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Biomedical subjects

R F Baugh

Publications and source records attributed to R F Baugh.

At least 37 records · Page 2Linked to original sources
PubMed1981

Identification of platelet receptors for bovine von Willebrand factor on human platelets by a new platelet receptor test.

A new test for the quantitation of platelet receptor activity for bovine von Willebrand factor in human platelet extracts is described. The test is based on the competition for the von Willebrand factor occurring between platelets, an antibody against von Willebrand factor, and platelet extracts containing the von Willebrand receptor. Bovine von Willebrand factor aggregates human platelets directly. In the presence of EDTA, anti-bovine von Willebrand factor antibody disaggregates platelet aggregates induced by bovine von Willebrand factor. Disaggregation is measured by following the decrease in light transmission accompanying disaggregation. Platelet extracts inhibited the disaggregating activity of the antibody, and the percent inhibition was directly proportional to the amount of the platelet extract added. The decrease in platelet disaggregating activity of the antibody was used as an indicator of platelet receptor activity in a system consisting of platelet-rich plasma, bovine von Willebrand factor, antibody and platelet extract. With this method we found von Willebrand factor receptors in the whole platelet extract, the Triton X-100 platelet membrane extract and in platelet extract material which bound to a bovine Willebrand factor-Sepharose 6MB affinity column.

Animals↗
PubMed1981

Characterization of a new mode of defective ristocetin-induced platelet aggregation.

A patient with a reduced response to the platelet-aggregating agent ristocetin and a prolonged bleeding time was found to have an abnormally high level of vWf as measured by Laurell immunoelectrophoresis. Characterization of the patient's vWf by disc-gel electrophoresis and crossed immunoelectrophoresis showed it to be indistinguishable from vWf isolated from normal plasma. The specific activity of the purified vWf in supporting RIPA was the same for both patient and normal vWf. The diminished RIPA was therefore not due to decreased levels of vWf or the presence of a modified form of the vWf. The patient's platelet-poor plasma inhibited the ristocetin-induced platelet aggregating activity of normal PRP, indicating the presence of an inhibitor. Fractionation of the plasma by ion-exchange chromatography showed the inhibitory activity to be in the patient's gamma globulin fraction. The gamma globulin was not directed against either the patient's vWf or against the patient's platelets but appeared to interfere with RIPA by binding ristocetin.

Aged↗
PubMed1978

The action of immobilized thrombin on factor VIII, fibrinogen and a synthetic tripeptide.

Bovine thrombin was insolubilized by attachment to cyanogen bromide-activated Sepharose (Sepharose-thrombin) or to activated (Affi-Gel 10) agarose containing a 10 A long arm (Affi-Gel-thrombin). Coupling in both instances approximated 7,000 units of thrombin per ml packed gel as determined by 125I-thrombin incorporation. The thrombin beads hydrolyzed the synthetic tripeptide Bz-Phe-Val-Arg-pNA (S-2160) at different rates, with the Sepharose-thrombin more active (220 esterase units per ml) than Affi-Gel thrombin (20.4 units per ml). The Km was significantly higher for the insolubilized thrombins (2 X 10(-3) M) than uncoupled thrombin (Km = 8 X 10(-5) M). The Sepharose-thrombin activated factor VIII significantly more rapidly than Affi-Gel-thrombin. Neither matrix-bound thrombin clotted a fibrinogen solution or liberated significant amounts of fibrinopeptides over 48 hr. This data indicates that a proteolysis of factor VIII, rather than a complex with thrombin, is the method of activation of factor VIII and that factor VIII is more accessible to the action of immobilized thrombin than is fibrinogen.

Animals↗
PubMed1978

The Passovoy defect: further characterization of a hereditary hemorrhagic diathesis.

We studied a coagulation abnormality present in 12 members of five kindreds who bruised easily and bled excessively after minor trauma. Their activated partial thromboplastin times were between 32 and 39 seconds (normal, 22.8 to 28.8 seconds). Prothrombin times, thrombin times, platelet-function tests and the levels of factors XII, XI, IX, VIII, prekallikrein and high-molecular-weight kininogen were normal. Within these kindreds inheritance of prolonged partial thromboplastin times followed an autosomal and probably dominant pattern. The prolonged thromboplastin times were corrected by normal plasma and by normal plasma adsorbed with celite, but there was no mutual correction between plasmas of the patients. These subjects shared a common defect in the intrinsic pathway of coagulation that we designate by the proband's surname, Passovoy.

Adolescent↗
PubMed1975

Plasma components which interfere with ristocetin-induced platelet aggregation.

Normal human plasma contains a component or components which interfere with ristocetin-induced platelet aggregation. Preliminary examination suggests a protein (or proteins) which binds ristocetin and competes more effectively for ristocetin than do the proteins involved in ristocetin-induced platelet aggregation. The presence of this protein in normal human plasma also prevents ristocetin-induced precipitation of plasma proteins at levels of ristocetin necessary to produce platelet aggregation (0.5-2.0 mg/ml). Serum contains an apparent two0fold increase of this component when compared with plasma. Heating serum at 56 degrees for one hour results in ad additional 2 to 4 forl increase. The presence of a ristocetin-binding protein in normal human plasma requires that this protein be saturated with ristocetin before ristocetin-induced platelet aggregation will occur. Variations in the ristocetin-binding protein(s) will cause apparent discrepancies in ristocetin-induced platelet aggregation in normal human plasmas.

Adsorption↗
PubMedDate not supplied

Vocal rehabilitation of tracheoesophageal speech failures.

Twenty-three tracheoesophageal speech failures were prospectively evaluated by clinical parameters and transnasal air insufflation at 3 L per minute. The results of testing allow an accurate indication of the etiology of the speech failure. Pharyngoesophageal spasm accounted for 79% of the failures; hypopharyngeal strictures for 26%. One patient was found to have both pharyngoesophageal spasm and a hypopharyngeal stricture. A modified air insufflation test result greater than 20 mm Hg reliably identified all tracheoesophageal speech failures prior to tracheoesophageal puncture. Clinical parameters were not helpful in identifying speech failures. Successful treatment of the specific etiology of the failure resulted in a reduction of the measured intraesophageal pressures. Ninety-one percent of the tracheoesophageal speech failures were successfully rehabilitated and achieved fluent tracheoesophageal speech. Successful rehabilitation was associated with long-term tracheoesophageal speech use.

Esophageal Spasm, Diffuse↗
PubMedDate not supplied

Small cell carcinoma of the head and neck.

Treatment methods for patients with small cell carcinoma of the head and neck are changing. Increasing clinical experience with these tumors and a better appreciation of patterns of recurrence, the need for thorough tumor staging, and the importance of chemotherapy as a form of primary therapy have contributed to these changes. Current concepts regarding small cell carcinoma arising in the head and neck are reviewed. Reported results of treatment for a variety of head and neck sites and site-specific relapse rates are summarized. New cases of small cell carcinoma arising in the hypopharynx, paranasal sinus, and from an unknown primary are added to the reported experience in the literature.

Adult↗