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Biomedical subjects

R A Walsh

Publications and source records attributed to R A Walsh.

At least 19 recordsLinked to original sources
PubMed2001

Quitting smoking in pregnancy.

Smoking doubles the risk of having a low-birthweight baby and significantly increases the rate of perinatal mortality and several other adverse pregnancy outcomes. The mean reduction in birthweight for babies of smoking mothers is 200 g. High quality interventions to help pregnant women quit smoking produce an absolute difference of 8.1% in validated late-pregnancy quit rates. If abstinence is not achievable, it is likely that a 50% reduction in smoking would be the minimum necessary to benefit the health of mother and baby. Healthcare providers perform poorly in antenatal interventions to stop women smoking. Midwives deliver interventions at a higher rate than doctors. The efficacy of nicotine replacement therapy has not been established in pregnancy. Currently, its use should only be considered in women smoking more than 10 cigarettes per day who have made a recent, unsuccessful attempt to quit and who are motivated to quit. Relapse prevention programs have shown little success in the postpartum period.

Female↗
PubMed2001

Sarcoplasmic reticulum Ca(2+) atpase (SERCA) 1a structurally substitutes for SERCA2a in the cardiac sarcoplasmic reticulum and increases cardiac Ca(2+) handling capacity.

Ectopic expression of the sarcoplasmic reticulum (SR) Ca(2+) ATPase (SERCA) 1a pump in the mouse heart results in a 2.5-fold increase in total SERCA pump level. SERCA1a hearts show increased rates of contraction/relaxation and enhanced Ca(2+) transients; however, the cellular mechanisms underlying altered Ca(2+) handling in SERCA1a transgenic (TG) hearts are unknown. In this study, using confocal microscopy, we demonstrate that SERCA1a protein traffics to the cardiac SR and structurally substitutes for the endogenous SERCA2a isoform. SR Ca(2+) load measurements revealed that TG myocytes have significantly enhanced SR Ca(2+) load. Confocal line-scan images of field-stimulated SR Ca(2+) release showed an increased rate of Ca(2+) removal in TG myocytes. On the other hand, ryanodine receptor binding activity was decreased by approximately 30%. However, TG myocytes had a greater rate of spontaneous ryanodine receptor opening as measured by spark frequency. Whole-cell L-type Ca(2+) current density was reduced by approximately 50%, whereas the time course of inactivation was unchanged in TG myocytes. These studies provide important evidence that SERCA1a can substitute both structurally and functionally for SERCA2a in the heart and that SERCA1a overexpression can be used to enhance SR Ca(2+) transport and cardiac contractility.

Animals↗
PubMed2001

Src and multiple MAP kinase activation in cardiac hypertrophy and congestive heart failure under chronic pressure-overload: comparison with acute mechanical stretch.

Activation of members of the mitogen-activated protein (MAP) kinase family and their downstream effectors has been proposed to play a key role in the pathogenesis of cell survival, ischaemic preconditioning, cardiac hypertrophy and heart failure. This study investigated the responses of Src kinase and multiple MAP kinases during the transition from compensated pressure-overload hypertrophy to decompensated congestive heart failure. Extracellular signal-regulated protein kinase (ERK) 1/2, p38, and Src were activated by chronic pressure-overload and their activity was sustained for 8 weeks after aortic banding. In contrast, while p90 ribosomal S6 kinase (90RSK) and big MAP kinase 1 (BMK1) were activated in compensated hypertrophy, their activities were significantly decreased in hearts with heart failure. No changes were found in C-Jun NH2 terminal kinase (JNK) activity after aortic banding. These data suggest that differential activation of MAP kinase family members may contribute to the transition from compensated to decompensated hypertrophy. We also examined acute effects of mechanical stretch on the activation of these kinases in normal and hypertrophied hearts. In the isolated coronary-perfused heart, a balloon in the left ventricle was inflated to achieve minimum end-diastolic pressure of 25 mmHg for 10-20 min. In normal guinea pig hearts, stretch activated ERK1/2, p90RSK, p38, Src, and BMK1 but not JNK. However in hypertrophied hearts, further activation of these kinases was not observed by acute mechanical stretch. Mechanical stretch-induced activation of ERK1/2 and p38 kinase in normal hearts was attenuated significantly by a protein kinase C inhibitor, chelerythrine. We demonstrate that ERK1/2, p90RSK, p38, Src, and BMK1 are activated by chronic pressure-overload and by acute mechanical stretch. These data suggest that Src, BMK1 and p90RSK play a role as novel signal transduction pathways leading to cardiac hypertrophy. In addition, the differential inhibition of p90RSK and BMK1 in hearts with congestive heart failure suggests the specific role of these two kinases to maintain cardiac function under chronic pressure-overload.

