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Biomedical subjects

W B Davis

Publications and source records attributed to W B Davis.

At least 55 records · Page 3Linked to original sources
PubMed1988

Stroke mortality maps. United States whites aged 35-74 years, 1962-1982.

We mapped average age-adjusted stroke mortality rates for white men and white women aged 35-74 years for state economic areas (counties or groups of counties) in the continental United States for three 7-year periods between 1962 and 1982. Despite the decline of national stroke mortality rates, rates in some areas failed to decline between 1962-1968 and 1969-1975. All areas experienced declines in 1976-1982, by which time some rates in the highest decile of the rate distribution were comparable to rates that had been in the lowest decile in 1962-1968. An east-west gradient of high-to-low stroke mortality rates was evident for both white men and white women in all three periods. Within the eastern part of the United States, high rates appeared more commonly in the South, and more so for white men than for white women. The "stroke belt" (area of very high stroke mortality rates in the coastal plain of the South) became less concentrated over the 2 decades, while a clustering of state economic areas with high rates along the Mississippi River and in the Ohio River valley became more pronounced.

Adult↗
PubMed1988

Purification and cytotoxic potential of myeloperoxidase in cystic fibrosis sputum.

The neutrophil myeloperoxidase-H2O2-halide enzyme system produces hypochlorous acid and chlorinated amine compounds capable of killing a variety of target cells. In the present study we hypothesized that the myeloperoxidase enzyme system is one mechanism for airway epithelial damage in patients with cystic fibrosis (CF). Enzyme linked immunosorbent assay detected high antigenic levels of myeloperoxidase in sputum samples of seven patients with CF. Myeloperoxidase was purified to homogeneity from CF sputum and from blood neutrophils by a three-step technique involving dialysis, gel filtration, and ion-exchange chromatography. CF sputum myeloperoxidase and neutrophil myeloperoxidase appeared identical by acid gel electrophoresis and Ouchterlony experiments. CF sputum myeloperoxidase also contained approximately the same enzymatic activity as neutrophil myeloperoxidase. The myeloperoxidase enzyme system was tested for its cytotoxic potential in a tracheal ring culture system. Myeloperoxidase-induced cytotoxicity for airway epithelium was confirmed by light microscopy and radiolabelling experiments. These findings suggest a possible role for neutrophil myeloperoxidase in CF lung disease.

Animals↗
PubMed1988

Enhanced cytotoxic potential of alveolar macrophages from cigarette smokers.

Cigarette smoking increases the numbers and oxidative metabolism of alveolar macrophages. Increased production of superoxide (O2-) and H2O2 by alveolar macrophages may contribute to the pathogenesis of cigarette-induced lung diseases. The cytotoxicity mediated by alveolar macrophages from smokers (n = 11) and nonsmokers (n = 13) was compared in an in vitro assay in which the target cells were chromium 51-labeled lung explants. The spontaneous cellular cytotoxicity mediated by smoker macrophages was significantly greater than that of nonsmoker macrophages (cytotoxic index 20.3% +/- 1.9% compared with 5.5% +/- 0.9%, P less than 0.001). Phorbol myristate acetate significantly increased the cytotoxic index of nonsmoker macrophages but did not cause further increases in smoker macrophage killing. The antioxidants superoxide dismutase and catalase produced partial inhibition of smoker macrophage cytotoxicity, suggesting that target cell killing was mediated in part by oxidant mechanisms. Supplementation of smokers' diets with high-dose oral vitamin E failed to decrease smoker alveolar macrophage cytotoxicity. These findings demonstrate that smoker alveolar macrophages possess enhanced cytotoxic potential for normal lung parenchymal cells.

Adult↗
PubMed1988

Decreased ceruloplasmin ferroxidase activity in cigarette smokers.

