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Biomedical subjects

B Adelman

Publications and source records attributed to B Adelman.

45 records · Page 3Linked to original sources
PubMed1985

Evaluation of platelet glycoprotein Ib by fluorescence flow cytometry.

Platelet glycoprotein Ib (GpIb), a receptor for von Willebrand's factor (vWF), was studied by way of fluorescence flow cytometry. Using a sandwich staining technique, GpIb was identified by a monoclonal antibody (6D1) directed against an epitope close to the vWF binding site. Platelets from normal individuals were symmetrically distributed with respect to GpIb content. Treatment of washed platelets with plasmin resulted in progressive loss of GpIb as measured by fluorescence flow cytometry and by loss of agglutination response when combined with ristocetin in the presence of vWF. In mixing experiments with GpIb-deficient and normal platelets, it was possible to detect a subpopulation of deficient cells comprising 2% of the total population. Streptokinase treatment of platelet-rich plasma caused loss of the agglutination response to ristocetin and the emergence of a population of GpIb-deficient platelets. Fluorescence flow cytometry appears to be an important new technique by which to study platelet surface receptors.

Blood Platelets↗
PubMed1985

The use of antithrombotic therapy in the elderly.

The elderly are predisposed to atherosclerosis and venous thrombosis, the conditions for which anticoagulants are used. Anticoagulants can be used safely in the elderly with little or no more risk of bleeding than exists in younger patients. The prescribing physician must know the mechanism of drug action, be attentive to potential side effects, and monitor drug activity adequately. The authors emphasize the oral anticoagulants and heparin because, in general, their use is associated with a greater degree of risk and more clearly defined benefits than would apply for the antiplatelet agents.

Aged↗
PubMed1985

Proliferation of smooth muscle cells in the thoracic aorta after injury to the abdominal aorta: evidence for a humoral mediator in experimental arteriosclerosis.

We tested the hypothesis that circulating humoral material(s) can induce vascular smooth muscle cells to synthesize DNA and to proliferate. Either the entire aorta or its abdominal segment was balloon de-endothelialized in four groups of rabbits. In the first group (control), the entire aorta was injured, and no further procedures were carried out. In a second group (reinjury), the abdominal aortic segment was reinjured 4 days after the initial de-endothelialization procedure. A third group (sham) had a second sham operation 4 days after initial injury. In a fourth group (abdominal only), the abdominal aortic segment was injured on two occasions 4 days apart. There was a rise in the specific activity of 3H-thymidine incorporation into smooth muscle cell DNA (DNA-SA) of the thoracic segments, which began 12 hours after reinjury, peaked within 24 hours at 335 +/- 63 dpm/micrograms DNA (+/- SEM), and returned to control level within 72 hours. The DNA-SA of the thoracic aorta of control rabbits and sham-operated animals 4.5 days after the initial injury was 86 +/- 19 and 48 +/- 8 dpm/micrograms DNA, respectively. There was no rise in DNA-SA in the thoracic aorta of animals in which the abdominal aorta was injured twice. Intimal cell nuclei per 0.1 mm internal elastic lamina were counted 3 days after the second injury and showed similar differences between doubly injured and control animals. Platelet accumulation, as measured by chromium 51 platelet attachment to the aortic surface, was increased in the abdominal segment 12 hours after reinjury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

The interaction of platelets with aortic subendothelium: inhibition of adhesion and secretion by prostaglandin I2.

We have studied the effect of prostaglandin I2 on platelet turnover, attachment to the subendothelium, and secretion following balloon deendothelialization of the rabbit aorta. Survival of 51Cr-labeled platelets in the balloon-injured animals remained normal. Thirty minutes after injury, there were 4.52 X 10(6) platelets/sq cm attached to the aortic surface, which was 87% covered by platelets. Although plasma platelet factor 4, as measured by radioimmunoassay, did not rise above the normal level of 6.8 +/- 2.6 ng/ml (mean +/- SEM) during the first hour after balloon injury, platelet factor 4 antigen was detected within the vessel wall by direct immunofluorescence within 30 min of injury. An infusion of 650-850 ng/kg/min prostaglandin I2 completely inhibited platelet aggregation and reduced surface coverage by 84% and platelet attachment by 63%. Animals given 50-100 ng/kg/min prostaglandin I2, which only partially inhibited platelet aggregation, had 70% of the aortic surface covered by platelets. Platelet factor 4 antigen was also detected within the aortic wall. Platelet attachment was normal in animals that had been given 850 ng/kg/min prostaglandin I2 prior to balloon injury but sacrificed after the infusion was stopped and ex vivo platelet aggregation had returned to normal.

Animals↗
PubMed1980

Rehabilitation in spinal cord injury: use of a patient-family group.

