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Biomedical subjects

F Green

Publications and source records attributed to F Green.

At least 55 records · Page 3Linked to original sources

Use of jacalin as a solid phase in ABO reverse grouping.

A major problem of using red cells as the solid phase in assay systems is the difficulty to bind them strongly to appropriate surfaces. We report here on a number of lectins of different specificities which were examined for their ability to bind red cells to polystyrene 96-well microtitre plates. The use of the Thomsen-Friedenreich antigen-specific lectins, jacalin, mushroom and Maclura pomifera agglutinin proved the most useful for ABO reverse grouping. Jacalin-coated plates were also compared with plates coated with poly-L-lysine and bovine serum albumin/glutaraldehyde for the binding of erythrocyte membranes and were found to be superior. We also describe the colorimetric detection of the solid phase red cell antibody reaction by using an indicator erythrocyte and peroxidase chromogenic substrate.

ABO Blood-Group System↗

Exogenous rh-urokinase modifies inflammation and Pseudomonas aeruginosa infection in a rat chronic pulmonary infection model.

The effect of recombinant human urokinase (rh-UK) in a rat model of chronic Pseudomonas aeruginosa pulmonary infection was studied. Efficacy was assessed by lung histology and quantitative bacteriology. Male Sprague-Dawley rats received 1 x 10(4) or 1 x 10(5) P. aeruginosa encapsulated in agar beads via the intratracheal route on day 1. Intratracheal administration of up to 12,500 units of rh-UK on day 21 led to a dose-dependent disappearance of viable organisms from the lungs by day 24 in rats receiving 10(4) organisms. In slightly longer term infections (30 days), rh-UK was still effective in facilitating the disappearance of the organisms from the lungs of most of the treated animals. rh-UK was effective in eliminating organisms when animals were infected with 10(4), but not 10(5) bacteria. In vitro analysis revealed that rh-UK was not directly toxic for the organisms. Histologically, lungs from short-term infected control animals exhibited acute inflammation, inflammatory cell infiltrates, and fibrin deposition. Histology of lungs from UK-treated, short-term infected rats revealed decreased airway inflammation and cellular infiltration compared with infected controls. Lungs from infected animals treated with 12,500 units of rh-UK were histologically indistinguishable from the lungs of uninfected control animals, except for the foreign body reaction. These results indicate that exogenous rh-UK may be efficacious in the treatment of pulmonary inflammation accompanying exposure to Gram-negative bacteria such as P. aeruginosa.

Animals↗

Surface properties of rat pulmonary surfactant studied with the captive bubble method: adsorption, hysteresis, stability.

Surface tension-area relations from pulmonary surfactant were obtained with a new apparatus that contains a leak free captive bubble of controllable size. Rat pulmonary surfactant was studied at phospholipid concentrations of 50, 200 and 400 micrograms/ml. At the highest concentration, adsorption was rapid, reaching surface tensions below 30 mN/m within 1 s, while at the lowest concentration, approximately 3 min were required. Upon a first quasi static or dynamic compression, stable surface tensions below 1 mN/m could be obtained by a film area reduction of approximately 50%. After three to four cycles the surface tension-area relations became stationary, and the tension fell from 25-30 to approximately 1 mN/m for a film area reduction of less than 20%. Hysteresis became negligible, provided the films were not collapsed by further area reduction. Under these conditions, the films could be cycled for more than 20 min without any noticeable loss in surface activity. After only three to four consecutive cycles, surfactant films exhibited the low surface tensions, collapse rates and compressibilities characteristic of alveolar surfaces in situ. Remarkably, surface tension and area are interrelated in the captive bubble which may promote low and stable surface tensions. If the surface tension of the captive bubble suddenly increases ('click') because of mechanical vibration or unstable surfactant, the bubble shape changes from flat to more spherical. The associated isovolumetric decrease in surface area prevents the surface tension from rising as much as it would have in a constant-area situation. This feedback mechanism may also have a favorable effect in stabilizing alveolar surface tension at low lung volumes.

Adsorption↗

Outbreak of hypersensitivity pneumonitis among mushroom farm workers.