Ceruloplasmin is one of the most important antioxidant proteins in serum. Ceruloplasmin functions as a ferroxidase that oxidizes iron to the Fe3+ state, thereby preventing Fe2+-catalyzed lipid peroxidation and cellular damage. Despite increased antigenic amounts of ceruloplasmin, cigarette smoker serum has previously been shown to exhibit significantly less antioxidant activity than non-smoker serum. We demonstrate that the decreased antioxidant activity of cigarette smoker serum may be explained by a decrease in ceruloplasmin ferroxidase activity. Smokers had a 14% decrease in serum ceruloplasmin ferroxidase activity (units per milliliter) compared with nonsmokers. There was a 24% decrease in ferroxidase activity per milligram of ceruloplasmin in smokers compared with nonsmokers (0.32 +/- 0.009 U/mg vs 0.42 +/- 0.020 U/mg, p less than 0.005). Smoker serum also contained significantly less ceruloplasmin-specific antioxidant activity than nonsmoker serum. These observations may explain the decrement in smoker serum antioxidant activity that could predispose cigarette smokers to increased oxidant injury.

Adult↗
PubMed1987

Music therapy in the 19th century America.

The history of music therapy in the United States has not been thoroughly investigated and documented. The few sources containing information on the historical uses of music in medicine concentrate primarily on 20th century practices, while virtually omitting 19th century contributions to the field. The purpose of this study was to analyze elected music therapy literature that appeared in 19th century medical journals and dissertations. The articles found in these publications indicated interest during this time in advocating the use of music to provide the patient an alternate, more holistic approach to treatment. The dissemination of music therapy ideas occurred almost exclusively through these publications, which unfortunately resulted in very limited proliferation of the topic because of the nature of the audience (i.e.,primarily physicians). Nine articles were analyzed; the study was based on primary evidence located in medical journals and dissertations written between 1804 and 1899. The sources were located in a variety of bibliographies found in books, journals, dissertations, and theses.

History, 19th Century↗
PubMed1987

Neutrophil collagenase in rheumatoid interstitial lung disease.

Ten patients with rheumatoid arthritis were evaluated by bronchoalveolar lavage. Five patients (group I) had interstitial lung disease by physiological and radiographic criteria, whereas five (group II) had no evidence of lung disease. Lavage fluid from four of the five group I patients contained an active collagenase which by inhibitory profile and substrate specificity appeared to be of neutrophil origin. None of the group II patients demonstrated lavage fluid collagenase. Treatment of lavage fluid with trypsin failed to uncover latent collagenase activity in either group, suggesting that the collagenase is present entirely in an active form. These findings parallel those observed in idiopathic pulmonary fibrosis and suggest a potential pathogenetic role for collagenase in rheumatoid interstitial lung disease.

Arthritis, Rheumatoid↗
PubMed1987

Detection of pulmonary lymphoma by bronchoalveolar lavage.

A patient with bilateral interstitial infiltrates was evaluated by bronchoalveolar lavage prior to open lung biopsy. The patient was found to have lymphocytic alveolitis (34 percent lymphocytes) in which 43 percent of lymphocytes were B cells. A clonal proliferation of these B cells was suggested by the finding of monoclonal kappa light chain on the B lymphocytes. A suspected diagnosis of primary pulmonary non-Hodgkin's lymphoma was later confirmed by open lung biopsy.

Biopsy↗
PubMed1986

Lung neutrophils in the adult respiratory distress syndrome. Clinical and pathophysiologic significance.

