Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chlamydia pneumoniae infection has been implicated in several chronic lung diseases by serology and direct antigen detection. Acute lower respiratory tract infection caused by C. pneumoniae seems often to precede attacks of asthma in both children and adults. Chlamydia pneumoniae is also involved in some exacerbations of chronic bronchitis and chronic obstructive lung disease but, more importantly, seems to be strongly associated with the latter irrespective of exacerbation status. Moreover, persistently elevated C. pneumoniae antibody titres have been observed in sarcoidosis and lung cancer.
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PMID:Chlamydia pneumoniae and chronic lung diseases. 925 79

Trends in mortality rates for respiratory disorders were investigated in Italy from 1979 to 1990, using data from the Italian Central Statistical Institute (ISTAT). Mortality from lung cancer increased in all age groups, except for those aged 45-64 yrs after 1985. Respiratory diseases showed a consistent reduction; in particular, mortality from emphysema decreased slowly, and mortality from chronic bronchitis showed a significant reduction in all age groups. However, mortality from asthma increased markedly in all age groups up to 1985, and then levelled off and slightly decreased, although remaining at a higher level than in the 1970s. In 1990, data stratified for age group and gender indicated a higher mortality rate in males, that tended to be age-dependent, with the highest rate ratio male/female in those aged 65-74 yrs. Overall, these data indicate a trend to increased mortality from lung cancer and asthma in Italy in the 1980s.
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PMID:Mortality rates for respiratory disorders in Italy (1979-1990). 927 Feb 43

The thickness of the basement membranes of bronchial epithelial cells varies under various pathological conditions. It has been reported that this membrane is thickened in patients with bronchial asthma. By light microscopy, this parameter was measured in biopsy specimens of bronchial mucosa obtained by fibre-optic bronchoscopy. These specimens were obtained from 171 patients who had undergone bronchial biopsy between 1984 and 1994. It was demonstrated that the thickness of the basement membrane of bronchial epithelial cells was weakly correlated with the patient's age, when thickness was examined in patients with lung cancer (r = 0.242, P = 0.0268). The basement membranes in patients with bronchial asthma (8.193 +/- 1.362 mu, mean +/- SEM) were significantly thicker than those without bronchial asthma (5.145 +/- 0.233 mu) (P = 0.0180, Mann-Whitney's U-test). In addition, it is noteworthy that the basement membranes in patients with diabetes mellitus (7.217 +/- 0.753 mu) were also significantly thicker than those without diabetes mellitus (4.968 +/- 0.235 mu) (P = 0.0038, Mann-Whitney's U-test). The background or underlying pathophysiology in such patients should be studied further, with attention directed towards the thickness of the bronchial basement membrane in bronchial biopsy specimens.
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PMID:Thickness of the basement membrane of bronchial epithelial cells in lung diseases as determined by transbronchial biopsy. 932 41

We have found that many synthetic selenoorganic compounds, including ebselen, have immunotropic activity. These studies were designed to assess the effect of the analog of ebselen bis[2-pyridyl (2-carbamoyl) phenyl]diselenide (AE-22) on human leukocytes that may express various activation states. The cells were obtained from bronchoalveolar lavage (BAL) cells of patients with various inflammatory lung diseases. The AE-22-treated BAL cells from patients with bronchial asthma (n = 6) and with small cell lung cancer (SCLC) (n = 6) were compared with these in the peripheral blood leukocytes (PBL) from the same donors. The control group comprised 5 patients who underwent diagnostic examination and were free of any cancer or concomitant diseases. Secretion of TNF-alpha, IL-6, and IFN-gamma was considered as a marker of BAL or PBL cell activation. Different response of the cells and various effects of AE-22 were observed in relation to the origin and functional state of leukocytes. It was established that AE-22 can induce TNF-alpha, IL-6, and IFN-gamma in a dose-dependent manner in BAL cells and PBL isolated from healthy individuals. However, BAL cells were found to be less reactive than PBL as cytokine producers. In contrast, AE-22 had no effect on BAL cells obtained from patients with lung cancer, which were found to be hyporeactive to phytohemagglutinin and bacterial lipopolysaccharide and did not produce TNF-alpha, IL-6, or IFN spontaneously. The spontaneous release of cytokines by BAL cells from bronchial asthma patients, but not by PBL from the same individuals, was significantly (p < 0.01) higher than that from the cultures of healthy control subjects. The high secretion of cytokines by the locally activated BAL cells was significantly (p < 0.01) reduced after administration of AE-22. The results suggest that AE-22 has immunomodulatory activity. AE-22 can downregulate the hyporeactive BAL cells from asthmatics, but it appears to be inactive in BAL cells of cancer patients who can tolerate the cytokine inducers.
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PMID:Modulation of cytokine production by a selenoorganic compound (AE-22) in hyperreactive or hyporeactive bronchoalveolar leukocytes of asthmatics or lung cancer patients. 935 62

