2024-03-28T09:05:13Zhttp://uobrep.openrepository.com/oai/requestoai:uobrep.openrepository.com:10547/2238132020-04-23T07:28:32Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Sculthorpe, Nicholas
author
Solomon, Andrew M.
author
Sinanan, Andrea C.M.
author
Bouloux, Pierre-Marc G.
author
Grace, Fergal
author
Lewis, Mark P.
department
University of Bedfordshire
2012-05-15T12:17:00Z
2012-04
Sculthorpe, N., Solomon, A.M., Sinanan, A.C., Bouloux, P.M., Grace, F., and Lewis, M.P. (2012)
'Androgens affect myogenesis in vitro and increase local IGF-1 expression', Medicine and Science in Sports and Exercise, 44(4) pp.610-5.
1530-0315
21946153
10.1249/MSS.0b013e318237c5c0
http://hdl.handle.net/10547/223813
Medicine and science in sports and exercise
The mechanism whereby anabolic androgens are associated with hypertrophy of skeletal muscle is incompletely understood but may involve an interaction with locally generated insulin-like growth factor (IGF) 1. The present investigation utilized a cell culture model of human skeletal muscle-derived cell maturation to test the hypothesis that androgens increase differentiation of human muscle precursor cells in vitro and to assess effects of androgen with or without IGF-1 on IGF-1 messenger RNA (mRNA) expression in human muscle precursor cells.
en
Archived with thanks to Medicine and science in sports and exercise
Androgenic Anabolic Steroids
C760 Biomolecular Science
Androgens affect myogenesis in vitro and increase local IGF-1 expression
Article
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oai:uobrep.openrepository.com:10547/2238122020-04-23T07:28:33Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Sculthorpe, Nicholas
author
Grace, Fergal
author
Jones, Peter
author
Davies, Bruce
department
University of Bedfordshire
2012-05-15T12:14:06Z
2010-12
Sculthorpe, N., Grace, F., Jones P., and Davies, B. (2010) 'Evidence of altered cardiac electrophysiology following prolonged androgenic anabolic steroid use', Cardiovascular toxicology, 10(4) pp. 239-43.
1559-0259
21038102
10.1007/s12012-010-9090-y
http://hdl.handle.net/10547/223812
Cardiovascular toxicology
The non-therapeutic use of androgenic anabolic steroids (AAS) is associated with sudden cardiac death. Despite this, there is no proposed mechanism by which this may occur. Signal-averaged ECG (SAECG) allows the assessment of cardiac electrical stability, reductions of which are a known risk factor for cardiac arrhythmias. The aim of the present study was to examine cardiac electrical stability using SAECG in a group (n = 15) of long-term AAS users (AAS use 21.3 ± 3.1 years) compared with a group (n = 15) of age-matched weight lifters (WL) and age-matched sedentary controls [C (n = 15)]. AS, WL and C underwent SAECG analysis at rest and following an acute bout of exercise to volitional exhaustion. SAECGs were analyzed using a 40 Hz filter and were averaged over 200 beats. Results indicate a non-significant trend for increased incidence of abnormal SAECG measures at rest in AS (P = 0.55). However, AS demonstrated a significantly higher incidence of abnormalities of SAECG following exercise than C or WL (P < 0.05). In conclusion, the higher incidence of abnormal SAECG measurements immediately post-exercise in the AAS group places them at a greater risk of sudden death. The present study provides a strong contraindication to the use of AAS.
en
Archived with thanks to Cardiovascular toxicology
B220 Toxicology
B120 Physiology
cardiac
androgenic anabolic steroids
Evidence of altered cardiac electrophysiology following prolonged androgenic anabolic steroid use.
Article
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URL
https://uobrep.openrepository.com/bitstream/10547/223812/1/2009_059519_sculthorpe.pdf
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2009_059519_sculthorpe.pdf.txt
oai:uobrep.openrepository.com:10547/2238042020-04-23T07:36:26Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Sculthorpe, Nicholas
author
Grace, Fergal
author
Jones, Peter
author
Fletcher, Iain M.
department
University of Bedfordshire
2012-05-15T12:19:00Z
2010-08
Sculthorpe, N., Grace, F., Jones, P., and Fletcher, I. (2010) 'The effect of short-term creatine loading on active range of movement', Applied physiology, nutrition, and metabolism, 35(4) pp.507-11.
1715-5312
20725117
10.1139/H10-036
http://hdl.handle.net/10547/223804
Applied physiology, nutrition, and metabolism = Physiologie appliquée, nutrition et métabolisme
During high-intensity exercise, intracellular creatine phosphate (PCr) is rapidly broken down to maintain adenosine triphosphate turnover. This has lead to the widespread use of creatine monohydrate as a nutritional ergogenic aid. However, the increase in intracellular PCr and the concomitant increase in intracellular water have not been investigated with regard to their effect on active range of movement (ROM). Forty male subjects (age, 24+/-3.2 years) underwent restricted randomization into 2 equal groups, either an intervention group (CS) or a control group (C). The CS group ingested 25 g.day(-1) of creatine monohydrate for 5 days, followed by 5 g.day(-1) for a further 3 days. Before (24 h before starting supplementation (PRE) and after (on the 8th day of supplementation (POST)) this loading phase, both groups underwent goniometry measurement of the shoulder, elbow, hip, and ankle. Data indicated significant reductions in active ROM in 3 movements: shoulder extension (57+/-11.3 degrees PRE vs. 48+/-11.2 degrees POST, p<0.01), shoulder abduction (183.4+/-6.8 degrees PRE vs. 180.3+/-5.1 degrees POST, p<0.05), and ankle dorsiflexion (14.2+/-4.7 degrees PRE vs. 12.1+/-6.4 degrees POST, p<0.01). There was also a significant increase in body mass for the CS group (83.6+/-6.2 kg vs. 85.2+/-6.3 kg, p<0.05). The results suggest that short-term supplementation with creatine monohydrate reduces the active ROM of shoulder extension and abduction and of ankle dorsiflexion. Although the mechanism for this is not fully understood, it may be related to the asymmetrical distribution of muscle mass around those joints.
en
Archived with thanks to Applied physiology, nutrition, and metabolism = Physiologie appliquée, nutrition et métabolisme
Nutrition
Muscle function
Flexibility
The effect of short-term creatine loading on active range of movement
Article
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oai:uobrep.openrepository.com:10547/2255552020-04-23T07:30:37Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Brown, William Michael
department
Queen Mary University of London
2012-05-23T10:24:44Z
2011-04
Brown, William M., (2011) 'The parental antagonism theory of language evolution: preliminary evidence for the proposal', Human Biology, 83(2) pp.213-45.
