Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenoid cystic carcinoma of the tracheobronchial tree in five patients was treated surgically and the clinicopathologic manifestations and histogenesis were examined in detail. Symptoms such as cough, dyspnea, hemoptysis, and atelectasis on chest X-ray were present in four patients, and the other patient was asymptomatic. Histologically, growth patterns were classified as tubular, cribriform, and solid. The solid pattern was the most aggressive with extensive perineural invasion. Immunohistochemically, secretory component, lactoferrin, and epithelial membrane antigen were present in the cells lining the gland-like lumen of tissues with the tubular and cribriform patterns, but was rare in those with a solid pattern. Desmin and S-100 protein were detected in the nonlining cells of tissues with all three patterns. These findings suggest that this tumor originates from the myoepithelial cells of the bronchial gland and that the solid pattern was the most poorly differentiated form.
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PMID:Adenoid cystic carcinoma of the tracheobronchial tree: clinicopathology and immunohistochemistry. 254 Dec 82

Normally the daily volume of lower respiratory tract secretions, in man, is probably less than 100 ml. In hypersecretory disease the volume increases sufficiently to cause cough and expectoration of secretions as sputum. The proportions which are sol or gel vary in disease as does the way in which constituent molecules partition in each phase. The constituent molecules and the cells which produce them (indicated in parentheses) may be classified as follows: 1. Mucus-glycoproteins present as droplets, or sheets (produced by mucous cells), periciliary fluid (serous or ciliated cell or a transudate), surface muco-substance (all epithelial cells) or surfactant hypophase (Clara or type II alveolar cells). 2. Proteins and peptides such as lysozyme (serous cell and macrophage), lactoferrin (serous cell and neutrophil), secretory piece (surface epithelium and submucosal glands), regulatory neuropeptides (dense-core granulated cell and both motor and sensory nerves) and fibronectin (alveolar macrophages). 3. Glycosaminoglycans such as heparan sulphate (epithelial membranes), heparin (mast cell), chondroitin sulphates and hyaluronate (connective tissue constituents). 4. Lipids including triglycerides (stored in cells) glycolipids (cell membrane), phospholipids (type II alveolar cells), sphingolipids (cell membrane), steroids (? Clara cells) and terpenes (cell membrane). 5. Anti-proteases and anti-oxidants such as bronchial protease inhibitors (serous anc Clara cells), alpha-2-macroglobulin (macrophage), alpha-1-antitrypsin (transudate) and anti-oxidants (type II alveolar cell and macrophage). 6. Other 'secretions' including ions and water (surface epithelium and submucosal glands), mediators of inflammation (migratory cell granules and their membranes), and serum proteins (present in transudate/exudate).
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PMID:The origins of secretions in the lower respiratory tract. 332 67

Pulmonary tuberculosis is one of the most prevalent infectious diseases in Japan. Host defense mechanisms may play an important role in every aspect of the disease, for example in acquiring the disease and/or in progression of the clinical course. Host defense mechanisms are constituted from mechanical protection such as cough or sneeze, chemical resistance such as complements or lactoferrin, nonspecific cellular defense such as macrophages or neutrophiles and specific immunological defense mechanisms such as immunoglobulins or immunocompetent cells. If there were any complicated disease other than pulmonary tuberculosis, the disease outcome might become different. We examined 44 patients whose sputa culture was continuously positive for one year or more, despite of administration of anti-tuberculous regimens. And we also analyzed clinical outcome of 556 patients with pulmonary tuberculosis (control group) who were discharged after bacteriological negative conversion. Diabetes mellitus is one of the most common complications in patients with pulmonary tuberculosis, 11/44 in continuously positive patients and 101/580 in control group. There was no statistical significance between these two. Next, the control group was divided into four subgroups, those were 1. no complication, 2. complicated with diabetes mellitus, 3. complicated with liver dysfunction, 4. complicated with the other diseases. Bacteriological negative conversion rate was analyzed in these four subgroups. At the first and the second month, there were significant difference in negative conversion rate between subgroup 1 and 2. But these differences disappeared as the time goes by.
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PMID:[From the aspects of complicated diseases]. 880 69

