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Biomedical subjects

J Gagnon

Publications and source records attributed to J Gagnon.

At least 37 records · Page 2Linked to original sources

Relationship of changes in maximal and submaximal aerobic fitness to changes in cardiovascular disease and non-insulin-dependent diabetes mellitus risk factors with endurance training: the HERITAGE Family Study.

The purpose of this study was to determine the relationship between changes in maximal oxygen uptake (VO2 max) and submaximal markers of aerobic fitness and changes in risk factors for cardiovascular disease (CVD) and non-insulin-dependent diabetes mellitus (NIDDM) consequent to a 20-week endurance training program. The 502 participants in this study were healthy and previously sedentary men (n = 250) and women (n = 252) of varying age (17 to 65 years) and race (blacks n = 142; whites n = 360) who had completed the HERITAGE Family Study testing and training protocol. Following baseline measurements, participants trained on cycle ergometers 3 days/week for a total of 60 exercise sessions starting at the heart rate (HR) associated with 55% of VO2 max for 30 minutes/session. This was progressively increased to the HR associated with 75% of VO2 max for 50 minutes/session, which was maintained during the last 6 weeks. VO2 max, heart rate at 50 W, power output at 60% of VO2 max, lipids and lipoproteins, resting blood pressure, body composition including abdominal fat (computed tomography [CT] scan), and blood glucose and insulin at rest and at peak following an intravenous glucose tolerance test (IVGTT) were determined both before and after training. Following training, there were significant increases in VO2 max (16%) and the power output at 60% of VO2 max and a significant decrease in HR at 50 W. These changes in markers of aerobic fitness were significantly correlated only to the changes in the body composition variables and the lipids and lipoproteins. Further, there was considerable individual variation in response for all variables studied. Finally, when risk factor data were analyzed by quartile of change in VO2 max, there were few significant relationships. It is concluded that there is a significant relationship between changes in markers of aerobic fitness and changes in several risk factors for CVD and NIDDM. However, the magnitude of these relationships is small.

Adolescent↗

Genome-wide linkage scan to detect loci influencing levels of dehydroepiandrosterones in the HERITAGE Family Study.

A genome-wide linkage scan was performed to identify genomic regions that influence levels of dehydroepiandrosterone (DHEA), DHEA sulfate (DHEAS), and DHEA fatty acid esters (DHEA-FA) at baseline and in response to 20 weeks of endurance exercise training in sedentary white and black participants in the HERITAGE Family Study. The baseline levels were log-transformed and adjusted for the effects of age and sex prior to genetic analysis. The training responses were adjusted for the effects of age, sex, and the baseline values. A total of 509 autosomal component polymorphic markers were used for the genome scan with an average spacing of 6.0 Mb. Multipoint variance components linkage analyses were performed in nuclear families containing 360 white and 106 black sibling pairs. We found 5 genomic regions with significant linkages for baseline DHEA-FA in whites, with log odd (LOD) scores over 3.6 (P < 2 x 10(-5)). They include (1) D1S468 (LOD 4.56, 2.533 Mb, 1p36.22); (2) D2S177 (LOD 5.65, 52.663 Mb, 2p16.3); (3) D4S2397 (LOD 3.98, 32.246 Mb, 4p15.2); (4) the paraoxonase loci (LOD 3.93 approximately 3.99, 101.544 approximately 102.933 Mb, 7q21.3), and D7S821 (LOD 3.88, 104.497 Mb, 7q22.1); and (5) D12S372 (LOD 4.66, 2.129 Mb, 12q13.33). In addition, we obtained evidence of suggestive linkages (2.2 < LOD < 3.6; 2 x 10(-5) < P < 7 x 10(-4)) on chromosomes 3p, 6q, and 8q for baseline DHEAS; on chromosomes 2q, 3p, 9q, 10p, 16q, and 17p for baseline DHEA-FA in whites; and on chromosomes 9q and 11p for baseline DHEA in blacks. This is the first genome-wide linkage scan searching for genomic regions influencing human DHEA levels. Several potential candidate genes are located in these genomic regions, which warrant further studies in HERITAGE and other cohorts.

