Biomedical subjects

B Wiggs

Publications and source records attributed to B Wiggs.

50 records · Page 3Linked to original sources

PubMed1986

Alveolar epithelial damage. A critical difference between high pressure and oleic acid-induced low pressure pulmonary edema.

The present study was designed to compare high pressure pulmonary edema (HPPE) and oleic acid-induced low pressure pulmonary edema (OAPE) in dogs when similar amounts of extra vascular water were present in the lung. The high pressure edema was produced by intravenous fluid overload and by inflating an aortic balloon catheter (n = 6). The low pressure edema was produced by the injecting 0.08 mg/kg oleic acid suspended in 5 ml saline (n = 6). Comparison of the difference between initial control measurements and final measurements in the edematous states showed that the animals with OAPE had a greater fall in percent oxygen saturation and a greater increase in shunt fractions. The light microscopic studies showed that OAPE was associated with greater amounts of alveolar flooding than HPPE where the edema fluid was located to a greater extent in the peribronchial interstitial space. The electron microscopy studies showed that the alveolar flooding in OAPE was associated with epithelial disruption, and tracer studies carried out in rabbits showed that dextran (150,000 mol wt) could pass from blood to airspace and that dextran (40,000 mol wt) could pass from air-space to blood in OAPE. We conclude that epithelial disruption is responsible for the excessive alveolar flooding in OAPE and that this results in a greater impairment in gas exchange.

Animals↗

PubMed1986

Cigarette smoke increases the penetration of asbestos fibers into airway walls.

For study of the penetration of asbestos fibers into airway walls, guinea pigs were given amosite asbestos by intratracheal instillation. Half of the animals were also exposed to cigarette smoke. Animals were sacrificed at 1 week and 1 month, and numbers of fibers in airway walls were counted in histologic sections. In both smoke-exposed and nonexposed groups, numbers of fibers per square millimeter of airway wall increased from 1 week to 1 month in the respiratory bronchioles. At each time period, smoke-exposed animals had significantly higher numbers of fibers in the airway walls, compared with nonexposed animals. It is concluded that 1) continued transport of fibers into interstitial tissues may be the reason that asbestosis can progress after cessation of exposure; 2) cigarette smoke increases the penetration of fibers into airway walls. This effect may play a role in the increased incidence of disease seen in smoking, compared with nonsmoking, asbestos workers.

Animals↗

PubMed1985

The Vancouver Lymphadenopathy-AIDS Study: 4. Effects of exposure factors, cofactors and HTLV-III seropositivity on number of helper T cells.

Results of testing for antibody to human T-lymphotropic virus (HTLV-III) and absolute numbers of helper T cells in 219 participants in the Vancouver Lymphadenopathy-AIDS (acquired immune deficiency syndrome) Study were analysed. The mean absolute helper T-cell counts in the 141 HTLV-III seronegative and the 78 seropositive men were 897/mL and 659/mL respectively (p less than 0.001). Established AIDS risk factors such as elevated lifetime number of male sexual partners and frequent receptive anal intercourse did not appear to have any significant effect on number of helper T cells that was independent of HTLV-III antibody status. Seropositive men with less than 100, 100 to 500 or more than 500 male sexual partners in their lifetime had mean absolute helper T-cell counts of 667/mL, 651/mL and 662/mL respectively. Most other risk factors, as well, did not appear to exert any effect on absolute number of helper T cells that was independent of the effect of HTLV-III antibody status. However, independent effects of a history of mononucleosis or hepatitis and of cigarette smoking were noted. The data support the hypothesis that no immune dysfunction beyond that due to the initial infection alone arises from repeated exposure to HTLV-III. Most risk factors appear to act as exposure factors, exerting their effect on the immune system merely by increasing the probability of contact with the agent. The independent effects of a history of mononucleosis or hepatitis suggest that viral agents may be cofactors in the production of immune dysfunction.

