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Biomedical subjects

A Churg

Publications and source records attributed to A Churg.

193 records · Page 11Linked to original sources
PubMed1976

Pulmonary tumorlet. A form of peripheral carcinoid.

Twenty cases of pulmonary tumorlet are presented. Approximately one-third of the tumors occurred in lungs severely scarred by bronchiectasis or other inflammatory processes; the other two-thirds were found in lungs with little to no scarring. In the former instances, tumorlets were found in large scars in which identifying architectural features had been destroyed. In the latter, the tumorlets were seen in minute fibrous nodules, surrounding or obliterating small bronchi or bronchioles. Argyrophilic granules were demonstrated in 14 of 15 cases; in the electron microscope these were consistent with neurosecretory granules. Their location, silver staining properties, and ultrastructure suggest that pulmonary tumorlets are minute peripheral carcinoid tumors.

Adult↗
PubMed1974

Induction of endometrial peroxidase synthesis and secretion by estrogen and estrogen antagonist.

Synthesis of peroxidase was induced in the uterine epithelium of immature rats by multiple doses over a 24-96-h period of either 17 beta-estradiol, the estrogen-antagonist Parke-Davis CI-628, or a combination of estradiol plus antagonist. Endogenous peroxidase activity first appeared in the cisternae of the rough endoplasmic reticulum of surface epithelial and glandular cells within 24-48 after the initial injection. Uterine peroxidase activity was also visible in the cisternae of the Golgi apparatus, in Golgi-derived secretory granules, and within the uterine and glandular lumen. Some cells of the epithelium produced little or no peroxidase, even after 96 h. Whereas the antagonist appeared to induce synthesis and secretion of peroxidase, neither the antagonist alone nor the combined treatment (estradiol plus antagonist) reproduced the estradiol-mediated growth in organ size and increased lumen diameter.

Animals↗
PubMed1972

Histochemical distribution of carbonic anhydrase after ligation of the pancreatic duct.

The distribution of carbonic anhydrase in the exocrine pancreas of the rat has been examined during the first 3 weeks after duct ligation. The normal pattern of positive reaction in ducts, centroacinar cells and capillaries changed, by the end of the first week, to one in which all the cells in the dilated ducts showed the enzyme. This situation persisted through the third week. By electron microscopy, the enzyme was found on the apical membranes of ductular, centroacinar and acinar cells, as well as on the surface membranes of the modified cells seen at 1 week. The significance of these findings with respect to function and cell origin is discussed.

Animals↗
PubMedDate not supplied

Ambient atmospheric particles in the airways of human lungs.

Epidemiologic studies linking particulate matter (PM) air pollution and adverse respiratory and cardiovascular effects have focused attention on the interactions of PM and lung cells. Information on the types, numbers, composition, sizes, and distribution of ambient particles in the airways is potentially useful for correlations with pathological and/or physiological changes, but relatively little is known about the extent to which ambient particles actually enter airway epithelial cells and are retained in airway walls and even less information is available about correlations with pathologic changes. Since many ambient particles are colorless and/or well below the level of resolution of light microscopy, definitive evaluation of particle burden in the airway wall requires analytical electron microscopy. Studies from the authors' laboratory suggest that in Vancouver, a city with relatively low PM levels, particle loads in the airway mucosa are nonetheless numerically substantial, typically in the range of 10(7) particles/g dry tissue. In most individuals particle concentrations in the larger airways show a clear increase in concentration with increasing airway generation (smaller airway diameter) as expected from deposition models; however, smoking disrupts this pattern in some subjects. Respiratory bronchioles accumulate particularly high particle loads, typically 25-100 times the concentrations seen in the mainstem bronchus. Similarly high concentrations are found in the large airway carinas, suggesting that these locations are likely sites for particle toxicity. The majority of particles in the airways in Vancouver lungs appear to be crustal in origin, with particular accumulation of silica in the airways compared to the parenchyma. Ultrafine particles, which have been postulated to be important in PM toxicity, are present in small numbers as singlet particles and are largely metals, perhaps representing combustion products, but carbonaceous chain aggregates are rarely found. Mean particle aerodynamic diameters vary from about 0.3 to 0.6 microm in different parts of the airways and, overall, the airways retain PM2.5 rather than PM10, a finding supporting the observation that, in some studies, adverse health effects appear to correlate better with PM2.5 than with PM10 concentrations. Preliminary examination of lungs of subjects from Mexico City, a location with relatively high ambient particle concentrations, indicates that the airway mucosa retains relatively large numbers of carbonaceous chain aggregates of ultrafine particles that appear to be combustion products and that presumably produce the numerous adverse effects documented for such products. Limited published data correlating visible particle load and airway mucus secretion, inflammation, and mural fibrosis suggest that high levels of air pollutant particles can induce chronic fibrotic responses in the airways, a phenomenon that might be linked to chronic airflow obstruction; this observation needs confirmation as well as correlation with specific types of particles.

