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Biomedical subjects

B F Feldman

Publications and source records attributed to B F Feldman.

At least 37 records · Page 2Linked to original sources

Effect of equine ehrlichial colitis on the hemostatic system in ponies.

Hemostatic function was determined in 10 ponies at various times after inoculation with Ehrlichia risticii to determine whether equine ehrlichial colitis (EEC) caused changes in the hemostatic system and to determine the prognostic value of hemostatic function tests during EEC. Mean platelet count; plasma fibrinogen, fibronectin, factor VIII: coagulant, alpha 2-antiplasmin, and plasminogen values; and serum concentrations of fibrin/fibrinogen degradation products changed significantly (P less than 0.05) from base line (day 0, before inoculation) during 18 days after inoculation with E risticii. Four ponies that died or were euthanatized because of severe clinical signs of EEC had significantly (P less than 0.05) greater mean plasma fibrinogen concentrations plasma factor VIII:coagulant values, and activated partial thromboplastin times immediately before death than did the 6 surviving ponies. Factor V concentrations were significantly (P less than 0.05) lower on postinoculation days 10 and 20 in nonsurvivors. Seemingly, changes in hemostasis took place during EEC. Ponies that did not survive EEC had greater laboratory evidence of coagulopathy.

Animals↗

A turbidimetric method for fibronectin assay in the dog.

An immunoturbidimetric method, using spectrophotometry, for the assay of canine plasma fibronectin concentration was compared with the immunoelectrophoretic method. The spectrophotometric method (S) correlated positively (r = 0.7) and significantly (P less than 0.01) with the immunoelectrophoretic method (I). The regression equation was S = 0.37I + 53. Ninety-five percent confidence levels for the regression line were calculated to allow detection, by spectrophotometry, of plasma fibronectin concentrations outside the normal range.

Animals↗

Plasma fibronectin concentration associated with various types of canine neoplasia.

Fibronectin, a large glycoprotein found in soluble form in plasma and in insoluble form in connective tissue matrices, has been implicated in cell-to-cell and cell-to-substratum interactions, inflammation and tissue repair, phagocytosis, hemostasis, and oncogenic cell transformation. Because fibronectin concentration is diminished or lacking on cell surfaces of many transformed cell lines and because decreased concentration of plasma fibronectin is associated with suboptimal mononuclear phagocyte system function and host defense, plasma fibronectin concentration was evaluated in 119 dogs with various forms of neoplasia. Included were 43 dogs with neoplasia of the skin and soft tissue, 18 with gastrointestinal tract neoplasia, 29 with mammary gland neoplasia, and 29 with various other types of neoplasia. Of the dogs studied, 44 (37%) had evidence of metastatic disease. This group had fibronectin concentration that differed significantly (P less than 0.01) from the plasma fibronectin concentration reference interval. Within this group, 9 dogs (20% of this group) had plasma fibronectin values within the reference interval, 33 (75%) had significantly (P less than 0.01) lower values than the reference interval, and 2 (5%) had significantly (P less than 0.01) higher values than the reference interval. These data suggested that fibronectin concentration determination, when results are abnormal, may be of diagnostic and prognostic interest.

Animals↗

Scanning electron microscope study of platelet release by canine megakaryocytes in vitro.

Megakaryocytes were isolated from bone marrow from healthy dogs, using a combination of density-gradient centrifugation and polysucrose-velocity sedimentation techniques. The 2-step separation technique resulted in a preparation comprising 30% to 35% megakaryocytes of total nucleated cells. Accessibility to large numbers of viable canine megakaryocytes allowed investigation of platelet release by these cells in short-term cultures. Megakaryocytes were observed to form long cytoplasmic processes that gradually developed segmental constrictions and subsequently fragmented into platelet-sized pieces. Some platelet-sized cytoplasmic pieces of megakaryocytes presumably underwent discoid transformation.

Animals↗

Circulating proplatelets: isolation and quantitation in healthy rats and in rats with induced acute blood loss.

A technique to isolate megakaryocyte proplatelet processes from blood of rats' hearts, using colloidal silica coated with polyvinylpyrrolidone density gradient, was developed. The proplatelet concentration in blood from right ventricles was significantly higher (P less than 0.001) than that in blood from left ventricles in healthy rats, as well as in rats with induced acute blood loss. The proplatelet concentration of blood from the heart, 24 hours after acute blood loss was induced was significantly (P less than 0.001) increased, indicating that platelet production was accelerated. The demonstration of proplatelets entering the pulmonary circulation indicates platelet release via proplatelet formation. Seemingly, proplatelets are fragmented in the lungs at predesignated locations along the proplatelet process.

Acetylcholinesterase↗

In vitro platelet release by rat megakaryocytes: effect of metabolic inhibitors and cytoskeletal disrupting agents.

Development of an in vitro visual assay facilitated the study of large numbers of megakaryocytes undergoing proplatelet formation in short-term cultures. Approximately 9% of megakaryocytes formed platelets during a 24-hour period. In the presence of an inhibitor of anaerobic glycolysis (NaF), proplatelet formation was inhibited, whereas inhibitors of respiration (NaCN) did not significantly (P greater than 0.05) decrease proplatelet formation. Presence of the microtubule-disrupting agents colchicine and vincristine sulfate in culture medium inhibited proplatelet formation, whereas the microfilament-disrupting agent cytochalasin B had a less pronounced inhibition.

Animals↗

In vitro platelet release by rat megakaryocytes: effect of heterologous antiplatelet serum.

