Testing the activitystat hypothesis: a randomised controlled trial.

BACKGROUND: It has been hypothesised that an 'activitystat' may biologically regulate energy expenditure or physical activity levels, thereby limiting the effectiveness of physical activity interventions. Using a randomised controlled trial design, the aim of this study was to investigate the effect of a six-week exercise stimulus on energy expenditure and physical activity, in order to empirically test this hypothesis. METHODS: Previously inactive adults (n = 129) [age (mean ± SD) 41 ± 11 year; body mass index 26.1 ± 5.2 kg/m(2)] were randomly allocated to a Control group (n = 43) or a 6-week Moderate (150 min/week) (n = 43) or Extensive (300 min/week) (n = 43) exercise intervention group. Energy expenditure and physical activity were measured using a combination of accelerometry (total counts, minutes spent in moderate to vigorous physical activity) and detailed time use recalls using the Multimedia Activity Recall for Children and Adults (total daily energy expenditure, minutes spent in moderate to vigorous physical activity) at baseline, mid- and end-intervention and 3- and 6-month follow up. Resting metabolic rate was measured at baseline and end-intervention using indirect calorimetry. Analysis was conducted using random effects mixed modeling. RESULTS: At end-intervention, there were statistically significant increases in all energy expenditure and physical activity variables according to both accelerometry and time use recalls (p < 0.001) in the Moderate and Extensive groups, relative to Controls. There was no significant change in resting metabolic rate (p = 0.78). CONCLUSION: Taken together, these results show no evidence of an "activitystat" effect. In the current study, imposed exercise stimuli of 150-300 min/week resulted in commensurate increases in overall energy expenditure and physical activity, with no sign of compensation in either of these constructs. TRIAL REGISTRATION NUMBER: ACTRN12610000248066  (registered prospectively 24 March 2010).

Spatial and temporal variability of Alexandrium cyst fluxes in the Gulf of Maine: Relationship to seasonal particle export and resuspension.

Quantification of Alexandrium cyst fluxes through the Gulf of Maine water column is central to understanding the linkage between the source and fate of annual Alexandrium blooms in the offshore waters. These blooms often lead to paralytic shellfish poisoning (PSP) and extensive closures of shellfish beds. We report here on time-series sediment trap deployments completed at four offshore locations in the gulf between 2005 and 2010 as components of two ECOHAB-GOM field programs. Data presented documents the substantial spatial and temporal fluctuations in Alexandrium fundyense cyst fluxes in the gulf. Cyst delivery out of the euphotic zone peaked primarily between July and August following annual spring-summer Alexandrium blooms and was greatest in the western gulf. At all sites, cyst flux maxima to the subsurface waters were rarely coincident with seasonal peaks in the total mass export of particulate material indicating that cyst delivery was primarily via individually sinking cysts. Where persistent benthic nepheloid layers (BNLs) exist, significant sediment resuspension input of cysts to the near-bottom water column was evidenced by deep cyst fluxes that were up to several orders of magnitude greater than that measured above the BNL. The largest cyst fluxes in the BNL were observed in the eastern gulf, suggesting greater resuspension energy and BNL cyst inventories in this region. Temporal similarities between peak cyst export out of the upper ocean and peak cyst fluxes in the BNL were observed and document the contribution of seasonal, newly formed cysts to the BNL. The data however also suggest that many Alexandrium cells comprising the massive, short-lived blooms do not transition into cysts. Time-series flow measurements and a simple 1D model demonstrate that the BNL cyst fluxes reflect the combined effects of tidal energy-maintained resuspension, deposition, and input of cysts from the overlying water column.

No change in hemoglobin mass after 40 days of physical activity in previously untrained adults.

