Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

LSP contents of sputum samples from patients with chronic airway diseases were measured by an enzyme-linked immunosorbent assay (ELISA) kit which was designed by Kuroki et al to examine whether a substance identical to lung surfactant contained in alveolar lining layer, is also contained in respiratory tract fluid or not in the ELISA kit. One antibody to LSP was conjugated to peroxidase and another one to LSP was fixed onto a bead. A neo-anionic detergent, Triton X-100 and an anionic detergent, sodium dodecyl sulfate (SDS) were added to extraction medium to separate LSP from lung surfactant, and LSP reaction of sputum sample was maximal when the ratio of Triton X-100 to SDS was in range of 1 to 4. Airway mucous glycoprotein (AMG) purified from sputum sample did not show any LSP reaction. In CsCl density gradient ultracentrifugation of whole sputum, the LSP reaction was detectable only in the top fraction with density of about 1.40 and AMG was located in the fraction with a density of about 1.50. These results indicate that the LSP reaction of sputum sample is not due to false reaction caused by nonspecific binding of viscous AMG to the two antibodies to LSP, but to the existence of LSP. Therefore it was concluded that lung surfactant is contained in respiratory tract fluid. In general, the LSP concentrations in sputum samples were lower in purulent sputa than in mucoid or mucopurulent sputa, and lower in patients with diffuse panbronchiolitis and bronchiectasia than in those with pulmonary emphysema and chronic bronchitis. It was shown that LSP was hydrolyzed by neutrophil leucocyte homogenate. These results suggest that LSP content of sputum is influenced by various factors such as infection and disease in the respiratory tract, and thus is useful to estimate pathological states of chronic airway diseases.
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PMID:[Lung surfactant apoprotein (LSP) content of sputum samples from patients with chronic airway diseases]. 221 2

In bronchial asthma, eosinophils and neutrophils are activated, so that the production of active oxygen species increases, causing airway epithelial injury. Suplatast tosilate (IPD Capsules) is a novel immunomodulating antiallergic drug that acts against bronchial asthma through a new mechanism. To evaluate the effects of suplatast tosilate on mononuclear cell-mediated IL-8 production, and neutrophil-mediated active oxygen species production at sites of inflammation, we collected peripheral blood from healthy subjects and separated the neutrophils as well as mononuclear cells. Suplatast tosilate was added at a concentration of 1 x 10(-6), 1 x 10(-7) or 1 x 10(-8) M, and cells were incubated for 10 min at 37 degrees C. Then, the neutrophils were stimulated with fMLP, and luminol-dependent chemiluminescence (LDCL) was measured, while IL-8 production was determined with an ELISA kit. Suplatast tosilate (1 x 10(-6) M) inhibited neutrophil-mediated active oxygen species production by 12.4% in terms of the peak, and by 16% in terms of the integral value. Moreover, it significantly inhibited mononuclear cell-mediated IL-8 production at concentrations of 1 x 10(-6), 1 x 10(-7) and 1 x 10(-8) M, in a concentration-dependent manner. This study indicated that suplatast tosilate may inhibit neutrophil infiltration by suppressing monocyte-mediated IL-8 production, and it may also inhibit the activation of neutrophils at sites of inflammation. These results suggest the possibility that suplatast tosilate may not only be of benefit for asthma, but may also prevent or control pulmonary fibrosis or emphysema, for which no effective treatment is presently available.
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PMID:Effects of suplatast tosilate (IPD Capsules) on the production of active oxygen by neutrophils and of IL-8 by mononuclear cells. 1140 12