1534-6617
21615287
10.3378/027.083.0205
http://hdl.handle.net/10547/225555
Human Biology
Language--as with most communication systems--likely evolved by means of natural selection. Accounts for the genetical selection of language can usually be divided into two scenarios, either of which used in isolation of the other appear insufficient to explain the phenomena: (1) there are group benefits from communicating, and (2) there are individual benefits from being a better communicator. In contrast, it is hypothesized that language phenotypes emerged during a coevolutionary struggle between parental genomes via genomic imprinting, which is differential gene expression depending on parental origin of the genetic element. It is hypothesized that relatedness asymmetries differentially selected for patrigene-caused language phenotypes to extract resources from mother (early in development) and matrigene-caused language phenotypes to influence degree of cooperativeness among asymmetric kin (later in development). This paper reports that imprinted genes have a high frequency of involvement in language phenotypes (~36%), considering their presumed rarity in the human genome (~2%). For example, two well-studied genes associated with language impairments (FOXP2 and UBE3A) exhibit parent-of- origin effects. Specifically, FOXP2 is putatively paternally expressed, whereas UBE3A is a maternally expressed imprinted gene. It is also hypothesized that the more unique and cooperative aspects of human language emerged to the benefit of matrilineal inclusive fitness. Consistent with this perspective, it is reported here that the X-chromosome has higher involvement in loci that have associations with language than would be expected by chance. It is also reported, for the first time, that human and chimpanzee maternally expressed overlapping imprinted genes exhibit greater evolutionary divergence (in terms of the degree of overlapping transcripts) than paternally expressed overlapping imprinted genes. Finally, an analysis of global language patterns reveals that paternally but not maternally silenced Alu elements are positively correlated with language diversity. Furthermore, there is a much higher than expected frequency of Alu elements inserted into the protein-coding machinery of imprinted and X-chromosomal language loci compared with nonimprinted language loci. Taken together these findings provide some support for parental antagonism theory. Unlike previous theories for language evolution, parental antagonism theory generates testable predictions at the proximate (e.g., neurocognitive areas important for social transmission and language capacities), ontogenetic (e.g., the function of language at different points of development), ultimate (e.g., inclusive fitness), and phylogenetic levels (e.g., the spread of maternally derived brain components in mammals, particularly in the hominin lineage), thus making human capacities for culture more tractable than previously thought.
en
The parental antagonism theory of language evolution: preliminary evidence for the proposal.
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
oai:uobrep.openrepository.com:10547/2255722017-10-24T13:31:36Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Consedine, Nathan S.
author
Magai, C.
author
Horton, D.
author
Brown, William Michael
department
University of Bedfordshire
2012-05-23T10:32:19Z
2012-05-23
Consedine, N. S., Magai, C., Horton, D., and Brown, W. M. (2012) 'The Affective Paradox: An Emotion Regulatory Account of Ethnic Differences in Self-Reported Anger', Journal of Cross-Cultural Psychology, 43(5), pp. 723-741.
0022-0221
10.1177/0022022111405659
http://hdl.handle.net/10547/225572
Journal of Cross-Cultural Psychology
en
anger
ethnic differences
emotion reporting
emotion regulation
repression
negative affect
social desirability
demand
bias
The affective paradox: an emotion regulatory account of ethnic differences in self-reported anger
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
oai:uobrep.openrepository.com:10547/2255732020-04-23T07:30:15Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Brown, William Michael
author
Price, M.E.
author
Kang, J.
author
Pound, N.
author
Zhao, Y.
author
Yu, H.
department
Brunel University
sponsor
Higher Education Funding Council; British Academy Grant
2012-05-23T10:46:44Z
2012-05-23
Brown, W. M., Price, M. E., Kang, J., Pound, N., Zhao, Y. and Yu, H. (2008) 'Fluctuating asymmetry and preferences for sex-typical bodily characteristics', Proceedings of the National Academy of Sciences, 105(35):12938.
0027-8424
10.1073/pnas.0710420105
http://hdl.handle.net/10547/225573
Proceedings of the National Academy of Sciences
Body size and shape seem to have been sexually selected in a variety of species, including humans, but little is known about what attractive bodies signal about underlying genotypic or phenotypic quality. A widely used indicator of phenotypic quality in evolutionary analyses is degree of symmetry (i.e., fluctuating asymmetry, FA) because it is a marker of developmental stability, which is defined as an organism's ability to develop toward an adaptive end-point despite perturbations during its ontogeny. Here we sought to establish whether attractive bodies signal low FA to observers, and, if so, which aspects of attractive bodies are most predictive of lower FA. We used a 3D optical body scanner to measure FA and to isolate size and shape characteristics in a sample of 77 individuals (40 males and 37 females). From the 3D body scan data, 360° videos were created that separated body shape from other aspects of visual appearance (e.g., skin color and facial features). These videos then were presented to 87 evaluators for attractiveness ratings. We found strong negative correlations between FA and bodily attractiveness in both sexes. Further, sex-typical body size and shape characteristics were rated as attractive and correlated negatively with FA. Finally, geometric morphometric analysis of joint configurations revealed that sex-typical joint configurations were associated with both perceived attractiveness and lower FA for male but not for female bodies. In sum, body size and shape seem to show evidence of sexual selection and indicate important information about the phenotypic quality of individuals.
en
Fluctuating asymmetry and preferences for sex-typical bodily characteristics
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oai:uobrep.openrepository.com:10547/2258322020-04-23T07:28:41Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Sharples, Adam P.
author
Al-Shanti, Nasser
author
Stewart, Claire E.
department
Manchester Metropolitan University
2012-05-24T15:58:58Z
2010-10
Sharples, A.P., Al-Shanti, N., and Stewart, C.E. (2010), 'C2 and C2C12 murine skeletal myoblast models of atrophic and hypertrophic potential: relevance to disease and ageing?', Journal of Cellular Physiology, 225(1) pp.240-50.