A visual assay to study megakaryocyte platelet release via proplatelet formation in vitro was established. Samples of megakaryocyte-enriched rat bone marrow were incubated (37 C) in RPMI-1640 medium with 15% autologous serum in specially prepared chambers. In the culture system, approximately 6% of megakaryocytes formed proplatelet processes within 24 hours. Inclusion of a heterologous antiplatelet antibody in the culture system inhibited proplatelet formation, compared with that in controls.

Animals↗

Effect of fibronectin supplementation in endotoxic shock in the dog.

An earlier study by our group demonstrated significant amelioration of hypotension, hypoglycemia, and acidosis in dogs treated with purified human plasma fibronectin prior to induction of endotoxic shock. The present study was completed to determine whether treatment with purified human plasma fibronectin 1 hr after induction of endotoxic shock would provide similar benefits. To this end, selected hemodynamic, pulmonary, acid-base, metabolic, hematological, and serum chemistry parameters were monitored for 6 hours in two groups of anesthetized dogs in Escherichia coli endotoxic shock. One group was given an intravenous injection of purified human plasma fibronectin, and the other received an equal volume of saline 1 hr after shock induction. Between-group analysis of the data revealed no significant differences between any parameter excepting modest differences in plasma glucose, albumin, alkaline phosphatase, and BUN concentrations. However, even these differences, although statistically significant, were sporadic and unimpressive. This study suggested that treatment of dogs with fibronectin during gram-negative endotoxic shock was not efficacious.

Animals↗

Immunoglobulin A myeloma in a cat with pleural effusion and serum hyperviscosity.

Immunoglobulin A myeloma, serum hyperviscosity, and septic pleuritis were diagnosed in a cat with pleural and peritoneal effusions. Serum hyperviscosity was determined by use of a WBC pipette, and clinical manifestations included retinopathy and cardiac changes. The presence of Salmonella typhimurium in the pleural fluid may have resulted from increased susceptibility to infection. Postmortem examination revealed plasma cell infiltration of the pleura, mesenteric lymph nodes, and the serosa of the intestine, liver, and spleen. This case represents an unusual form of myeloma in the cat.

Animals↗

Platelet dysplasia associated with megakaryoblastic leukemia in a dog.

In a case of megakaryoblastic leukemia in a dog, definitive diagnosis was made through use of specific cytochemical stains of circulating and bone marrow blast cells. Morphologic and functional abnormalities of platelets were revealed through transmission electron microscopy and in vitro aggregation of platelets after addition of adenosine diphosphate.

Animals↗

Drug-induced thrombocytopenia.

A variety of drugs may cause thrombocytopenia. Although it occurs more often than drug-induced anemia it is less well understood because techniques for studying drug-platelet-immune interactions have been unavailable until recently. The mechanisms by which drugs cause thrombocytopenia are varied. Bone marrow suppression or increased peripheral destruction of platelets could be involved. Nonimmunologic as well as immunologic mechanisms may also occur. These different mechanisms of drug-induced thrombocytopenia are reviewed. Diagnostic methods and treatment are also summarized.

Animals↗

An enzyme immunoassay to measure canine circulating fibronectin.

A competitive enzyme immunoassay has been used to detect and quantitate fibronectin in canine plasma. In this test, purified fibronectin, bound to microtiter plates, competes with plasma fibronectin for the conjugated antibody, rabbit-anticanine, fibronectin-horseradish peroxidase. The assay could detect fibronectin in purified standards from 58 ng/ml to 580 microgram/ml. The range of 1-100 microgram/ml was linear for plasma samples diluted 1:10, allowing samples with fibronectin concentrations from 10-1000 microgram/ml to be easily measured by this method. The mean normal fibronectin concentration of 132 dogs, by this method, was determined to be 320 +/- 74 microgram/ml.

Journal Article↗

Haemostatic abnormalities in canine Cushing's syndrome.

Selected parameters of the haemostatic system were evaluated in 12 consecutive cases of canine Cushing's syndrome. The dogs did not exhibit evidence of thromboembolic complications. Levels of factors V and X were increased significantly (P less than 0.01) and fibrinogen concentration was increased modestly (P less than 0.05) in these dogs. Levels of factors IX and VIII:C remained in the reference range. Antithrombin III (ATIII) and plasminogen concentrations were markedly elevated (P less than 0.001). The low factor VIII:C and elevated ATIII levels in the plasma were not consistent with characteristics of a hypercoagulable state. These results demonstrated that haemostatic abnormalities which occur in canine Cushing's syndrome do not necessarily represent a state predisposed to thrombosis.

Animals↗

Scanning electron microscopic studies of megakaryocytes and platelet formation in the dog and rat.

Megakaryocyte morphology and platelet formation in canine and murine bone marrows were studied by scanning electron microscopy. In situ-fixed bone marrow preparations and cell suspensions of bone marrow provided complementary information for the 2 species (dogs and rats). Cylindrical processes (proplatelets) of variable length and thickness, originating from the megakaryocyte surface, were in the larger marrow sinusoids and the central vein. Regional constrictions along the length of proplatelets, particularly near their apical region, and the presence of fragments of such processes supported the concept of platelet formation through segmentation of proplatelets. Megakaryocytes presented varied morphology. Surface features resembling platelets were observed on megakaryocytes, indicating that platelets may have been released through surface budding. In conclusion, megakaryocytes formed long proplatelet processes that actively migrated to venous sinusoids to release platelets by fragmentation. Scanning electron microscopy analysis revealed a complex and variable megakaryocyte surface topography. The platelet-like structures on megakaryocyte surfaces may represent platelet release by a budding mechanism. The similarity between murine platelet release and canine platelet release demonstrates that data from rodent models may be applicable to nonrodents.

Animals↗