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Query: UMLS:C0242379 (lung cancer)
71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological evidence suggests that cadmium (Cd) exposure causes pulmonary damage such as emphysema and lung cancer. However, relatively little is known about the mechanisms involved in Cd pulmonary toxicity. In the present study, the effects of Cd exposure on human fetal lung fibroblasts (MRC-5 cells) were evaluated by determination of lipid peroxidation, intra-cellular production of reactive oxygen species (ROS), and changes of mitochondrial membrane potential. A time- and dose-dependent increase of both lactate dehydrogenase leakage and malondialdehyde formation was observed in Cd-treated cells. A close correlation between these two events suggests that lipid peroxidation may be one of the main pathways causing its cytotoxicity. It was also noted that Cd-induced cell injury and lipid peroxidation were inhibited by catalase and superoxide dismutase, two antioxidant enzymes. By using the fluorescent probe 2',7'-dichlorofluorescin diacetate, a significant increase of ROS production in Cd-treated MRC-5 cells was detected. The inhibition of dichlorofluorescein fluorescence by catalase, not superoxide dismutase, suggests that hydrogen peroxide is the main ROS involved. Moreover, the significant dose-dependent changes of mitochondrial membrane potential in Cd-treated MRC-5 cells, demonstrated by increased fluorescence of rhodamine 123 examined using a laser-scanning confocal microscope, also indicate the involvement of mitochondrial damage in Cd cytotoxicity. These findings provide in vitro evidence that Cd causes oxidative cellular damage in human fetal lung fibroblasts, which may be closely associated with the pulmonary toxicity of Cd.
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PMID:Cadmium-induced oxidative cellular damage in human fetal lung fibroblasts (MRC-5 cells). 929 17

The mechanism(s) by which high-linear energy transfer a particles, like those emitted by inhaled radon and radon daughters, cause lung cancer has not been elucidated. Conceivably, DNA damage that is induced by a particles may be mediated by the metabolic generation of reactive oxygen species (ROS), in addition to direct a particle-DNA interactions and hydroxyl radical-DNA interactions. Using normal human lung fibroblasts, we investigated the hypothesis that densely ionizing alpha particles may induce the intracellular generation of superoxide (O2.-) and hydrogen peroxide (H2O2). Ethidium bromide and 2',7'-dichlorofluorescein, fluorescent products of the membrane-permeable dyes hydroethidine and 2',7'-dichlorofluorescin diacetate, respectively, were used to monitor the intracellular production of O2.- and H2O2, respectively, by flow cytometry. Compared to sham-irradiated cells, fibroblasts that were exposed to alpha particles (0.4-19 cGy) had significant increases in intracellular O2.- production, along with concomitant increases in H2O2 production. Further analyses suggest that the plasma membrane-bound NADPH-oxidase is primarily responsible for this increased intracellular generation of ROS and that the ROS response does not require direct nuclear or cellular "hits" by the a particles. In this latter regard, we additionally report that unirradiated cells also show the ROS response when they are incubated with serum-containing culture medium that has been exposed to a particles or when they are incubated with supernatants from a-irradiated cells. Our overall results support the possibility that a particles, at least in part, may mediate their DNA-damaging effects indirectly via a ROS-related mechanism.
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PMID:Alpha particles initiate biological production of superoxide anions and hydrogen peroxide in human cells. 930 80

Seven patients who had undergone a pneumonectomy for lung cancer developed a second tumor in the remaining lung after a mean time of 28.5 months and underwent a further resection. Preoperative evaluation was based on standard functional tests and on the "stair climbing test". Three patients were operated on using an extracorporeal oxygenator to work on a collapsed lung, three using standard anesthesiologic techniques, and one using high-frequency jet ventilation. There was no operative mortality. Complications occurred in two patients, requiring a temporary tracheostomy in one case. No patient required home oxygen supplementation. Four patients died of metastatic disease after 4, 8, 10, and 12 months, while two patients are alive and free of disease after 83 and 9 months, one is alive and free of symptoms but with a local recurrence after 29 months. Lung resection for bronchogenic carcinoma on a single lung can be safely performed provided that careful clinical judgment is used; long-term survival can be achieved with the resection of the new tumor.
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PMID:Lung resection on single residual lung after pneumonectomy for bronchogenic carcinoma. 947 58

