Search PubMed⌕ Search

Biomedical subjects

B A Bradlow

Publications and source records attributed to B A Bradlow.

At least 19 recordsLinked to original sources
PubMed1995

Response of hypercholesterolemic subjects to administration of tocotrienols.

The cholesterol-suppressive actions of Palmvitee and gamma-tocotrienol were assessed in hypercholesterolemic subjects after acclimation to the American Heart Association Step 1 dietary regimen for four and eight weeks, respectively. The four-week dietary regimen alone elicited a 5% decrease (P < 0.05) in the cholesterol level of the 36 subjects. Subjects continuing on the dietary regimen for a second four-week period experienced an additional 2% decrease in their cholesterol levels. Dietary assessments based on unanticipated recalls of 24-h food intake records suggest that significant reductions in energy and fat, predominantly in saturated fat, intakes are responsible. The subjects experienced significant Palmvitee- and gamma-tocotrienol-mediated decreases in cholesterol. The group of subjects acclimated to the dietary regimen for four weeks responded to Palmvitee (a blend of tocols providing 40 mg alpha-tocopherol, 48 mg alpha-tocotrienol, 112 mg gamma-tocotrienol, and 60 mg delta-to-cotrienol/day for four weeks) with a 10% decrease in cholesterol (P < 0.05). Dietary assessments showed no further change in energy and fat intakes. alpha-Tocopherol attenuated the cholesterol-suppressive action of the tocotrienols. The second group of subjects, acclimated to the dietary regimen for eight weeks, received 200 mg gamma-tocotrienol/d for four weeks. The cholesterol-suppressive potency of this alpha-tocopherol-free preparation was calculated to be equivalent to that of the mixture of tocotrienols (220 mg) used in the prior study. Cholesterol levels of the 16 subjects in the second group decreased 13% (P < 0.05) during the four-week trial. Plasma apolipoprotein B and ex vivo generation of thromboxane B2 were similarly responsive to the tocotrienol preparations, whereas neither preparation had an impact on high density lipoprotein cholesterol and apolipoprotein A-1 levels.

Adult↗
PubMed1991

An analysis of duplicate testing of prothrombin time and activated partial thromboplastin time assays.

An evaluation of duplicate prothrombin time (PT) and activated partial thromboplastin time (aPTT) assays determined by the MCA 110 coagulation analyzer was undertaken to develop analytical duplicate performance criteria to quantitate the risks associated with single versus duplicate procedures. Included in the study were 1,277 patient samples. On the basis of the currently recommended therapeutic range for prothrombin ratios, a variation of approximately 10% or more between duplicates was considered to be unacceptable. For aPTT assays, the recommended therapeutic range for heparin therapy was usually 1.5 to 2.5 times the baseline value, and variations of up to 25% might be considered acceptable. With these relatively lenient criteria, approximately 2% of PT and 1.3% of aPTT assays had differences between duplicate values that were unacceptable. From this data the authors concluded that the frequency of errors produced by single estimations was too great for satisfactory clinical practice.

Humans↗
PubMed1989

Plasma fibrinolytic activity after ingestion of omega-3 fatty acids in human subjects.

Plasma fibrinolytic activity was measured in human volunteers after 30 day periods of ingestion of a fish oil product (Max Vita) containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and a wheat germ oil product containing alpha linolenic acid. Compliance was confirmed by significant increases in plasma levels of EPA and DHA and by significant falls in serum triglyceride levels. Platelet aggregation in platelet rich plasma and in whole blood was not altered significantly by fish oil or wheat germ oil. Neither fish oil or wheat germ oil caused any significant change in tissue plasminogen activator (tPA) or its inhibitor (PAI) measured enzymatically or in tPA antigen measured by an ELISA method. All these analytes (tPA, PAI, and tPA antigen) were measured before and after venous compression.

Adult↗
PubMed1988

Evaluation of Leu-M5 (CD11c) in hairy cell leukemia by the alkaline phosphatase anti-alkaline phosphatase technique.

The concomitant presence of B antigens and of the antigen recognized by the monoclonal antibody Leu-M5 (CD11c) on neoplastic lymphoid cells has been reported to be largely restricted to hairy cell leukemia (HCL). The authors studied Leu-M5 reactivity of neoplastic cells from 59 patients whose specimens were referred with a stated diagnosis of HCL by using the alkaline phosphatase anti-alkaline phosphatase technique on peripheral blood (PB) and bone marrow (BM) specimens. Tartrate-resistant acid phosphatase (AcP-T) activity was also studied. In 49 patients, HCL had been confirmed previously by BM biopsy, and specimens were evaluated for disease status during or after therapy with interferon (IFN) or 2'-deoxycoformycin. The remaining ten patients were newly referred for confirmation of the diagnosis of HCL before therapy. In all 55 patients in whom the BM biopsy demonstrated HCL, virtually every leukemic cell was Leu-M5 reactive, and the reaction proved, in some cases, to be helpful in the detection of small numbers of hairy cells in PB or BM preparations. AcP-T reactivity was demonstrated in the neoplastic cells of 52 of these 55 patients, including all but 3 of those receiving IFN, and was helpful in confirming persistent leukemia when interpretation of BM biopsy sections was difficult because the numbers of hairy cells were small. However, in four of the ten newly referred patients, BM biopsy showed features of splenic lymphoma with villous lymphocytes, rather than HCL. The neoplastic cells of these four patients were of B-cell origin and in three were Leu-M5 reactive. The authors' study indicates that Leu-M5 is present in nearly all hairy cells, but its presence in conjunction with other B-cell markers is not specific for HCL.

