounding radiolucent halos. In the center of the mass several linear radiolucent densities were seen with the appearance of a conglomerated well-circumscribed mass such as fibroadenoma. These linear radiolucent densities were consistent with the fat between the fibrous sclerosis in pathologic specimen. Ultrasonogram showed a well-circumscribed mass with homogeneous low echogenicity, partial posterior enhancement, and bilateral acoustic shadowings.
Acoustics ; Adult ; Breast* ; Female ; Fibroadenoma ; Humans ; Sclerosis ; Shadowing (Histology) ; Ultrasonography

Dengue fever is an important health problem for international travelers to all endemic areas. The steadily increasing numbers of tourists visiting endemic areas raise the risk of exposure, and imported dengue cases are increasingly observed in nonendemic area. Dengue has a wide spectrum of clinical presentations, often with unpredictable clinical evolution and outcome. While most patients recover following a self-limiting, non-severe clinical course, a small proportion progress to severe disease such as dengue hemorrhagic fever or dengue shock syndrome. Therefore, it is important to suspect dengue fever in every febrile patient returning from the tropics. Whenever it is suspected, a quick diagnosis and adequate managements are essential to avoid complications. We report two cases of imported dengue fever in Korean children presenting with fever, headache, nausea, and rash.
Child ; Dengue ; Dengue Hemorrhagic Fever ; Exanthema ; Fever ; Headache ; Humans ; Korea ; Nausea ; Philippines

New evidence is emerging that airway smooth muscle (ASM) may act as an immunomodulatory cell by providing pro-inflammatory cytokines and chemokines, polypeptide growth factors, extracellular matrix proteins, cell adhesion receptors and co-stimulatory molecules. ASM can promote the formation of the interstitial extracellular matrix, and potentially contribute to the alterations within the extracellular matrix in asthma. In addition, extracellular matrix components can alter the proliferative, survival, and cytoskeletal synthetic function of ASM cells through integrin-directed signaling. Increased ASM mass is one of the most important features of the airway wall remodeling process in asthma. Three different mechanisms may contribute to the increased ASM mass: cell proliferation, increased migration and decreased rate of apoptosis. The major signaling pathways of cell proliferation activated by ASM mitogens are those dependent on extracellular signal-regulated kinase and phosphoinositide 3'-kinase. The key signaling mechanisms of cell migration have been identified as the p38 mitogen-activated protein kinase and the p21-activated kinase 1 pathways. ASM cells contain beta2-adrenergic receptors and glucocorticoid receptors. They may represent a key target for beta2- adrenergic receptor agonist/corticosteroid interactions which have antiproliferative activity against a broad spectrum of mitogens.
Apoptosis ; Asthma* ; Cell Adhesion ; Cell Movement ; Cell Proliferation ; Chemokines ; Cytokines ; Extracellular Matrix ; Extracellular Matrix Proteins ; Intercellular Signaling Peptides and Proteins ; Mitogens ; Muscle, Smooth* ; p21-Activated Kinases ; Phosphotransferases ; Protein Kinases ; Receptors, Adrenergic ; Receptors, Glucocorticoid

Asthma comprises a heterogeneous group of disorders characterized by airway inflammation, airway obstruction, and airway hyperresponsiveness (AHR). Airway inflammation, which induces AHR and recurrence of asthma, is the main pathophysiology of asthma. The fractional exhaled nitric oxide (FeNO) level is a noninvasive, reproducible measurement of eosinophilic airway inflammation that is easy to perform in young children. As airway inflammation precedes asthma attacks and airway obstruction, elevated FeNO levels may be useful as predictive markers for risk of recurrence of asthma. This review discusses FeNO measurements among early-childhood wheezing phenotypes that have been identified in large-scale longitudinal studies. These wheezing phenotypes are classified into three to six categories based on the onset and persistence of wheezing from birth to later childhood. Each phenotype has characteristic findings for atopic sensitization, lung function, AHR, or FeNO. For example, in one birth cohort study, children with asthma and persistent wheezing at 7 years had higher FeNO levels at 4 years compared to children without wheezing, which suggested that FeNO could be a predictive marker for later development of asthma. Preschool-aged children with recurrent wheezing and stringent asthma predictive indices also had higher FeNO levels in the first 4 years of life compared to children with wheezing and loose indices or children with no wheeze, suggesting that FeNO measurements may provide an additional parameter for predicting persistent wheezing in preschool children. Additional large-scale longitudinal studies are required to establish cutoff levels for FeNO as a risk factor for persistent asthma.
Airway Obstruction ; Asthma ; Child* ; Child, Preschool ; Cohort Studies ; Eosinophils ; Humans ; Inflammation ; Longitudinal Studies ; Lung ; Nitric Oxide* ; Parturition ; Phenotype* ; Recurrence ; Respiratory Function Tests ; Respiratory Sounds* ; Risk Factors