Between April 1982 and August 1985, seven cases of mushroom worker's lung (MWL), a form of hypersensitivity pneumonitis, were diagnosed among workers at one mushroom farm in Florida. The cases suffered from episodic shortness of breath, cough, fever and chills, myalgia, malaise, and difficulty breathing. Pulmonary function testing revealed restrictive ventilatory impairment and reduced diffusing capacity; chest radiographs exhibited diffuse interstitial pulmonary infiltrates. The seven cases occurred among workers from different farm operations, suggesting that workers throughout the farm were exposed to the disease causing agent(s). Six of the affected workers left employment at the farm in order to remain free of symptoms. The other affected worker was able to continue working at the farm, but only by remaining in a maintenance shop which was physically separated from the rest of the farm facilities. An industrial hygiene survey demonstrated that farm workers from every work area were exposed to organic dust constituents suspected of causing MWL, but no specific antigens were identified as the cause of the cases. Of the remaining workers who participated in a cross-sectional respiratory morbidity survey at the farm, approximately 20% of the more heavily exposed workers reported occasionally experiencing symptoms consistent with MWL. Approximately 10% of the workers had below normal spirometry test results, but interpretation was hampered by the diverse racial makeup of the population and lack of an adequate comparison group. No abnormalities consistent with either acute or chronic MWL were seen on the chest radiographs. Serologic tests demonstrated that almost all workers had been exposed to antigens capable of causing MWL, but the results were not associated with health status. At the time of the cross-sectional survey, no workers were found to be suffering acute respiratory problems consistent with MWL.

Adult↗

Morphologic aspects of pericardial heart disease: Part I.

Pericardial heart disease is a common entity at necropsy. Frequently, focal areas of fibrin deposits or parietal-visceral pericardial adhesion are observed at necropsy without previous clinical evidence of pericardial dysfunction. Some of these instances are related to clinically silent acute or healed myocardial infarction, but the vast majority of cases are incidental (idiopathic) findings. The purpose of this review is to summarize various morphologic responses of the pericardium and to provide an etiologic framework for these responses. Part I will review general morphologic responses of pericardial layers.

Heart Diseases↗

Morphologic aspects of pericardial heart disease: Part II.

Pericardial heart disease is a common entity at necropsy. Frequently, focal areas of fibrin deposits or parietal-visceral pericardial adhesion are observed at necropsy without previous clinical evidence of pericardial dysfunction. Some of these instances are related to clinically silent acute or healed myocardial infarction but the vast majority of cases are incidental (idiopathic) findings. The purpose of this review is to summarize various morphologic responses of the pericardium and to provide an etiologic framework for these responses. Part II will review specific morphologic responses of pericardial layers to selected diseases.

Cardiac Surgical Procedures↗

Genetic and environmental determinants of factor VII coagulant activity in ethnic groups at differing risk of coronary heart disease.

It has been shown previously that individuals possessing the Gln353 allele of factor VII have significantly lower factor VIIc levels. In this population based study of Europeans, Afro-Caribbeans and Gujarati Indians, the Gln353 allele was associated with lower factor VIIc in all groups, carriers having factor VIIc levels 20-25% below the group mean. Although the Afro-Caribbeans had the lowest factor VIIc levels, the frequency of the Gln353 allele was not different from the European sample. However, in the Gujaratis, the frequency of the Gln353 allele was significantly higher than in the Europeans (0.25 compared to 0.09, P less than 0.001). Factor VIIc is known to be positively correlated with plasma triglyceride levels, although the Gujaratis, having the highest mean triglyceride levels, did not have the highest mean factor VIIc levels. On examination of the relationship between triglycerides and factor VIIc in the Gujaratis there was a correlation (r = 0.23, P = 0.13) in individuals homozygous for the factor VII Arg353 allele, but no correlation (r = 0.001, P = 0.5) among Gln353 carriers. This striking difference suggests that the effect of triglycerides on factor VIIc is genotype specific and thus provides an example of gene-environment interaction. The high frequency of the Gln353 allele, with its associated lack of relationship between triglyceride and factor VIIc levels, may explain the lower than expected factor VIIc levels in the Gujaratis.

Africa↗

Decentralization of the superior cervical ganglia and the immediate hypersensitivity response.