Acid Phosphatase↗
PubMed1985

Long-term ultra-low-dose aspirin therapy and platelet function.

The effect of ultra-low-dose aspirin on platelet aggregation and thromboxane B2 (TXB2) production was studied in two groups of normal subjects. Group 1 received 162 mg/d and group 2 received 20 mg/d for 4 weeks. For the first 2 weeks the effects were similar in the two groups, namely inhibition of aggregation and inhibition of TXB2 production. However, after 4 weeks there was significantly less inhibition of platelet aggregation in those receiving 20 mg/d. Inhibition of TXB2 production in the two groups was not significantly different. Two of 9 individuals receiving 20 mg/d showed an escape from the aspirin effect by the 4th week. When 40 mg/d was given to these 2 individuals they again responded. A daily dose of 20 mg aspirin is therefore too small to maintain adequate inhibition of platelet function in normal subjects.

Adenosine Diphosphate↗
PubMed1984

Mother-infant prothrombin precursor status at birth.

Previous work from this laboratory has suggested there is a risk of hemorrhagic disease of the newborn (HDNB) in approximately one-third of term neonates, presumably as a result of vitamin K deficiency. Using the same assay for PIVKA (protein induced by vitamin K absence, prothrombin precursor), we studied 46 normal mother-infant pairs at term to investigate the relationship between neonatal and maternal PIVKA status. PIVKA was found in 13 infants (28%) and in seven mothers (15%). Maternal PIVKA status correlated with infant status (p less than 0.03). These data suggest that fetal vitamin K deficiency and risk of HDNB may be a consequence of maternal deficiency of the vitamin.

Adult↗
PubMed1984

Acarboxy prothrombin in cord plasma from normal neonates.

Acarboxy prothrombin was detected in the plasma of 48 of 128 umbilical cord plasma samples and in all of 65 patients receiving coumadin. None was found in 20 normal adults. Although the prevalence was the same in blacks, whites, and neonates of mixed origin, levels were significantly higher in blacks. There was a negative correlation between the level of acarboxy prothrombin and the prothrombin index. There was no correlation between maternal age, birth weight, gestational age, obstetrical complications, race, socioeconomic status, albumen, or alpha-foetoprotein and the incidence of cord plasma acarboxy prothrombin.

Adult↗
PubMed1983

Oral anticoagulants in the 1980s. A reassessment of indications, dosage and laboratory control.

Oral anticoagulants were introduced into clinical practice in the late 1940s. An initial wave of enthusiasm was followed by a period of scepticism in the late 1950s and 1960s. During the 1970s and recently a number of studies have revealed new evidence of clinical benefits in many thrombo-embolic conditions. The importance of correct dosage based on sound laboratory control has been recognized as a fundamental prerequisite for efficient use of this form of therapy. A reassessment of the correct therapeutic range based on prothrombin assays which conform to an international standard has resulted in more effective dosage within acceptable limits of safety. Currently accepted indications for oral anticoagulation therapy and the optimal therapeutic ranges for various thromboplastin preparations are reviewed.

Administration, Oral↗
PubMed1983

Warfarin therapy--a practical guide.

Efficient anticoagulation with warfarin therapy requires optimal dosage. An international programme of standardization of prothrombin time tests has been developed in order to achieve correct dosage and efficient anticoagulation. Many South African laboratories use a more conservative therapeutic range for the prothrombin time than that recommended by international bodies. Consequently, warfarin dosage is often lower in the RSA than in many other countries. The use of a slightly lower therapeutic range in the RSA would improve anticoagulation without increasing the risk of haemorrhage. Practical guidelines for efficient warfarin therapy, including induction and maintenance dosage, therapeutic range, management of overdosage, contraindications and use during pregnancy and lactation, are discussed.

Female↗
PubMed1983

The effect of low-dose aspirin and platelet aggregation in familial hypercholesterolaemia.

