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Biomedical subjects

J L Wright

Publications and source records attributed to J L Wright.

At least 163 records · Page 9Linked to original sources
PubMed1987

Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig.

In order to assess the effects of cigarette smoke and asbestos exposure, we divided guinea pigs into 4 groups: smoking or nonsmoking, and asbestos-exposed or not asbestos-exposed groups. Asbestos-exposed animals were given a single intratracheal instillation of 5 mg UICC amosite, a dose and method of administration that we have previously shown produces morphologic changes in the small airways as well as minimal interstitial fibrosis. Animals were smoked 5 days per week for 6 months. By itself, smoking did not affect lung collagen content, small airways wall thickness, or the volume fraction of tissue surrounding airways, but it did cause a significant increase in alveolar mean linear intercept (Lm). Asbestos alone increased collagen content, airway wall thickness, and tissue volume fraction surrounding airways, the latter measure used to assess interstitial fibrosis. An unexpected finding was that asbestos also increased Lm. The two agents administered together caused more severe changes of all types than were produced by either agent alone, and the interaction between the 2 was generally synergistic. Smoke-exposed animals retained 3 times the asbestos fiber burden of those not smoke-exposed; the increase in retention was greater for short than for long fibers. We conclude that cigarette smoke can potentiate the fibrosis induced by asbestos, possibly because of increased fiber retention. As well, in this model, asbestos or asbestos plus cigarette smoke produces increases in alveolar size.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

A comparison of bronchiolitis obliterans with organizing pneumonia, usual interstitial pneumonia, and small airways disease.

This report is based on 43 cases where a diagnosis of either bronchiolitis obliterans with organizing pneumonia (BOOP), usual interstitial pneumonia (UIP), or small airways disease (SAD) was established by lung biopsy. The severity of histologic abnormalities in the peripheral airways and interstitial spaces were measured on these biopsies using semiquantitative techniques and compared with the clinical data available in 42 of 43 cases, preoperative chest radiographs in 31 of 43, and preoperative pulmonary function tests in 29 of 43. The data show that when a diagnosis of BOOP was made, there was a higher total pathologic score for membraneous bronchiolitis (MB) and respiratory bronchiolitis (RB) than for UIP and SAD (p less than 0.005). This was due to peribronchiolar inflammation and the presence of loose connective tissue in the RB lumen. The pathologic changes in the interstitial space were less severe in SAD than in BOOP or UIP (p less than 0.005). Clubbing was more frequent in UIP (p less than 0.01), and symptoms were of shorter duration in BOOP (p less than 0.05). The radiographic assessment showed that the characteristic finding in BOOP was patchy air-space consolidation, a finding that was not present in UIP or SAD.

Bronchial Diseases↗
PubMed1987

Carcinoembryonic antigen and milk-fat globule protein staining of malignant mesothelioma and adenocarcinoma of the lung.

Immunohistologic markers have been of considerable value in differentiating malignant mesothelioma from adenocarcinoma. Recently, staining for milk-fat globule (MFG) protein has been suggested as a useful diagnostic test for this separation, but subsequent reports have been conflicting, with some authors finding clearcut differences, while others showed similar marking of both tumor types. To examine this technique further, we studied lung carcinomas and mesotheliomas with commercially available anti-MFG, and compared these results with those obtained with anticarcinoembryonic antigen (CEA), a commonly used immunomarker of carcinoma. We found that carcinomas showed strong cytoplasmic staining for MFG and CEA; however, a greater percentage of carcinomas were more strongly positive for CEA than for MFG. Mesotheliomas did not, for the most part, stain strongly with either antibody. In addition, carcinomas from different hospitals stained differently for MFG, but not for CEA. We conclude that although strong cytoplasmic staining for MFG is a reasonably reliable indicator of carcinoma, CEA staining provides a better separation and is considerably easier to interpret in lung cancer specimens.

Adenocarcinoma↗
PubMed1987

Effects of cigarette smoke exposure on retention of asbestos fibers in various morphologic compartments of the guinea pig lung.