Alkaloids↗
PubMed2001

Src family kinase and adenosine differentially regulate multiple MAP kinases in ischemic myocardium: modulation of MAP kinases activation by ischemic preconditioning.

Recent studies suggest that ischemia activates Src and members of the mitogen-activated protein (MAP) kinase superfamily and their downstream effectors, including big MAP kinase 1 (BMK1) and p90 ribosomal S6 kinase (p90RSK). It has also been reported that adenosine is released during ischemia and involved in triggering the protective mechanism of ischemic preconditioning. To assess the roles of Src and adenosine in ischemia-induced MAP kinases activation, we utilized the Src inhibitor PP2 (4-Amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) and the adenosine receptor antagonist 8-(p-sulfophenyl) theophylline (SPT) in perfused guinea pig hearts. PP2 (1 microm) inhibited ischemia-induced Src, BMK1 and JNK activation but not JAK2 and p38 activation. SPT inhibited ischemia-mediated p38 and JNK activation. These results demonstrate that Src family kinase and adenosine regulate MAP kinases by parallel pathways. Preconditioning significantly improved both recovery of developed pressure and dp/dt in isolated guinea pig hearts. Since the protective effect of preconditioning was blocked by PP2 (1 microm) and SPT (50 microm), we next investigated the regulation of Src, MAP kinases and p90RSK during preconditioning. The activity and time course of ERK1/2 was not changed, but p90RSK activation by reperfusion was completely inhibited by preconditioning. In contrast, the activation by ischemia of Src, BMK1, p38 and JNK was significantly faster in preconditioned hearts. Maximal BMK1 activation by ischemia was also significantly enhanced by preconditioning. These data suggest important roles for Src family kinases and adenosine in mediating preconditioning, and suggest specific roles for individual MAP kinases in preconditioning.

Adenosine↗
PubMed2001

Preventive and other interactional skills of general practitioners, surgeons, and physicians: perceived competence and endorsement of postgraduate training.

BACKGROUND: Perceived competencies and support for formal postgraduate training across a range of preventive and other interactional skills were examined in three medical groups. METHODS: All eligible final year students and recent graduates of the three major Australian medical colleges (n = 767) were mailed a questionnaire examining communication skills in four domains: preventive, educational, therapeutic, and general. RESULTS: Overall consent rate was 45%. For most items, at least one-third of each group reported low competence. On preventive items, low competence ratings ranged from 5 to 39% in general practice, 38 to 67% in surgery, and 33 to 51% in the speciality physician group. Significant intergroup differences occurred on eight competence items. Agreement with training on preventive topics ranged from 80 to 91% in general practice, 48 to 69% in surgery, and 72 to 82% in the specialty physician group. On all 11 training items where significant differences occurred, the general practice group reported the highest level and the surgeon group the lowest level of endorsement for formal training and assessment. CONCLUSIONS: Substantial proportions in the general practice, surgery, and the physician specialty report lack of competence in common interactional skills. There were high levels of support for formal training in preventive and other interactional skills. The strong endorsement supports the development of effective, tailored interactional skills training programs.

Adult↗
PubMed2001

Differential uptake of a smoking cessation programme disseminated to doctors and midwives in antenatal clinics.