A high hemoglobin mass (Hb(mass)) is associated with a high maximum aerobic power (VO(2max)), however, the extent to which Hb(mass) is influenced by training is currently unclear. Accordingly, this study monitored changes in Hb(mass) and VO(2max) in 12 previously untrained adults (aged 18-25 years) following 40 days of regular physical activity. Hb(mass) and VO(2max) were assessed at the start and end of a 40-day physical activity program, which comprised of approximately 40 min of daily, moderate-intensity physical activity. Relative VO(2max) increased by 11.3%, yet there was no significant change in relative Hb(mass) (1.7%) and body mass (0.2%) during the 40-day period. There was a significant correlation between Hb(mass) and VO(2max) at the start of the study (r=0.58, P=0.05), but not between the change in relative VO(2max) and the change in relative Hb(mass) (r=-0.07, P=0.83). Our results support the concept of relative stability in Hb(mass) with approximately 1 month of moderate-intensity physical activity suggesting that Hb(mass) may be used for talent identification and possibly for anti-doping purposes.

High molecular weight kininogen inhibits fibrinogen binding to cytoadhesins of neutrophils and platelets.

Fibrinogen inhibited 125I-high molecular weight kininogen (HMWK) binding and displaced bound 125I-HMWK from neutrophils. Studies were performed to determine whether fibrinogen could bind to human neutrophils and to describe the HMWK-fibrinogen interaction on cellular surfaces. At 4 degrees C, the binding of 125I-fibrinogen to neutrophils reached a plateau by 30 min and did not decrease. At 23 and 37 degrees C, the amount of 125I-fibrinogen bound peaked by 4 min and then decreased over time because of proteolysis of fibrinogen by human neutrophil elastase (HNE). Zn++ (50 microM) was required for binding of 125I-fibrinogen to neutrophils at 4 degrees C and the addition of Ca++ (2 mM) increased the binding twofold. Excess unlabeled fibrinogen or HMWK completely inhibited binding of 125I-fibrinogen. Fibronectin degradation products (FNDP) partially inhibited binding, but prekallikrein and factor XII did not. The binding of 125I-fibrinogen at 4 degrees C was reversible with a 50-fold molar excess of fibrinogen or HMWK. Binding of 125I-fibrinogen, at a concentration range of 5-200 micrograms/ml of added radioligand, was saturable with an apparent Kd of 0.17 microM and 140,000 sites/cell. The binding of 125I-fibrinogen to neutrophils was not inhibited by the peptide RGDS derived from the alpha chain of fibrinogen or by the mAb 10E5 to the platelet glycoprotein IIb/IIIa heterodimer. Fibrinogen binding was inhibited by a gamma-chain peptide CYGHHLGGAKQAGDV and by mAb OKM1 but was not inhibited by OKM10, an mAb to a different domain of the adhesion glycoprotein Mac-1 (complement receptor type 3 [CR3]). HMWK binding to neutrophils was not inhibited by OKM1. These observations were consistent with a further finding that fibrinogen is a noncompetitive inhibitor of 125I-HMWK binding to neutrophils. Fibrinogen binding to ADP-stimulated platelets was increased twofold by Zn++ (50 microM) and was inhibited by HMWK. These studies indicate that fibrinogen specifically binds to the C3R receptor on the neutrophil surface through the carboxy terminal of the gamma-chain and that HMWK interferes with the binding of fibrinogen to integrins on both neutrophils and activated platelets.

The prevention of thymic lymphomas in transgenic mice by human O6-alkylguanine-DNA alkyltransferase.

Nitrosoureas form O6-alkylguanine-DNA adducts that are converted to G to A transitions, the mutation found in the activated ras oncogenes of nitrosourea-induced mouse lymphomas and rat mammary tumors. These adducts are removed by the DNA repair protein O6-alkylguanine-DNA alkyltransferase. Transgenic mice that express the human homolog of this protein in the thymus were found to be protected from developing thymic lymphomas after exposure to N-methyl-N-nitrosourea. Thus, transgenic expression of a single human DNA repair gene is sufficient to block chemical carcinogenesis. The transduction of DNA repair genes in vivo may unravel mechanisms of carcinogenesis and provide therapeutic protection from known carcinogens.

The thrombin receptor extracellular domain contains sites crucial for peptide ligand-induced activation.