Adult↗

Changes in ventilatory threshold with exercise training in a sedentary population: the HERITAGE Family Study.

UNLABELLED: The purpose of this study was to evaluate the effect of exercise training intensity relative to the ventilatory threshold (VT) on changes in work (watts) and VO2 at the ventilatory threshold and at maximal exercise in previously sedentary participants in the HERITAGE Family Study. We hypothesized that those who exercised below their VT would improve less in VO2 at the ventilatory threshold (VO2vt) and VO2max than those who trained at an intensity greater than their VT. Supervised cycle ergometer training was performed at the 4 participating clinical centers, 3 times a week for 20 weeks. Exercise training progressed from the HR corresponding to 55% VO2max for 30 minutes to the HR associated with 75% VO2max for 50 minutes for the final 6 weeks. VT was determined at baseline and after exercise training using standardized methods. 432 sedentary white and black men (n = 224) and women (n = 208), aged 17 to 65 years, were retrospectively divided into groups based on whether exercise training was initiated below, at, or above VT. RESULTS: 1) Training intensity (relative to VT) accounting for about 26% of the improvement in VO2vt (R2 = 0.26, p < 0.0001). 2) The absolute intensity of training in watts (W) accounted for approximately 56% of the training effect at VT (R2 = 0.56, p < 0.0001) with post-training watts at VT (VT(watts)) being not significantly different than W during training (p > 0.70). 3) Training intensity (relative to VT) had no effect on DeltaVO2max. These data clearly show that as a result of aerobic training both the VO2 and W associated with VT respond and become similar to the absolute intensity of sustained (3 x /week for 50 min) aerobic exercise training. Higher intensities of exercise, relative to VT, result in larger gains in VO2vt but not in VO2max.

Adolescent↗

Cardiac output and stroke volume changes with endurance training: the HERITAGE Family Study.

PURPOSE: The purpose of this study was to determine the magnitude of changes in cardiac output (Qc), stroke volume (SV), and arterial-mixed venous oxygen difference (a-vO2 diff) during submaximal exercise following a 20-wk endurance training program, with the primary focus on identifying differences in response by race, sex, and age. METHODS: The participants in this study (N = 631) were healthy and previously sedentary men (N = 277) and women (N = 354) of varying age (17-65 yr) and race (blacks, N = 217; whites, N = 414) who had completed the HERITAGE Family Study protocol. After baseline measurements, participants trained on cycle ergometers 3 d x wk(-1) for a total of 60 exercise sessions starting at the HR associated with 55% of maximal oxygen uptake (VO2max) for 30 min/session and building to the HR associated with 75% of VO2max for 50 min/session, which was maintained during the last 6 wk. HR, Qc (CO2 rebreathing), and SV (Qc/HR) were determined in duplicate at 50 W and at 60% of VO2max on two different days both before and after training. RESULTS: After training, there were significant decreases in HR and Qc, and significant increases in SV and a-vO2 diff at 50 W (except for no change in a-vO2 diff in black men). The changes in HR differed by sex and age, and the changes in SV, Qc, and a-vO2 diff differed by race. Qc decreased by 0.6 L x min(-1) at 50 W for the total sample, consistent with the decrease in VO2 at this power output. At 60% of VO2max HR decreased, and SV, Q, and a-VO2 diff increased. There were small differences in response by sex (HR and SV), race (HR), and age (HR and Qc). CONCLUSION: It is concluded that the cardiovascular systems of men and women, blacks and whites, and younger and older subjects are not limited in their ability to adapt to endurance training.

Adolescent↗

Heart rate and blood pressure changes with endurance training: the HERITAGE Family Study.