A 1-day group meeting for spinal cord injured individuals and their families was initiated approximately 3 years ago with emphasis on providing information and sharing mutual concerns and feelings. From the results of tests administered before and after the program and of evaluation forms filled out by all participants, the Family Group has been found to be a useful adjunct to the rehabilitation program. Family members are effectively and meaningfully involved in the total rehabilitation process with the added benefit of decreasing their feelings of anxiety, helplessness and isolation. Evaluation suggests that the Family Group increases the individual's knowledge and awareness of a disability and its implications. It has introduced important topics of discussion within the family unit and has aided in more open communication among family members surrounding these issues. All of these benefits, combined, have resulted in more effective, realistic and appropriate discharge planning for patients.

Adolescent↗
PubMed1976

Synthesis of basement membrane collagen by cultured human endothelial cells.

Studies were performed to determine if cultured human endothelial cells synthesized basement membrane collagen. In culture, endothelial cells were attached to grossly visible membranous structures which on light microscopy were composed of ribbons of dense, amorphous material. On transmission electron microscopy, these membranous structures consisted of amorphous basement membrane, and material morphologically similar to microfibrils and elastic fibers. By immunofluorescence microscopy, these membranous structures stained brightly with antisera to human glomerular basement membrane. Cultured endothelial cells incorporated [3H]proline into protein; 18% of the incorporated [3H]proline was solubilized by purified collagenase. When endothelial cells were cultured with [14C]proline, 7.1% of the incorporated counts were present as [14C]hydroxyproline. Cultured endothelial cells were labeled with [3H]glycine and [3H]proline and digested with pepsin. The resulting fractions on analysis by SDS-polyacrylamide gel electrophoresis contained two radioactive protein peaks of mol wt 94,200 and 120,500. Both these peaks disappeared after digestion with purified collagenase. The peak of mol wt 120,500 corresponds to that of alpha1 (IV) collagen; the peak of the mol wt 94,200 probably corresponds to that of alpha1 (III) collagen. Thus, cultured human endothelial cells synthesize material which is morphologically and immunologically like amorphous basement membrane and biochemically like basement membrane collagen. Cultured endothelial cells probably also synthesize material which is morphologically similar to microfibrils and elastic fibers.

Basement Membrane↗
PubMedDate not supplied

In vivo imaging and evaluation of platelet accumulation vs. time at arterial injury site.

The feasibility of quantitatively imaging platelet deposition over time following angioplasty of the abdominal aorta in a rabbit model, with and without antiplatelet treatment, was investigated. Ten male 3-4 kg rabbits were balloon de-endothelialized and placed on 2% cholesterol diet for eight weeks. Group A was untreated. In Group B, donors and recipients were treated with aspirin (5 mgm/kg) prior to and after angioplasty. Platelets were labelled with indium-111. Labelled platelets were injected just prior to PTA and images of 100,000 counts were obtained immediately and at 30 minutes, 1 hour, and 24 hours. In Group A, increased activity of angioplasty site vs. nonangioplastied aorta was seen immediately. This focal increase became more marked in hypercholesterolemic animals over the 24-hour period. In Group B, both hypercholesterolemic and normocholesterolemic, no focal uptake could be documented on sequential scans. This method and model are promising for in vivo evaluation of platelet-vessel wall interactions, in the setting of angioplasty and antiplatelet therapy.

Angioplasty, Balloon↗
PubMedDate not supplied

Interaction of platelets and fibrin with injured rabbit aortic neointima. Effect of prostaglandin I2 and heparin.

Following aortic balloon deendothelialization, rabbits develop a neointima composed of smooth muscle cells and extracellular connective tissue. Injury of this neointima with a balloon catheter results in the accumulation of platelet aggregates and fibrin on the vessel surface. We studied platelet attachment and secretion following injury of the neointima and also the effect of prostaglandin I2 (PGI2) and heparin on these events. Platelet factor 4 was detected within the neointima by indirect immunofluorescence 30 minutes after neointimal injury. By using 51Cr-labeled platelets, it was possible to quantitate total platelet attachment following neointimal injury. When animals were sacrificed 30 minutes after reinjury, there were 4.46 X 10(6) platelets/cm2 of aortic surface in animals injured 10 days after initial balloon deendothelialization, and 3.75 X 10(6) platelets/cm2 of aortic surface in animals injured 29 days after initial injury. In these two groups, infusion of 850 ng/kg/min PGI2, along with a single infusion of 2500 units of heparin, inhibited fibrin deposition and reduced platelet attachment by 71% and 76%, respectively. Although infusion of heparin alone prevented fibrin deposition, neither heparin nor PGI2 individually reduced platelet attachment as profoundly as did their combined use.

Aminophylline↗