Lung disease is the leading and second-leading cause of death in women and men in Taiwan, respectively. Epidemiological studies conducted in Taiwan have shown that cigarette smoking is the principal risk factor of lung disease, but little is known about the association between apoptosis and cigarette smoke (CS)-induced lung pathogenesis. We designed an animal exposure system to study signal proteins involved in the process of apoptosis induced by smoking in rat terminal bronchiole. Rats were exposed to CS in doses of 5, 10, and 15 cigarettes, respectively, and the exposure lasted for 30 min, twice a day, 6 days a week for 1 month. Following which the rats were sacrificed and the lung tissues were analyzed by histopathological methods. The terminal bronchioles revealed mild to severe inflammation according to the doses of CS and marked lipid peroxidation, lymphocyte infiltration, congestion, and epithelial emphysema of alveolar spaces were also noted. Using an in situ cell death detection kit (TA300), the association of CS with apoptosis was determined in a concentration-dependent manner. Immunohistochemical evaluation showed that CS treatment produced an increase in the cellular levels of Bax, t-Bid, cleaved caspase-3, phospho-p53, phospho-JNK, and FasL but a decline in Bcl-2 and Mcl-1 (p<0.001 for all) in rat terminal bronchioles. The results provided evidences suggesting that exposure to CS not only induced apoptosis, but also involved p53/Bax and JNK/FasL cascade pathway.
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PMID:Immunohistochemical detection of apoptotic proteins, p53/Bax and JNK/FasL cascade, in the lung of rats exposed to cigarette smoke. 1634 95

Cigarette smoke (CS), a major risk factor in emphysema, causes cell death by incompletely understood mechanisms. Death-inducing signaling complex (DISC) formation is an initial event in Fas-mediated apoptosis. We demonstrated cigarette smoke extract (CSE) induced DISC formation in human lung fibroblasts (MRC-5). The aim of this study was to investigate the involvement of extracellular signal-regulated kinase (ERK) MAPK activation in CSE induced DISC formation. Immunoprecipitation (IP) for Fas and Western Immunoblot (IB) analysis for caspase 8 were then performed to show DISC. Lactate dehydrogenase (LDH) release was measured using a cytotoxicity detection kit. MTT assay was used as a measure of cell viability. We demonstrated that CSE induces DISC formation in MRC-5 using IP for Fas and IB for caspase 8. ERK was expressed in MRC-5 exposed to CSE. MEK-1 inhibitor (PD98059) decreased DISC formation in MRC-5 exposed to 20% CSE at 1 hr, and cell viability, as assessed by colorimetric MTT assay, was increased in MEK-1 inhibitor treated MRC-5 cells after 24 hr CSE exposure compared to the control. Inhibiting ERK significantly decreased the caspase-3,-8 activity in MEK-1 inhibitor treated MRC-5 cells compared to the control.The DISC formation, initial event of extrinsic apoptotic pathway, is a primary component of CSE- induced death in MRC-5, and ERK activation plays an active role in the DISC formation and downstream pathway. These results suggest that modulation of ERK may have therapeutic potential in the prevention of smoke-related lung injury.
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PMID:Extracellular signal-regulated kinase (ERK) inhibition attenuates cigarette smoke extract (CSE) induced-death inducing signaling complex (DISC) formation in human lung fibroblasts (MRC-5) cells. 2011 22

Percutaneous dilatational tracheotomies (PT) are commonly performed in the ICU. The procedure carries the risk of complications, among them severe events as loss of airway or pneumothorax. In this case report we describe complications related to a PT procedure in the ICU. The procedure was performed with a single dilator kit, and by visual guidance of a bronchoscope. Because of difficulties with the insertion of the tracheal cannula, the procedure was aborted, and the endotracheal tube (ET) reinserted. After placement of the ET, subcutaneous emphysema emerged. Upon digital exploration in the tracheotomy incision the tube was found to exit from the trachea, the tube-tip being situated para-tracheally. The tube position was corrected using a finger in the incision, and the patient could again be ventilated. Poor visual conditions may occur during PT because of bleeding. Importantly, there is a risk for the ET to exit an incision in the trachea when reintubating during a PT procedure, or after decannulation. This can be prevented using digital occlusion of the tracheal opening.
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PMID:Paratracheal placement of orotracheal tube: a complication when aborting percutaneous tracheotomy. 2174 35