An overlap of breast-feeding and late pregnancy is associated with decreased intake of human milk and reduced infant growth. We evaluated the association of an overlap with macronutrient and immunological components of milk, infant urinary IgA, and infant and maternal morbidity. On d 2 and 1 mo postpartum, staff measured 24-h intake of breast milk and collected samples from 133 Peruvian women; 68 had breast-fed during the last trimester of pregnancy (BFP) and 65 had not breast-fed during pregnancy (NBFP). Data on maternal and infant anthropometry and health were collected for 1 mo. On d 2, lactose and lysozyme concentrations were higher, total lysozyme intake was higher and concentration and total intake of lactoferrin were lower in the BFP than the NBFP group (P < 0.05). The total 1-mo IgA intake was lower among BFP than NBFP infants (P = 0.01). Urinary IgA concentration was correlated with breast milk IgA concentration (r = 0.29; P = 0.01) but not with breast-feeding during pregnancy. An overlap was not associated with diarrhea but BFP infants were 5 times as likely to have a cough for at least 7 d than NBFP infants (P < 0.05). Reported mastitis was rare and occurred only in the NBFP group (P = 0.05). An overlap of breast-feeding and late pregnancy was associated with changes in milk composition, an increased frequency in symptoms of infant respiratory illness but decreased reported mastitis. Further in-depth studies are warranted to determine the cumulative effects associated with a breast-feeding/pregnancy overlap on infant and maternal outcomes.
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PMID:An overlap of breastfeeding during late pregnancy is associated with subsequent changes in colostrum composition and morbidity rates among Peruvian infants and their mothers. 1288 42

The mechanisms of bronchial secretion are an important part of the innate defense system that protects the airways against pathogens and environmental toxins. Bronchial secretions are mainly produced by goblet cells and submucosal glands but also small amounts of surfactant from clara cells and some other fluids are part of the airway epithelium fluid. Together with the ciliary system the bronchial secretions are essential for the bronchial clearance ("mucociliary clearance"). Cilia beat within a periciliary layer with low viscosity ("sol-phase"). They move the overlying mucous sheet ("gel-phase") by their tips towards the nose to remove those mucous particles together with foreign material and pathogens from the airways. The gel-layer of the airway epithelium fluid is formed mainly by water, mucins (MUC) and free proteins. Mucins are highly glycosylated macromolecules, to date more than 18 different MUC-genes have been described. In addition the airway epithelium fluids contains many antibacterial proteins and peptides including lysozyme, lactoferrin, secretory IgA, complement, beta-defensines as well as many others. Acute inflammatory or toxic stimuli can promote hypersecretion of mucins mediated by a large variety of cytokines and chemokines or even directly like some toxins. Chronic inflammatory conditions like asthma or COPD are associated with hyperplasia of goblet cells and submucosal glands thus increasing the secretory capacity of the airways. The system of mucociliary clearance forms a functional unit together with the coughing mechanisms discussed elsewhere in this journal.
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PMID:[Physiology and pathophysiology of bronchial secretion]. 1831 75

This study reported detailed clinical effects of bovine lactoferrin on 2 canine littermates (1 female and 1 male) with familial neutrophil dysfunction and an investigation of their genetic background. Clinical signs caused by severe upper respiratory bacterial infections were observed in these dogs. Oral administration of bovine lactoferrin for a long duration improved their clinical signs (severe uveitis in the female dog and coughing from pneumonia in the male dog). Their backcross dogs that have the same father didn't show clinical signs of bacterial infection. Neutrophil function tests revealed that the backcross dogs didn't have any disorders. It is likely that abnormal clinical signs are associated with neutrophil dysfunction in the colony, and the mother dog of these cases might be the genetic carrier of this dysfunction.
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PMID:Clinical effects of bovine lactoferrin on two canine cases with familial neutrophil dysfunction. 2253 Nov 2

We report a case of localized bronchial lactoferrin amyloidosis. A 47-year-old man presented with a complaint of persistent dry cough for two months. Chest computed-tomography revealed a calcification shadow of the right main bronchus; hence, a biopsy was performed, showing layered spheroid-type eosinophilic deposits in the bronchial wall. These deposits were positive for Congo red staining, exhibiting apple-green birefringence under polarized light. In addition, an electron microscopic examination demonstrated that this layered structure was formed by very thin cord-like amyloid deposits. By proteomics analysis using liquid chromatography-tandem mass spectrometry and immunohistochemistry, we confirmed that the deposited amyloid was composed of lactoferrin. While lactoferrin is known to be a precursor protein of localized corneal and seminal vesicle amyloidosis, localized lactoferrin amyloidosis of the bronchus has not been reported in the English literature. Our pathological findings suggested that localized lactoferrin amyloidosis may be caused by long-term tissue damage, and the characteristic spheroid-type appearance is thought to be associated with unique, thin cord-like amyloid deposits.
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PMID:A case of spheroid-type localized lactoferrin amyloidosis in the bronchus. 3077 53