AIMS: Two methods of dissemination (simple and intensive) were used to disseminate a smoking cessation programme to doctors and midwives working in antenatal clinics. This paper describes the differential uptake of the smoking cessation programme by doctors and midwives. It investigates whether the number of smoking cessation interventions used differ due to the type of dissemination. It also examines the frequency with which doctors and midwives provide smoking cessation interventions after dissemination. DESIGN: Clinics were randomized to the method of dissemination (simple or intensive). Pre-post test design was used to examine the relationship between dissemination method and professional status at baseline and follow-up. A baseline survey collected data on the use of smoking cessation intervention in the clinics prior to dissemination. A follow-up survey was conducted 18 months after the dissemination. SETTING: Twenty-three public hospital antenatal clinics in NSW. PARTICIPANTS: All clinical staff (midwives and doctors) working in the clinic during the 1-2-week survey period prior to dissemination and 18 months after the dissemination were asked to participate. The response rate was 63% (223) at baseline and 64% (182) at follow-up. Only 48% of midwives and doctors at follow-up were working in the original clinic. MEASURES: The proportion of clinicians who initially adopted the programme; the proportion of clinicians who had used one or more programme components in the last week); the number of types of smoking cessation intervention provided (maximum = 13), and the estimated proportion of clients offered smoking cessation intervention. FINDINGS: More midwives than doctors "ever used" the programme (76% vs. 25%) and continued to implement (58% vs. 22%) the programme 18 months after dissemination. Both midwives and doctors increased the number of types of smoking cessation intervention offered at follow-up compared to baseline (mean difference 2.8). Midwives provided more smoking cessation interventions than doctors at baseline (mean difference 0.9) and at follow-up (1.6), regardless of method used to disseminate the programme. Midwives' mean estimates of the proportion of clients offered interventions were greater than doctors' (midwives' 59% vs. doctors' 35%) at follow-up. CONCLUSION: The dissemination of a smoking cessation programme increased the level of smoking cessation interventions used by doctors and midwives. Doctors and midwives differ in their uptake of smoking cessation programmes. This information can be used to plan programme dissemination strategies in the future.

Analysis of Variance↗
PubMed2001

Cardiac hypertrophy and failure: lessons learned from genetically engineered mice.

Congestive heart failure is a major and growing public health problem. Because of improved survival of myocardial infarction patients produced by thrombolytic therapy or per-cutaneous revascularization it represents the only form of cardiovascular disease with significantly increased incidence and prevalence. Clinicians view this clinical syndrome as the final common pathway of diverse pathologies such as myocardial infarction and haemodynamic overload. Insights into mechanisms for heart failure historically derived from physiological and biochemical studies which identified compensatory adaptations for the haemodynamic burden associated with the pathological condition including utilization of the Frank Starling mechanism, augmentation of muscle mass, and neurohormonal activation to increase contractility. Therapy has largely been phenomenological and designed to prevent or limit the deleterious effects of these compensatory processes. More recently insights from molecular and cell biology have contributed to a more mechanistic understanding of potential causes of cardiac hypertrophy and failure. Many different analytical approaches have been employed for this purpose. These include the use of conventional animal models which permit serial observation of the onset and progression of heart failure and a sequential analysis of underlying biochemical and molecular events. Neonatal murine cardiomyocytes have been a powerful tool to examine in vitro subcellular mechanisms devoid of the confounding functional effects of multicellular preparations and heterogeneity of cell type. Finally, significant progress has been made by utilizing tissue from human cardiomyopathic hearts explanted at the time of orthotopic transplantation. Each of these methods has significant advantages and disadvantages. Arguably the greatest advance in our understanding of cardiac hypertrophy and failure over the past decade has been the exploitation of genetically engineered mice as biological reagents to study in vivo the effects of alterations in the murine genome. The power of this approach, in principle, derives from the ability to precisely overexpress or ablate a gene of interest and examine the phenotypic consequences in a cardiac specific post-natal manner. In contrast to conventional animal models of human disease which employ some form of environmental stress, genetic engineering involves a signal known molecular perturbation which produces the phenotype.

Animals↗
PubMed2001

Interactional skills of students from traditional and non-traditional medical schools before and after alcohol education.

OBJECTIVE: To compare alcohol-related intervention and general interactional skills performance of medical students from a traditional (Sydney) and a non-traditional (Newcastle) medical school, before and after participation in an alcohol education programme about brief intervention. DESIGN: In two controlled trials, students received either a didactic alcohol education programme or didactic input plus skills-based training. Prior to and after training, all students completed videotaped interviews with simulated patients. SETTING: The Faculties of Medicine at the University of Newcastle and the University of Sydney, Australia. SUBJECTS: Fifth-year medical students (n=154). RESULTS: Both alcohol-related intervention and general interactional skills scores of the Newcastle students were significantly higher than those of the Sydney students at pre-test but not after training. Although alcohol-related interactional skills scores improved after training at both universities, they did not reach a satisfactory level. The educational approach used had no effect on post-test scores at either university. CONCLUSIONS: Significant baseline differences in interactional skills scores favouring non-traditional over traditional students were no longer evident after both groups had been involved in an alcohol education programme. Further research is required to develop more effective alcohol intervention training methods.