Although neutrophils are of pathogenetic importance in various animal models of acute lung injury, their role in the adult respiratory distress syndrome (ARDS) is unclear. To study the significance of lung neutrophils in this disorder, patients with ARDS (n = 11) were evaluated by bronchoalveolar lavage within 24 h of admission to the intensive care unit. Patients with non-ARDS respiratory failure requiring mechanical ventilation (n = 4) and normal volunteers (n = 12) were also studied. Neutrophils constituted 67.6 +/- 9.8% of recovered lavage cells in patients with ARDS compared with only 4.0 +/- 2.4% of cells in mechanically ventilated control patients and 0.8 +/- 0.2% in normal volunteers (p less than 0.005, both comparisons). Furthermore, in patients with ARDS (n = 6) evaluated serially by bronchoalveolar lavage at 72-h intervals, neutrophil percentages decreased from 91 +/- 3.2% (initial lavage) to 42.8 +/- 12% (final lavage) (p less than 0.005). Lung neutrophils also predicted the severity of abnormalities in gas exchange and lung protein permeability. That is, the percentage of neutrophils correlated directly with the alveolar-arterial Po2 difference (r = 0.69, p less than 0.01) and lavage fluid total protein concentrations (r = 0.62, p less than 0.01). Because large numbers of lung neutrophils were present in these patients, ARDS lavage fluid was assayed for neutrophil mediators relevant to the pathogenesis of acute lung injury. Neutrophil elastase activity was not detected in any ARDS lavages, although elastase was antigenically present in most samples and appeared to be complexed to alpha-1-antitrypsin. In contrast to elastase, neutrophil collagenase was readily detectable in ARDS fluid.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Deficiency of vitamin E in the alveolar fluid of cigarette smokers. Influence on alveolar macrophage cytotoxicity.

Cigarette smoking produces oxidant-mediated changes in the lung important to the pathogenesis of emphysema. Since vitamin E can neutralize reactive oxygen species and prevent peroxidation of unsaturated lipids, it may constitute an important component of the lung's defense against oxidant injury. To better characterize the antioxidant protective role of vitamin E, young asymptomatic smokers and nonsmokers were evaluated by bronchoalveolar lavage before and immediately after a 3-wk course of oral vitamin E (2,400 IU/d). Smoker alveolar fluid at baseline was relatively deficient in vitamin E compared with nonsmoker fluid (3.1 +/- 0.7 ng/ml vs. 20.7 +/- 2.4 ng/ml, P less than 0.005). Although smoker alveolar fluid vitamin E levels increased to 9.3 +/- 2.3 ng/ml after supplementation, the levels remained significantly lower than nonsmoker baseline levels (P less than 0.01). This deficiency was explained, in part, by the increased oxidative metabolism of vitamin E to the quinone form in the lungs of smokers compared with nonsmokers. Although the significance of a lower concentration of alveolar fluid vitamin E is unclear, it may compromise the antioxidant protection afforded by the alveolar fluid as it coats the lung's epithelial surface. The protective role of vitamin E was assessed by cytotoxicity experiments, which demonstrated that the killing of normal rat lung parenchymal cells by smoker alveolar macrophages was inversely related to the vitamin E content of the parenchymal cells. These findings suggest that vitamin E may be an important lower respiratory tract antioxidant, and that the deficiency seen in young smokers may predispose them to an enhanced oxidant attack on their lung parenchymal cells.

Cell Survival↗
PubMed1986

Protein permeability in the adult respiratory distress syndrome. Loss of size selectivity of the alveolar epithelium.

Small amounts of plasma protein normally reach the alveolar epithelial surface by a size-selective process that restricts the passage of very large molecules. Size selectivity may be compromised in the lungs of patients with the adult respiratory distress syndrome (ARDS). To assess this question, bronchoalveolar lavage fluid (BALF) from normal volunteers (n = 11), cardiac edema patients (n = 3), and ARDS patients (n = 8) was compared. Mean total protein in ARDS BALF was greater than 12 times the levels in normals or cardiac edema patients. BALF/plasma total protein ratios and measurements of epithelial lining fluid protein also separated the patients groups. The large proteins IgM and alpha 2-macroglobulin were found in ARDS BALF at greater than 90 times the concentrations of normal or cardiac edema fluid. The relationship of distribution coefficient vs. log molecular weight for seven proteins (54,000-900,000 mol wt) hyperbolically increased in normals but was flat in ARDS patients. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed a paucity of high molecular weight proteins in normal and cardiac edema BALF, but demonstrated the full spectrum of plasma proteins in ARDS BALF. We conclude that normal size selectivity is preserved in cardiac edema but is destroyed by the alveolar-capillary injury of ARDS.