Prevention of the initiation of tobacco use, which is associated with increased risk of developing cancer of the lung, the oral cavity, larynx, and emphysema, should target middle school-age children because that is where experimentation with tobacco use usually begins. Millions of children attending school do not receive proper education regarding the biological science of the human respiratory system coupled with the impact that tobacco use has at the cell, tissue, and organ levels of biological organization because their teachers are ill-prepared and ill-equipped to teach this normal and cancer-related content. The University of Arkansas for Medical Sciences has a statewide outreach program that provides middle school teachers training in a "Healthy Lungs" curriculum that covers the normal functional anatomy of the respiratory system as a basis for adding the effect of tobacco use and its associated cancers and emphysema. This training also provides each participant a resource kit of supplies, materials, and items of equipment. A long-term implementation survey identified a high degree of transference of content and use of the resource kit items into new classroom learning activities for the trainee's students for both the normal functional anatomy of the human respiratory system and associated general and cell/tissue/organ-specific cancer biology.
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PMID:Healthy Lungs: cancer education for middle school teachers using a "train and equip" method. 2193 99

The qualitative and quantitative deficiency of alpha-1-antitrypsin (A1AT) is an inherited factor of susceptibility to a number of conditions including chronic obstructive disease of lungs and primary emphysema and liver affection. The study was carried out to evaluate analysis of alpha-1-fraction (A1F) using zonal electrophoresis technique for detecting patients with alpha-1-antitrypsin insufficiency (A1ATI). The patients with decreased (group I) and normal (group II) A1F on proteinogram. The electrophoresis was applied using the system of capillary electrophoresis Capillaris-2 Flex Piercing (Sebia, France) and also system for electrophoresis in agarose gel SAS-1/SAS-2 (Helena Biosciences, Great Britain). The commercial kit Sentinel diagnostics (Italy) and biochemical analyzer A15 (Biosystems, Spain) were used for quantitative detecting of A1AT The study results demonstrated that decreasing of A1F on proteinogram correlated with lessening of concentration of A1ATI in blood serum and with presence of its pathological phenotype. The average values of concentration of A1AT in group I and group II made up to 1148 and 1738 mg/I correspondingly. The total rate of pathological phenotypes made up to 76% (19/25) in group I that reliably differed from indicators in group II--7.1% (2/28). Thereby, electrophoresis of proteins of blood serum can be sufficiently informative for primary selection of patients requiring examination for presence of A1ATI.
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PMID:[THE COMPARISON OF TECHNIQUES OF ELECTROPHORESIS, IMMUNE TURBIDYNAMIC MEASUREMENT AND PHENOTYPING OF ALPHA-1-ANTITRYPSIN FOR DIAGNOSTIC OF ALPHA-1-ANTITRYPSIN INSUFFICIENCY]. 2684 69

A 76-year-old woman with right mandibular gingival cancer was scheduled for surgery. A percutaneous tracheostomy kit was used for tracheostomy under intravenous sedation. After puncturing the cricothyroid membrane, a dilator was inserted along a guidewire. Bucking was observed at the time of insertion of the dilator, despite intratracheal lidocaine spray applied before insertion. After that, the tracheostomy tube was inserted, but no capnographic waveforms appeared when the tube was connected to the anesthesia circuit. Direct macroscopic observation revealed a perforation extending from the posterior wall of the trachea to the anterior wall of the esophagus, which prompted us to request assistance from a thoracic surgeon for treatment before reinserting the tracheostomy tube. After verifying capnographic waveforms on the monitor, anesthesia was induced. Because arterial oxygen saturation was 96% under the administration of pure oxygen, chest radiography was conducted revealing a right pneumothorax. A chest tube was inserted and the patient transported to a nearby general hospital. We suspect that pneumothorax was induced when the integrity of the mediastinal pleura was compromised by mediastinal emphysema because of the injury to the posterior tracheal wall complicated by bucking at the time of insertion of the dilator.
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PMID:Tension Pneumothorax After Percutaneous Tracheostomy. 2860 85