1097-4652
20506232
10.1002/jcp.22252
http://hdl.handle.net/10547/225832
Journal of Cellular Physiology
Reduced muscle mass and increased susceptibility to TNF-induced degradation accompany inflamed ageing and chronic diseases. Furthermore, C(2) myoblasts display diminished differentiation and increased susceptibility to TNF-alpha-induced cell death versus subcloned C(2)C(12) cells, providing relevant models to assess: differentiation (creatine kinase), growth (protein), death (trypan-blue) and anabolic/catabolic parameters (RT-PCR) over 72 h +/- TNF-alpha (20 ng ml(-1)). At 48 and 72 h, respectively, larger myotubes and significantly higher CK activity (320.26 +/- 6.82 vs. 30.71 +/- 2.5, P < 0.05; 544.94 +/- 27.7 vs. 39.4 +/- 3.37 mU mg ml(-1), P < 0.05), fold increases in myoD (21.45 +/- 3.12 vs. 3.97 +/- 1.76, P < 0.05; 31.07 +/- 3.1 vs. 6.82 +/- 1.93, P < 0.05) and myogenin mRNA (241.8 +/- 40 vs. 36.80 +/- 19.3, P < 0.05; 440 +/- 100.5 vs. 201.1 +/- 86, P < 0.05) were detected in C(2)C(12) versus C(2). C(2)C(12) showed significant increases in IGF-I mRNA (243.05 +/- 3.87 vs. 105.75 +/- 21.95, P < 0.05), reduced proliferation and significantly lower protein expression (1.21 +/- 0.28 vs. 1.79 +/- 0.29 mg ml(-1), P < 0.05) at 72 h versus C(2) cells. Significant temporal reductions in C(2)C(12) IGFBP2 mRNA (28.02 +/- 15.44, 13.82 +/- 8.07, 6.92 +/- 4.37, P < 0.05) contrasted increases in C(2)s (4.31 +/- 3.31, 13.02 +/- 9.92, 82.9 +/- 58.9, P < 0.05) at 0, 48 and 72 h, respectively. TNF-alpha increased cell death in C(2)s (2.67 +/- 1.54%, 34.42 +/- 5.39%, 29.71 +/- 5.79% (0, 48, 72 h), P < 0.05), yet was without effect in C(2)C(12)s at 48 h but caused a small significant increase at 72 h (9.88 +/- 4.02% (TNF-alpha) vs. 6.17 +/- 0.749% (DM), 72 h). TNF-alpha and TNFRI mRNA were unchanged; however, larger reductions in IGF-I (8.2- and 7.5-fold vs. 4.5- and 4.1-fold (48, 72 h)), IGF-IR (2-fold vs. no-significant reduction (72 h)) and IGFBP5 (3.24 vs. 1.38 (48 h) and 2.21 vs. 1.71 (72 h), P < 0.05) mRNA were observed in C(2) versus C(2)C(12) with TNF-alpha. This investigation provides insight into regulators of altered basal hypertrophy and TNF-induced atrophy, providing a model for future investigation into therapeutic initiatives for ageing/wasting disorders.
en
Archived with thanks to Journal of cellular physiology
C2 and C2C12 murine skeletal myoblast models of atrophic and hypertrophic potential: relevance to disease and ageing?
Article
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oai:uobrep.openrepository.com:10547/2259322020-04-23T07:28:41Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Sharples, Adam P.
author
Al-Shanti, Nasser
author
Lewis, Mark P.
author
Stewart, Claire E.
department
University of Bedfordshire
2012-05-25T08:53:26Z
2011-12
Sharples A.P., Al-Shanti N., Lewis M.P., and Stewart C.E., (2011) 'Reduction of myoblast differentiation following multiple population doublings in mouse C2 C12 cells: a model to investigate ageing?', Journal of Cellular Biochemistry, 112(12) pp.3773-85.
1097-4644
21826704
10.1002/jcb.23308
http://hdl.handle.net/10547/225932
Journal of Cellular Biochemistry
Ageing skeletal muscle displays declines in size, strength, and functional capacity. Given the acknowledged role that the systemic environment plays in reduced regeneration (Conboy et al. [2005] Nature 433: 760-764), the role of resident satellite cells (termed myoblasts upon activation) is relatively dismissed, where, multiple cellular divisions in-vivo throughout the lifespan could also impact on muscular deterioration. Using a model of multiple population doublings (MPD) in-vitro thus provided a system in which to investigate the direct impact of extensive cell duplications on muscle cell behavior. C(2) C(12) mouse skeletal myoblasts (CON) were used fresh or following 58 population doublings (MPD). As a result of multiple divisions, reduced morphological and biochemical (creatine kinase, CK) differentiation were observed. Furthermore, MPD cells had significantly increased cells in the S and decreased cells in the G1 phases of the cell cycle versus CON, following serum withdrawal. These results suggest continued cycling rather than G1 exit and thus reduced differentiation (myotube atrophy) occurs in MPD muscle cells. These changes were underpinned by significant reductions in transcript expression of: IGF-I and myogenic regulatory factors (myoD and myogenin) together with elevated IGFBP5. Signaling studies showed that decreased differentiation in MPD was associated with decreased phosphorylation of Akt, and with later increased phosphorylation of JNK1/2. Chemical inhibition of JNK1/2 (SP600125) in MPD cells increased IGF-I expression (non-significantly), however, did not enhance differentiation. This study provides a potential model and molecular mechanisms for deterioration in differentiation capacity in skeletal muscle cells as a consequence of multiple population doublings that would potentially contribute to the ageing process.
en
Archived with thanks to Journal of cellular biochemistry
Reduction of myoblast differentiation following multiple population doublings in mouse C2 C12 cells: a model to investigate ageing?