Adult↗
PubMed1986

Eosinophilic alveolitis in acute respiratory failure. A clinical marker for a non-infectious etiology.

Two patients with acute respiratory failure requiring mechanical ventilation were found to have eosinophilic alveolitis on bronchoalveolar lavage and lung biopsy studies. Neither patient had evidence of lung infection or parasitic disease and both rapidly improved following treatment with corticosteroids. Lung eosinophilia in this setting is unusual, since the stress reaction that accompanies severe illness usually causes a rapid drop in circulating eosinophil levels. Eosinophilic alveolitis in such patients may be a useful clinical marker for non-infectious acute lung injury that is responsive to corticosteroid therapy.

Acute Disease↗
PubMed1985

Geographic variation in declining ischemic heart disease mortality in the United States, 1968-1978. I. Rates and change, whites aged 35-74 years.

Despite the well known geographic pattern for heart disease mortality, studies of the decline in ischemic heart disease have not provided a comprehensive examination of its spatial component. In this study, the authors computed and mapped mean rates and per cent change in ischemic heart disease mortality for whites aged 35-74 years, for the period of the Eighth Revision (1968-1978) of the International Classification of Diseases. Visual evidence of clustering and markedly different spatial patterns were found for mean rate and per cent change among the state economic areas of the United States.

Adult↗
PubMed1985

Experimental polymyxin B-induced interstitial lung disease characterized by an accumulation of cytotoxic eosinophils in the alveolar structures.

A variety of lung disorders are associated with the accumulation of eosinophils in the alveolar structures. To help understand the role of eosinophils in these disorders, an animal model of eosinophilic lung disease was developed. Administration of an aerosol of polymyxin B to guinea pigs (3 times per wk for 4 wk) produced diffuse interstitial lung disease with alveolar wall thickening and an alveolitis characterized by marked increases in eosinophils and alveolar macrophages. Bronchoalveolar lavage confirmed the presence of significantly increased numbers of eosinophils and alveolar macrophages in polymyxin-B-treated animals compared with those in control animals. Using density gradient centrifugation, approximately 10(7) eosinophils could be purified from the lungs of a single polymyxin-B-treated animal. Importantly, eosinophils purified from the lungs from polymyxin B-treated animals exhibited significant spontaneous cellular cytotoxicity for human fetal lung fibroblasts. In contrast, neither eosinophils from control animals nor alveolar macrophages from either group of animals were cytotoxic. These findings demonstrate that eosinophils possess effector processes capable of injuring the lung parenchyma and suggest that eosinophils can contribute to the pathogenesis of the interstitial lung disease.

Aerosols↗
PubMed1985

Adult bronchiolitis. Evaluation by bronchoalveolar lavage and response to prednisone therapy.

Four adult patients with biopsy-proven bronchiolitis were identified and prospectively evaluated. Each patient presented with the rapid onset (weeks to months) of severe respiratory disease that was clinically distinct from asthma, chronic bronchitis, bronchiectasis, cystic fibrosis, and emphysema. Bronchiolitis patients were evaluated by pulmonary function testing and bronchoalveolar lavage (BAL) before and after two months of treatment with 1 mg/kg/day of prednisone. Initial BAL results of bronchiolitis patients were compared to those of cigarette smokers with chronic bronchitis (n = 4), asymptomatic cigarette smokers (n = 5), and normal nonsmoking volunteers (n = 5). Neutrophils comprised 53 +/- 13 percent of the cells recovered by BAL in bronchiolitis patients but only 3 +/- 2 percent of the cells in chronic bronchitis patients, 1.5 +/- 0.6 percent of the cells in asymptomatic smokers, and 0.3 +/- 0.3 percent of the cells in normal volunteers (p less than 0.01, all comparisons). Moreover, prednisone produced a striking decrease in lower respiratory tract neutrophils (53 +/- 13 percent to 8 +/- 3 percent, p less than 0.05) in all bronchiolitis patients while lung function either improved (two patients) or remained unchanged (two patients). These findings suggest a central role for the neutrophil in bronchiolitis and argue that BAL may be clinically useful in the diagnosis and management of these patients.

