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Biomedical subjects

S A Lonky

Publications and source records attributed to S A Lonky.

11 recordsLinked to original sources

Speculoscopy.

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Female↗

Amino acid analysis of elastin hydrolysates using a lithium citrate gradient: quantification of elastin from whole lung.

A method to quantitate the elastin content in lungs is described. Desmosine and isodesmosine, the cross-linking amino acids unique to elastin, were measured directly from acid hydrolysates of hamster and human lungs by amino acid analysis. A Durrum D-500 (Dionex) amino acid analyzer, with a modified lithium citrate buffer gradient was used. Results compared favorably with those obtained by gravimetric and microenzymatic techniques, and the method described could be used for the quantification of elastin in biopsy specimens

Amino Acids↗

Stimulation of human leukocyte elastase by platelet factor 4. Physiologic, morphologic, and biochemical effects on hamster lungs in vitro.

The purpose of this study was to determine if human platelet factor 4 (PF4) stimulates human leukocyte elastase (HLE) against lung elastin. Lung elastin was purified from hamster lungs and tritiated by reduction with NaB3H4. We found that HLE activity against this substrate is increased by concentrations of PF4 as low as 1.6 microgram/ml, and that this stimulation increased linearly with additional PF4. Lungs removed from hamsters and inflated with solutions containing buffer alone, low dose HLE, HLE plus PF4, or PF4 alone were incubated for 2 h at 37 degrees C. Whereas low-dose HLE failed to lower lung elastin when compared to control animals, HLE stimulated by PF4 lowered lung elastin by 20%. PF4 alone had no effect. Furthermore, low-dose HLE failed to alter the mechanical properties of hamster lungs as measured by pressure-volume curves in saline, although there was a significant loss of lung elasticity in the mid- and high-lung volume ranges in lungs treated with HLE and PF4. Morphologic studies revealed that low dose HLE resulted in a minimal emphysemalike lesion whereas HlE plus PF4 caused a significantly more severe lesion. PF4 is capable of stimulating HLE against lung elastin, and this effect may have a role in the pathogenesis of emphysema.

Animals↗

Protease and antiprotease responses in lung and peripheral blood in experimental canine pneumococcal pneumonia.

We studied the effects of pulmonary infection with type III pneumococcus in dogs on the degree of granulocyte elastase-like esterase activity and on the degree of antiproteases in peripheral blood and lung lavage fluid. In 9 infected dogs the peripheral blood granulocyte esterase activity increased from a preinfection level of 361.3 +/- 51 units/10(8) leukocytes to 593.8 +/- 80 units/10(8) leukocytes (mean +/- SE) 24 h after pneumonia had been induced (p less than .02). Parallel changes were measured in granulocytes obtained from bronchial lavage fluid. The antitrypsin activity and esterase inhibitory activity of peripheral blood increased by 15% after infection was induced. The esterase inhibitory activity of lung lavage fluid increased from a preinfection level of 776 +/- 160 units/mg of lavage protein to 1,390 +/- 200 units/mg of lavage protein (p less than .05). These findings indicate that whereas both circulating and lung lavage granulocytes contain increased concentrations of proteolytic activity during infection, serum antiproteases and, to a larger extent, lung antiproteases, also are increased.

Animals↗

Determining changes in airway caliber in asthma: the role of submaximal expiratory flow rates.

Sixteen patients with suspected reversible airway obstruction who had previously demonstrated an increase in specific airway conductance after isoproterenol, but who had not demonstrated an increase in forced expiratory flow were studied using a measurement of submaximal flow. Flow during tidal breathing (VTV) was measured spirometrically, and VTV increased in all 16 patients from a value of 0.61 L/sec before isoproterenol to 0.80 L/sec after isoproterenol. In addition, each of these 16 patients experienced a significant increase in vital capacity and a significant decompression of functional residual capacity after isoproterenol. If plethysmography is not available, the measurement of VTV may provide evidence of bronchodilatation. The mechanism responsible for the dichotomy between maximal and submaximal flow is the compression of airways by high positive pleural pressure which is present during maximal, but not submaximal maneuvers.

Adolescent↗

Acute coccidioidal pleural effusion.

Acute coccidioidal pleural effusions were studied in 28 patients. Coccidioidal pleural effusion appeared to be secondary to direct spread of contigous parenchymal infection, rather than to hematogenous dissemination, in more than 90 per cent of these patients. Only 2 of 28 patients had the concomitant development of disseminated infection, and both patients possessed factors known to predispose to dissemination. Because of the excellent prognosis in most patients, therapy in patients with coccidioidal pleural effusion should be expectant. This is true even when substantial increases occur in complement fixation titers; such elevations were frequent in this series. Cultures of pleural biopsy specimens were the most rewarding cultural source in this series, being positive in all 8 patients in whom such biopsy specimens were cultured. Dermal hypersensitivity, including erythema nodosum and erythema multiforme, was commin in patients whose clinical course was uncomplicated.

Adolescent↗

Combined hyertrophic subaortic stenosis and calcific aortic valvular stenosis.

A well documented case of combined hypertrophic subaortic stenosis and calcific aortic stenosis is reported. Detection of multilevel involvement in cases of left ventricular outflow obstruction requires a high index of suspicion and precise hemodynamic and angiographic documentation. Careful analysis of the total data base is necessary for proper management of the patient. The pathogenesis of this combined lesion is unclear: Asymmetrical septal hypertrophy may occur as a consequence of the valvular stenosis, or it may be that abnormal leaflet motion in patients with hypertrophic obstruction produces leaflet thickening, calcification, deformity and stenosis.

Aged↗