Article
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oai:uobrep.openrepository.com:10547/2259552020-04-23T07:30:00Zcom_10547_132196col_10547_132226col_10547_132228
University of Bedfordshire Repository
author
Taylor, Lee
author
Hillman, Angela R.
author
Midgley, Adrian W.
author
Peart, Daniel J.
author
Chrismas, Bryna C.
author
McNaughton, Lars R.
department
University of Bedfordshire
2012-05-25T09:04:53Z
2012-03-23
Taylor L., Hillman A.R., Midgley A.W., Peart D.J., Chrismas B., and McNaughton L.R., (2012) 'Hypoxia-mediated prior induction of monocyte-expressed HSP72 and HSP32 provides protection to the disturbances to redox balance associated with human sub-maximal aerobic exercise.' Amino Acids
1438-2199
22441647
10.1007/s00726-012-1265-3
http://hdl.handle.net/10547/225955
Amino Acids
HSP72 is rapidly expressed in response to a variety of stressors in vitro and in vivo (including hypoxia). This project sought a hypoxic stimulus to elicit increases in HSP72 and HSP32 in attempts to confer protection to the sub-maximal aerobic exercise-induced disturbances to redox balance. Eight healthy recreationally active male subjects were exposed to five consecutive days of once-daily hypoxia (2,980 m, 75 min). Seven days prior to the hypoxic acclimation period, subjects performed 60 min of cycling on a cycle ergometer (exercise bout 1-EXB1), and this exercise bout was repeated 1 day post-cessation of the hypoxic period (exercise bout 2-EXB2). Blood samples were taken immediately pre- and post-exercise and 1, 4 and 8 h post-exercise for HSP72 and immediately pre, post and 1 h post-exercise for HSP32, TBARS and glutathione [reduced (GSH), oxidised (GSSG) and total (TGSH)], with additional blood samples obtained immediately pre-day 1 and post-day 5 of the hypoxic acclimation period for the same indices. Monocyte-expressed HSP32 and HSP72 were analysed by flow cytometry, with measures of oxidative stress accessed by commercially available kits. There were significant increases in HSP72 (P < 0.001), HSP32 (P = 0.03), GSSG (t = 9.5, P < 0.001) and TBARS (t = 5.6, P = 0.001) in response to the 5-day hypoxic intervention, whereas no significant changes were observed for GSH (P = 0.22) and TGSH (P = 0.25). Exercise-induced significant increases in HSP72 (P < 0.001) and HSP32 (P = 0.003) post-exercise in EXB1; this response was absent for HSP72 (P ≥ 0.79) and HSP32 (P ≥ 0.99) post-EXB2. The hypoxia-mediated increased bio-available HSP32 and HSP72 and favourable alterations in glutathione redox, prior to exercise commencing in EXB2 compared to EXB1, may acquiesce the disturbances to redox balance encountered during the second physiologically identical exercise bout.
Hypoxia-mediated prior induction of monocyte-expressed HSP72 and HSP32 provides protection to the disturbances to redox balance associated with human sub-maximal aerobic exercise.
Article
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oai:uobrep.openrepository.com:10547/2313342020-04-23T07:28:42Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Sharples, Adam P.
author
Stewart, Claire E.
department
University of Bedfordshire
department
Manchester Metropolitan University
2012-06-28T15:36:06Z
2011-05
Sharples, A. P. and Stewart, C. E. (2011) 'Myoblast models of skeletal muscle hypertrophy and atrophy', Current opinion in clinical nutrition and metabolic care, 14(3) pp. 230-236.
1473-6519
21460719
10.1097/MCO.0b013e3283457ade
http://hdl.handle.net/10547/231334
Current opinion in clinical nutrition and metabolic care
To highlight recent breakthroughs and controversies in the use of myoblast models to uncover cellular and molecular mechanisms regulating skeletal muscle hypertrophy and atrophy.
en
Archived with thanks to Current opinion in clinical nutrition and metabolic care
muscle precursor cell
satellite cell
IGF-I
myostatin
three-dimensional muscle constructs
hypertrophy
atrophy
ageing
cachexia
Akt
mTOR
MAPK
mafbx
murf
foxo
igfbp2
FAK
Myoblast models of skeletal muscle hypertrophy and atrophy.
Article
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
URL
https://uobrep.openrepository.com/bitstream/10547/231334/1/Sharples%20and%20Stewart%20%282010%29%20Pre-review%20version-Myoblast%20models%20of%20atrophy%20and%20hypertrophy.pdf
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application/pdf
Sharples and Stewart (2010) Pre-review version-Myoblast models of atrophy and hypertrophy.pdf
URL
https://uobrep.openrepository.com/bitstream/10547/231334/8/Sharples%20and%20Stewart%20%282010%29%20Pre-review%20version-Myoblast%20models%20of%20atrophy%20and%20hypertrophy.pdf.txt
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MD5
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Sharples and Stewart (2010) Pre-review version-Myoblast models of atrophy and hypertrophy.pdf.txt
oai:uobrep.openrepository.com:10547/2283532020-04-23T08:39:54Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Brown, William Michael
author
Consedine, Nathan S.
department
Long Island University
2012-06-11T11:21:50Z
2004
Brown, W.M. and Consedine, N.S. (2004) 'Just how happy is the happy puppet? An emotion signaling and kinship theory perspective on the behavioral phenotype of children with Angelman syndrome'. Medical hyposthesis. 63(3) pp. 377-85
0306-9877
15288352
10.1016/j.mehy.2004.05.010
http://hdl.handle.net/10547/228353
Medical hypotheses
The favored level of parental investment in a child may differ for genes of maternal and paternal origin in the child. This conflict can be expressed in the phenomenon of genomic imprinting that refers to situations in which the same gene is differentially expressed depending on its parent of origin. Two disorders that show the effects of genomic imprinting--both at 15q11-q13--are Angelman Syndrome (AS) which is due to the absence of expression of maternally-inherited genes and Prader-Willi syndromes (PWS) which is due to the absence of expression of paternally-inherited genes. However, although both disorders can arise from the deletion of the same genetic region, the gustatory, behavioral, and affective characteristics of AS and PWS children are remarkably distinct. Recent research inspired by kinship theory has suggested the origins of these phenotypic differences may lie in the differential investment of each parent's genome in the AS or PWS child. Specifically, it is thought that each set of parental genes have different 'ideas' regarding how the child should behave towards the mother and how much investment they should look to extract. In normal cases, the trade-off between the competing parental genomes produces a behavioral equilibrium in the child. However, in pathological instances, particularly where gene expression is one-sided, the evolved behavioral strategies favored by the contributing genome will dominate the child's behavior. To date, research in the area of genomic conflict in AS and PWS children has primarily focusing on differences in post-natal nutrition-related behaviors. The current paper extends this framework by offering an emotion and evolutionary signaling interpretation of the affective characteristics of AS children. A review of the affective characteristics of the two syndromes (PWS and AS) is presented before kinship and emotions theory are used to examine the functions that differential affect expression may serve in altering maternal investment. We expected that because the ultimate goal of paternal genes is to increase the child rearing burden of mothers, the Angelman behavioral phenotype should exhibit the emotion signaling characteristics that elicit levels of investment more consistent with paternal genetic interests. AS children display more positive, relative to negative, affect expressions (i.e. AS children laugh and smile more frequently than PWS children). In affect signaling theories, positive affect signals (i.e., smiling, laughing) have evolved to manipulate the sensory systems of receivers to increase social resources. In contrast, because the expression of some negative affects may indicate to the mother that the infant is not viable, negative affect expression is characteristically low among AS children. However, AS children may nonetheless have high levels of non-expressed anxiety because of its role in assisting the child (and its paternal genome) to maintain vigilance for changes in investment on the part of the mother. Overall, our kinship and emotion signaling analysis of AS children suggests that their global pattern of affect signaling represents one manifestation of an array of possible evolved strategies within the parental genome. Specifically, because AS exhibits the effects of paternally-inherited genes unhindered by the expression of maternally-inherited genes, the AS infant manifests a pattern of expression and non-expression that maximize maternal investment and thus paternal fitness. This theory is a significant departure from the standard but erroneous conjecture that a mother and child's inclusive fitness interests are one and the same.