A thrombin receptor (TR) demonstrating a unique activation mechanism has recently been isolated from a megakaryocytic (Dami) cell line. To further study determinants of peptide ligand-mediated activation phenomenon, we have isolated, cloned, and stably expressed the identical receptor from a human umbilical vein endothelial cell (HUVEC) library. Chinese hamster ovary (CHO) cells expressing a functional TR (CHO-TR), platelets, and HUVECs were then used to specifically characterize alpha-thrombin- and peptide ligand-induced activation responses using two different antibodies: anti-TR34-52 directed against a 20-amino acid peptide spanning the thrombin cleavage site, and anti-TR1-160 generated against the NH2-terminal 160 amino acids of the TR expressed as a chimeric protein in Escherichia coli. Activation-dependent responses to both alpha-thrombin (10 nM) and peptide ligand (20 microM) were studied using fura 2-loaded cells and microspectrofluorimetry. Whereas preincubation of CHO-TR with anti-TR34-52 abolished only alpha-thrombin-induced [Ca2+]i transients, preincubation with anti-TR1-160 abrogated both alpha-thrombin- and peptide ligand-induced responses. This latter inhibitory effect was dose dependent and similar for both agonists, with an EC50 of approximately 90 micrograms/ml. Anti-TR1-160 similarly abolished peptide ligand-induced [Ca2+]i transients in platelets and HUVECs, whereas qualitatively different responses characterized by delayed but sustained elevations in [Ca2+]i transients were evident using alpha-thrombin. Platelet aggregation to low concentrations of both ligands was nearly abolished by anti-TR1-160, although some shape change remained; anti-TR34-52 only inhibited alpha-thrombin-induced aggregation. These data establish that a critical recognition sequence for peptide ligand-mediated receptor activation is contained on the NH2-terminal portion of the receptor, upstream from the first transmembrane domain. Furthermore, alpha-thrombin-induced activation of HUVECs and platelets may be partially mediated by an alternative mechanism(s) or receptor(s).

Thromboerythrocytes. In vitro studies of a potential autologous, semi-artificial alternative to platelet transfusions.

In an attempt to overcome the limitations and drawbacks of using fresh platelets for transfusion therapy of thrombocytopenic patients, we have performed in vitro experiments on an autologous, semi-artificial alternative to platelet transfusions. Based on our previous studies of the interactions of unactivated and activated platelets with beads coated with peptides of various lengths, all of which contained the arginine-glycine-aspartic acid (RGD) cell recognition sequence, the peptide Ac-CGGRGDF-NH2 was chosen for covalent coupling to erythrocytes. A heterobifunctional crosslinking reagent (N-maleimido-6-aminocaproyl ester of 1-hydroxy-2-nitrobenzene-4-sulfonic acid) was used to crosslink via the peptide's free sulfhydryl group and the erythrocyte's surface amino groups. Approximately 0.5-1.5 x 10(6) peptide molecules bound per erythrocyte after 2 h of incubation, and most of the peptides appeared to crosslink to glycophorin A. The resulting cells, termed thromboerythrocytes, interacted selectively with activated platelets to form mixed aggregates. Studies with fluid phase RGD peptides and monoclonal antibodies indicated that the RGD peptides on the thromboerythrocytes interacted with the GPIIb/IIIa receptors on activated platelets. Thromboerythrocytes could also bind to platelets adherent to collagen. There was minimal erythrocyte hemolysis during the formation of thromboerythrocytes and studies of thromboerythrocyte osmotic fragility and cellular deformability showed no significant changes from control erythrocytes. Whereas there is a 20:1 ratio of erythrocytes to platelets in the circulation of normal individuals, the erythrocytes from as little as 50 ml of blood could be transformed into the equivalent of 2 U of platelets by numbers (equivalent to 18 U of platelets by mass), and reinfused into the same individual within several hours. These data encourage us to proceed to in vivo studies to assess the hemostatic efficacy of thromboerythrocytes in thrombocytopenic animals.

Comparison of global positioning and computer-based tracking systems for measuring player movement distance during Australian football.