Air Pollutants↗
PubMedDate not supplied

Exogenous mineral particles in the human bronchial mucosa and lung parenchyma. I. Nonsmokers in the general population.

We extracted mineral particles from 7 different regions of the bronchial tree and 4 regions of lung supplied by these airways from 11 morphologically normal adult autopsy right lungs. All patients were nonsmokers. Particles were identified, counted, and sized by analytical electron microscopy. Both particle concentration and particle size showed a significant negative correlation with airway diameter; detailed analysis showed that the correlation for concentration was only true of large particles. Distance from the carina (pathlength) showed a weaker correlation with particle concentration. The lowest particle concentration was found in the mainstem bronchi, and there was a consistent (case to case) increase in particle concentration with airway generation. Parenchyma supplied by the apical segmental bronchus had a higher particle concentration than that in other sample sites. Segmental bronchial particle size was consistently larger than particle size in the supplied lung tissue, and particles from both upper-lobe tissue sample sites were slightly larger than those from the two lower-lobe sample sites. Bronchial mucosa from all sites showed a predominance of silica, whereas tissue sites appeared to preferentially concentrate silicates, especially kaolin and mica. These observations suggest that in morphologically normal lungs from lifetime nonsmokers (1) in the noncarinal portions of the larger airways, airway diameter and, to a much lesser extent, pathlength are the major influences on long-term bronchial particle concentration and size; (2) tissue particle concentration does not appear to relate to pathlength; (3) the airways accumulate very specific sizes and types of particles compared to the parenchyma, an effect that may influence the location of specific pathologic lesions; and (4) the pattern of long-term particle concentration appears to be fairly similar to acute bronchial deposition patterns seen in experimental human systems, an observation that may imply that long-term burden is the result of translocation of a fraction of the locally deposited particles to the interstitial tissues.

Aged↗
PubMedDate not supplied

Effect of long-term cigarette smoke exposure on pulmonary vascular structure and function in the guinea pig.

To investigate the effect of chronic exposure to cigarette smoke on the structure and function of the pulmonary vasculature, we used a guinea pig model of cigarette smoke-induced emphysema, in which groups of guinea pigs were exposed to smoke for periods of 1, 3, 6, and 12 months. We found that the mean pulmonary artery pressure in smokers was increased at one month, a time at which there was no evidence of emphysema. Although the vascular pressures remained elevated, they did not progressively increase, even though there was progressive lung destruction. Pulmonary hypertension was associated with muscularization of the arterioles, seen as an increase in the percentage of small pulmonary vessels with double elastic lamina. We conclude that chronic exposure to cigarette smoke will produce pulmonary hypertension in the guinea pig, and that the hemodynamic changes are accompanied by alteration of the structure of the small pulmonary arterioles and arteries. The apparent dissociation of pulmonary hypertension and emphysema suggests that the pulmonary hypertension is not due to destruction of the lung capillary bed. The etiology of this process may be smoke-induced inflammation with release of vasoactive substances as well as proteolytic enzymes.

Animals↗
PubMedDate not supplied

Calcium-containing particles as a marker of cigarette smoke exposure in autopsy lungs.