The harmful effects of passive smoking are well known and proved. A cause-and-effect relationship between involuntary inhalation of cigarette smoke and increased number of various respiratory diseases either in children or in adults is now clearly established. Many publications indicate that the respiratory consequences of passive smoking in humans may include nonmalignant disease in addition to lung cancer. It has been observed that children exposed to cigarette smoke have more frequently asthma and other wheezing diseases. An influence of the passive smoking on the pulmonary function tests has been also widely examined. A functional disorders especially of bronchioles have been detected. Since adverse effects of passive smoking on human health are proved there is a necessity to enable life in the environment free from cigarette smoke.
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PMID:[The influence of passive smoking on the respiratory tract]. 938 Aug 12

Lung diseases, defined by ICD-9 diagnoses on medical insurance claims, were studied through the combined use of administrative records, private health insurance, and workers' compensation claims for a cohort of 10,938 active union carpenters between 1989 and 1992. The cohort defined the study base for a nested case-control study, in which cases (n = 220) were initially identified by an ICD-9 code for asthma in private health insurance or workers' compensation files. A questionnaire was used to collect information on respiratory history and potential home and workplace exposures. Questions used by Burney et al. to define a discriminant function predictor (DFP) of a bronchial response to histamine were used to reclassify cases and controls for further exploratory analyses. Bronchitis accounted for over 50% of the lung disease cases among this cohort followed by asthma, chronic obstructive airway disease, and chronic bronchitis. Incidence density rates of asthma, chronic bronchitis, and chronic obstructive airway disease adjusted for age, sex, and time in the union increased with increasing age. Using Surveillance, Epidemiology, and End Results (SEER) Program data to estimate expected lung cancer cases in our cohort, an elevated standardized incidence rate (SIR) was seen among male carpenters between the ages of 45-54. Smoking history was not available for the entire cohort. Using the ICD-9 or Burney case definition of asthma, odds ratios were significantly elevated for exposure to hay, epoxy paints, enzymes, animals, and molds. Additional exposures associated with asthma using Burney's definition, are ones to which a majority of these carpenters were exposed including cement, drywall, and demolition dusts.
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PMID:Respiratory diseases among union carpenters: cohort and case-control analyses. 943 46

To study the mechanisms contributing to the recruitment of a selective leukocyte subset in allergic inflammation involving the airways as may occur in asthma, we examined whether allergic exposure induces the expression of cell adhesion molecules (CAMs) on the bronchial endothelium of passively sensitized human bronchi. Human bronchial tissue obtained from patients undergoing lung cancer surgery was passively sensitized with serum from patients with atopic asthma who were sensitive to house dust mite. We incubated the tissues for 30, 120, 240, and 480 min in the presence or absence of the dust mite allergen. The tissues were stained immunohistochemically for intercellular adhesion molecule 1 (ICAM-1), E-selectin, and vascular cell adhesion molecule 1 (VCAM-1). ICAM-1 was constitutively expressed in both the epithelium and endothelium in all tissues but after allergen stimulation significantly increased at 240 and 480 min. E-selectin expression also existed constitutively and increased significantly at 120 and 240 min with allergen exposure. The constitutive expression of VCAM-1 was less than that of ICAM-1 and E-selectin. Following allergen exposure, VCAM-1 expression increased significantly at 30, 120, 240, and 480 min, and at 480 min reached an almost 3.5-fold increase from baseline expression. The TNF-alpha level in the supernatants significantly increased at 120 min after allergen stimulation, and the interleukin (IL)-1beta level increased in 4 of 15 samples. We also examined the induction of CAMs by TNF-alpha, IL-1beta, and IL-4 on human bronchial tissue. TNF-alpha and IL-1beta increased the expression of ICAM-1, E-selectin, and VCAM-1, whereas IL-4 induced only that of VCAM-1. In addition, neutralizing antibody against TNF-alpha and IL-1beta partially blocked the upregulation of CAMs on passively sensitized bronchial tissue after allergen exposure. Thus, both an IgE-dependent allergic response and selected cytokines are able to upregulate endothelial CAMs in human bronchial tissue. These observations provide further evidence that leukocyte infiltration into the site of allergic inflammation as occurs in atopic asthma is in part regulated by the expression of ICAM-1, VCAM-1, and E-selectin.
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PMID:Allergen exposure induces the expression of endothelial adhesion molecules in passively sensitized human bronchus: time course and the role of cytokines. 944 41