For investigation of mechanisms whereby smoking might potentiate asbestos-related disease, guinea pigs were given 0.5 mg UICC amosite by intratracheal instillation. Half the animals were subsequently exposed to cigarette smoke. Animals were sacrificed at 1 day, 7 days, and 1 month after exposure. Lungs were lavaged and macrophages separated from the lavage fluid. Lung fiber concentration, numbers of fibers in macrophages, and fiber sizes from tissue (TFs), macrophages (MFs), and macrophage-free lavagate (FFs) were determined by electron microscopy. Smoke-exposed animals retained greater numbers of fibers in lung tissue by 1 month but had greater total numbers of fibers in macrophages at all time periods. In both smokers and nonsmokers, fibers in the three morphologic compartments had distinctly different lengths: the longest fibers were found associated with the lung tissue; the macrophages always contained the shortest fibers; and the macrophage-free lavagate had fibers of intermediate size. However, fiber widths and aspect ratios did not show the same clear separation by anatomic compartment, suggesting that in both smoking and nonsmoking animals length is the size parameter which is most important in determining fiber clearance. Smoking did not affect the lengths of MFs but did produce a progressive reduction in the lengths of FFs and TFs with time. These data indicate that smoking causes a marked increase in the number of fibers retained in the lung within macrophages and suggest that either macrophage removal via the mucociliary escalator or macrophage mobility is impaired by cigarette smoke. However, smoking does not change the sizes of fibers in macrophages and does not appear to depress phagocytic capacity. These observations imply that failure of macrophage clearance and subsequent re-release of fibers into the medium may at least partially explain the changes in fiber sizes and eventual increases in tissue fiber concentrations in smoke-exposed animals.

Animals↗
PubMed1987

Legislation.

Explore the source record for details and available documents.

Humans↗
PubMed1986

Malignant mesothelioma caused by childhood exposure to long-fiber low aspect ratio tremolite.

A 41-year-old man was found to have a malignant mesothelioma of the pleura. During childhood in Corsica, he had been exposed at home to chrysotile ore from the Canari mine. Analysis of lung mineral content revealed background levels of chrysotile but an elevated level of tremolite and actinolite asbestos. The latter had a geometric mean length of 3.7 microns, a value considerably longer than we have found for tremolite and actinolite from Quebec chrysotile miners but roughly the same as the mean length of amosite and crocidolite in workers with occupational amphibole exposure. No tremolite or actinolite fibers of length greater than 8 microns microns and width less than 0.25 micron were observed. The mean aspect ratio of the tremolite and actinolite fibers was 7, a value similar to that found in chrysotile miners with mesothelioma but considerably less than the mean aspect ratio of amosite and crocidolite from those with occupational exposure. These data suggest that long-fiber tremolite is a potential mesothelial carcinogen in humans, and that fiber length is more important than fiber aspect ratio in this regard.

Adult↗
PubMed1986

Interactions in the solid state. II: Interaction of sodium bicarbonate with substituted benzoic acids in the presence of moisture.

The interaction of an organic acid with sodium bicarbonate in water produces an effervescent reaction. The reaction products are carbon dioxide, water, and the sodium salt of the acid. The kinetic rate-determining step for this reaction is the dehydration of carbonic acid. The solid-solid interaction with known amounts of moisture was followed by quantitatively determining carbon dioxide evolution as a function of time. The aqueous solubilities, diffusion coefficients, dissociation constants, and solid-solid interaction rates of six different substituted benzoic acids were determined. Using a model based on diffusion of the organic acid through the aqueous layer coupled with chemical reaction, predicted rates and levels of carbon dioxide production were compared with experimental results. Included in the model were the effects of the reaction products on the solution properties of the reactants. It was found that high concentrations of substituted sodium benzoate were generated very quickly and affected the solubility of the reactants, diffusion coefficient of the acid, and the carbonic acid dehydration rate constant. Moisture content was found to have a profound influence on the interaction rate. Water provides a medium for diffusion of the reacting species as well as the reaction solvent.

Benzoates↗
PubMed1986

Pulmonary capillary hemangiomatosis.

Pulmonary capillary hemangiomatosis (PCH) is a rare cause of pulmonary hypertension; only three cases have been reported. Four additional cases are described in this report. All of the patients in this study presented with signs and symptoms of pulmonary hypertension, and in none was a correct morphologic diagnosis made during life. Histologically, the most striking feature was the presence of numerous cytologically benign thin-walled capillary-sized blood vessels proliferating diffusely through alveolar walls and in and around larger vessels and airways. Venous infiltration was associated with intimal fibrosis and secondary veno-occlusive disease (VOD). Because of the presence of hemorrhage, the apparent interstitial widening and inflammation, and the venous changes, the condition in these cases was initially misdiagnosed as interstitial fibrosis or VOD. However, the identification of proliferating and invasive capillaries, which are unique to PCH, led to the correct diagnosis. Although the nature of PCH is unknown, it behaves like a low-grade vascular neoplasm.

Adolescent↗
PubMed1986

Two unusual pathological reactions to nitrofurantoin: case reports.

Idiosyncratic pulmonary reactions to nitrofurantoin are not unusual, often presenting as eosinophilic pneumonia. We report two cases of uncommon pathological reactions, one resembling a hypersensitivity pneumonitis and the other mimicking a giant cell interstitial pneumonia.