Sports scientists require a thorough understanding of the energy demands of sports and physical activities so that optimal training strategies and game simulations can be constructed. A range of techniques has been used to both directly assess and estimate the physiological and biochemical changes during competition. A fundamental approach to understanding the contribution of the energy systems in physical activity has involved the use of time-motion studies. A number of tools have been used from simple pen and paper methods, the use of video recordings, to sophisticated electronic tracking devices. Depending on the sport, there may be difficulties in using electronic tracking devices because of concerns of player safety. This paper assesses two methods currently used to measure player movement patterns during competition: (1) global positioning technology (GPS) and (2) a computer-based tracking (CBT) system that relies on a calibrated miniaturised playing field and mechanical movements of the tracker. A range of ways was used to determine the validity and reliability of these methods for tracking Australian footballers for distance covered during games. Comparisons were also made between these methods. The results indicate distances measured using CBT overestimated the actual values (measured with a calibrated trundle wheel) by an average of about 5.8%. The GPS system overestimated the actual values by about 4.8%. Distances measured using CBT in experienced hands were as accurate as the GPS technology. Both systems showed relatively small errors in true distances.

Profile of movement demands of national football players in Australia.

Descriptive data on game movement demands of contemporary players in the Australian National Soccer League (NSL, now the A League) are lacking. The purpose of this study was to profile movement demands of NSL games and specifically analyse distance covered, time in various speed categories (e.g., walking, jogging, striding, etc.), number of sprint speed efforts and overall mean player speed. Video tapes of 45 players from the 2002 to 2003 NSL season were analysed for whole- and half-game movement patterns and game statistics using Trak Performance software. Bivariate and ANOVA statistics were used for between game halves and positional comparisons. Results showed no changes to the frequency and speed of high intensity demands in both halves of the game. However, a 14% slower overall speed in the second half of the game when compared with the first half was attributed to fewer observations of the low intensity movements (9.0% less walking and 12.4% less jogging) and more stationary periods. Engagement in game events such as kicking and passing was also 11.2% less frequent in the second versus first half of games. Position-specific results of higher movement speeds of midfield players (7.2kmh(-1)), compared with defenders (6.1kmh(-1)), agree with previous results from international professional leagues. The results provide position-specific directions for future conditioning drills and benchmark fitness requirements in high level soccer players. The results also highlight the challenge to ensure consistency of second-half performances for elite level soccer players in Australia.

Characterization of new pancreatic cancer-reactive monoclonal antibodies directed against purified mucin.

Although mucins have been found to be useful in the diagnosis of pancreatic cancer, the carbohydrate and peptide structures of pancreatic mucins are still not well characterized. Monoclonal antibodies were produced using mucins purified from xenografts of a human pancreatic cancer cell line as the immunogen. One of these, Ia3, reacted with almost all pancreatic, gastric, and colorectal carcinomas examined by immunoperoxidase staining, but with few normal tissues. Ia3 antigen was elevated in sera of 50.4% of individuals with gastrointestinal tumors, but its levels did not correlate with those of CA15-3, CA19-9, or DU-PAN-2. Serum Ia3 antigens migrated more slowly in sodium dodecyl sulfate-polyacrylamide gel electrophoresis than the polymorphic epithelial mucins recognized by DF3 or 115D8. Ia3 reacted only with native, and not with partially deglycosylated, pancreatic cancer xenograft mucins. Periodate or neuraminidase treatment destroyed this reactivity, but protease had little effect. The antigen recognized by another antibody, Nd2, was not detected in normal pancreatic, colonic, or gastric tissues but was present in approximately 60% of the pancreatic and gastric carcinomas examined. Nd2 reactivity with native and partially deglycosylated mucin was lost after pretreatment with protease and beta-mercaptoethanol. We conclude that, while Ia3 reacts with carbohydrates, Nd2 reactivity appears to be dependent on the integrity of the mucin protein core. The antigenic determinants of Ia3 and Nd2 are different from those of B72.3, CA19-9, DU-PAN-2, SPan-1, and several breast cancer mucin-directed antibodies. These results suggest that the malignancy-associated structures identified by Ia3 and Nd2 may provide new information on the carbohydrate and peptide structure of pancreatic cancer mucins.