Respiratory transfer impedance (Ztr) measured using the forced oscillation technique requires virtually no patient cooperation and provides a noninvasive approach for acquiring data reflective of lung mechanics. Also, model analysis of Ztr provides reliable estimates of separate airway and tissue properties (1), but only if data out to 64 Hz are acquired. The current study evaluated the clinical utility of Ztr from 1-80 Hz for assessing the degree and type of impaired lung function. Spirometry and Ztr measurements were made on 37 individuals: 11 healthy subjects and 26 patients with lung disease including chronic obstructive pulmonary disease (COPD), asthma, lung cancer, and sarcoidosis. Over the entire patient group, 12 were also smokers. We first established normal ranges for several Ztr features and model estimated mechanical properties. The COPD and smokers groups showed significant differences in portions of their Ztr spectra from that of the healthy group. Key Ztr spectral features included R0, the frequency at which the real part of impedance is zero; and Re4, the real part of impedance at 4 Hz. The key model parameter was airway resistance, Raw. We found Raw, Re4, and R0 to be significantly elevated during disease (p < 0.0005) and to significantly decrease with bronchodilator therapy (p < 0.025). Moreover, we found moderate to strong correlations between R0, Raw, and Re4 versus FVC and R0 versus FEV1. After bronchodilator, changes in R0, Re4, and Raw were correlated with changes in several spirometric indices. The R0 feature has not been previously evaluated since it is typically above 32 Hz (well above 32 Hz in diseased individuals) and not encompassed in previous clinical studies.
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PMID:Use of transfer impedance measurements for clinical assessment of lung mechanics. 947 55

The aim of this study was to systematically compare the interaction of the long-acting beta2-adrenoceptor agonists formoterol and salmeterol with short-acting beta2-adrenoceptor agonists in contracted human bronchi. Human bronchi were obtained at thoracotomy from patients with lung cancer. Formoterol or salmeterol at concentrations inducing up to 92 and 94% of their maximal relaxant effect, respectively, were added to bronchial rings contracted with carbachol (10(-6) M). After a time period of 30 min, concentration-response curves for the short-acting beta2-adrenoceptor agonists, salbutamol, terbutaline, isoprenaline and fenoterol were recorded. Administration of equieffective concentrations of salmeterol and formoterol, resulted in only salmeterol inducing a shift to the right of isoprenaline, terbutaline, fenoterol and salbutamol concentration-response curves. The rank order of shift was salbutamol > fenoterol > terbutaline > isoprenaline. Formoterol, up to concentrations of 3x10(-9) M induced submaximal relaxation resulting in no shift in short-acting beta2-adrenoceptor agonist concentration-response curves. Salmeterol but not formoterol appears to antagonize the relaxation of human contracted bronchi induced by short-acting beta2-agonists. These results obtained in vitro cannot be translated in clinical terms. This study, however, highlights the need for clinical studies on the interaction of long-acting and short-acting beta2-adrenoceptor agonists in acute severe asthma.
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PMID:Long- and short-acting beta2 adrenoceptor agonists: interactions in human contracted bronchi. 959 6

Asthma is a common chronic childhood disease yet not much is known about factors that determine its outcome. Cigarette smoke has been associated with lung cancer in adults but its effects on children has hitherto been underestimated and not well studied. Cigarette smoke has been noted through various research studies to influence the development and or the exacerbation of asthma in childhood. Furthermore the prevalence of childhood asthma is higher among the children of smoking parents, more so when both parents are smokers as compared to those of non-smoking parents. Corroborative evidence indicates elevated urine cotinine levels amongst children of smoking parents than those of non-smoking parents. There is a corresponding increase in prevalence and exacerbation of asthma symptoms among children with raised urine cotinine levels than those with low levels. The presence of other risk factors increases the risk of development and exacerbation of bronchial asthma in children exposed to tobacco smoke than those not exposed. Cigarette smoking is on the increase, especially in developing countries due to aggressive advertising and exportation by the tobacco industry from developed countries. International legislation is needed to regulate the production and exportation of tobacco products. However, this may be resisted by the influential tobacco industry and may not get the support from the developing countries due to economic gains from the sale of tobacco products. This scenario poses major health problems for the developing countries in the future.
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PMID:Relationship between exposure to tobacco smoke and bronchial asthma in children: a review. 960 35


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