PURPOSE: The purpose of this study was to determine the magnitude of change in resting and exercise heart rate (HR) and blood pressure (BP), by race, sex, and age, after a 20-wk endurance training program in 507 healthy and previously sedentary subjects from the HERITAGE Family Study. METHODS: After baseline measurements, subjects exercised on cycle ergometers 3 d x wk(-1) for a total of 60 exercise sessions starting at 55% of VO2max for 30 min x session(-1) and building to 75% of VO2max for 50 min x session(-1) for the last 6 wk. HR and BP at rest and during exercise (50 W, 60% of VO2max maximal exercise) were each determined in duplicate on two different days both before and after training (resting values at 24-h and 72-h posttraining). RESULTS: After the period of training, there was a small decrease in resting HR (-2.7 to -4.6 beats x min(-1) across groups at 72-h posttraining), and small changes (i.e., < 3 mm Hg) in resting systolic (SBP), diastolic (DBP), and calculated mean BP (MBP), which varied by race, sex, and age. During exercise at the same absolute work rate (50 W), HR, SBP, DBP, and MBP were all significantly reduced, with greater reductions in HR in women compared with men, and greater reductions in BP in blacks and older subjects compared with whites and younger subjects, respectively. At the same relative work rate (60% VO2max), HR, DBP, and MBP were reduced, but SBP remained unchanged. Blacks had a greater reduction in DBP, but whites had a greater reduction in HR. Finally, at maximal exercise, there was a small decrease in HR, with men and whites decreasing more than women and blacks; an 8 mm Hg increase in SBP, with men increasing more than women; a 4 mm Hg decrease in DBP, with blacks decreasing more than whites; and no change in MBP. CONCLUSION: In conclusion, the reductions in resting HR and BP with training were generally small, but the reductions during exercise were substantial and clinically important, with the older and the black populations experiencing greater reductions.

Adolescent↗

Fitness, fatness, and estimated coronary heart disease risk: the HERITAGE Family Study.

PURPOSE: To determine the contributions of fatness and fitness to the estimated risk of future coronary heart disease (CHD). METHODS: The sample consisted of 212 black and 411 white adult sedentary participants. Percent body fat (%BF) was measured using densitometry, whereas maximal oxygen uptake (VO(2max)) was measured on a cycle ergometer. Risk of future CHD was estimated using the revised Framingham Heart Study algorithm. RESULTS: For fatness, the odds ratios for risk of future CHD were 1.83 and 1.70 for the moderate and high tertiles, respectively, compared with the low tertile. Similarly, the odds ratios for VO(2max) were 1.29 (NS) and 1.62, for the moderate and low tertiles, respectively. Removing VO(2max) from the full model had no effect; however, removing %BF resulted in a significantly weaker model (chi(2) = 10.38, P < 0.01). CONCLUSION: Both fatness and fitness are important predictors of risk of future CHD, based on the Framingham index.

Adipose Tissue↗

Familial aggregation of submaximal aerobic performance in the HERITAGE Family study.

PURPOSE: This study examines the contribution of genetic factors to submaximal aerobic performance phenotypes measured before and after 20 wk of endurance training. METHODS: Submaximal oxygen consumption (VO(2)) at three power outputs, 50 W (VO(2)50W), 60% (VO(2)60%) and 80% (VO(2)80%) of VO(2max) and power outputs at 60% (PO60%) and 80% (PO80%) of VO(2max) were measured during cycle ergometer exercise tests in 483 subjects from 99 white families participating in the HERITAGE Family study. The baseline phenotypes were adjusted for the effects of age, sex, and body mass using stepwise multiple regression procedures. The response phenotypes, computed as the difference (Delta) between the posttraining and baseline measures, were adjusted for age, sex, and the baseline value. RESULTS: All submaximal exercise phenotypes measured at baseline and in response to training were characterized by a significant familial resemblance. Maximal heritabilities of the baseline phenotypes range from 48% to 74% with significant spouse, sibling, and parent-offspring correlations. The hypothesis of maternal inheritance where mother-offspring and sibling correlations were forced to be equal was found to fit the data for VO(2)60%, VO(2)80% and PO80%. For the response phenotypes, the maximal heritabilities tended to be lower (23--57%) with a significant maternal inheritance for Delta VO(2)60%, Delta PO60%, and Delta PO80%. CONCLUSION: These results suggest that the submaximal working capacities of sedentary subjects and their responses to endurance training are influenced by familial/genetic factors with a significant contribution of maternal inheritance.