Acquired Immunodeficiency Syndrome↗

PubMed1985

Relation of HTLV-III seropositivity and lymphadenopathy.

Testing for antibody to human T-lymphotropic retrovirus (HTLV-III) was carried out in five groups of homosexual men: 250 without lymphadenopathy (control group), 37 with slight or nonpersistent lymph node enlargement (intermediate group), 141 with persistent generalized lymphadenopathy, 32 with persistent generalized lymphadenopathy who underwent biopsy and 11 in whom acquired immune deficiency syndrome (AIDS) was diagnosed. The rates of HTLV-III seropositivity in the five groups were 18%, 32%, 61%, 94% and 91% respectively.

Acquired Immunodeficiency Syndrome↗

PubMed1985

The Vancouver Lymphadenopathy-AIDS Study: 2. Seroepidemiology of HTLV-III antibody.

Testing for antibody to human T-lymphotropic retrovirus (HTLV-III) was carried out in 448 participants in the Vancouver Lymphadenopathy-AIDS (acquired immune deficiency syndrome) Study. The overall prevalence rate of seropositivity was 34%. Of 130 seronegative subjects followed for an average of 8.5 months, 14 became seropositive; thus, the approximate annual seroconversion rate was 15%. More than 100 male sexual partners in one's lifetime, frequent receptive anal intercourse, fisting, a history of gonorrhea or hepatitis, and frequent sexual contact in clubs were found to be independent risk factors for HTLV-III seropositivity.

Acquired Immunodeficiency Syndrome↗

PubMed1985

Mineral particles, mineral fibers, and lung cancer.

The total fibrous and nonfibrous mineral content of the lung has been analyzed in a series of 14 men with lung cancer but no history of occupational dust exposure, and in a series of 14 control men matched for age, smoking history, and general occupational class. The lung cancer patients had an average of 525 +/- 369 X 10(6) exogenous mineral particles and 17.4 +/- 19.6 X 10(6) exogenous mineral fibers/g dry lung, while the controls had averages of 261 +/- 175 mineral particles and 4.7 +/- 3.2 X 10(6) mineral fibers/g dry lung. These differences are statistically significant for both particles and fibers. Kaolinite, talc, mica, feldspars, and crystalline silica comprised the majority of particles of both groups. Approximately 90% of the particles were smaller than 2 micron in diameter and approximately 60% smaller than 1 micron; the mean particle size in the cancer group was 1.1 +/- 0.2 micron and in the control group 1.3 +/- 0.2 micron. In both groups, patients who had smoked more than 35 pack years had greater numbers of particles than patients who had smoked less than 35 pack years. It is concluded that, in this study, lungs from patients with lung cancer had statistically greater numbers of mineral particles and fibers than lungs from controls, and that smoking influences total long-term retention of particles from all sources.

Aged↗

PubMed1985

Histamine dose-response curves in guinea pigs.

Histamine dose-response curves were performed on anesthetized tracheostomized guinea pigs that were paralyzed and mechanically ventilated at a constant tidal volume and breathing frequency. The dose was calculated by generating an aerosol of known concentration and measuring the volume delivered to the lung. Increasing the dose was accomplished by increasing the number of breaths of aerosol delivered. The response to each dose was determined by measuring the change in airway resistance (RL) and dynamic compliance (Cdyn) using the method of Von Neergaard and Wirz (Z. Klin. Med. 105: 51-82, 1927). With increasing doses of histamine, RL increased and reached a plateau at approximately five times the base-line value and Cdyn fell to approximately 20% of its initial value. The variability in the base-line and maximum response as well as the calculated sensitivity and reactivity was less than that previously reported. Propranolol pretreatment increased resting RL and shifted the dose-response curve for RL to the left of the controls, increasing reactivity but not sensitivity. Atropine shifted the dose-response curve to the right of the control, decreasing sensitivity but without changing reactivity. The data for Cdyn showed that atropine pretreatment caused a higher resting value and propranolol pretreatment a lower value at the highest histamine dose but no differences in either sensitivity or reactivity.