Enhanced repair of O6-methylguanine DNA adducts in the liver of transgenic mice expressing the ada gene.

The capacity to repair O6-methylguanine-DNA adducts was measured in the liver of transgenic mice expressing a chimeric gene consisting of the inducible P-enolpyruvate carboxykinase (GTP) promoter linked to the bacterial O6-alkylguanine-DNA alkyltransferase (ada) gene. Under induced conditions, total hepatic alkyltransferase reached 32.8 +/- 4.2 (SE) fmol/micrograms DNA compared to 7.8 +/- 1.1 fmol/micrograms DNA in nontransgenic mice. Administration of methylnitrosourea or nitrosodimethylamine to both groups of mice produced O6-methylguanine-DNA adducts which resulted in repair-mediated depletion of total hepatic alkyltransferase in a dose-dependent fashion. In nontransgenic mice, depletion of hepatic alkyltransferase occurred at lower doses of carcinogen, and recovery of alkyltransferase activity occurred later than in ada+ transgenic mice. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of residual alkyltransferase activity after methylating agent exposure indicated that the bacterial as well as endogenous mammalian alkyltransferases were functioning as DNA repair proteins in hepatocytes in vivo. Analysis of O6-methylguanine- and N7-methylguanine-DNA adducts in the liver of transgenic and nontransgenic mice after treatment with one dose of 50 mg/kg methylnitrosourea i.p. revealed that transgenic mice repaired in situ O6-methylguanine-DNA adducts approximately 3 times faster than nontransgenic mice, commensurate with the increase in alkyltransferase activity. Thus, ada+ transgenic mice treated with methylnitrosourea have lower levels of persistent mutagenic O6-methylguanine adducts than ada- nontransgenic mice. Hepatic expression of bacterial alkyltransferase appears to protect mice from the DNA-damaging effects of N-nitroso compounds in vivo.

Disrupting Mating Behavior of Diaphorina citri (Liviidae).

Severe economic damage from citrus greening disease, caused by 'Candidatus Liberibacter asiaticus' bacteria, has stimulated development of methods to reduce mating and reproduction in populations of its insect vector, Diaphorina citri (Hemiptera: Liviidae). Male D. citri find mating partners by walking on host plants, intermittently producing vibrational calls that stimulate duetting replies by receptive females. The replies provide orientational feedback, assisting the search process. To test a hypothesis that D. citri mating can be disrupted using vibrational signals that compete with and/or mask female replies, courtship bioassays were conducted in citrus trees with or without interference from female reply mimics produced by a vibrating buzzer. Statistically significant reductions occurred in the rates and proportions of mating when the buzzer produced reply mimics within 0.4 s after male courtship calls compared with undisturbed controls. Observations of courtship behaviors in the two bioassays revealed activity patterns that likely contributed to the reductions. In both disruption and control tests, males reciprocated frequently between structural bifurcations and other transition points where signal amplitudes changed. Males in the disruption bioassay had to select among vibrational signals combined from the buzzer and the female at each transition point. They often turned towards the buzzer instead of the female. There was a statistically significant reduction in the proportion of males mating if they contacted the buzzer, possibly due to its higher vibration amplitude and duration in comparison with female replies. Potential applications of D. citri mating disruption technology in citrus groves are discussed.

Analysis of the physicochemical interactions between Clostridium difficile toxins and cholestyramine using liquid chromatography with post-column derivatization.

