Was the literature "corrupted"?
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Biomedical subjects
Publications and source records attributed to P C Pratt.
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Several lines of evidence indicate that neutrophil elastase and oxidants secreted by phagocytic inflammatory cells play key roles in the development of centrilobular emphysema. A recent report suggests that ethanol consumption may have a protective role against this disease in smokers. The aim of this study was to examine the effect of ethanol consumption on neutrophil elastase activity and superoxide production of peripheral blood neutrophils. These activities were measured in neutrophils from 52 male intoxicated patients and compared to activities in neutrophils from 20 male volunteers. Neutrophils from intoxicated patients contained 31% less elastase activity than that found in controls, 0.99 +/- 0.27 versus 1.44 +/- 0.23 micrograms/10(6) neutrophils (p less than 0.0001) and produced 25 to 27% less superoxide than controls in response to phorbol 12-myristate-13-acetate, 0.90 +/- 0.17 versus 1.2 +/- 0.21 nmol/min/10(6) PMN (p less than 0.0001) or N-formylmethionylleucylphenylalanine, 0.64 +/- 0.19 versus 0.88 +/- 0.24 (p less than 0.001). In follow-up studies of 10 patients admitted for acute alcoholism, elastase activity and superoxide production remained low for 2 to 4 days. After 6 to 10 days, elastase activity and superoxide production were significantly greater than they were at Day 0 and approached normal levels. Neutrophils isolated from blood samples of healthy abstaining donors, which had been exposed to ethanol or to plasma from inebriated patients for 16 to 20 h, showed no loss of elastase activity or superoxide production.(ABSTRACT TRUNCATED AT 250 WORDS)
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Pulmonary emphysema is an extraordinarily prevalent disease, especially among men, and is found in about 40% of all autopsies at this Veterans Medical Center. However, in the great majority of cases, it is an incidental finding, and the individual has died of another lesion, either pulmonary or in another organ system. These facts have permitted the authors to examine the interrelationships between presence or absence of emphysema and the cause of death in a consecutive series of 1033 autopsies. Results show that chronic renal disease is much less common as a cause of death in persons with, than in those without, emphysema. Since emphysema is closely associated with smoking, the data also show a reduction in risk of death from renal disease in smokers. These trends persist, even when individuals who have died from smoking-related diseases are eliminated from the population. Further analyses suggest that it is the presence of emphysema which is mainly responsible for this effect. A likely mechanism for it is proposed.
Although recognizing that the subject is controversial, most authors of textbooks about diagnostic radiology conclude that chest radiography is of little value for either confirmation or exclusion of the diagnosis of emphysema. Yet several reports in the literature show a high degree of accuracy in the interpretation of films for presence of this disease. Some of the controversy results from continuing confusion over the current definition of emphysema in terms of lung structure rather than symptoms or physiologic evidence relating to impaired ventilation. Many autopsy studies have shown that emphysema is often present at postmortem examination and can involve as much as 30 percent of the lung tissue, even in subjects with no respiratory symptoms or impairment during life. Since radiographs deal with structure rather than function, interpreters of chest films should have the intention to recognize the presence of structural emphysema. The correct recognition of emphysema is useful even in a patient without symptoms, and the ability to exclude this diagnosis in symptomatic patients is of equal, if not greater value. The degree of success reported in various studies depends upon the criteria used and the strictness applied by the authors in matching their interpretations to the presence or absence of structural emphysema. This review of existing literature deals solely with papers in which radiographic observations have been related to morphologic evidence of emphysema in inflation-fixed autopsy lung specimens. It identifies reasons for discrepancies among reports and emphasizes the very high predictive value of validated radiographic criteria. Applications of radiographic interpretation both for diagnosis and for exclusion of emphysema in clinical situations are described.
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The essential point of this analysis is that, although arterial deficiency was shown to be virtually useless as a diagnostic criterion for emphysema, it does not follow that use of other validated radiographic criteria for diagnosing and excluding emphysema, using conventional films, should be abandoned. Interested readers can find further detailed information in reference 1.