Aerosols↗

PubMed1985

Small airways disease and mineral dust exposure. Prevalence, structure, and function.

Previously we described a lesion of the small airways that appears related to mineral dust exposure and is found in asbestos and nonasbestos dust-exposed populations. To determine the usefulness of this lesion as a marker for mineral dust exposure, and to determine whether it produces functional consequences, we examined a group of 53 workers who had been either hard rock miners or in the asbestos, construction, and shipyard industries. The specific lesion (mineral dust airways disease (MDAD] consists of marked fibrosis and pigmentation of the respiratory bronchioles and was found in 13 of 53 workers with dust exposure, but only in 1 of 121 without dust exposure. Compared with age and smoking-matched dust-exposed control subjects, patients with this lesion had significant abnormalities of forced expiratory volume in one second (FEV1), forced expiratory flow during the middle half of the forced vital capacity (FEF25-75), vital capacity (VC), and nitrogen washout. In addition to fibrosis in the walls of respiratory bronchioles, these patients also had significant increases of fibrosis in the walls of membranous bronchioles, indicating that changes in the small airways are widespread in this subset of workers. We conclude that markedly abnormal small airways are present in some workers with mineral dust exposure; pathologic observation of this lesion is a good indicator of dust exposure, and its presence is associated with abnormalities of air flow greater than those induced by smoking alone. The presence of this lesion in only a portion of dust-exposed workers may account for contradictory results in past studies that attempted to demonstrate air flow abnormalities associated with mineral dust exposure.

Aged↗

PubMed1985

A morphologic grading scheme for membranous and respiratory bronchioles.

We describe a system for grading pathologic changes in the small airways. This system consists of determining a score of 0 to 3 using a set of pictorial reference standards for any or all of the following variables: wall inflammation, fibrosis, muscle hypertrophy, pigment deposition, epithelial goblet and squamous metaplasia, and intralumenal macrophages. Grading of this type is much faster and easier than formal morphometric analysis. This system has produced a good correlation with pulmonary function test abnormalities, indicating obstruction in cigarette smokers and has also been used to detect lesions produced by other inhaled agents such as mineral dusts.

Bronchi↗

PubMed1984

The detection of small airways disease.

In order to investigate the relationship between pulmonary function and disease of the membranous and respiratory bronchioles, we studied 96 patients who required lobectomy for removal of a solitary pulmonary nodule. A subgroup of patients with forced expiratory volume in one second (FEV1) greater than 80% predicted were further analyzed to determine if abnormalities in tests designed to detect peripheral airways disease actually correlated with the pathology found in these airways. Analysis of the data shows that inflammation in both respiratory and membranous bronchioles, goblet cell metaplasia of the epithelium in membranous bronchioles, and decreasing muscle in the respiratory bronchioles are the pathologic features that are associated with deterioration of the FEV1. When the FEV1 is greater than 80% of the predicted value, inflammation of the respiratory bronchioles and fibrosis of both membranous and respiratory bronchioles increase with decreasing FEV1. Tests of specialized pulmonary function appear to correlate with epithelial pathologic parameters of membraneous bronchioles and inflammation and fibrosis of respiratory bronchioles. When patients with FEV1 greater than 80% predicted were subdivided according to the number of abnormal tests of small airways function, there was a significant increase in inflammation of the walls of respiratory bronchioles when 2 tests were abnormal and increases in both airway wall and intralumenal inflammatory cells as well as increased wall fibrosis when 3 tests were abnormal. We conclude that when the FEV1 is greater than 80% predicted, abnormalities in the tests for small airway disease reflect pathologic changes in the respiratory bronchioles.

Adolescent↗

PubMed1984

Lung asbestos content in chrysotile workers with mesothelioma.