A potential therapy for antibiotic-associated pseudomembranous colitis is to bind Clostridium difficile toxins A and B using cholestyramine, a hydrophobic anion exchange medium. Frontal analysis in isotonic phosphate buffer was studied using post-column derivatization with o-phthalaldehyde, which gave a highly sensitive (> or =30 ng) flow-through analysis. Following load (1.5-3.0 microg toxin/3.6 mg), toxin A was bound at a slightly higher capacity than B, due to slower kinetics. A salt gradient eluted roughly 20% of bound toxin A with 0.6 M NaCl and toxin B with 1.1 M NaCl, hence toxin A showed weaker electrostatic affinity. The remainder of toxin A (65%) and some of toxin B (10% out of 50%) were eluted using a subsequent gradient to 60% acetonitrile in normal saline, which measured predominantly hydrophobic binding. Low and high affinity populations of both toxins were observed. Glycocholic acid or amino acids were competitive binders, although these components had little effect on the toxin A population bound primarily through ionic interactions. Competitive protein constituents in hamster cecal contents were also profiled. These results help to explain the variable clinical response in using cholestyramine to treat colitis. Using quaternary amine-polyhydroxymethacrylate (PHM) ion exchange chromatography, a trend for increased binding at higher pH was observed, especially for toxin A. Binding to strong cation exchange resins (sulfonate-PHM) was not observed. A range of reversed phase media retained both toxins, although recovery was very poor relative to protein standards. Size exclusion chromatography with light scattering detection showed that toxin B exists in different aggregation states, while toxin A remains monomeric.

Structural and functional characterization of major platelet membrane components derived by limited proteolysis of glycoprotein IIIa.

The authors isolated a product of proteolytic degradation of glycoprotein IIIa (GPIIIa) which is formed on the surface of human platelets during incubation with chymotrypsin and which was previously described as the 66 kDa platelet membrane component. This component migrated with an apparent Mr 62,400 in a non-reduced system of sodium dodecyl sulfate polyacrylamide gel electrophoresis. In a reduced system it yielded two major subunits migrating with apparent Mr 14,000-17,000 and 65,000. The low-molecular weight component began with the NH2-terminal sequence of GPIIIa (GPNICTTR...) and the larger component with residue 348 of GPIIIa (GKIRSKKA...) as deduced from a cDNA clone of this glycoprotein. The two subunits appeared to be linked by one or more S-S bridges supporting the contention that GPIIIa is a highly folded molecule on the platelet membrane. In contrast to GPIIIa, the '66 kDa component' did not bind to GRGDSPK-agarose, to fibrinogen-agarose nor to insolubilized monoclonal antibody recognizing the GPIIb/IIIa complex. The exposure of fibrinogen receptors during the course of incubation of platelets with chymotrypsin preceded the formation of the '66 kDa component' characterized in this study. An intermediate product of GPIIIa proteolysis migrating with an apparent Mr 120,000 in a non-reduced system and Mr 80,000 in a reduced system was identified as a precursor of the '66 kDa component'. The '120 kDa component' was not retained on GRGDSPK-agarose or on fibrinogen-agarose but it was retained on insolubilized antibody recognizing the GPIIb/IIIa complex. Incubation of platelets with porcine pancreatic elastase or human granulocytic elastase resulted in the formation of similar proteolytic degradation fragments.

Determination of amino acids in diverse polymeric matrices using HPLC, with emphasis on agars and agaroses.

Determination of amino acids in polymers with varying structure and charge was performed using vapor phase acid hydrolysis and subsequent precolumn derivatization with 6-aminoquinolyl-N-hydroxysuccinimidyl carbamate (AQC). Percent load of neutral, cationic and anionic peptide-modified synthetic polymers was accurately determined using this technique. Assay utility was shown for glycosaminoglycans and other sulfated polymers, neutral carbohydrate polymers such as agar, agarose, and cellulose, and polymers such as lipopolysaccharide and deoxyribonucleic acid. The carboxylated and sulfated molecules included chondroitin sulfate, hyaluronic acid, dermatan sulfate, and heparin, and the sulfated polymers included fucoidan, carrageenan, and dextran sulfate, as examples. Assayed cumulative amino acid concentrations (i.e. protein levels) are reported, although amino acid distribution data was also available from the analysis. Recovery was acceptable for the various compounds tested and did not correlate with structure. However, different sample sizes were necessary to achieve acceptable recovery, depending on the level of protein present in the matrix. While some matrices contained peaks in addition to the amino acids and amino sugars, they were not found to interfere using the standard gradient separation. Assayed amino acid profiles were compared for agaroses with differing electroendosmosis values and for agar samples from different parts of the globe. While the amounts of protein varied depending on source, the relative distribution of amino acids was very similar across the agar samples surveyed.