Background : Recurrent wheezing in infants is manifested in a number of disease spectrums and gastroesophageal reflux ( GER ) has been known to be associated with apnea, recurrent pneumonia, asthma, chronic cough, and wheezing. The prevalence of GER in infants with recurrent wheezing and the relationship between atopy and GER in infantile asthmatics have not yet been established, but it was hypothesized that microaspiration of food allergen could induce food-induced wheezing. Objective : To evaluate the prevalence of GER in infants with recurrent wheezing episodes, and to determine whether the presence of atopy affects the prevalence of GER in infantile asthmatics. Method : Seventy infants with recurrent wheezing episodes were evaluated for GER using 24 hour continuous esophageal pH monitoring. Patients were classified into five groups, : 12 atopic asthmatics : 20 nonatopic asthmatics : 15 infants with recurrent bronchiolitis : 8 infants with recurrent pneumonia : and 15 infants with chronic lung disease ( CLD ) of prematurity. GER was considered to be prevalent when reflux index was higher than 95 percentile of normal values by Vandenplas, 1991. Result : The prevalence of GER in infants with recurrent wheezing was 21.4%. The prevalence of GER in each group was 25% in atopic asthmatics, 20% in nonatopic asthmatics, 6.7% in infants with recurrent bronchiolitis, 12.5% in infants with recurrent pneumonia, and 40% in infants with CLD of prematurity. There were no significant differences in prevalence of GER between atopic asthmatics and nonatopic asthmatics, between asthmatics with atopic dermatitis and those without, and between asthmatics with family history of allergy and those without. CONCLUSION: The prevalence of GER in infants with recurrent wheezing was high, especially in infantile asthmatics and infants with chronic lung disease of prematurity. The presence of atopy may not affect the prevalence of GER in infantile asthmatics.
Apnea ; Asthma ; Bronchiolitis ; Cough ; Dermatitis, Atopic ; Esophageal pH Monitoring ; Gastroesophageal Reflux* ; Humans ; Hypersensitivity ; Infant* ; Lung Diseases ; Pneumonia ; Prevalence* ; Reference Values ; Respiratory Sounds*

OBJECTIVE: To evaluate the basophil histamine releasability in response to IgE- and non- IgE-mediated stimuli in children with atopic asthma. Met: Basophil histamine releasability was measured in Dermatophagoides farinae (D. farinae)-sensitive atopic asthmatics, D.farinae-sensitive healthy atopics, non-atopic asthmatics, and healthy non-atopics. Basophils were stimulated with D.farinae, goat antihuman IgE antibody, formyl-Met-Leu-Phe(fMLP), and Calcium ionophore A23187. Histamine was measured by automated fluorometric technique. RESULTS: Sponianeous histamine release was higher in atopic asthmatics compared to healthy non-atopics. Histamine release by D.farinae and by anti-IgE antibody was higher in atopic asthmatics compared to the other groups. There was no difference in histamine release by fMLP among all groups. Histamine release by Calcium ionophore was higher in healthy atopics and non-atopic asthmatics compared to healthy non-atopics. The atopics showed correlation between histamine release by D.farinae, by anti-IgE antibody and total serum IgE levels. CONCLUSIONS: Spontaneous and IgE-mediated histamine release were related to the presence of both atopy and asthma, whereas non-IgE mediated histamine release was different depending on the stimuli.
Asthma* ; Basophils* ; Calcimycin ; Calcium ; Child* ; Dermatophagoides farinae ; Goats ; Histamine Release ; Histamine* ; Humans ; Immunoglobulin E

Airway smooth muscle (ASM) hypertrophy and hyperplasia, important pathological features in chronic severe asthma, contribute to irreversible airflow obstruction. ASM, which had been known to be a structural cell, may act as an immunomodulatory cell by providing pro- inflammatory cytokines and chemokines, polypeptide growth factors, extracellular matrix proteins, cell adhesion receptors and co-stimulatory molecules. ASM can promote the formation of the interstitial extracellular matrix, and potentially contribute to the alterations within the extracellular matrix in asthma. In addition, extracellular matrix components can alter the proliferative, survival, and cytoskeletal synthetic function of ASM cells through integrin- directed signaling. Increased ASM mass is one of the most important features of the airway wall remodeling process in asthma. Despite considerable research effort, the precise cellular mechanisms that modulate ASM growth remain unknown. Three different mechanisms may contribute to the increased ASM mass: cell proliferation or hypertrophy, increased migration and decreased rate of apoptosis. The major signaling pathways of cell proliferation activated by ASM mitogens are those dependent on extracellular signal-regulated kinase and phosphoinositide 3'-kinase. The key signaling mechanisms of cell migration have been identified as the p38 mitogen-activated protein kinase and the p21-activated kinase 1 pathways. ASM cells contain beta2-adrenergic receptors and glucocorticoid receptors. They may represent a key target for beta2-adrenergic receptor agonist/corticosteroid interactions which may have antiproliferative activity against a broad spectrum of mitogens. But corticosteroid itself, with or without beta2-adrenergic receptor agonist, cannot inhibit or reduce ASM cell proliferation completely. Future therapy should focus on blocking intracellular signal pathway which regulates proliferation.
Apoptosis ; Asthma* ; Cell Adhesion ; Cell Movement ; Cell Proliferation ; Chemokines ; Cytokines ; Extracellular Matrix ; Extracellular Matrix Proteins ; Hyperplasia ; Hypertrophy ; Intercellular Signaling Peptides and Proteins ; Mitogens ; Muscle, Smooth* ; p21-Activated Kinases ; Phosphotransferases ; Protein Kinases ; Receptors, Glucocorticoid ; Signal Transduction

