No abstract available.
Asthma*

BACKGROUND: Rhinovirus infection of the airways results in increased permeability of the airway vascular endothelium with the influx of plasma proteins, including lipids such as LDL. In vitro studies on the effect of oxLDL on leukocytes has shown many proinflammatory effects on multiple leukocytes. We hypothesized that oxLDL is one mechanism for recruiting granulocytes to the airways during a RV infection. Therefore, chemotaxis and transendothelial migration, in response to nLDL, was determined for these granulocytes. METHODS: nLDL was oxidized with 5mM Cu2SO4 for 20-24 hours. 3-5×10(5) cells were loaded into the Transwell filter while the chemotatic agonists were placed in the lower well for chemotaxis. Confluent monolayers on HPMEC were grown on Transwell filters for transendothelial migration. The filters were washed and eosinophils and neutrophils loaded on to the filter with the chemotatic agonist was were placed in the lower well. The wells were incubated for 3 hours. The number of migrating cells was counted on a hemocytometer. RESULTS: OxLDL, but not nLDL, is chemotatic for eosinophils and neutrophils. The level of granulocytes chemotaxis was dependent on both the concentration of LDL and its degree of oxidation. OxLDL stimulates eosinophil and neutrophils migration across HPMEC monolayers (±IL-1β preactivation) in a dose dependent manner. CONCLUSION: Increased vascular permeability during a RV infection may lead to the influx and oxidation of LDL. The resulting oxLDL. is one possible mechanism for the recruitment of neutrophils and eosinophils to the airway interstitial matrix. Once in the airways, granulocytes can further interact with oxLDL to promote airway inflammation.
Blood Proteins ; Capillary Permeability ; Chemotaxis ; Endothelium, Vascular ; Eosinophils* ; Granulocytes ; Inflammation ; Leukocytes ; Neutrophils* ; Permeability ; Rhinovirus ; Transendothelial and Transepithelial Migration

The aspergillus tracheobronchitis is distinctive manifestation of invasive aspergillosis, in which infection is limited completely or predominantly to the tracheobronchial tree. It accounts for about 7 to 10 percent of cases of invasive disease. Grossly, such disease may take the mucosal exudate and obstruct partially the airway lumen or completely the occlusive mucous/fungus plugs. Microscopically, the superficial portion of the airway wall is acutely inflamed and contain fungal hyphae. However, infection is often limited to the mucosa. We report a case of aspergillus tracheobrochits in a 54 year-old man who presented cough, progressive dyspnea with wheezing, and mucus plug. Bronchoscopy showed mucosal exudate and plug.Bronchoscopic biopsy showed aspergillus hyphae and inflammation in the mucosa. He was successfully treated with itraconazole.
Aspergillosis ; Aspergillus* ; Biopsy ; Bronchoscopy ; Cough ; Dyspnea ; Exudates and Transudates ; Humans ; Hyphae ; Inflammation ; Itraconazole ; Mucous Membrane ; Mucus ; Respiratory Sounds ; Trees

No abstract available.
Toluene* ; Xylenes*

Pulmonary aspergillosis is classified as a saprophytic, allergic, and invasive disease. Chronic necrotizing pulmonary aspergillosis is categorized as an invasive pulmonary aspergillosis. Most invasive pulmonary aspergillosis have acute and toxic clinical features but chronic necrotizing pulmonary aspergillosis is characterized by a sub-acute infection, most commonly seen in patients with altered local defense system from preexisting pulmonary disease of in mild immunocompromised patients. Pulmonary artery aneurysm due to this infection is termed as a mycotic aneurysm, etiology of which are tuberculosis, syphilis, bacteria and fungus. We report a case chronic necrotizing pulmonary aspergillosis complicating pulmonary aneurysm is a 62 year-old man who was presented with cough, sputum, and fever. Chest radiographs showed a rapid, progressive cavitary lesion and pulmonary artery aneurysm. Angioinvastion of aspergillus was revealed by pathology after operative removal of left upper lobe containing the pulmonary artery aneurysm. He was treated with itraconazole.
Aneurysm* ; Aneurysm, Infected ; Aspergillus ; Bacteria ; Cough ; Fever ; Fungi ; Humans ; Immunocompromised Host ; Invasive Pulmonary Aspergillosis* ; Itraconazole ; Lung Diseases ; Pathology ; Pulmonary Artery* ; Pulmonary Aspergillosis ; Radiography, Thoracic ; Sputum ; Syphilis ; Tuberculosis