en
Just how happy is the happy puppet? An emotion signaling and kinship theory perspective on the behavioral phenotype of children with Angelman syndrome.
Article
oai:uobrep.openrepository.com:10547/2283522017-10-24T13:30:20Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Brown, William Michael
2012-06-11T11:17:10Z
2012-06-11
Brown, W. M. (2001) 'Genomic Imprinting and the Cognitive Architecture Mediating Human Culture', Journal of Cognition and Culture, 1(3) pp. 251-258
1567-7095
10.1163/156853701753254396
http://hdl.handle.net/10547/228352
Journal of Cognition and Culture
Archived with thanks to Journal of Cognition and Culture
Genomic imprinting and the cognitive architecture mediating human culture
Article
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
oai:uobrep.openrepository.com:10547/2951032020-04-23T07:30:21Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Fletcher, Iain M.
2013-07-03T08:22:23Z
2013
Fletcher, I.M. (2013) 'An Investigation into the Effect of a Pre-performance Strategy on Jump Performance', Journal of Strength and Conditioning Research, 27(1), pp.107-115
1064-8011
10.1519/JSC.0b013e3182517ffb
http://hdl.handle.net/10547/295103
Journal of Strength and Conditioning Research
The aim of this study was to explore the effect that different components, making up a commonly used pre-performance preparation strategy, have on jump height performance. Sixteen male collegiate athletes (age, 21.38 ± 0.52 years; height, 1.79 ± 0.07 m; and body mass, 75.1 ± 5.26 kg) performed a preparation strategy involving a cycle ergometer warm-up, followed by a dynamic stretch component, and finishing with heavy back squats. This intervention was repeated to test countermovement, squat or drop jump performance after each component of the preparation strategy, with electromyographic activity measured during each jump test. Significant increases (p < 0.05) in jump height and electromyographic activity were noted, with a stepwise increase in performance from pre- to post-warm-up, increased further by the dynamic stretch component and again increased after the back squat.
en
Archived with thanks to Journal of Strength and Conditioning Research
C600 Sports Science
An investigation into the effect of a pre-performance strategy on jump performance
Article
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
oai:uobrep.openrepository.com:10547/2961662020-04-23T07:30:28Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Soubry, Adelheid
author
Schildkraut, Joellen M.
author
Murtha, Amy
author
Wang, Frances
author
Huang, Zhiqing
author
Bernal, Autumn J.
author
Kurtzberg, Joanne
author
Jirtle, Randy L.
author
Murphy, Susan K.
author
Hoyo, Cathrine
department
Duke University Medical Center
2013-07-16T10:15:07Z
2013
Soubry, A., Schildkraut, J.M., Murtha, A. et al. (2013) 'Paternal obesity is associated with IGF2 hypomethylation in newborns: results from a Newborn Epigenetics Study (NEST) cohort', BMC medicine, 11 (1) pp.1-10.
1741-7015
23388414
10.1186/1741-7015-11-29
http://hdl.handle.net/10547/296166
BMC medicine
Data from epidemiological and animal model studies suggest that nutrition during pregnancy may affect the health status of subsequent generations. These transgenerational effects are now being explained by disruptions at the level of the epigenetic machinery. Besides in vitro environmental exposures, the possible impact on the reprogramming of methylation profiles at imprinted genes at a much earlier time point, such as during spermatogenesis or oogenesis, has not previously been considered. In this study, our aim was to determine associations between preconceptional obesity and DNA methylation profiles in the offspring, particularly at the differentially methylated regions (DMRs) of the imprinted Insulin-like Growth Factor 2 (IGF2) gene.
en
Archived with thanks to BMC medicine
epigenetics
DNA methylation
obesity
Paternal obesity is associated with IGF2 hypomethylation in newborns: results from a Newborn Epigenetics Study (NEST) cohort
Article
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URL
https://uobrep.openrepository.com/bitstream/10547/296166/2/1741-7015-11-29.pdf
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https://uobrep.openrepository.com/bitstream/10547/296166/8/1741-7015-11-29.pdf.txt
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1741-7015-11-29.pdf.txt
oai:uobrep.openrepository.com:10547/2961882020-04-23T07:34:26Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Bernal, Autumn J.
author
Dolinoy, Dana C.
author
Huang, Dale
author
Skaar, David A.
author
Weinhouse, Caren
author
Jirtle, Randy L.
2013-07-16T10:15:57Z
2012
Bernal, A.J., Dolinoy, D.C., Huang, D. et al. (2012) 'Adaptive radiation-induced epigenetic alterations mitigated by antioxidants', FASEB Journal, 27(2), pp.665-671
0892-6638
10.1096/fj.12-220350
http://hdl.handle.net/10547/296188
FASEB Journal
Humans are exposed to low-dose ionizing radiation (LDIR) from a number of environmental and medical sources. In addition to inducing genetic mutations, there is concern that LDIR may also alter the epigenome. Such heritable effects early in life can either be positively adaptive or result in the enhanced formation of diseases, including cancer, diabetes, and obesity. Herein, we show that LDIR significantly increased DNA methylation at the viable yellow agouti (A(vy)) locus in a sex-specific manner (P=0.004). Average DNA methylation was significantly increased in male offspring exposed to doses between 0.7 and 7.6 cGy, with maximum effects at 1.4 and 3.0 cGy (P<0.01). Offspring coat color was concomitantly shifted toward pseudoagouti (P<0.01). Maternal dietary antioxidant supplementation mitigated both the DNA methylation changes and coat color shift in the irradiated offspring. Thus, LDIR exposure during gestation elicits epigenetic alterations that lead to positive adaptive phenotypic changes that are negated with antioxidants, indicating they are mediated in part by oxidative stress. These findings provide evidence that in the isogenic A(vy) mouse model, epigenetic alterations resulting from LDIR play a role in radiation hormesis, bringing into question the assumption that every dose of radiation is harmful.
en
Archived with thanks to The FASEB Journal
DNA methylation
agouti mice
hormesis
reactive oxygen species
Adaptive radiation-induced epigenetic alterations mitigated by antioxidants
Article
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
oai:uobrep.openrepository.com:10547/2961672020-04-23T07:30:28Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Skaar, David A.
author
Li, Yue
author
Bernal, Autumn J.
author
Hoyo, Cathrine
author
Murphy, Susan K.
author
Jirtle, Randy L.