BACKGROUND: Community-acquired pneumonia (CAP) is a common respiratory disorder in children, which necessitates hospitalization. Bacterial pneumonia, especially lobar pneumonia and parapneumonic effusions, is associated with considerably severe clinical course and extensive alveolar infiltrates. Serum procalcitonin (PCT) level has been used to distinguish bacterial from viral infections, but its usefulness is disputed. The diagnostic accuracy and usefulness of PCT, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and white blood cell (WBC) count were determined by comparing their values in the patients with CAP with those in healthy controls. METHODS: The serum PCT levels, as well as CRP level, ESR, and WBC counts, were measured in 76 hospitalized patients with CAP (lobar pneumonia, 16; bronchopneumonia, 60) and 18 healthy controls. Serum PCT level was measured using VIDAS(R) BRAHMS PCT (Biomerieux, France), and ROC curve analysis was performed to evaluate its diagnostic accuracy. RESULTS: Serum PCT levels were higher in the patients with CAP than in healthy controls, especially in the patients with lobar pneumonia than in those with bronchopneumonia. Serum CRP level was also significantly elevated in the patients with CAP, especially in those with lobar pneumonia. The diagnostic accuracy of serum PCT level for the diagnosis of lobar pneumonia was better than those of serum CRP level and ESR. The serum PCT level was significantly correlated with the CRP level, ESR, and WBC count. CONCLUSIONS: Serum PCT level was a better marker than CRP level or ESR for the diagnosis of lobar pneumonia in children with CAP.
Adolescent ; Biological Markers/blood ; Blood Sedimentation ; Bronchopneumonia/complications ; C-Reactive Protein/analysis ; Calcitonin/*blood ; Child ; Child, Preschool ; Community-Acquired Infections/complications/*diagnosis ; Female ; Humans ; Infant ; Infant, Newborn ; Leukocyte Count ; Male ; Pneumonia/complications/*diagnosis ; Protein Precursors/*blood ; ROC Curve

PURPOSE: Obesity is a major risk factor for asthma and it influences airway smooth muscle function and responsiveness. Adiponectin is inversely associated with obesity and its action is mediated through at least 2 cell membrane receptors (AdipoR1 and AdipoR2). Leptin is positively associated with obesity. We investigated whether human airway smooth muscle (ASM) cells express adiponectin receptors and whether adiponectin and leptin regulate human ASM cell proliferation and vascular endothelial growth factor (VEGF) release. MATERIALS AND METHODS: Human ASM cells were growth-arrested in serum-deprived medium for 48 hours and then stimulated with PDGF, adiponectin and leptin. After 48 hours of stimulation, proliferation was determined using a cell proliferation ELISA kit. Human AdipoR1 and -R2 mRNA expressions were determined by RT-PCR using human-specific AdipoR1 and -R2 primers. Concentrations of VEGF, monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-1alpha in cell culture supernatant were determined by ELISA. RESULTS: Both AdipoR1 and AdipoR2 mRNA were expressed in the cultured human ASM cells. However, adiponectin did not suppress PDGF-enhanced ASM cell proliferation, nor did leptin promote ASM cell proliferation. Leptin promoted VEGF release by human ASM cells, while adiponectin did not influence VEGF release. Neither leptin nor adiponectin influenced MCP-1 secretion from human ASM cells. Adiponectin and MIP-1alpha were not secreted by human ASM cells. CONCLUSION: Human ASM cells expressed adiponectin receptors. However, adiponectin did not regulate human ASM cell proliferation or VEGF release, while leptin stimulated VEGF release by human ASM cells.
Adiponectin/metabolism/*pharmacology/physiology ; Cell Proliferation/*drug effects ; Cells, Cultured ; Chemokine CCL2/metabolism ; Chemokine CCL3/metabolism ; Humans ; Leptin/metabolism/*pharmacology/physiology ; Myocytes, Smooth Muscle/cytology/drug effects/*metabolism ; Obesity/metabolism ; Platelet-Derived Growth Factor/metabolism ; Receptors, Adiponectin/*metabolism ; Respiratory System/cytology/metabolism ; Vascular Endothelial Growth Factor A/metabolism