Adult↗

Familial resemblance in ventilatory threshold: the HERITAGE Family Study.

PURPOSE: This study investigates the familial resemblance of VO2 at the ventilatory threshold (VO2vt) from 199 nuclear families (100 White and 99 Black) participating in the HERITAGE Family Study. METHODS: VO2vt (mL x min(-1)) was determined in the sedentary state and again after 20 wk of aerobic cycle ergometer exercise training in 339 individuals (131 parents and 228 of their offspring), aged between 17 and 65 yr. VO2vt was adjusted for weight, age, fat mass, and fat-free mass by using regression methods. RESULTS: There was evidence for significant familial resemblance in the sedentary state for VO2vt (maximal heritability = 58% in White and 54% in Black families) and VO2vt/VO2max (maximal heritability = 38% in White and 39% in Black families). Spouse, sibling, and parent-offspring relationships for VO2vt were significant at baseline, suggesting that both genetic and shared environmental factors may contribute to the familial resemblance in the sedentary state. There was a moderate familial component in the response of VO2vt to aerobic exercise training in Whites (22%) and a larger component in Blacks (51%). In Blacks, the familial effect for VO2vt/VO2max appeared to be accounted for by fat and fat-free mass. CONCLUSION: These results show a strong familial contribution to VO2vt in the sedentary state and to the response of VO2vt to aerobic exercise training.

Adolescent↗

Angiogenin gene-race interaction for resting and exercise BP phenotypes: the HERITAGE Family Study.

We examined the association between an angiogenin gene polymorphism and blood pressure (BP) at rest and in response to acute exercise before and after a 20-wk endurance-training program. Subjects were 737 normotensive and borderline hypertensive subjects (257 black and 480 white). The polymorphism was detected by PCR and digestion with AvaII, yielding an allele of 253 bp or a rare allele of 194 + 59 bp. Resting and exercise [50 W; 60, 80, and 100% of maximal O2 consumption (VO2 max)] systolic (SBP) and diastolic BP were determined before and after training. Among blacks, adjusted SBP in the sedentary state was significantly lower in carriers of the rare allele at rest and exercise intensities of 60, 80, and 100% of VO2 max. In the trained state, carriers of the rare allele had a significantly (P < 0.05) lower SBP than did noncarriers at rest and at 80 and 100% of VO2 max. The genotypic effect observed among blacks was not evident among whites. Furthermore, change in BP (after--before) was not significantly associated with the genotype. In conclusion, the angiogenin gene AvaII polymorphism is associated with a lower SBP at rest and in response to acute high-intensity exercise in blacks but not in whites.

Adult↗

Age, sex, race, initial fitness, and response to training: the HERITAGE Family Study.

Effects of age, sex, race, and initial fitness on training responses of maximal O(2) uptake (VO(2 max)) are unclear. Data were available on 435 whites and 198 blacks (287 men and 346 women), aged 17-65 yr, before and after standardized cycle ergometer training. Individual responses varied widely, but VO(2 max) increased significantly for all groups. Responses by men and women and by blacks and whites of all ages varied widely. There was no sex difference for change (Delta) in VO(2 max) (ml. kg(-1). min(-1)); women had lower initial values and greater relative (%) increases. Blacks began with lower values but had similar responses. Older subjects had a lower Delta but a similar percent change. Baseline VO(2 max) correlated nonsignificantly with DeltaVO(2 max) but significantly with percent change. There were high, medium, and low responders in all age groups, both sexes, both races, and all levels of initial fitness. Age, sex, race, and initial fitness have little influence on VO(2 max) response to standardized training in a large heterogeneous sample of sedentary black and white men and women.

Adolescent↗

Genomic scan for genes affecting body composition before and after training in Caucasians from HERITAGE.