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Diseases associated with asbestos exposure include asbestosis, malignant mesothelioma, carcinoma of the lung, and parietal pleural plaques. In this study the asbestos content of lung tissue was examined in groups of cases representing each of these diseases and in several cases with non-occupational idiopathic pulmonary fibrosis. Asbestos bodies (AB), which are the hallmark of asbestos exposure, were present in the lungs of virtually everyone in the general population and present at increased levels in individuals with asbestos associated diseases. The highest numbers of AB occurred in individuals with asbestosis, all of whom had levels greater than or equal to 2000 ABs/g wet lung tissue. Every case with a content of 100,000 ABs/g or higher had asbestosis. Intermediate levels occurred in individuals with malignant mesothelioma and the lowest levels in patients with parietal pleural plaques. There was no overlap between the asbestos content of lung tissue from patients with asbestosis and those with idiopathic pulmonary fibrosis. Lung cancer was present in half the patients with asbestosis, and the distribution of histological patterns did not differ from that in patients with lung cancer without asbestosis. The asbestos body content in patients with lung cancer was highly variable. Control cases had values within our previously established normal range (0-20 ABs/g). There was a significant correlation (p less than 0.001) between AB counted by light microscope and AB and uncoated fibres counted by scanning electron microscopy. The previous observation that the vast majority of asbestos bodies isolated from human tissues have an amphibole core was confirmed.
Over a 5-year period, 25 patients who had undergone chest computed tomography (CT) died and were autopsied. Their lungs were fixed in the inflated state and were assessed for the presence and severity of centrilobular emphysema (CLE). Three radiologists independently evaluated the CT scans for nonperipheral low-attenuation areas, peripheral low-attenuation areas, pulmonary vascular pruning, pulmonary vascular distortion, and pulmonary density gradient. The CT criterion that best correlated with the presence and severity of CLE was the nonperipheral low-attenuation area. With this CT criterion, lung destruction was correctly identified in 13 of 15 cases. The absence of this criterion resulted in correct identification of eight of ten normal lungs. These preliminary data suggest that CLE can be reliably identified and quantified with current CT scanners.
The subserosal stroma of hernia sacs consistently contains birefringent particulate material, in amounts greater than those observed in other intra-abdominal organs. The major component of this material was shown in the present study to be talc; thus, it cannot be of endogenous origin. Cellular response to this foreign material is remarkably slight. Possible sources of the material and mechanisms of access to the hernia sac were examined in a search of the available literature. It is proposed that the probable source is ingestion with food or, more likely, medications and that the particles reach the peritoneal cavity by migration through the intact intestinal wall. They probably reach the hernia by sedimentation in peritoneal fluid and subsequently migrate into the subserosa. The virtual absence of response to the particles is attributed to their composition (silicate) and their relatively small size (up to about 10 microns) compared with the particles in talc granulomas (up to at least 50 microns).
Clinical, radiological, and pathologic data for nine children with adult respiratory distress syndrome (ARDS) were reviewed. The children ranged in age from 7 months to 15 years (mean age, 7.4 yrs). Underlying diseases and precipitating events included sepsis, pneumonia, near drowning, aspiration pneumonia, central nervous system trauma, and malignancy. All patients had the rapid onset of diffuse bilateral lung opacification, required assisted ventilation for periods of 5-86 days (mean, 25.2 days), and received high levels of inspired oxygen for 2-41 days (mean, 12.7 days). Eight patients manifested air leak complications; these problems persisted until the patients died or were weaned from the respirator. Five of the nine patients died. Autopsy in three patients demonstrated alveolar duct fibrosis characteristic of the late proliferative phase of ARDS and consistent with oxygen toxicity. Two survivors demonstrated mild restrictive changes on follow-up pulmonary function tests and showed persistent linear densities on chest radiographs.
All studies of toxic effects must compare normal conditions with those existing after contact with the toxin. If the effects to be studied involve alterations of gross, microscopic or ultramicroscopic structures, then a knowledge of normality at each of these levels is essential. This understanding is equally true for every organ of the body from the skin to the bones. Our interest today is in the pulmonary effects of phosgene; consequently, this discussion of basic morphology will be directed entirely at the lower respiratory tract. While most of the research to be presented in subsequent papers will relate to experimental studies in animals of various species, all are probably intended to have relevance to human responses to contact with phosgene. This discussion, therefore, will be concerned with the human lung and with examples of two animal species, rats and dogs. Since any single author can do relatively little of the vast range of studies necessary to establish normal morphology, this discussion is necessarily derived largely from the literature. Rather than present copies of illustrations and charts, which would require extensive copyright negotiations, and many of which would lose detail in reproduction, its seems best to refer the reader to the original publications. Most of these are readily available in medical libraries.