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Biomedical subjects

H Wohl

Publications and source records attributed to H Wohl.

At least 19 recordsLinked to original sources
PubMed1981

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↗
PubMed1981

Plasma calcitonin as a marker of disease activity in patients with small cell carcinoma of the lung.

To evaluate the usefulness of plasma calcitonin as an index of tumor burden and disease activity, we undertook a prospective study of serial calcitonin measurements in a group of patients with small cell carcinoma of the lung from diagnosis throughout a period of intensive therapy. Plasma calcitonin was significantly elevated in 84% of patients with extensive small cell carcinoma of the lung and was not elevated in patients with limited disease at the time of diagnosis. The elevated values fell significantly in response to chemotherapy and radiation therapy, and reflected regression of followable disease and improvement in clinical status. A significant correlation existed between plasma calcitonin and extent of disease. Relapse was generally associated with an increase in elevated plasma calcitonin levels, and calcitonin appeared to reflect tumor burden. The serial measurement of plasma calcitonin is useful in the management of the patient with small cell carcinoma of the lung.

Calcitonin↗
PubMed1981

Platelet markers of thromboembolic disease.

Platelets may be useful as markers of thromboembolic disease. When labeled with indium 111 they allow external imaging of localized clots. Indium 111 is much superior to chromium 51 for this procedure. Detection of circulating platelet aggregates also appears to be a simple means of determining the presence of thromboembolic disorders. In response to injury or involvement in clotting, platelets release several unique proteins not normally found in the plasma. Therefore, elevated levels of these proteins suggest the presence of such damage. Platelet factor 4 and beta-thromboglobulin are the most widely studied of these proteins, and both can be quantitated by radioimmunoassay. Such assays are now commercially available. Elevated levels have been demonstrated in such diverse disorders as deep venous thrombosis, atherosclerosis and diabetes. However, blood must be drawn with great care to avoid in vitro damage to platelets and false elevation of these markers. All of these procedures are promising at present, but their precise role and value await further study.

Beta-Globulins↗
PubMed1978

Platelet factor 4: an inhibitor of collagenase.

Human platelet factor 4 (PF4) is known to bind to heparin and inhibit its anticoagulant effect. This factor also inhibits the enzyme collagenase derived from cultured human skin and collagenase extracted from human granulocytes. The addition of heparin to the PF4-collagenase assay system has no effect on the observed inhibition of collagenase. Thus PF4 inhibits collagenase, in addition to neutralizing heparin.

Blood Coagulation Factors↗
PubMed1976

Human platelet factor 4: Purification and characterization by affinity chromatography. Purification of human platelet factor 4.

Platelet factor 4 is a low molecular weight protein contained in the storage granules of platelets and released during aggregation with a variety of aggregating agents. In vitro, it is a potent antiheparin. This property has been used for a rapid, simple purification procedure using affinity chromatography on heparin epsilon-aminocaproic aced Sepharose. Supernatants collected from outdated platelet concentrates, or platelet extracts prepared from washed, outdate platlets themselves, are first precipitated with 50% ammonium sulfate. The supernatant is dialyzed and applied to the affinity column. Contaminating proteins are washed from the column with 0.5 M NaCl in 0.005 M sodium barbital buffer, pH 7.4 and the column is then eluted with a gradient of 0.5 to 3.0 M NaCl in 0.005 M sodium barbital buffer, pH 7.4. When prepared from platelet extracts, a single protein peak with high platelet factor 4 activity is eluted at 0.9 to 1.0 M NaCl. The peak fractions demonstrate a single band on Na dodecyl-SO4-polyacrylamide gel electrophoresis. The molecular weight as determined by Na dodecyl-SO4 gel electrophoresis was 11,600 +/- 330, and was 40,000 by gel filtration.

Amino Acids↗