2013-07-16T10:16:50Z
2012-12
Skaar, D.A., Li, Y., Bernal, A.J. et al. (2012) 'The human imprintome: regulatory mechanisms, methods of ascertainment, and roles in disease susceptibility', ILAR journal, 53(3-4), pp.341-358
1930-6180
23744971
10.1093/ilar.53.3-4.341
http://hdl.handle.net/10547/296167
ILAR journal
Imprinted genes form a special subset of the genome, exhibiting monoallelic expression in a parent-of-origin-dependent fashion. This monoallelic expression is controlled by parental-specific epigenetic marks, which are established in gametogenesis and early embryonic development and are persistent in all somatic cells throughout life. We define this specific set of cis-acting epigenetic regulatory elements as the imprintome, a distinct and specially tasked subset of the epigenome. Imprintome elements contain DNA methylation and histone modifications that regulate monoallelic expression by affecting promoter accessibility, chromatin structure, and chromatin configuration. Understanding their regulation is critical because a significant proportion of human imprinted genes are implicated in complex diseases. Significant species variation in the repertoire of imprinted genes and their epigenetic regulation, however, will not allow model organisms solely to be used for this crucial purpose. Ultimately, only the human will suffice to accurately define the human imprintome.
en
Archived with thanks to ILAR journal / National Research Council, Institute of Laboratory Animal Resources
differential methylation
histone modification
imprinted gene
The human imprintome: regulatory mechanisms, methods of ascertainment, and roles in disease susceptibility
Article
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
oai:uobrep.openrepository.com:10547/2961682020-04-23T07:30:29Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Zhang, Aiping
author
Skaar, David A.
author
Li, Yue
author
Huang, Dale
author
Price, Thomas M.
author
Murphy, Susan K.
author
Jirtle, Randy L.
2013-07-16T10:17:45Z
2011
Zhang, A., Skaar, D.A., Li,Y, et al. (2011) 'Novel retrotransposed imprinted locus identified at human 6p25', Nucleic Acids Research, 39(13), pp.5388-5400
0305-1048
10.1093/nar/gkr108
http://hdl.handle.net/10547/296168
Nucleic Acids Research
Differentially methylated regions (DMRs) are stable epigenetic features within or in proximity to imprinted genes. We used this feature to identify candidate human imprinted loci by quantitative DNA methylation analysis. We discovered a unique DMR at the 50-end of FAM50B at 6p25.2. We determined that sense transcripts originating from the FAM50B locus are expressed from the paternal allele in all human tissues investigated except for ovary, in which expression is biallelic. Furthermore, an antisense transcript, FAM50B-AS, was identified to be monoallelically expressed from the paternal allele in a variety of tissues. Comparative phylogenetic analysis showed that FAM50B orthologs are absent in chicken and platypus, but are present and biallelically expressed in opossum and mouse.
en
Archived with thanks to Nucleic Acids Research
Novel retrotransposed imprinted locus identified at human 6p25
Article
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oai:uobrep.openrepository.com:10547/2961642020-04-23T07:30:28Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Ratkevicius, Aivaras
author
Carroll, Andrew M.
author
Kilikevicius, Audrius
author
Venckunas, Tomas
author
McDermott, Kevin T.
author
Gray, Stuart R.
author
Wackerhage, Henning
author
Lionikas, Arimantas
2013-07-16T10:10:09Z
2010
Ratkevicius, A., Carroll, A.M., Kilikevicius, A. et al. (2010) 'H55N polymorphism as a likely cause of variation in citrate synthase activity of mouse skeletal muscle', Physiological Genomics, 42A (2), pp.96-102
1094-8341
10.1152/physiolgenomics.00066.2010
http://hdl.handle.net/10547/296164
Physiological Genomics
The aim of this study was to investigate the mechanisms underlying low activity of citrate synthase (CS) in A/J mice compared with other inbred strains of mice. Enzyme activity, protein content, and mRNA levels of CS were studied in the quadriceps muscles of A/J, BALB/cByJ, C57BL/6J, C3H/HeJ, DBA/2J, and PWD/PhJ strains of mice. Cytochrome c protein content was also measured. The results of the study indicate that A/J mice have a 50–65% reduction in CS activity compared with other strains despite similar levels of Cs mRNA and lack of differences in CS and cytochrome c protein content. CS from A/J mice also showed lower Michaelis constant (Km) for both acetyl CoA and oxaloacetate compared with the other strains of mice.
en
Archived with thanks to Physiological Genomics
inbred strains
oxidative phosphorylation
polymorphisms
H55N polymorphism as a likely cause of variation in citrate synthase activity of mouse skeletal muscle
Article
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oai:uobrep.openrepository.com:10547/5529122020-12-08T02:23:22Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Brown, William Michael
department
University of Bedfordshire
2015-05-15T08:19:55Z
2015-03-30
Brown, William M. (2015) 'Exercise-associated DNA methylation change in skeletal muscle and the importance of imprinted genes: a bioinformatics meta-analysis', British Journal of Sports Medicine, 49, pp.1567-1578.