An autosomal genomewide search for genes related to body composition and its changes after a 20-wk endurance-exercise training program has been completed in the HERITAGE Family Study. Phenotypes included body mass index (BMI), sum of eight skinfold thicknesses, fat mass (FM), fat-free mass, percent body fat (%Fat), and plasma leptin levels. A maximum of 364 sib-pairs from 99 Caucasian families was studied with the use of 344 markers with single-point and multipoint linkage analyses. Evidence of significant linkage was observed for changes in fat-free mass with the S100A and the insulin-like growth factor I genes (P = 0.0001). Suggestive evidence (2.0 < or = Lod < 3.0; 0.0001 < P < or = 0.001) was also observed for the changes in FM and %Fat at 1q31 and 18q21-q23, in %Fat with the uncoupling protein 2 and 3 genes, and in BMI at 5q14-q21. At baseline, suggestive evidence was observed for BMI at 8q23-q24, 10p15, and 14q11; for FM at 14q11; and for plasma leptin levels with the low-density lipoprotein receptor gene. This is the first genomic scan on genes involved in exercise-training-induced changes in body composition that could provide information on the determinants of weight loss.

Adipose Tissue↗

Evidence of LPL gene-exercise interaction for body fat and LPL activity: the HERITAGE Family Study.

Evidence of a gene-exercise interaction for traits related to body composition is limited. Here, the association between the lipoprotein lipase (LPL) S447X polymorphism and changes in body mass index, fat mass, percent body fat, abdominal visceral fat measured by computed tomography, and post-heparin plasma LPL activity in response to 20 wk of endurance training was investigated in 741 adult white and black subjects. Changes were compared between carriers and noncarriers of the X447 allele after adjustment for the effects of age and pretraining values. No evidence of association was observed in men. However, white women carrying the X447 allele exhibited greater reductions of body mass index (P = 0.01), fat mass (P = 0.01), and percent body fat (P = 0.03); in black women, the carriers exhibited a greater reduction of abdominal visceral fat (P = 0.05) and a greater increase in post-heparin LPL activity (P = 0.02). These results suggest that the LPL S447X polymorphism influences the training-induced changes in body fat and post-heparin LPL activity in women but not in men.

Adult↗

TGF-beta(1) gene-race interactions for resting and exercise blood pressure in the HERITAGE Family Study.

We examined the possible association between a transforming growth factor (TGF)-beta(1) gene polymorphism in codon 10 and blood pressure (BP) at rest, in acute response to exercise in the pretrained (sedentary) and trained states, as well as in its training response (Delta) to 20 wk of endurance exercise. Subjects were 257 black and 480 white, healthy sedentary normotensive subjects from the HERITAGE Family Study. The polymorphism was detected by polymerase chain reaction and digestion with the Msp A1 I endonuclease yielding a wild (leucine-10) and a mutant (proline-10) allele. Resting and exercise [50 W plus 60, 80, and 100% maximal oxygen consumption (VO(2)(max))] BP were determined before and after training. Significant (P < 0.05) race-genotype interactions were found for systolic (S) BP in both the sedentary and trained states. Among whites but not in blacks, the TGF-beta(1) genotypes were significantly (P < 0.05) associated with sedentary-state SBP at rest, at 50 W, and at 60 and 100% VO(2)(max)as well as with trained-state SBP at rest and at 80 and 100% VO(2)(max). The leucine-10 homozygotes had significantly (P < 0.05) lower SBP than proline-10 homozygotes. DeltaBP was not significantly associated with genotype. These results support the hypothesis of an association between the TGF-beta(1) marker in codon 10 and SBP at rest and in response to acute exercise in whites but not in blacks.

Adult↗

Genomic scan for exercise blood pressure in the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) Family Study.