Adult↗
PubMed2001

Effect of angiotensin type I-receptor blockade on left ventricular remodeling in pressure overload hypertrophy.

BACKGROUND: The renin-angiotensin system is involved in cardiac remodeling. In contrast to the well-recognized salutary effects of angiotensin-converting enzyme inhibition, the value of angiotensin II type I (AT(1))-receptor blockade on left ventricular (LV) hypertrophy and dysfunction is controversial. METHODS AND RESULTS: Descending thoracic aorta-banded and sham-operated guinea pigs were given either losartan (30 mg x kg(-1) x day(-1) intraperitoneally) or vehicle for 8 weeks (n = 7 in each group). LV end-diastolic and end-systolic dimensions and wall thicknesses were measured echocardiographically, and LV fractional shortening, relative wall thickness, and LV mass normalized by body weight were calculated. Isolated heart function (Langendorff perfusion) was studied 8 weeks after surgery, and LV performance was assessed by maximum LV pressure and +/-dP/dt normalized by LV mass. Eight weeks after banding guinea pigs developed concentric LV hypertrophy and had decreased maximum LV pressure and +/-dP/dt normalized by LV mass; LV end-diastolic dimension and LV fractional shortening were unchanged. In band-operated guinea pigs treatment with losartan had no significant effects on any of these measurements. CONCLUSIONS: In guinea pigs with descending aortic banding, treatment with losartan for 8 weeks neither attenuates progression of pressure overload hypertrophy nor significantly improves impaired mass-normalized pressure-derived indices of LV contraction and relaxation.

Angiotensin Receptor Antagonists↗
PubMed2000

Disruption of a single copy of the SERCA2 gene results in altered Ca2+ homeostasis and cardiomyocyte function.

A mouse model carrying a null mutation in one copy of the sarcoplasmic reticulum (SR) Ca(2+)-ATPase isoform 2 (SERCA2) gene, in which SERCA2 protein levels are reduced by approximately 35%, was used to investigate the effects of decreased SERCA2 level on intracellular Ca(2+) homeostasis and contractile properties in isolated cardiomyocytes. When compared with wild-type controls, SR Ca(2+) stores and Ca(2+) release in myocytes of SERCA2 heterozygous mice were decreased by approximately 40-60% and approximately 30-40%, respectively, and the rate of myocyte shortening and relengthening were each decreased by approximately 40%. However, the rate of Ca(2+) transient decline (tau) was not altered significantly, suggesting that compensation was occurring in the removal of Ca(2+) from the cytosol. Phospholamban, which inhibits SERCA2, was decreased by approximately 40% in heterozygous hearts, and basal phosphorylation of Ser-16 and Thr-17, which relieves the inhibition, was increased approximately 2- and 2.1-fold. These results indicate that reduced expression and increased phosphorylation of phospholamban provides compensation for decreased SERCA2 protein levels in heterozygous heart. Furthermore, both expression and current density of the sarcolemmal Na(+)-Ca(2+) exchanger were up-regulated. These results demonstrate that a decrease in SERCA2 levels can directly modify intracellular Ca(2+) homeostasis and myocyte contractility. However, the resulting deficit is partially compensated by alterations in phospholamban/SERCA2 interactions and by up-regulation of the Na(+)-Ca(2+) exchanger.

Animals↗
PubMed2000

Transgenic overexpression of constitutively active protein kinase C epsilon causes concentric cardiac hypertrophy.

To test the hypothesis that activation of the protein kinase C (PKC) epsilon isoform leads to cardiac hypertrophy without failure, we studied transgenic mice with cardiac-specific overexpression of a constitutively active mutant of the PKCepsilon isoform driven by an alpha-myosin heavy chain promoter. In transgenic mice, the protein level of PKCepsilon in heart tissue was increased 9-fold. There was a 6-fold increase of the membrane/cytosol ratio, and PKC activity in the membrane fraction was 4.2-fold compared with wild-type mice. The heart weight was increased by 28%, and upregulation of the mRNA for beta-myosin heavy chain and alpha-skeletal actin was observed in transgenic mouse hearts. Echocardiography demonstrated increased anterior and posterior wall thickness with normal left ventricular function and dimensions, indicating concentric cardiac hypertrophy. Isolated cardiomyocyte mechanical function was slightly decreased, and Ca(2+) signals were markedly depressed in transgenic mice, suggesting that myofilament sensitivity to Ca(2+) was increased. No differences were observed in either the levels of cardiac Ca(2+)-handling proteins or the degree of cardiac regulatory protein phosphorylation between wild-type and transgenic mice. Unlike mice with PKCbeta(2) overexpression, transgenic mice with cardiac-specific overexpression of the active PKCepsilon mutant demonstrated concentric hypertrophy with normal in vivo cardiac function. Thus, PKC isoforms may play differential functional roles in cardiac hypertrophy and failure.

