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A B Fraser

Publications and source records attributed to A B Fraser.

8 recordsLinked to original sources
PubMed2003

Combined hormonal versus nonhormonal versus progestin-only contraception in lactation.

BACKGROUND: Contraception for women who are breastfeeding is a public health issue of global importance. Each year over 100 million women make decisions about beginning or resuming contraception after childbirth. These decisions include both the choice of contraceptive method and the time at which its use begins, both of which continue to be debated by experts. Choices of contraception may be limited for lactating women due to concerns about hormonal effects on quality and quantity of milk, passage of hormones to the infant, and infant growth. Ideally, the contraceptive method chosen should not interfere with lactation. Additionally, because the return of menstruation and ovulation can be unpredictable in breastfeeding women, the timing of contraception initiation is important. OBJECTIVES: To determine the effect of combined oral contraceptives and progestin-only contraceptives on lactation. The a priori hypothesis is that combined oral contraception impairs lactation, making it less appropriate than progestin-only or nonhormonal contraception for breastfeeding women. SEARCH STRATEGY: We used PUBMED, POPLINE, EMBASE, LILACS, and Cochrane Controlled Trials Register computer searches, supplemented by review articles and contact with investigators. SELECTION CRITERIA: We sought all randomized controlled trials, reported in any language, that included any form of hormonal contraception compared with another form of hormonal contraception, nonhormonal contraception, or placebo during lactation. Hormonal contraception could include combined oral or injectable contraceptives, progestin-only oral or injectable contraceptives, hormonal implants, or hormonal intrauterine devices. Study participants included breastfeeding women of any age or parity who desired contraception. DATA COLLECTION AND ANALYSIS: We evaluated the methodological quality of each report and sought to identify duplicate reporting of data from multicenter trials. We abstracted data onto data collection forms. Principal outcome measures included quantity of milk; biochemical analysis of milk composition; initiation, maintenance and duration of lactation; infant growth; efficacy of contraceptive method while breastfeeding; and timing of contraception initiation and its effects on lactation. Because the trials did not have uniform interventions, often lacked quantifiable outcomes, and had poor methodological quality, we could not aggregate the data in a meta-analyses. MAIN RESULTS: Seven reports from five randomized controlled trials met our inclusion criteria. Most of the five trials did not specify their method used to generate a random sequence, method of allocation concealment, blinding of treatments, or use of an intention-to-treat analysis. Additionally, high loss to follow-up rates invalidated at least two studies. The findings from two reports comparing oral contraceptives to placebo during lactation were conflicting. Another trial found no inhibitory effects on lactation from progestin-only contraceptives. Finally, the WHO trial found no effect of progestin-only contraceptives on lactation but a decline in breast milk volume from combination contraceptives during lactation. High loss to follow-up rates, however, undermine the credibility of the WHO trial. No significant differences in infant growth or weight appeared in any of the included trials as a result of the use of hormonal contraception during lactation. REVIEWER'S CONCLUSIONS: Evidence from randomized controlled trials on the effect of hormonal contraceptives during lactation is limited and of poor quality; results should be interpreted with caution. The existing randomized controlled trials are insufficient to establish an effect of hormonal contraception, if any, on milk quality and quantity. Evidence is inadequate to make recommendations regarding hormonal contraceptive use for lactating women. At least one properly conducted randomized controlled trial of adequate size is urgently needed to address this question.

Contraceptives, Oral, Combined↗
PubMed2003

Hormonal contraception during lactation. systematic review of randomized controlled trials.

Contraception choices may be limited for lactating women due to concerns about hormonal effects on quality and quantity of milk, passage of hormones to the infant and infant growth. We conducted a systematic review of randomized controlled trials to determine the effect of hormonal contraception on lactation. We sought all randomized controlled trials, reported in any language, that included any form of hormonal contraception compared with another form of hormonal contraception, nonhormonal contraception or placebo during lactation. Seven reports from five randomized controlled trials met the inclusion criteria. Most of the five trials did not specify their method used to generate a random sequence, method of allocation concealment, blinding of treatments or use of an intention-to-treat analysis. Additionally, high loss-to-follow-up rates invalidated at least two trials. The findings from two trials comparing oral contraceptives to placebo during lactation were conflicting. Another trial found no inhibitory effects on lactation from progestin-only contraceptives. Finally, the World Health Organization trial found a statistically significant decline in breast milk volume in women using combined oral contraceptives compared to women using progestin-only pills. However, infant growth for the two groups did not differ. The limited evidence from randomized controlled trials on the effect of hormonal contraceptives during lactation is of poor quality and insufficient to establish an effect of hormonal contraception, if any, on milk quality and quantity. At least one properly conducted randomized controlled trial of adequate size is urgently needed to make recommendations regarding hormonal contraceptive use for lactating women.