It has been recently reported that the major inorganic particle components of cigarette smoke are calcium and potassium carbonates, potassium sulfate and chloride, and quartz. To determine whether any of these particles might serve as a marker of cigarette smoke exposure in human lungs, we used analytical electron microscopy to compare the mineral particle content in two parenchymal sites and two large bronchi from five nonsmoker autopsy lungs and five age- and sex-matched smoker autopsy lungs. Potassium carbonate, sulfate, and chloride were not identified in any lung. The percentage of quartz was the same in both smoker and nonsmoker lungs. However, lungs from smokers contained a large percentage (average 23% of all particles) of particles composed of calcium, carbon, and oxygen (probably calcium carbonate) in all sample sites, whereas lungs from nonsmokers usually contained no such particles or only minute numbers (average 0.1%). We conclude that calcium-containing particles of this type may serve as a marker of cigarette smoke exposure in humans and may prove useful for examining the distribution of smoke particles in the normal and diseased lung.

Adult↗
PubMedDate not supplied

Effect of long-term exposure to cigarette smoke on the small airways of the guinea pig.

Smoke-induced airway abnormalities are a common feature of the lungs of cigarette smokers. We examined the small airways from guinea pigs exposed to cigarette smoke for periods of 1, 3, 6, and 12 months, and compared these data to those obtained from age-matched, nonexposed animals. We found that there was no change in the structure of the airway walls, and that similar numbers of peribronchiolar alveolar attachments were present in both groups. However, the airway epithelium of animals exposed to smoke for 3, 6, and 12 months had greater numbers of secretory cells/mm length basement membrane. We conclude that this guinea pig model of cigarette smoke-induced lung disease mimics the human condition in that there is alteration of the cellular population of the small airway epithelium. However, the lack of structural changes in the airway wall, with no evidence of peribronchiolar alveolar destruction, suggests that the airflow obstruction seen in these animals is most likely due to emphysematous parenchymal destruction with loss of elastic recoil.

Airway Obstruction↗
PubMedDate not supplied

Mineral particles in the human bronchial mucosa and lung parenchyma. II. Cigarette smokers without emphysema.

The effects of cigarette smoke on the microanatomic deposition and retention pattern of exogenous mineral particles is unknown. To determine how cigarette smoke affects long-term particle retention in those with minimal smoke-related disease, we selected autopsy lungs from ten smokers without evidence of emphysema at autopsy, and used analytical electron microscopy to examine exogenous mineral particle concentration in the mucosa of seven different bronchi of varying sizes and four parenchymal sites fed by those bronchi. These data were compared with values from twelve lifetime nonsmokers. Overall, total mean particle burden in the parenchyma in the smokers and nonsmokers was similar, but there was a markedly decreased particle load retained in the smokers' airways. The consistent increase in particle burden seen in nonsmokers as airways became narrower and more distant from the carina was lost in many, but not all, of the smokers, especially for particles larger than 1 micron, and this effect did not appear to depend on amount of smoking. Rare polonium particles were found but were too sparse to use as a smoke distribution marker. However, calcium-containing particles, previously suggested by us to represent calcium carbonate actually derived from the smoke, were present in greatest concentration in the larger airways and distal parenchyma. These observations indicate the following in smokers without parenchymal smoke-induced structural damage: (1) Overall, cigarette smoking disrupts the normal retention (? deposition) pattern of particles in the airways. (2) Cigarette smoking leads to markedly decreased long-term retention of exogenous mineral particles in the airways without significantly affecting overall tissue particle retention. (3) The distribution of calcium particles in the airways and parenchyma in smokers is similar to that predicted in a recently published model of smoke particle deposition, and further supports the idea that calcium-containing particles can be used as a direct tracer of smoke particle deposition. In the present study this distribution indicates that the large airways and parenchyma receive the greatest smoke deposition. (4) Within the group of smokers, some people appear resistant to the disruptive effects of smoke on particle retention patterns, whereas other people smoking comparable amounts show markedly abnormal retention patterns. The latter may have unusual sensitivity to cigarette smoke and perhaps susceptibility to smoke-induced diseases.

Aged↗
PubMedDate not supplied

Lung cancer cell type and asbestos exposure.

It is often claimed that adenocarcinoma is the most frequent type of lung cancer seen in workers exposed to asbestos. Careful review of the published data, however, fails to support this claim. Rather, it seems that all types of lung cancers occur in asbestos workers, and the presence or absence of a specific cell type cannot be used to prove or disprove an association of carcinoma and asbestos exposure.

Adenocarcinoma↗