Bilateral decentralization of the superior cervical ganglia protects against pulmonary inflammation when measured 8 hr after induction of anaphylaxis in rats sensitized to the nematode, Nippostrongylus brasiliensis. Since anaphylactic shock produces immediate perturbations to the cardiovascular and respiratory systems, we examined whether bilateral decentralization of the superior cervical ganglia modified the responses of these two systems during the first 4 hr of the anaphylactic response. With the exception of the bronchioles, decentralization did not protect against anaphylaxis-associated increases in extravasation of albumin, and the small changes in respiratory function induced by anaphylaxis were unaffected by the denervation. Decentralization did not alter anaphylaxis-induced reductions in blood flow to the gastrointestinal tract; however, blood flow to the kidneys and spleen of decentralized rats was restored more rapidly to normal values. These results suggest that the protective effect of decentralization on the late phase pulmonary inflammation of anaphylaxis is unrelated to early changes in respiratory mechanics, although the protection may be facilitated by the more rapid re-establishment of normal cardiovascular homeostasis.

Analysis of Variance↗

Cytokine production by cholesterol-loaded human peripheral monocyte-macrophages: the effect on fibrinogen mRNA levels in a hepatoma cell-line (HepG2).

Conditioned medium from human monocyte-macrophages incubated under various conditions was tested for its ability to stimulate fibrinogen mRNA levels in the hepatoma cell line HepG2. Recombinant human interleukin-6 (IL-6) stimulated fibrinogen mRNA levels 4.4-fold over control levels; this response was blocked by an anti-IL-6 antibody. Conditioned medium from 3-day-cultured monocyte-macrophages produced a slight stimulation of fibrinogen synthesis in HepG2 cells which was enhanced when the monocyte-macrophages had been treated with lipopolysaccharide (LPS). This stimulation was blocked by the anti IL-6 antibody. The cytokines, interleukin-1 (IL-1) and tumour necrosis factor (TNF) were also detected in the conditioned medium from the 3-day-cultured monocyte-macrophages. Monocyte-macrophages were cultured for 17 days and then incubated with acetylated low density lipoprotein (AcLDL) for 48 h. Such cells were 'foamy' in appearance and showed a 4-fold increase in apoE mRNA and a 10 to 50-fold increase in apoE secretion. This increase in apoE production was suppressed by almost a third when cells were coincubated with AcLDL and LPS. Conditioned medium from these 17-day-cultured AcLDL-treated human monocyte-macrophages did not stimulate fibrinogen mRNA synthesis in HepG2 cells, nor did the conditioned medium contain detectable levels of cytokines. These results suggest that cytokine production from foam cells in the atherosclerotic lesion is unlikely to be a major contributing factor in determining the elevated fibrinogen levels seen in the plasma of patients with IHD.

Antibodies↗

Catheter balloon valvuloplasty of stenotic aortic valves. Part I: Anatomic basis and mechanisms of balloon dilation.

Catheter balloon valvuloplasty of stenotic aortic valves has met with generally poor short- and long-term clinical results. Part of this problem resides with the lack of recognition of various etiologies of aortic stenosis. Part I of this review discusses the various etiologies of aortic stenosis and provides an anatomic basis for successful valve dilation. Results of an in vitro study indicate stenotic aortic valves are dilated by various mechanisms (cracking, stretching) based in part upon the etiology of the aortic valve stenosis.

Adult↗

Pathology of pulmonary parasitic migration: morphological and bronchoalveolar cellular responses following Nippostrongylus brasiliensis infection in rats.

Nippostrongylus brasiliensis has an obligatory migratory phase through the lungs during its development in rats. This migration is associated with marked tissue damage and pronounced cellular reaction. Given that cells from the lower respiratory tract, especially alveolar macrophages, can adhere to and kill larvae of N. brasiliensis in vitro, we studied the time course of morphological changes associated with parasitic migration. Compared to a primary infection, a secondary infection resulted in significant changes in the pulmonary tissue characterized by an early acute inflammation leading to granulomatous reaction in the parenchyma and a leucocytosis in the bronchoalveolar lavage fluids with an anamnestic increase in absolute numbers of neutrophils, alveolar macrophages, eosinophils, and lymphocytes. Scanning electron microscopy showed that inflammatory cells, especially alveolar macrophages, granulocytes, lymphocytes, erythrocytes, and platelets, adhered to the larvae following secondary infection and this adhesion was associated with disruption of cuticular surface in some larvae. Secondary infection also resulted in retention of larvae in granulomatous lesions in the lungs even up to 21 days postinfection. There was mast cell and type II pneumocyte hyperplasia and these cells appeared to be activated. Thus, the histopathological changes in lungs correlated with the bronchoalveolar cellular responses and further document the inflammatory and immunological reactions during the migration of N. brasiliensis larvae.