No abstract available.
Inhalation* ; Lung Injury* ; Lung*

BACKGROUND: Infectious complications frequently occur after cardiac arrest and may be even more frequent after therapeutic hypothermia. Pneumonia is the most common infectious complication associated with therapeutic hypothermia, and it is unclear whether prophylactic antibiotics administered during this intervention can decrease the development of early-onset pneumonia. We investigated the effect of antibiotic prophylaxis on the development of pneumonia in cardiac arrest patients treated with therapeutic hypothermia. METHODS: We retrospectively reviewed the medical records of patients who were admitted for therapeutic hypothermia after resuscitation for out-of-hospital cardiac arrest between January 2010 and July 2015. Patients who died within the first 72 hours or presented with pneumonia at the time of admission were excluded. Early-onset pneumonia was defined as pneumonia that developed within 5 days of admission. Prophylactic antibiotic therapy was defined as the administration of any parenteral antibiotics within the first 24 hours without any evidence of infection. RESULTS: Of the 128 patients admitted after cardiac arrest, 68 were analyzed and 48 (70.6%) were treated with prophylactic antibiotics within 24 hours. The frequency of early-onset pneumonia was not significantly different between the prophylactic antibiotic group and the control group (29.2% vs 30.0%, respectively, p = 0.945). The most commonly used antibiotic was third-generation cephalosporin, and the class of prophylactic antibiotics did not influence early-onset pneumonia. CONCLUSION: Antibiotic prophylaxis in cardiac arrest patients treated with therapeutic hypothermia did not reduce the frequency of pneumonia.
Anti-Bacterial Agents ; Antibiotic Prophylaxis* ; Heart Arrest* ; Humans ; Hypothermia* ; Medical Records ; Out-of-Hospital Cardiac Arrest ; Pneumonia* ; Resuscitation ; Retrospective Studies

BACKGROUND: Pulmonary fibrosis is the most common pulmonary complication in patients with end stage renal disease undergoing hemodialysis. The diffusing capacity is sensitive and reliable methods for diagnosis for pulmonary fibrosis. The aim of this study was to investigate the change of diffusing capacity for dialysis duration and membranes (synthetic vs cellulosynthetic) in maintenance hemodialysis patients. METHODS: We evaluated prospectively pulmonary diffusing capacity (DLCO/VA) of the patients who had been receiving regular hemodialysis for a period of at least 3 months at Gyeongsang National University Hospital from April 1, 2002 to June 30, 2003. Seventy one patients were divided into two groups by dialysis duration: less than 24 months; more than 24 months. Also, we divided patients into two groups by dialysis membrane: cellulosynthetic membrane (Hemophan); synthetic membrane (Polysulfone). RESULTS: The diffusing capacity and dialysis durations were presented for negative correlation [r= -0.321 (p=0.01) in DLCO/VA]. According to dialysis membranes, DLCO/VA values were significantly decreased in patients in Hemophan group rather than Polysulfone Group [92.4+/-20.5% vs 107.5+/-19.3%, (p= 0.01)]. According to dialysis durtation and membranes, DLCO/VA values were significantly decreased in patients in Hemophan group rather than Polysulfone group at duration for more than 24 months [84.9+/-20.1% vs 105.2+/-20.8%, (p=0.003)]. CONCLUSION: Patients undergoing long-term maintenance hemodialysis showed a gradual reduction in lung diffusing capacity for dialysis duration. Our results suggested that lung diffusing capacity was more severely reduced in hemodialysis patients using bioincompatible membrane rather than biocompatible membrane.
Diagnosis ; Dialysis* ; Humans ; Kidney Failure, Chronic ; Lung* ; Membranes* ; Prospective Studies ; Pulmonary Diffusing Capacity ; Pulmonary Fibrosis ; Renal Dialysis*

No abstract available.
Surgery, Oral* ; Transplants* ; Veins*

BACKGROUND: Arterial hypoxemia has been noted in patients with liver cirrhosis because of bronchial vessel dilatation. Cabenes et al. reported that bronchial hyperresponsiveness to the metacholine inhalation was observed in patients of left side heart failure, he suggested that one of the mechanism was bronchial vessel dilatation. We hypothesized that patients of liver cirrhosis might have bronchial hyperresponsiveness to metacholine inhalation due to portal hypertension. We evaluate the relationship between bronchial responsiveness and severity of liver cirrhosirs, severity of portal hypertension. METHODS: In the 22 patients of the liver cirrhosis with clinical portal hypertension metacholine provocation test was done and determined PC20 FEV1. We classified lifter cirrhosis according to Pugh- Child classification Esophagogastroscopies were performed for the evaluation of the relationship between bronchial hyperresponsiveness and severity of esophageal varix. RESULTS: In the 22 cases of the liver cirrhosis with clinical portal hypertension. The causes of liver cirrhosis, alcoholic hepatitis was 9 cases. hepatitis B virus was 12 cases, hepatitis C virus was 1 case. and 151 cases (68.18%) of total 22 cases were positive in metacholine provocation test. In positive cases There was no significant relationship between PC20FEV1 and severity of liver cirrhosis which were classified by Pugh-Child classification or severity of esophageal varix(p<0.05). CONCLUSION: we observed that bronchial responsiveness to metacholine increased in the patients of liver cirrhosis and there was no significant relationship between the severity of liver cirrhosis and the severity of esophageal varix.
Anoxia ; Child ; Classification ; Dilatation ; Esophageal and Gastric Varices ; Fibrosis ; Heart Failure ; Hepacivirus ; Hepatitis ; Hepatitis B virus ; Humans ; Hypertension, Portal ; Inhalation ; Liver Cirrhosis* ; Liver Cirrhosis, Alcoholic ; Liver*