Animals↗
PubMed2000

Changes in Ca(2+) cycling proteins underlie cardiac action potential prolongation in a pressure-overloaded guinea pig model with cardiac hypertrophy and failure.

Ventricular arrhythmias are common in both cardiac hypertrophy and failure; cardiac failure in particular is associated with a significant increase in the risk of sudden cardiac death. We studied the electrophysiologic changes in a guinea pig model with aortic banding resulting in cardiac hypertrophy at 4 weeks and progressing to cardiac failure at 8 weeks using whole-cell patch-clamp and biochemical techniques. Action potential durations (APDs) were significantly prolonged in banded animals at 4 and 8 weeks compared with age-matched sham-operated animals. APDs at 50% and 90% repolarization (APD(50) and APD(90) in ms) were the following: 4 week, banded, 208+/-51 and 248+/-49 (n = 15); 4 week, sham, 189+/-68 and 213+/-69 (n = 16); 8 week, banded, 197+/-40 and 226+/-40 (n = 21); and 8 week, sham, 156+/-42 and 189+/-45 (n = 22), respectively; P<0.05 comparing banded versus sham-operated animals. We observed no significant differences in the K(+) currents between the 2 groups of animals at 4 and 8 weeks. However, banded animals exhibited a significant increase in Na(+) and Na(+)-Ca(2+) exchange current densities compared with controls. Furthermore, we have found a significant attenuation in the Ca(2+)-dependent inactivation of the L-type Ca(2+) current in the banded compared with sham-operated animals, likely as a result of the significant downregulation of the sarcoplasmic reticulum Ca(2+) ATPase, which has been documented previously in the heart failure animals. Our data provide an alternate mechanism for APD prolongation in cardiac hypertrophy and failure and support the notion that there is close interaction between Ca(2+) handling and action potential profile.

Action Potentials↗
PubMed2000

Cardiac-specific overexpression of calsequestrin results in left ventricular hypertrophy, depressed force-frequency relation and pulsus alternans in vivo.

Cardiac-specific overexpression of calsequestrin has been shown to result in significant decreases in contractile parameters and intracellular Ca(2+)transients in vitro. Therefore, the purpose of the present study was to determine the effects of calsequestrin overexpression on basal cardiac function and the force-frequency relation in vivo. Calsequestrin overexpression mice (CSQ-OE, n=20) and their isogenic controls (WT) were studied with an integrative approach using transthoracic echocardiography, stress-shortening relations, and invasive hemodynamics in intact closed-chest mice. M-mode echocardiography indicated that calsequestrin overexpression resulted in concentric hypertrophy (+52%) and an increase in LV ejection phase indices. However, mean end-systolic stress-shortening coordinates revealed that at matched end-systolic wall-stress, fractional shortening was depressed in CSQ-OE mice. This was confirmed by depressed indices of LV isovolumic contraction and relaxation in CSQ-OE v. WT mice. Furthermore, overexpression of calsequestrin resulted in a downward and leftward shift of the biphasic force-frequency relation; thus, the critical heart (HR(crit)) was significantly lower in calsequestrin-overexpression mice (264+/-15 bpm) than in wild-type controls (365+/-21 bpm). Surprisingly, calsequestrin overexpression was associated with the induction of pulsus alternans in every animal (at an average heart rate of 428+/-26 bpm), whereas none of the wild-type controls displayed this phenomenon. We conclude that: (i) although increased levels of calsequestrin result in decreased myocardial contractility and a depressed force-frequency relation, LV wall stress is reduced and chamber function is normal, and (ii) an increase in SR Ca(2+)storage capacity induces pulsus alternans in the intact anesthetized mouse.

Animals↗
PubMed2000

beta2-adrenergic receptor polymorphisms at amino acid 16 differentially influence agonist-stimulated blood pressure and peripheral blood flow in normal individuals.