Since the platelets of patients with familial hypercholesterolaemia (FH) are hyperaggregable, the inhibitory effect of low-dose aspirin on platelet aggregation in response to adenosine diphosphate, collagen, adrenaline and arachidonic acid was tested in 9 young adult patients with FH and compared with that in 9 normal subjects. After a single oral dose (150 mg) of aspirin the degree of inhibition of platelet aggregation was the same in the two groups, as was the recovery time (in days) for full restoration of platelet aggregation . In a second experiment in which 162 mg aspirin was administered daily for 28 days, inhibition of platelet aggregation was sustainable in both the patient and the control groups. These results suggest that despite the recognized hyperaggregability of platelets from patients with FH, daily low-dose aspirin ingestion effectively inhibits their in vitro aggregation and may therefore prove beneficial as supplemental therapy to reduce the rate of myocardial infarction in this high-risk group.

Adult↗
PubMed1983

The effects of a vegetarian diet on platelet function and fatty acids.

Nine healthy subjects taking an average mixed "Western" diet were placed on a vegetarian diet poor in arachidonic acid for four weeks. All animal and marine foods except for cows milk and milk products were excluded. Platelet aggregation responses to arachidonic acid and epinephrine increased slightly whereas responses to ADP and collagen were unchanged. Platelet thromboxane production, platelet counts, serum LDL cholesterol and triglycerides did not change but total and HDL serum cholesterol levels fell significantly. There was a significant rise in platelet arachidonic acid content but other platelet fatty acids did not change significantly. A reduction in dietary arachidonic acid did not inhibit platelet aggregation or thromboxane production.

Adult↗
PubMed1983

The effects of a mixed fish diet on platelet function, fatty acids and serum lipids.

Eight healthy subjects were fed a diet containing 1-4 g eicosapentaenoic acid (EPA) daily for 8-21 days. The EPA was derived from 300-400 g per day of sardines, pilchards, herring and/or kabeljou. Sources of arachidonic acid (AA) in the diet were reduced. At the end of the experimental period there was an increase in the ratio of EPA to AA in the platelets and a decrease in platelet aggregation to ADP, epinephrine and collagen. Aggregation to AA was not reduced. Thromboxane production in response to all four agonists was reduced. Serum total and HDL cholesterol levels fell significantly but platelet counts, LDL cholesterol and triglyceride values did not change. We conclude that even a relatively modest intake of EPA derived from a mixed fish diet together with a reduction in AA intake can alter in vitro platelet function and serum lipids significantly. A long term controlled trial of a palatable mixed fish diet to assess possible antithrombotic and antiatherogenic effects is justifiable.

Adenosine Diphosphate↗
PubMed1983

Identification of a heparin activated amidolytic enzyme in carp (Cyprinus carpio) plasma.

A heparin activated amidolytic enzyme capable of cleaving synthetic thrombin sensitive chromogenic substrates was identified from the plasma of the carp (Cyprinus carpio). Activation was inhibited by KCl, protamine sulphate and human plasma. Heparin was not required for the continued action of the enzyme. Active enzyme was irreversibly inhibited by DFP. The pH and temperature optima was studied and the enzyme semi purified by Sephadex G100 superfine and Sephadex A50 chromatography. An approximate MW of 62,000 was found. Activity generated by as little as 0.002 units of heparin per ml carp plasma was detected. The trivial name carpamidase is proposed for the enzyme.

Animals↗
PubMed1982

Dosage frequency for suppression of platelet function by low dose aspirin therapy.

A study of platelet aggregation and MDA production after an oral dose of 300 mg aspirin indicated that partial recovery of platelet function occurred when approximately one third of the circulating platelets had been replaced by new (uninhibited) platelets. In vitro studies on mixtures of normal and aspirin inhibited platelets indicated partial restoration of platelet aggregation and thromboxane B2 production with as little as 10% of normal platelets in some subjects. Restoration of full function required a higher proportion of normal platelets. There was considerable variation between subjects. These data suggest that complete suppression of platelet functions in all normal subjects requires daily administration of the drug.

Adenosine Diphosphate↗
PubMed1982

Platelet function in familial hypercholesterolaemia in South Africa and the effects of probucol.

Patients with Familial Hyperlipoproteinaemia Type II showed evidence of increased platelet aggregability when compared to normal controls. This abnormality was not influenced by oral therapy with probucol whether or not the serum cholesterol levels were lowered during the study period. Probucol assays indicated adequate compliance during the study period but did not demonstrate any uptake of the drug by platelets. In vitro studies also failed to demonstrate any inhibition of platelet function at therapeutic drug levels although higher levels were inhibitory.

Adolescent↗
PubMed1982

A rapid chromogenic method for the determination of prothrombin precursor in plasma.

A method was described for the quantitation of precursor prothrombin using a chromogenic substrate S2238 and Dispholidus typus venom. Prothrombin precursor was detected in the adsorbed plasma of all 65 patients on coumadin therapy tested, but was absent in 20 controls. The technic offered a rapid and sensitive method for determining if a prolonged prothrombin time is due to vitamin K antagonism or deficiency.

Adsorption↗