Adult↗
PubMed1985

Peritonitis, dialysate infusion and lung function in continuous ambulatory peritoneal dialysis (CAPD).

Pulmonary function tests were done in seven CAPD patients with acute peritonitis on the day of admission to the hospital and after recovery. Subsequently, the effect of dialysate infusion alone on lung function was studied in 19 patients initiated on CAPD and nine of these patients were restudied 7.6 +/- 4.1 months later. Peritonitis was associated with a 30% reduction in vital capacity and a significant fall in arterial oxygen tension (7 to 11 mmHg) (p less than 0.01). Dialysate infusion alone decreased functional residual capacity (FRC) and produced small changes in PaO2 which were more pronounced in the supine position. The decrease in PaO2 observed in changing from sitting prior to dialysate infusion, to supine after dialysate infusion was due to the development of airways closure at resting lung volumes. Follow-up studies in nine patients demonstrated a continued and significant fall in FRC with dialysate infusion, without however, any changes in PaO2. We conclude that peritonitis in CAPD patients is accompanied by significant changes in lung function which are probably due to a decrease in diaphragmatic mobility resulting in atelectasis and underventilation of dependent lung zones. In CAPD patients without peritonitis, dialysate infusion in the supine position produces significant changes in PaO2, but with time, compensatory mechanisms develop to abolish the changes in PaO2.

Adult↗
PubMed1984

Eosinophil-mediated injury to lung parenchymal cells and interstitial matrix. A possible role for eosinophils in chronic inflammatory disorders of the lower respiratory tract.

Eosinophils are a common component of the inflammation of the lower respiratory tract that characterizes the interstitial lung disorders. Bronchoalveolar lavage analyses (n = 680) of 251 patients with interstitial lung disease demonstrated that eosinophils represented greater than 5% of the effector cells comprising the alveolitis in 20% of all lavages. In contrast, lavage of normal individuals (n = 117) showed that eosinophils were never greater than 5% of the total effector cells recovered. To evaluate a possible role for eosinophils in mediating some of the cellular and connective tissue matrix derangements of the lung parenchyma found in interstitial disease, eosinophils were evaluated for the presence of proteases capable of cleaving connective tissue proteins found in the lung and for the ability to mediate cytotoxicity to lung parenchymal cells. Evaluation of guinea pig and human eosinophils demonstrated that eosinophil granules contained a collagenase that specifically cleaved human collagen types I and III, the two major connective tissue components of the human lung parenchyma. In contrast, the eosinophil did not contain an elastase or a nonspecific neutral protease. The eosinophil collagenase appeared to be a metalloprotease, as it was inhibited by ethylenediaminetetraacetate but not by phenylmethanesulfonyl-fluoride or alpha 1-antitrypsin. The eosinophil also has the capacity to injure lung parenchymal cells. Without further stimulation, eosinophils purified from peritoneal exudates of guinea pigs demonstrated spontaneous cytotoxicity for human lung fibroblasts (HFL-1), cat lung epithelial cells (AK-D) and rat lung mesothelial cells (I6B). Under identical conditions, the epithelial cells were more sensitive to eosinophil-mediated cytotoxicity than the fibroblasts or mesothelial cells (P less than 0.01), consistent with the clinical observation that in the interstitial disorders, the alveolar epithelial cells are damaged more commonly than fibroblasts or pleural cells. The eosinophil-mediated cytotoxicity could be partially inhibited by the antioxidants catalase and dimethylsulfoxide suggesting that toxic oxygen radicals play a role in mediating the cellular damage. Importantly, eosinophils purified from bronchoalveolar lavage of human interstitial lung disease also demonstrated spontaneous cytotoxicity for lung epithelial cells. These observations demonstrate that eosinophils are frequent participants of the alveolitis of the interstitial lung disorders and suggest that these cells have the potential to damage the parenchymal cells and collagen matrix of the lower respiratory tract.

Animals↗