1473-0480
25824446
10.1136/bjsports-2014-094073
http://hdl.handle.net/10547/552912
British Journal of Sports Medicine
BACKGROUND: Epigenetics is the study of processes-beyond DNA sequence alteration-producing heritable characteristics. For example, DNA methylation modifies gene expression without altering the nucleotide sequence. A well-studied DNA methylation-based phenomenon is genomic imprinting (ie, genotype-independent parent-of-origin effects). OBJECTIVE: We aimed to elucidate: (1) the effect of exercise on DNA methylation and (2) the role of imprinted genes in skeletal muscle gene networks (ie, gene group functional profiling analyses). DESIGN: Gene ontology (ie, gene product elucidation)/meta-analysis. DATA SOURCES: 26 skeletal muscle and 86 imprinted genes were subjected to g:Profiler ontology analysis. Meta-analysis assessed exercise-associated DNA methylation change. DATA EXTRACTION: g:Profiler found four muscle gene networks with imprinted loci. Meta-analysis identified 16 articles (387 genes/1580 individuals) associated with exercise. Age, method, sample size, sex and tissue variation could elevate effect size bias. DATA SYNTHESIS: Only skeletal muscle gene networks including imprinted genes were reported. Exercise-associated effect sizes were calculated by gene. Age, method, sample size, sex and tissue variation were moderators. RESULTS: Six imprinted loci (RB1, MEG3, UBE3A, PLAGL1, SGCE, INS) were important for muscle gene networks, while meta-analysis uncovered five exercise-associated imprinted loci (KCNQ1, MEG3, GRB10, L3MBTL1, PLAGL1). DNA methylation decreased with exercise (60% of loci). Exercise-associated DNA methylation change was stronger among older people (ie, age accounted for 30% of the variation). Among older people, genes exhibiting DNA methylation decreases were part of a microRNA-regulated gene network functioning to suppress cancer. CONCLUSIONS: Imprinted genes were identified in skeletal muscle gene networks and exercise-associated DNA methylation change. Exercise-associated DNA methylation modification could rewind the 'epigenetic clock' as we age. TRIAL REGISTRATION NUMBER: CRD42014009800.
en
C400 Genetics
C420 Human Genetics
C431 Medical Genetics
C440 Molecular Genetics
C182 Evolution
C600 Sports Science
C120 Behavioural Biology
bioinformatics
DNA methylation
excercise
Exercise-associated DNA methylation change in skeletal muscle and the importance of imprinted genes: a bioinformatics meta-analysis
Article
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Br J Sports Med-2015-Brown-bjsports-2014-094073.pdf.txt
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oai:uobrep.openrepository.com:10547/5947622020-04-23T07:34:19Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Mehta, Sanjeev R.
author
Louise Thomas, Elizabeth
author
Patel, Nayna
author
Crofton, Mary E.
author
McCarthy, John
author
Eliahoo, Joseph
author
Morin, Stanislas X.
author
Fitzpatrick, Julie
author
Durighel, Giuliana
author
Goldstone, Anthony P.
author
Johnston, Desmond G.
author
Bell, Jimmy D.
author
Taylor-Robinson, Simon D.
department
Hammersmith Hospital
2016-01-25T10:25:20Z
2010-04
Mehta, S.R. et al (2010) 'Proton magnetic resonance spectroscopy and ultrasound for hepatic fat quantification'. Hepatology Research 40 (4):399
1386-6346
20236356
10.1111/j.1872-034X.2009.00620.x
http://hdl.handle.net/10547/594762
Hepatology Research
Aim: The increasing prevalence of fatty liver disease requires routine assessment methods. Proton magnetic resonance spectroscopy (1H MRS) is increasingly used for steatosis measurement, but due to cost, is unlikely to become a widely-used screening tool. Ultrasound is cheaper and more widely available, although subject to observer variability. Our aim was to determine the sensitivity and specificity of ultrasound against 1H MRS, using MRS as a gold standard, for the detection and quantification of hepatic fat content. Methods: Fifty adults participated (43 men, seven women) in this study. Hepatic steatosis was assessed by ultrasound and 1H MRS. Images were graded by two independent radiologists to classify severity and distribution of liver fat. Results: Ultrasound detected liver fat infiltration in 82% of cases measurable by 1H MRS, while liver fat was detectable in 44% of cases graded absent by ultrasound. Ultrasound grading was subjective, with the radiologists in agreement in 53% of cases (κ = 0.39, P = 0.002). Considerable overlap in intrahepatocellular lipid content was observed between different grades: absent (0.0–1.58%), mild (2.2–16.2%), moderate (4.9–26.7%) and severe (8.1–76.8%) steatosis. Ultrasound could not detect liver fat levels below 2% as measured by 1H MRS Conclusion: Ultrasound is less sensitive than 1H MRS in detecting very low levels of liver fat content, but is sensitive to fatty infiltration greater than 2%. There is a tendency of higher ultrasound grades to correlate with higher degrees of fatty infiltration, although some overlap exists. Our findings are still consistent with ultrasound being useful as a low cost screening tool.