Aged↗
PubMed1986

Comparison of the cell content of lung lavage fluid with the presence of emphysema and peripheral airways inflammation in resected lungs.

This study was designed to investigate the relationship between the cellular components of lung lavage fluid and the presence of airways disease and emphysema in resected lung specimens, primarily from current and ex-smokers. Since standard bronchopulmonary lavage cannot be performed on these specimens, an intrapulmonary lavage technique was developed and compared to the results of bronchoalveolar lavage performed prior to surgery on the lung or lobe opposite to the one resected. The specimen lavage produced inflammatory cell differential counts similar to those obtained by bronchopulmonary lavage, and studies on postmortem lungs showed that the fluid washed alveoli, respiratory and membranous bronchioles, and small cartilaginous bronchi. The results show that the variation in peripheral airways inflammation and extent of lung destruction by emphysema did not correlate with the variation in cell content observed in the lavage fluid. Similarly, the differential counts performed in the lavage fluid did not correlate with the smoking habits of the patient. We conclude that the changes in cell content of the lavage fluid do not reflect the extent or severity of the inflammatory disease and lung destruction present in the lungs of this group of patients.

Body Fluids↗
PubMed1986

Nonspecific airway reactivity in cigarette smokers. Relationship to airway pathology and baseline lung function.

To examine the relationship of cigarette smoking, starting airway caliber, and airway pathology to nonspecific airway reactivity, we performed inhalation dose-response curves in 40 patients prior to lung surgery. Airway reactivity was assessed by the provocative concentration of methacholine (n = 30) or histamine (n = 10) resulting in a 20% fall in FEV1 (PC20). All patients had measurements of maximal expiratory flow, diffusing capacity, and lung volumes preoperatively. After resection, the specimens were graded for small and large airways pathology and emphysema. The patients were divided into 4 groups: PC20 less than or equal to 1 mg/ml (n = 6), PC20 1 mg/ml to less than or equal to 4 mg/ml (n = 11), PC20 4 mg/ml to less than or equal to 16 mg/ml (n = 14), and PC20 greater than 16 mg/ml (n = 9). Subjects with PC20 less than or equal to 1 mg/ml had reduced measurements of maximal expiratory flow (FEV1, FEV1/FVC, Vmax50, and Vmax25). There were no differences in measurements of cartilaginous airway disease among the 4 reactivity groups. We found significant independent correlations of cigarette consumption, membranous bronchiole inflammation, and maximal expiratory flow rates (FEV1 and Vmax50) to PC20. The data suggest that cigarette smoking, starting airway caliber, and airway inflammation are associated with nonspecific airway reactivity and that each exerts an effect on airway reactivity that is not dependent on the contribution of the other 2 factors.

Aged↗
PubMed1986

Smoking inhibits asbestos clearance.

To determine whether smoking affects the clearance of asbestos fibers, guinea pigs were given amosite asbestos by intratracheal instillation and divided into 3 groups: (1) nonsmokers, (2) animals exposed to smoke only after asbestos instillation, and (3) animals exposed to smoke both before and after asbestos instillation. Asbestos fiber concentrations and sizes were measured at 1 wk and 1 month after exposure. Between 1 wk and 1 month the asbestos burden in nonsmokers decreased on average 6-fold, whereas both smoking groups failed to show a significant decrease. Over this time period, the mean length of retained fibers increased in the nonsmokers but decreased in both smoking groups. This phenomenon was seen in tissue samples and lavage samples, although lavaged fibers were consistently shorter than tissue fibers. We conclude that in this model, cigarette smoking impedes asbestos clearance, largely by increasing retention of short fibers. This increased pulmonary fiber burden may be important in the increased disease rate seen in asbestos workers who smoke.

Animals↗
PubMed1986

Pathophysiologic correlations in asbestos-induced airway disease in the guinea pig.