Animals↗

Marked antiinflammatory effects of decentralization of the superior cervical ganglia.

Intravenous challenge with parasite antigens in Nippostrongylus brasiliensis-sensitized rats resulted in anaphylactic shock and, in some animals, death. Surviving animals showed significant drop in mean arterial blood pressure, cardiac output, and blood flow to the trachea, bronchioles, and mesentery. After anaphylaxis, changes in the cellular and protein composition in bronchoalveolar lavage fluids (BALF) were assessed. 8 h after antigen challenge, there was significant influx of inflammatory cells and an increase in the levels of histamine and serum-derived immunoglobulins (IgG and IgM) in BALF. Chemotactic activity for neutrophils was also present in BALF. Once we established this anaphylaxis-induced model of pulmonary inflammation, we sought to determine whether or not the superior cervical ganglia (SCG) modulate this inflammation. We performed bilateral superior cervical ganglionectomy or decentralization of the SCG. Our results show that decentralization significantly reduced mortality (by 68%) after anaphylaxis. Furthermore, the increases in levels of serum-derived proteins, histamine, and influx of cells (especially neutrophils) observed in BALF after anaphylaxis were attenuated by both decentralization and ganglionectomy. By contrast, hemodynamic parameters in the respiratory tract and the presence of neutrophil chemotactic activity in BALF were not influenced by decentralization. Thus, the severity of pulmonary inflammation initiated by systemic anaphylaxis is depressed by bilateral ganglionectomy or decentralization of SCG.

Animals↗

Surfactant displaces particles toward the epithelium in airways and alveoli.

This study was designed to investigate the early stages of particle deposition on airway and alveolar surfaces. To do this we used morphometric studies of aerosol deposition, in situ measurements of surface tension, and in vitro assays of particle displacement and mathematical modelling. We observed that latex particles, equal or less than 6 microns in diameter deposited in hamster lungs were submerged in the subphase of the alveolar lining layer and became completely coated with an osmiophilic film. Similar results were obtained for particles deposited in the conductive airways which were also covered with a surface active film, having a surface tension of 32 +/- 2 dyn.cm-1. In vitro experiments showed that pulmonary surfactant promotes the displacement of particles from air to the aqueous phase and that the extent of particle immersion depends on the surface tension of the surface active film. The lower the surface tension the greater is the immersion of the particles into the aqueous subphase. Mathematical analysis of the forces acting on a particle deposited on an air-fluid interface show that for small particles (less than 100 microns) the surface tension force is several orders of magnitude greater than forces related to gravity. Thus, even at the relatively high surface tension obtained in the airways (32 +/- 2 dyn.cm-1) particles will still be displaced into the aqueous subphase. Particles in peripheral airways and alveoli likely are below the surfactant film and submerged in the subphase. This may promote clearance by macrophages. In addition, particle displacement into the subphase is likely to increase the contact between the epithelial cell and particle. Toxic or allergenic particles would be available to interact with epithelial cells and this may be important in the pathophysiology of airway disease.

Administration, Inhalation↗

Capsaicin pretreatment modifies hydrogen sulphide-induced pulmonary injury in rats.

One of the major target organs of hydrogen sulphide gas is the lung. Exfoliation of upper respiratory epithelia and pulmonary edema are prominent effects. Various neuropeptides contained in afferent C-fibres are intimately associated with the epithelia of the conducting airways and are liberated upon exposure to noxious gases. We sought to determine their role in the pathogenesis of hydrogen-sulphide-induced pulmonary injury by pretreating rats with the neurotoxin, capsaicin, which is known to ablate a subpopulation of vagal afferent C-fibres. Groups of capsaicin and saline (control) pretreated Fischer 344 rats were exposed to an edemogenic concentration of hydrogen sulphide (525-559 mg/m3) for 4 hr. Mortality was significantly greater (p less than 0.01) in the capsaicin treated rats (12/12) compared to the control animals (2/12). Pulmonary injury was also more severe in the capsaicin pretreated animals as assessed by lung water content, histological grade of pulmonary edema and protein in the broncho-alveolar fluid. Animals depleted of substance P exhibited a significantly greater (p less than 0.01) degree of bronchial epithelial cell exfoliation and ulceration following exposure to hydrogen sulphide. These experiments indicate that capsaicin sensitive sensory nerves may play a major role in pulmonary defense against the effects of inhaled toxic gases such as hydrogen sulphide.

Animals↗