The antioxidative effect of CuZnSOD, which catalyzes the dismutation of superoxide anion (O2-), provides a defense against the oxygen toxicity. The object of the study is to evaluate the erythrocytes superoxide dismutase (SOD) activity in two groups of persons (Group I, healthy blood donors; Group II, lung cancer patients), using the spectrophotometric assay of NADH oxidation and the indirect method. The effect of trace elements, such as Al3-, Cr3+, Fe3+, Hg2+, NI2+, and Pb2+ (producing free radicals oxygen and present in pollution and smoke) is also evaluated. The results show the decrease of SOD activity in lung cancer patients with respect to healthy individuals. Likewise, in those patients the enzymatic activity is bigger in early stage (I,II) with respect to advanced one (III) (p < 0.05). The lesser activity when the samples are incubated with Ni or Pb point out that these metals play a role in neoplasm development. In short, the oxidant-antioxidant balance is altered in lung cancer patients.
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PMID:Assay for erythrocyte superoxide dismutase activity in patients with lung cancer and effects on pollution and smoke trace elements. 949 59

Approximately three million workers in the United States are estimated to be exposed to silica, man-made mineral fibers, and asbestos. The lung is the primary target organ of concern. Each of these substances is composed predominantly of silicon and oxygen; asbestos and silica are crystalline, and asbestos and man-made mineral fibers are fibers. Man-made mineral fibers and asbestos are used as insulating agents, with the former having generally replaced the latter in recent years. Silica is used in foundries, pottery, and brick making, and is encountered by miners. A meta-analysis of 16 of the largest studies with well-documented silica exposure and low probability of confounding by other occupational exposures, indicates a relative risk (RR) of 1.3 (95 percent confidence interval [CI] = 1.2-1.4). Lung cancer risks are highest and most consistent for silicotics, who have received the highest doses (RR = 2.3, CI = 2.2-2.4, across 19 studies). The data for mineral fibers continue to support the International Association for Research on Cancer's 1988 judgment that mineral fibers are a possible human carcinogen (Group 2B). Recent epidemiologic studies provide little evidence for lung carcinogenicity for either glass wool or rock/slag wool. Ceramic fibers, a much less common exposure than glass wool and rock/slag wool, are of concern because of positive animal studies, but there are insufficient human data. Regarding asbestos, its carcinogenicity for the lung and mesothelium is well established. With regard to the controversy over chrysotile and mesothelioma, the data suggest chrysotile does cause mesothelioma, although it may be less potent than amphibole asbestos.
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PMID:Silica, asbestos, man-made mineral fibers, and cancer. 949 6

The management of primary lung cancer relies on sophisticated imaging methods to assist in the diagnosis, staging, and evaluation of tumor regression during treatment. The information provided is generally anatomical in nature, except for that provided by positron emission tomography with [18F]fluorodeoxyglucose, a modality that yields physiological data that have been shown to be useful in identifying neoplasia, based on an elevated glucose metabolic rate. Because the metabolism of malignant tissue depends intimately on neovascularization to provide oxygen and glucose in sufficient quantities to allow tumor growth, the characterization of tumor vascular physiology could be an important tool for assessing and predicting the likely effectiveness of treatment. Our goal was to show the feasibility and practical value of parameters of tumor vascular physiology obtained using dynamic T1-weighted magnetic resonance imaging (MRI), to correlate them with glucose metabolism and to demonstrate changes in these parameters during and after treatment in patients with lung cancer. Parameters of vascular physiology [permeability-surface area (PS) product and extracellular contrast agent distribution volume] and glucose metabolism were assessed in 14 patients with lung cancer. Glucose metabolism was measured by using [18F]fluorodeoxyglucose-positron emission tomography. Vascular physiology was assessed by dynamic T1-weighted, contrast-enhanced MRI. The mean PS product in tumor was 0.0015 +/- 0.0002 s(-1) (n = 13) before, 0.0023 +/- 0.0003 s(-1) (n = 3, P = 0.053) midway through, and 0.00075 +/- 0.0002 s(-1) (n = 5, P < 0.03) 2 weeks after treatment. Values for the extracellular contrast distribution space were 0.321 +/- 0.03 before, 0.289 +/- 0.02 midway through, and 0.195 +/- 0.02 (P < 0.01) 2 weeks after therapy. The glucose metabolic rate was significantly correlated with the PS product (P < 0.01) but not with the extracellular contrast distribution space. Our results demonstrate that tumor PS product correlates with glucose metabolism, that chemo- and radiotherapy induce observable and quantifiable changes in these parameters, and that such changes can be measured by in vivo dynamic MRI. Quantitative dynamic T1-weighted MRI of tumor vascular physiology may have a useful role in the clinical management of lung cancer.
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PMID:Dynamic T1-weighted magnetic resonance imaging and positron emission tomography in patients with lung cancer: correlating vascular physiology with glucose metabolism. 956 89