The role of chrysotile asbestos in the genesis of mesotheliomas in humans is disputed. We analyzed the asbestos content of the lung in 6 long-term chrysotile miners and millers who had pleural mesotheliomas. In five patients, only chrysotile ore components (chrysotile and tremolite/actinolite/anthophyllite types of amphibole asbestos) were found, while the sixth patient presented both chrysotile ore components and amosite, a type of asbestos that is not derived from the mining process. The mean number of fibers/g dry lung for the 5 patients with mesothelioma containing only chrysotile ore components was higher (chrysotile 64 X 10(6) and tremolite group 540 X 10(6] than in a group of long-term chrysotile miner control subjects who had no asbestos-related disease (chrysotile 23 X 10(6), tremolite group 58 X 10(6], but some patients with mesothelioma had fiber burdens near the mean of the control range. Fiber sizes and aspect ratios in the mesothelioma group were approximately the same as those in the control subjects, and analysis of fiber distribution failed to show any preferential localization in the periphery of the lung. However, the concentration ratio of tremolite in the lungs of the mesothelioma cases compared to the control cases was 9.3, while the ratio of chrysotile was only 2.8. Our findings provide strong evidence that chrysotile mine dust (chrysotile and amphibole components) can produce mesotheliomas in humans; the greater relative amounts of tremolite group amphiboles present in the patients with mesothelioma raise the possibility that these fibers may be important in the pathogenesis of the tumors.

Aged↗

PubMed1984

Fiber size and number in amphibole asbestos-induced mesothelioma.

Numbers and sizes of fibers from the lungs of 10 patients who had an amphibole asbestos-induced malignant pleural mesothelioma were analyzed. Amosite was found in 10 lungs and crocidolite in 9; the average ratio of amosite to crocidolite was approximately 14:1. In the 8 patients who were not long-time asbestos insulators , the mean number of amosite fibers was 2.3 X 10(6) fibers/g dry lung, and of crocidolite fibers, 0.2 X 10(6)/g; these values represent an approximately 250-fold increase over those found in the general population. Crocidolite fibers were significantly narrower than amosite fibers (mean width, 0.13 versus 0.23 mu), were significantly shorter (mean length, 4.0 versus 5.8 mu), and had a significantly higher mean aspect (length to width) ratio (48 versus 34). Aspect ratios in general increased with increasing fiber length and decreasing fiber width, but the highest values were found for thin amosite fibers at about 13 mu in length, and thin crocidolite fibers at 8 or 15-17 mu in length. Comparison with data from other asbestos-exposed populations indicates that mesothelioma can be induced by relatively small numbers of amphibole fibers and also indicates that amosite is an effective mesothelial carcinogen in humans. Comparison of these data with epidemiologic and experimental predictions of carcinogenic size ranges for mesothelioma induction implies that either the carcinogenic size range is much broader than has been claimed (in particular, fibers considerably shorter than 8 mu and broader than 0.05 mu can produce mesothelioma), or, alternately, that extraordinarily small absolute numbers of fibers in certain size ranges can induce tumors in humans.

Aged↗

PubMedDate not supplied

Static bone histomorphometry in preterm and term babies.

The nature and pathophysiology of the bone loss which occurs in term and especially preterm neonates are poorly understood, and it is unclear whether this neonatal osteopenia results from impaired bone formation or increased bone resorption. This study compared the static bone histomorphometry of preterm and term babies, employing iliac crest bone biopsy specimens obtained postmortem. All the babies died within the first 6 days of life and none had any clinical, biochemical or radiologic evidence of metabolic bone disease. The trabecular bone volume, as well as static parameters of bone formation (OV/TV, OV/BV, OS/BS, OB.S/BS) did not differ significantly in preterm and term babies. Although time-spaced tetracycline labelling could not be employed in the present study, evidence of rickets was not apparent. Parameters of bone resorption in preterm babies were, however, significantly higher (p = 0.01) than those of term babies, suggesting that increased bone resorption and not impaired formation, underlies the development of osteopenia in the preterm neonate.

Biopsy↗

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↗