To determine whether asbestos-induced changes in the structure of the walls of small airways might be associated with abnormalities of pulmonary function, guinea pigs were given 10 mg of amosite asbestos (test group) or saline (control group) by intratracheal instillation. Pulmonary function tests performed 6 months later revealed significant increases in FRC, RV, and TLC in the test group. Measurement of airway wall thickness showed that both membranous and respiratory bronchioles were significantly thickened in the test group; this group also had airways of smaller internal diameter than the controls. Analysis for lung collagen content as hydroxyproline showed a 50% increase in the asbestos exposed animals. There was, however, only minimal and very focal interstitial fibrosis (asbestosis) in the lung parenchyma. Analysis of fiber size indicated that the fibers obtained by digestion of the tissue or from the lavage fluid were significantly longer and wider than those in the original asbestos sample; however, the tissue contained considerably larger fibers than the lavage fluid. We conclude that: Asbestos can produce airway fibrosis and narrowing causing air trapping on pulmonary function examination; this process occurs in the absence of significant interstitial fibrosis of the parenchyma (asbestosis), implying that abnormalities of pulmonary function which are consistent with airflow obstruction in asbestos exposed animals can be caused by pathologic changes in the small airways alone; long asbestos fibers are preferentially retained in the lung, and the longest fibers appear to be in a compartment inaccessible to lavage, presumably, in this model, in airway walls. Enhanced penetration of long fibers into tissue may be one reason why long fibers are more pathogenic than short ones.

Animals↗
PubMed1986

Surgical treatment of lung cancer: promise and problems of early diagnosis.

Recent studies have shown that the survival of patients with lung cancer is improved if the tumour is resected before it becomes larger than 3 cm in diameter and before it spreads to lymph nodes. While this suggests a positive benefit from early detection, recent mass-screening studies have claimed that the benefit obtained from this procedure is illusory because it relates to a lead-time bias. This study reports the results of surgical resection of 143 primary lung cancers. The data confirmed that the predicted 5-year survival was greatest (74%) following resection of lesions that were less than 3 cm in diameter without node involvement. Analysis showed that the age of these patients was 63 +/- 8 years, the same as in patients with larger tumours and more extensive node involvement. This suggests that tumours progress rapidly from a stage at which resection is beneficial to stages at which it is not. Although it is desirable that tests predict the presence of small tumours, the high requirements for sensitivity and specificity at current prevalence rates for lung cancer make this goal impractical.

Adenocarcinoma↗
PubMed1986

Ranking the severity of emphysema on whole lung slices. Concordance of upper lobe, lower lobe, and entire lung ranks.

This study describes a modification of a standard method for grading emphysema that was originally described by Thurlbeck for postmortem lungs. The study was based on pneumonectomy specimens that were fixed in inflation and sliced sagittally. The midsagittal slice was impregnated with barium sulphate and examined under water by 2 observers on 2 separate occasions. It was then re-examined on 2 additional occasions with either the upper or the lower lobe covered and the grade assigned using the uncovered lobe. In each case, the grade was assigned by comparing the specimen with the panel of pictures of paper sections of lung provided by Thurlbeck and coworkers. The data showed good agreement between grades assigned on separate observations of the same lobe. They also showed that the order of cases from no emphysema to severe emphysema was changed little when the grade was assigned by observing either the upper or the lower lobe. We conclude that this modification of the previous technique described by Thurlbeck and coworkers provides a simple reliable method of ranking surgical lung specimens as to the severity of emphysema present.

Emphysema↗
PubMed1985

Reassessment of inflammation of airways in chronic bronchitis.

The term chronic bronchitis has been criticised because it is associated with hypersecretion of mucus rather than bronchial inflammation. This study was designed to establish the presence or absence of clinical chronic bronchitis and measure pulmonary function in 45 patients about to undergo resection of the lung. The condition in the cartilaginous and small airways and the severity of the emphysema were then measured in the resected specimen. The results from 20 patients who had clinical chronic bronchitis were compared with those in 25 patients who did not. The data show that patients with chronic bronchitis had greater inflammation (a) on mucosal surfaces (p less than 0.05) of all bronchi larger than 2 mm luminal diameter and (b) around glands (p less than 0.005) and gland ducts (p less than 0.05) in bronchi larger than 4 mm diameter. A variable degree of inflammation was present in the submucosa of smaller bronchi. The groups had equivalent proportions of mucous glands and Reid's indices in central airways, and no differences were noted in measurements of pulmonary function, condition of small airways, or emphysema. These data show that the term chronic bronchitis is justified by inflammation of cartilaginous airways and suggest that this abnormality may be the cause of the chronic productive cough.

Bronchi↗
PubMed1985

Airways disease: evolution, pathology, and recognition.

Obstruction to airflow in the lung was studied in 150 patients who presented with coin lesions necessitating surgical resection of the lung. Pulmonary function tests were performed before surgery, and the structure of the lung or lobe was analysed by means of morphometric techniques. The evolution of obstructive airways disease appeared to be based on a progressive chronic inflammatory reaction in the respiratory and membranous bronchioles. This led to progressive airway obstruction and was associated with destruction of the lung surface. The early pulmonary vascular problems appeared to be related to progressive airways obstruction that may have increased pulmonary artery pressure by causing alveolar pressure to increase more than pleural pressure during the hyperventilation of exercise.

Adult↗