Contraceptives, Oral, Combined↗
PubMed2000

An automated, handheld biosensor for aflatoxin.

A new immunoaffinity fluorometric biosensor has been developed for detecting and quantifying aflatoxins, a family of potent fungi-produced carcinogens that are commonly found in a variety of agriculture products. They have also been cited as a biological agent under weapons development. The handheld, self-contained biosensor is fully automatic, highly sensitive, quick, quantitative, and requires no special storage. Approximately 100 measurements can be made before refurbishment is required, and concentrations from 0.1 parts per billion (ppb) to 50 ppb can be determined in <2 min with a 1 ml sample volume. The device operates on the principles of immunoaffinity for specificity and fluorescence for a quantitative assay. The analytic procedure is flexible so that other chemical and biological analytes could be detected with minor modifications to the current device. Advances in electro-optical components, electronics, and miniaturized fluidics were combined to produce this reliable, small, and versatile instrument.

Aflatoxins↗
PubMed2000

Endothelin receptor antagonism does not prevent the development of in vivo glyceryl trinitrate tolerance in the rat.

There is evidence that increased endothelial production of endothelin-1 (ET-1) may contribute to glyceryl trinitrate (GTN) tolerance. We used the competitive ET(A) receptor antagonist ZD2574 to determine whether chronic ET(A) receptor blockade affected the biochemical and functional responses to GTN during the development of GTN tolerance in vivo. Tolerance induced using transdermal GTN patches resulted in a 5.3 +/- 1.2-fold increase in the EC(50) value for GTN relaxation in isolated aorta from GTN-tolerant rats. Coadministration of ZD2574 (100 mg kg(-1) t.i.d. for 3 days) during tolerance induction had no effect on GTN-induced relaxation. This dose of ZD2574 markedly blunted the pressor response to ET-1, indicating effective blockade of ET(A) receptors, and also abolished the initial transient depressor response to ET-1, indicating that blockade of endothelial ET(B) receptors also occurred using this dosage regimen for ZD2574. Consistent with the relaxation data, coadministration of ZD2574 had no effect on the decrease in GTN-induced cGMP accumulation or on the decrease in GTN biotransformation that occurred in aortae from GTN-tolerant animals. Radioimmunoassay data indicated that the GTN tolerance induction protocol caused a 2.3 +/- 0.4-fold and a 2.2 +/- 0.5-fold increase in total tissue ET-1 levels in tolerant aorta and vena cava, respectively. These data suggest that chronic inhibition of ET receptors by ZD2574 was not sufficient to prevent or diminish the tolerance-inducing effects of GTN, and that the increase in ET-1 levels observed in tolerant tissues may occur as a consequence of the vascular changes that occur during chronic GTN exposure.

Animals↗
PubMed1975

The interaction of heavy meromyosin and subfragment 1 with actin. Physical measurements in the presence and absence of adenosine triphosphate.

Viscosity, turbidity, and laser-light fluctuation autocorrelations of acto-heavy merymyosin (HMM) and acto-subfragment 1 (S-1) solutions were measured under conditions where the actin-activated ATPase is close to its maximal value. The results were compared to similar data obtained in the absence of ATP where the actin and myosin fragments were completely domplexed, and in the presence of ATP but at 0.1 M KLC where the actin and HMM or S-1 were almost completely dissociated. It was found that at maximal actin activation, the viscosity, turbidity, and autocorrelation data were all much closer to the values for the completely dissociated systems than to the values for the completely complexed systems. Assuming that viscosity, turbidity, and autocorrelation measurements approximate a linear measure of binding between actin and HMM or S-1, the results suggest that at maximal actin activation less than 10% of the HMM or S-1 are bound to the actin. Therefore as was suggested previously by ultracentrifuge and kinetics studies, it appears that under conditions of maximal actin activation, most of the HMM and S-1 occur in a refractory state unable to bind to actin.

Actins↗