Agenome-wide linkage scan was performed for genes affecting submaximal exercise systolic blood pressure (SBP) and diastolic blood pressure (DBP) in the sedentary state and their responses to a standardized endurance training program. A total of 344 polymorphic markers were used, and 344 pairs of siblings from 99 white nuclear families and 102 sibling pairs from 105 black family units were available for the study. All subjects were healthy but sedentary at baseline. SBP and DBP were measured during exercise tests at 2 different intensities: 50 W (SBP50 and DBP50) and 80% of maximal oxygen consumption (SBP80 and DBP80). Baseline blood pressure phenotypes were adjusted for age, gender, and body mass index, and the training responses (after training minus baseline [Delta]) were adjusted for age, gender, baseline body mass index, and baseline blood pressure. Two analytical strategies were used: a multipoint variance-components linkage analysis using all the family data and a single-point linkage analysis using pairs of siblings. In whites, promising linkages (lod score >1.75) were detected for baseline SBP80 on 10q23-q24 and for DeltaSBP50 on 8q21. In addition, several chromosomal regions with suggestive evidence of linkage (lod score 1.0 to 1.75) were observed for SBP50 (22q11.2-q13), DBP50 (6q23-q27), SBP80 (2p24, 2q21, 14q11.1-q12, and 16q21), DBP80 (6q13-q21), DeltaSBP50 (7p12-p13), and DeltaDBP50 (5q31-q32). In blacks, DBP50, DBP80, and DeltaDBP80 showed promising quantitative trait loci on 18p11.2, 11q13-q21, and 10q21-q23, respectively. Suggestive linkages were evident for DBP50 on 2p22-p25, 11p15.5, and 18q21.1; for SBP80 on 6q21-q21, 6q31-q36, 12q12-q13, 15q12-q13, and 17q11-q12; and for DBP80 on 8q24, 10q21-q24, and 12p13. All the detected chromosomal regions include several potential candidate genes and therefore warrant further studies in the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) cohort and other studies.

Blood Pressure↗

Effects of endurance exercise training on plasma HDL cholesterol levels depend on levels of triglycerides: evidence from men of the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) Family Study.

High density lipoprotein (HDL) cholesterol concentrations have been shown to increase with regular endurance exercise and, therefore, can contribute to a lower risk of coronary heart disease in physically active individuals compared with sedentary subjects. Although low HDL cholesterol levels are frequently observed in combination with hypertriglyceridemia, some individuals may be characterized by isolated hypoalphalipoproteinemia, ie, low HDL cholesterol levels in the absence of elevated triglyceride (TG) concentrations. The present study compared the responses of numerous lipoprotein-lipid variables to a 20-week endurance exercise training program in men categorized on the basis of baseline TG and HDL cholesterol concentrations: (1) low TG and high HDL cholesterol (normolipidemia), (2) low TG and low HDL cholesterol (isolated low HDL cholesterol), (3) high TG and high HDL cholesterol (isolated high TGs), and (4) high TGs and low HDL cholesterol (high TG/low HDL cholesterol). A series of physical and metabolic variables was measured before and after the training program in a sample of 200 men enrolled in the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) Family Study. At baseline, men with high TG/low HDL cholesterol had more visceral adipose tissue than did men with isolated low HDL cholesterol and men with normolipidemia. The 0.4% (not significant) exercise-induced increase in HDL cholesterol levels in men with isolated low HDL cholesterol suggests that they did not benefit from the "HDL-raising" effect of exercise. In contrast, men with high TG/low HDL cholesterol showed a significant increase in HDL cholesterol levels (4.9%, P<0.005). Whereas both subgroups of men with elevated TG levels showed reductions in plasma TGs ( approximately -15.0%, P<0.005), only those with high TG/low HDL cholesterol showed significantly reduced apolipoprotein B levels at the end of the study (-6.0%, P<0.005). Multiple regression analyses revealed that the exercise-induced change in abdominal subcutaneous adipose tissue (10.6%, P<0.01) was the only significant correlate of the increase in plasma HDL cholesterol with training in men with high TG/low HDL cholesterol. Results of the present study suggest that regular endurance exercise training may be particularly helpful in men with low HDL cholesterol, elevated TGs, and abdominal obesity.

Adult↗

Age, body mass index, race and other determinants of steroid hormone variability: the HERITAGE Family Study.