Connection between histological type of lung cancer and existence of clinical and spirometric symptoms of COPD was analysed in 110 lung cancer patients (64 small cell, 23 adenocarcinoma, and 23 squamous). It was shown that adenocarcinoma was significantly more frequent among subjects with values of FEV1%VC over 70 than among subjects with small cell and squamous lung cancer. Also subjects with values of FEV1% VC over 70 had significantly higher oxygen blood pressure, and clinical and radiological symptoms of COPD were less intensive than in subjects with values of this index below 70. There was no correlation between histological type of lung cancer and bronchoscopic symptoms of bronchitis and radiological symptoms of emphysema.
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PMID:[Coexistence of obstructive lung diseases and lung cancer]. 965 83

This article shows the results of a 10-year follow-up study conducted on a cohort of 870 patients affected by severe chronic airflow obstruction (CAO) on spirometric tests. The main aims of the study were to identify those factors associated with reduced survival in CAO patients and to evaluate the effectiveness of a care program on patients' survival. The analysis compared the survival time and causes of death between patients who showed adherence and patients who did not show adherence to the care program. The most important results can be summarized as follows: (1) CAO patients have a high mortality rate for acute respiratory failure, cor-pulmonale, and lung cancer; (2) patient's age at the time of selection to enter follow-up influences the death hazard; (3) patients who need long-term oxygen treatment (LTOT) have a higher death hazard than those who don't need it; (4) the higher is FEV1 or PaO2 value at the time of selection, the lower the death hazard; (5) patients who need, and regularly take, long-term oxygen treatment have a lower death hazard compared to those who need it, but do not take it properly; and (6) patients with a partial reversible airway obstruction (pRAO) who regularly attend the clinic for planned check-ups, have a lower death hazard compared to those who have the same characteristics, but do not show adherence to the care program. These results indicate that an organized program to treat severe CAO patients may improve their survival.
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PMID:Predictors of survival in a group of patients with chronic airflow obstruction. 967 61

The 8-hydroxydeoxyguanosine (8-OH-dG) levels in the peripheral parts of human lung tissues were compared between lung cancer patients (n=70) and non-cancer patient controls (n=15). An increased level of 8-OH-dG was observed in the lung cancer group, in both the adenocarcinoma and non-adenocarcinoma (mainly squamous cell carcinoma) groups, as compared to the non-cancer control group. This result suggests that reactive oxygen species are partly involved in the induction of lung carcinomas (both adenocarcinoma and non-adenocarcinoma).
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PMID:Lung cancer patients have increased 8-hydroxydeoxyguanosine levels in peripheral lung tissue DNA. 973 74

Whatever facts we gather and no matter how many we have, you and I must eventually put the journal down and pick up our stethoscope, pen, and prescription pad and go to work. Hopefully we can do better than, "Therapy is not uniform and specific antibiotic regimens are usually selected based on local tribal custom." We can discard an old paradigm, "The absence of data bears no relation to the strength of opinion." Personally, I have used these new scientific data before I reached my conclusion. I have developed 10 points to structure my new approach. I invite you to compare my conclusions to yours. 1. In acute bronchitis, in otherwise healthy adults, my preference is to not prescribe an antibiotic. If I do, it is not over the phone. You should want to see and examine the patient. If there are no helpful hints to etiology, I choose a newer macrolide for those under age 50 and use a short course, five-seven days. For patients over age 50, especially if they are "healthy smokers," consider a short course of cefuroxime. (You can see, even in these acute bronchitis patients, you want an antibiotic effective against today's pathogens.) 2. In all chronic bronchitis patients, prevention of further damage to the airways should be attempted by instituting a program of smoking cessation and appropriate immunizations against influenza and pneumococcus. 3. Treatment outcomes will also improve if we recognize that in some patients the progressing SOB, cough, and increasing sputum production are due to congestive heart failure and not due to infection. I try to think about congestive heart failure in all of my patients, but especially in those with known heart disease and cardiomegaly on their chest x-ray. 4. Routine pulmonary function testing is important in smoking patients. Physicians underestimate the degree of obstruction present when they rely on physical exam alone. Hopefully long before the patient's acute illness you have established whether or not obstruction is present. This information helps identify the high risk patient for not only recurrent bouts of infection but also those at increased risk for lung cancer. 5. We will have more success in treating AECB when we elect to use an antibiotic only for patients with at least two of the following three cardinal symptoms: increased dyspnea, increased sputum production, and increased purulent sputum. COPD patients have many days when they feel more SOB. To use this or any one sign as the sole indication for starting an antibiotic has been proven not to make a statistically significant difference in outcome in most patients. Also, the value of prophylactic antibiotic therapy has not been established. 6. When airflow obstruction is moderately severe or more pronounced, AECB should usually be treated with oral steroids. Other measures such as chronic bronchodilator therapy, supplemental and home oxygen use, and pulmonary rehabilitation have been extensively reviewed elsewhere.
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PMID:Challenging questions in treating bronchitis. 979 74


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