Evidence for secular trends in children's physical activity behaviour.

It is not clear whether the global increase in weight problems in children is the result of excessive energy intake or decreasing energy expenditure. Methodological limitations have made it difficult to analyse. There is evidence that at least part of the problem may lie with increasing energy consumption, but it is important to examine the other side of the energy equation also. However, it is not possible to conclusively describe physical activity trends because of the absence of suitable baseline data. One solution is to summate all available evidence in as many areas of daily activities as possible and then draw tentative conclusions. This review summarises available trend data on direct representations of physical activity in a range of contexts, together with indirect measures such as sedentariness, fitness, and attitudes. The conclusions drawn are: physical activity in clearly defined contexts such as active transport, school physical education, and organised sports is declining in many countries; young people would like to be active but are often constrained by external factors such as school policy or curricula, parental rules in relation to safety and convenience, and physical environmental factors.

A decrease in the association between the physical activity patterns of Australian parents and their children; 1985-1997.

The present study investigated the interactions between parents' and children's physical activity levels by examining whether or not parents who exercise have children who participate in sport. Of primary interest was an investigation of trends in these interactions over time. Information was collected from 10-13 y old children in 1985 (n = 2463) and then again in 1997-99 (n = 1469), about their sports participation and their perceptions of parents' exercise habits. Boys' participation in at least one sport declined from 87% in 1985 to 76% in 1997/1999 while, among girls, participation fell from 80% to 71%. According to their children's perceptions, mothers exercising regularly fell from 36% to 31% between surveys, while fathers exercising regularly fell from 39% to 32%. Interactions between parents' and children's exercise and sports behaviours were examined employing chi-square analysis techniques. Results showed gender-specific relationships for the 1985 sample, such that active fathers were associated with increased participation in sports by boys, and inactive mothers were associated with less participation in sports by girls. These interactions seemed to diminish over time. It is possible that changes in social structures during this time may be affecting familial behaviour relationships, such as the role modelling of active behaviours.

A comparison of patients relapsing to addictive drug use with non-relapsing patients following residential addiction treatment in Antigua.

The outcome of a 29-day residential addiction treatment programme for persons from Antigua and Barbuda with addiction to drugs or alcohol was assessed. All 100 patients entering the drug and alcohol treatment programme at Crossroads Centre Antigua between November 1998 and October 2002 were included. All patients were assessed with regards to drug or alcohol use or abstinence in November 2002 using telephone and mail follow-up as well as informal follow-up with families and other community contacts. Crossroads Centre Antigua is a 35 bed, 29-day residential treatment centre for drug and alcohol addiction serving patients from developed countries (85%) and from the Caribbean region (15%). Patients records were also reviewed to obtain age, gender, ethnicity, drug of choice, years of problematic use, completion of the 29 day programme, family member participation at Crossroads Centre Antigua (a four-day programme) and acceptance of halfway house placement. Of the 100 Antiguan patients admitted, 46 (46%) were abstinent (non-relapsers) at average 20.7+/-14.7 months after treatment. Abstinence did not have to be continuous. Forty-nine were known to be using drug or alcohol (49%) and five (5%) were lost to follow-up and considered to be using drugs (relapsers). Age (37.5 vs 41.1 years), gender (28% vs 22% female), ethnicity (87% vs 87% Afro-Caribbean), years of harmful use (12.7 vs 12.5 years) did not differ significantly between relapsers and non-relapsers. Crack cocaine use (67% vs 65%) and alcohol use (26% vs 31%) as primary addiction did not differ significantly between relapsers and non-relapsers. Relapsers were significantly less likely to complete the 29- day programme (81% vs 100%, p < 0.01), have family members participate at Crossroads (32% vs 54%, p < 0.05) or accept halfway house placement (4% vs 54%, p < 0.001). In conclusion, abstinence was achieved in 46% of those entering treatment, in 51% completing treatment, in 60% whose families participated and in 92% of those accepting halfway house placement.