OBJECTIVE AND METHODS: To investigate from the HERITAGE Family Study database, 13 steroid hormones (androstane-3alpha, 17beta-diol glucuronide, androsterone glucuronide, cortisol, dehydroepiandrosterone (DHEA), DHEA ester (DHEAE), DHEA sulfate (DHEAS), dihydrotestosterone (DHT), estradiol, 17-hydroxyprogesterone, progesterone, pregnenolone ester, sex hormone binding globulin (SHBG) and testosterone in each sex for their relationships with age, body mass index (BMI), race and key lifestyle variables. Sample sizes varied from 676 to 750 per hormone. Incremental regression methods were used to examine the contributions of the variables to steroid hormone variability. RESULTS: Age was a major predictor for most steroid hormones. The greatest contribution of age was a negative relationship with DHEAS (R(2)=0.39). BMI was also associated with the variability of several steroid hormones, being the most important predictor of SHBG (R(2)=0.20) and of testosterone (R(2)=0.12) concentrations. When age and BMI were included, race still contributed significantly to the variations in cortisol (R(2)=0.02 for men and 0.04 for women), DHT (R(2)=0.02 for men and 0.03 for women), and progesterone (R(2)=0.03 for women). Nevertheless, race appeared to be less important than age and BMI. In addition, lifestyle indicators (food and nutrient intakes, smoking and physical activity) influenced steroid hormone variability. Their contributions, however, were minor in most cases once age, BMI and race had been taken into account. CONCLUSIONS: We conclude that age was the most important factor, followed by BMI, race and lifestyle factors in explaining steroid hormone variability.

Adolescent↗

Familial resemblance for free androgens and androgen glucuronides in sedentary black and white individuals: the HERITAGE Family Study. Health, Risk Factors, Exercise Training and Genetics.

Familial correlation analyses were used to evaluate the familial aggregation of plasma androgens and androgen glucuronides (testosterone (TESTO), dihydrotestosterone (DHT), androstane-3 alpha,17 beta-diol glucuronide (3 alpha-DIOL-G), and androsterone glucuronide (ADT-G)) in 505 members of 99 white families and 296 members of 111 black families participating in the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) Family Study. Each of these four measures was determined by RIA after separation of conjugated and unconjugated steroid using C18 column chromatography. All participants were sedentary prior to being including in this study. Significant spouse correlations, as well as parent-offspring and sibling correlations, were found for TESTO, DHT, 3 alpha-DIOL-G, and ADT-G in the white sample, suggesting that common familial environments and genes contribute to the familial resemblance. In the black sample, significant sibling and parent-offspring correlations were found for all four phenotypes, while the spouse correlation was marginally significant for 3 alpha-DIOL-G and not significant for TESTO, DHT, and ADT-G. The non-significance of spouse correlations in the black individuals may be due to the small number of spouse pairs. The maximal heritability estimates of TESTO, DHT, 3 alpha-DIOL-G, and ADT-G were 69%, 87%, 74%, and 56% for white individuals and 70%, 73%, 62%, and 48% for black individuals respectively. Sex differences in heritability estimates were found in the white individuals, but they were less dramatic in the black individuals. In conclusion, plasma levels of androgens and androgen glucuronides are highly heritable in both white individuals and black individuals. There are notable sex differences in the white individuals.

Adolescent↗

Comparison of the PR mutant with the wild-type strain of proteus mirabilis brings insight into peroxide resistance factors and regulation of catalase expression.

The peroxide resistant mutant (PR) of Proteus mirabilis was characterized by an increased constitutive catalase activity concomitant with a large production of specific mRNA. Survival toward hydrogen peroxide during exponential phase was increased by H2O2 pretreatment in the wild type but not in the mutant, although the catalase of both strains was not inducible under these conditions. In the mutant, besides catalase, over-produced proteins comprised two different alkyl hydroperoxide reductase subunit C (AhpC) proteins and a protein homologous to the stationary phase transcription factor SspA of Escherichia coli. Conversely, the flagellin A (FlaA) of P. mirabilis was repressed in the PR mutant. Genomic DNA fragments of 2.9 kb carrying the catalase gene (katA) together with the 5' and 3' flanking regions were isolated from both strains and found to be identical. Upstream of katA, a Fur box-like sequence was found, but surprisingly, restricting iron in the culture medium caused a decrease in catalase production. The PR mutant presents similarities with other peroxide resistant mutants, but the regulation of catalase biosynthesis in P. mirabilis seems somewhat different from other close species such as E. coli.

Adhesins, Bacterial↗