Empyema of the thorax in adults: review of 105 cases.
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Biomedical subjects
Publications and source records attributed to G L Snider.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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Quantum-dot cellular automata (QCA), a computation paradigm based on the Coulomb interactions between neighboring cells. The key idea is to represent binary information, not by the state of a current switch (transistor), but rather by the configuration of charge in a bistable cell. In its molecular realization, the QCA cell can be a single molecule. QCA is ideally suited for molecular implementation since it exploits the molecule's ability to contain charge, and does not rely on any current flow between the molecules. We have examined using an UHV-STM some of the QCA molecules like silicon phthalocyanines and Fe-Ru complexes on Au (111) and Si (111) surfaces, which are suitable candidates for the molecular QCA approach.
Localized collection of fluid in an interlobar fissure as a consequence of congestive heart failure is a well-known entity. It has been termed vanishing tumor because of its appearance as a mass lesion in the lung and its propensity to resolve with diuretic therapy. We report a case of loculated pleural effusion in the subcostal pleural space without interlobar fluid collection. This was initially thought to represent an occult metastatic malignancy; however, the cause of the density became obvious when it disappeared with therapy of heart failure and recurred concurrent with cardiac decompensation. Loculated pleural effusion must be included in the differential diagnosis of roentgenographic densities in the chest when seen in subcostal as well as in interlobar locations.
An intratracheal instillation of human neutrophil elastase (HNE) causes accumulation of an excess number of secretory granules in the epithelial secretory cells lining the hamster bronchus. This chronic lesion, which we refer to as secretory cell metaplasia (SCM), is not seen in the trachea or bronchioles. Because luminal cell surface lectin binding is much higher in the trachea than in the bronchus, we concluded that tracheal resistance may be due to a protective glycoconjugate coat. In the present ultrastructural study, we analyzed the lectin-binding capability of bronchiolar epithelial cells to determine whether their luminal cell surface glycoconjugate layer is similar to tracheal epithelial cells. None of the six ferritin-conjugated lectins showed higher binding in bronchioles compared to the bronchus, suggesting that a high level of surface oligosaccharides is not necessary for resistance to the metaplastic effects of HNE. HNE caused a significant reduction in bronchiolar surface binding of the gold-labeled, secretory cell-specific lectin, Helix pomatia agglutinin. The principal granulated secretory cell type in bronchioles was ultrastructurally similar to a form of bronchial Clara cell that converts to a mucous cell phenotype in response to HNE. The results suggest that absence of bronchiolar SCM is not attributable to a protective layer of cell surface oligosaccharides, a lack of cellular contact by HNE, or the presence of a morphologically distinct population of epithelial cells in bronchioles.
Hamster airway epithelial secretory cells were investigated by light and electron microscopic cytochemistry to study possible changes in their carbohydrate content induced by human neutrophil elastase (HNE), an agent known to cause replacement of Clara cells by mucous cells in hamster bronchi. Characterization of secretory cell carbohydrates by the AB/PAS, PA-TCH-SP, HID-TCH-SP, and LID-TCH-SP sequences indicated the existence of periodate-reactive acidic glycoconjugates, but the absence of sulfated or carboxylated glycoconjugates in both treated and control animals. Differences were seen in the quality and quantity of historeactive carbohydrates throughout various regions in the lower respiratory tract. This was especially evident in the HNE-treated animals. It is concluded that the HNE-induced expression of the mucous cell phenotype is associated with an increase in the amount of neutral and acidic nonsulfated and noncarboxylated polysaccharides stored in the secretory granules of these cells.
A single intratracheal instillation of human neutrophil elastase (HNE) into hamsters causes granule discharge from bronchial secretory cells followed by marked accumulation of granules, visible by light microscopy at 21 days and persisting through 18 months. To determine whether persistence of this secretory cell metaplasia (SCM) is due to inability of the metaplastic secretory cells to secrete their granules, hamsters having HNE-induced SCM were challenged with the potent secretagogue HNE. Four groups of 10 hamsters each received 300 micrograms HNE intratracheally. Twenty-one days later, hamsters were intratracheally treated with HNE or saline; the groups were designated HNE-HNE and HNE-SAL, respectively. Hamsters were killed 2 h or 21 days following the second treatment. Using light microscopy, nucleated epithelial cells were counted in plastic sections of the left main intrapulmonary bronchus. Cells were classified as ciliated (C), basal (B), indeterminate (IN), or secretory. Secretory cells were subcategorized as S0 (0 granules), S1 (1-4 granules), S2 (> or = 5 granules with intervening cytoplasm), and S3 (abundant granules completely filling the cytoplasm). At 2 h, S3 cell frequency in the HNE-HNE group was 13.0 +/- 2.2 (% mean +/- SE), significantly lower than in the 2 h HNE-SAL group (31.1 +/- 4.5). Concomitantly, higher cell frequencies were seen in the other secretory categories of the HNE-HNE group compared to the HNE-SAL group; S2 17.1 +/- 1.9 compared to 9.4 +/- 1.9, S1 2.4 +/- 0.4 compared to 1.1 +/- 0.5, and S0 2.4 +/- 0.5 compared to 1.1 +/- 0.5, respectively. The S3 cell frequency of the 21-day HNE-HNE group was 25.4 +/- 4.7, increased significantly compared to the 2 h HNE-HNE group; this change was concomitant with significant decrease in the frequency of the S0 secretory cells. Cell frequencies of C, B, and IN were not affected by treatment or time. It is concluded that metaplastic secretory cells discharge their granules in response to HNE; SCM returns to its original state after HNE rechallenge; persistent SCM is not due to the inability of metaplastic secretory cells to discharge their granules.
BACKGROUND: Recent reports of a high frequency of theophylline toxicity, which usually occurs at theophylline blood levels > 20 micrograms/mL, coupled with the recent addition of metered-dose, inhaled anticholinergics to the beta-2 agonist inhalers already available for treatment of chronic obstructive pulmonary disease, has led some authors to suggest that theophylline should no longer be used in the ambulatory management of this disease. OBJECTIVE: The author suggests an alternate approach to theophylline dosing as a means of resolving the current controversy. SUMMARY: Because of the log-linear relationship between bronchodilation and blood level, little bronchodilator efficacy is lost by using a target therapeutic theophylline blood level of 10 +/- 2 micrograms/mL. This target provides a greater range between therapeutic and toxic blood levels than the 17 +/- 2 micrograms/mL therapeutic target blood level that has also been recommended. CONCLUSIONS: Because theophylline has a different mode of action than the sympathomimetic or anticholinergic drugs, it continues to have a useful place in the ambulatory management of chronic obstructive pulmonary disease.
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