BACKGROUND: The Gly16 beta(2)-adrenergic receptor (beta(2)AR) polymorphism is a common variant of the beta(2)AR that displays depressed function caused by enhanced receptor downregulation in vitro compared with the Arg16 receptor. METHODS AND RESULTS: We studied 20 healthy, normotensive, nonsmoking white individuals who were homozygous for either the Arg16 (n = 10) or the Gly16 (n = 10) genotype. Plethysmographic lower-limb blood flow, blood pressure, and 2-dimensional echocardiograms were recorded at baseline and after 15-minute incremental infusions of terbutaline (100 to 300 ng/kg per minute). Baseline heart rates, blood pressures, and flows were similar in both groups, but at the maximum dose of terbutaline, limb blood flow was less (P <.05), calculated vascular resistance was greater (P <.05), and systolic and diastolic blood pressures were greater in patients with Gly16 than in those with Arg16 (both P <.05). In contrast, terbutaline-stimulated heart rates were not different. In a separate group of 20 homozygous individuals (12 Arg16, 8 Gly16), there were no differences in 2-dimensional echocardiographically determined ventricular function. CONCLUSIONS: We conclude that the Gly16 beta(2)AR polymorphism imparts attenuated vasodilatory responses to catecholamines in normal human beings and is an important genetic component in the regulation of peripheral blood flow and systemic arterial pressure.

Adrenergic beta-2 Receptor Agonists↗
PubMed2000

Alterations in Ca2+ cycling proteins and G alpha q signaling after left ventricular assist device support in failing human hearts.

OBJECTIVE: Left ventricular assist device support mechanically unloads the failing ventricle with resultant improvement in cardiac geometry and function in patients with end-stage heart failure. Activation of the G alpha q signaling pathway, including protein kinase C, appears to be involved in the progression of heart failure. Similarly down-regulation of Ca2+ cycling proteins may contribute to contractile depression in this clinical syndrome. Thus we examined whether protein kinase C activation and decreased Ca2+ cycling protein levels could be reversed by left ventricular assist device support. METHODS: Left ventricular myocardial specimens were obtained from seven patients during placement of left ventricular assist device and heart transplantation. We examined changes in protein levels of G alpha q, phospholipase C beta 1, regulators of G protein signaling (RGS), sarcoplasmic reticulum Ca2+ ATPase, phospholamban and translocation of protein kinase C isoforms (alpha, beta 1, and beta 2). RESULTS: The paired pre- and post-left ventricular assist device samples revealed that RGS2, a selective inhibitor of G alpha q, was decreased (P < 0.01), while the status of G alpha q, phospholipase C beta 1, RGS3 and RGS4 were unchanged after left ventricular assist device implantation. Translocation of protein kinase C isoforms remained unchanged. Left ventricular assist device support increased sarcoplasmic reticulum Ca2+ ATPase protein level (P < 0.01), while phospholamban abundance was unchanged. CONCLUSIONS: We conclude that altered protein expression and stoichiometry of the major cardiomyocyte Ca2+ cycling proteins rather than reduced phospholipase C beta 1 activation may contribute to improved mechanical function produced by left ventricular assist device support in human heart failure.

Adolescent↗
PubMed2000

Process measures in an antenatal smoking cessation trial: another part of the picture.

Data on provider and patient compliance can be crucial in understanding the degree of a health education program's effectiveness, as well as in identifying areas where the program requires modification. However, such data are rarely systematically reported in randomized trials. This report assesses the degree to which doctors and midwives complied with intervention protocols in a hospital antenatal smoking cessation trial, and also examines the program's acceptability to patients. Provider compliance was assessed principally via consultation audiotapes and provider-completed checklists. The audiotape analysis identified substantial compliance problems. For example, in relation to six specific smoking-related pregnancy risks, the proportions of Experimental Women informed about each individual risk ranged from 26 to 38% and the proportions receiving counselling items ranged from 52 to 79%. Doctors only informed a minority of Experimental Women of the increased risk of Sudden Infant Death Syndrome (28%) and of the presence of toxic chemicals in tobacco (21%). Comparison of compliance data from audiotapes and provider checklists revealed there was no significant agreement in three of four cases tested. Experimental Patients completed questionnaires to assess recall of smoking advice and to rate 12 program features. Of specific Experimental Program elements, the videotape (85%) received the highest level of positive patient ratings and the lottery (42%) the lowest. The process evaluation indicated that the Experimental Program needed some modification to increase its suitability for routine application. The findings also support the value of including an objective measure of provider compliance.

Female↗