en
Archived with thanks to Hepatology Research
fatty liver disease
proton magnetic resonance spectroscopy
hepatic fat
Proton magnetic resonance spectroscopy and ultrasound for hepatic fat quantification
Article
Tk9OLUVYQ0xVU0lWRSBESVNUUklCVVRJT04gTElDRU5TRQoKQnkgc2lnbmluZyBhbmQgc3VibWl0dGluZyB0aGlzIGxpY2Vuc2UsIHlvdSAodGhlIGF1dGhvcihzKSBvciBjb3B5cmlnaHQKb3duZXIpIGdyYW50cyB0byB0aGUgVW5pdmVyc2l0eSBvZiBCZWRmb3Jkc2hpcmUgUmVwb3NpdG9yeSAgKFVPQlJFUCkgdGhlIG5vbi1leGNsdXNpdmUgcmlnaHQgdG8gcmVwcm9kdWNlLAp0cmFuc2xhdGUgKGFzIGRlZmluZWQgYmVsb3cpLCBhbmQvb3IgZGlzdHJpYnV0ZSB5b3VyIHN1Ym1pc3Npb24gKGluY2x1ZGluZwp0aGUgYWJzdHJhY3QpIHdvcmxkd2lkZSBpbiBwcmludCBhbmQgZWxlY3Ryb25pYyBmb3JtYXQgYW5kIGluIGFueSBtZWRpdW0sCmluY2x1ZGluZyBidXQgbm90IGxpbWl0ZWQgdG8gYXVkaW8gb3IgdmlkZW8uCgpZb3UgYWdyZWUgdGhhdCBVT0JSRVAgbWF5LCB3aXRob3V0IGNoYW5naW5nIHRoZSBjb250ZW50LCB0cmFuc2xhdGUgdGhlCnN1Ym1pc3Npb24gdG8gYW55IG1lZGl1bSBvciBmb3JtYXQgZm9yIHRoZSBwdXJwb3NlIG9mIHByZXNlcnZhdGlvbi4KCllvdSBhbHNvIGFncmVlIHRoYXQgVU9CUkVQIG1heSBrZWVwIG1vcmUgdGhhbiBvbmUgY29weSBvZiB0aGlzIHN1Ym1pc3Npb24gZm9yCnB1cnBvc2VzIG9mIHNlY3VyaXR5LCBiYWNrLXVwIGFuZCBwcmVzZXJ2YXRpb24uCgpZb3UgcmVwcmVzZW50IHRoYXQgdGhlIHN1Ym1pc3Npb24gaXMgeW91ciBvcmlnaW5hbCB3b3JrLCBhbmQgdGhhdCB5b3UgaGF2ZQp0aGUgcmlnaHQgdG8gZ3JhbnQgdGhlIHJpZ2h0cyBjb250YWluZWQgaW4gdGhpcyBsaWNlbnNlLiBZb3UgYWxzbyByZXByZXNlbnQKdGhhdCB5b3VyIHN1Ym1pc3Npb24gZG9lcyBub3QsIHRvIHRoZSBiZXN0IG9mIHlvdXIga25vd2xlZGdlLCBpbmZyaW5nZSB1cG9uCmFueW9uZSdzIGNvcHlyaWdodC4KCklmIHRoZSBzdWJtaXNzaW9uIGNvbnRhaW5zIG1hdGVyaWFsIGZvciB3aGljaCB5b3UgZG8gbm90IGhvbGQgY29weXJpZ2h0LAp5b3UgcmVwcmVzZW50IHRoYXQgeW91IGhhdmUgb2J0YWluZWQgdGhlIHVucmVzdHJpY3RlZCBwZXJtaXNzaW9uIG9mIHRoZQpjb3B5cmlnaHQgb3duZXIgdG8gZ3JhbnQgVU9CUkVQIHRoZSByaWdodHMgcmVxdWlyZWQgYnkgdGhpcyBsaWNlbnNlLCBhbmQgdGhhdApzdWNoIHRoaXJkLXBhcnR5IG93bmVkIG1hdGVyaWFsIGlzIGNsZWFybHkgaWRlbnRpZmllZCBhbmQgYWNrbm93bGVkZ2VkCndpdGhpbiB0aGUgdGV4dCBvciBjb250ZW50IG9mIHRoZSBzdWJtaXNzaW9uLgoKSUYgVEhFIFNVQk1JU1NJT04gSVMgQkFTRUQgVVBPTiBXT1JLIFRIQVQgSEFTIEJFRU4gU1BPTlNPUkVEIE9SIFNVUFBPUlRFRApCWSBBTiBBR0VOQ1kgT1IgT1JHQU5JWkFUSU9OIE9USEVSIFRIQU4gVEVTVE9SLCBZT1UgUkVQUkVTRU5UIFRIQVQgWU9VIEhBVkUKRlVMRklMTEVEIEFOWSBSSUdIVCBPRiBSRVZJRVcgT1IgT1RIRVIgT0JMSUdBVElPTlMgUkVRVUlSRUQgQlkgU1VDSApDT05UUkFDVCBPUiBBR1JFRU1FTlQuCgpVT0JSRVAgd2lsbCBjbGVhcmx5IGlkZW50aWZ5IHlvdXIgbmFtZShzKSBhcyB0aGUgYXV0aG9yKHMpIG9yIG93bmVyKHMpIG9mIHRoZQpzdWJtaXNzaW9uLCBhbmQgd2lsbCBub3QgbWFrZSBhbnkgYWx0ZXJhdGlvbiwgb3RoZXIgdGhhbiBhcyBhbGxvd2VkIGJ5IHRoaXMKbGljZW5zZSwgdG8geW91ciBzdWJtaXNzaW9uLgo=
oai:uobrep.openrepository.com:10547/5947322020-04-23T07:38:57Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Watson, R.A.
author
Pride, N.B.
author
Thomas, E. Louise
author
Fitzpatrick, Julie
author
Durighel, Giuliana
author
McCarthy, John
author
Morin, Stanislas X.
author
Ind, P.W.
author
Bell, Jimmy D.
department
National Heart and Lung Institute
department
Imperial College London
2016-01-25T10:31:54Z
2010-03-18
Watson, R.A. et al (2010) 'Reduction of total lung capacity in obese men: comparison of total intrathoracic and gas volumes'. Journal of Applied Physiology 108 (6):1605
8750-7587
20299612
10.1152/japplphysiol.01267.2009
http://hdl.handle.net/10547/594732
Journal of Applied Physiology
PMC2886677
Restriction of total lung capacity (TLC) is found in some obese subjects, but the mechanism is unclear. Two hypotheses are as follows: 1) increased abdominal volume prevents full descent of the diaphragm; and 2) increased intrathoracic fat reduces space for full lung expansion. We have measured total intrathoracic volume at full inflation using magnetic resonance imaging (MRI) in 14 asymptomatic obese men [mean age 52 yr, body mass index (BMI) 35–45 kg/m2] and 7 control men (mean age 50 yr, BMI 22–27 kg/m2). MRI volumes were compared with gas volumes at TLC. All measurements were made with subjects supine. Obese men had smaller functional residual capacity (FRC) and FRC-to-TLC ratio than control men. There was a 12% predicted difference in mean TLC between obese (84% predicted) and control men (96% predicted). In contrast, differences in total intrathoracic volume (MRI) at full inflation were only 4% predicted TLC (obese 116% predicted TLC, control 120% predicted TLC), because mediastinal volume was larger in obese than in control [heart and major vessels (obese 1.10 liter, control 0.87 liter, P = 0.016) and intrathoracic fat (obese 0.68 liter, control 0.23 liter, P < 0.0001)]. As a consequence of increased mediastinal volume, intrathoracic volume at FRC in obese men was considerably larger than indicated by the gas volume at FRC. The difference in gas volume at TLC between the six obese men with restriction, TLC < 80% predicted (OR), and the eight obese men with TLC > 80% predicted (ON) was 26% predicted TLC. Mediastinal volume was similar in OR (1.84 liter) and ON (1.73 liter), but total intrathoracic volume was 19% predicted TLC smaller in OR than in ON. We conclude that the major factor restricting TLC in some obese men was reduced thoracic expansion at full inflation.
en
magnetic resonance imaging
restricted total lung capacity
lung capacity
mediastinal volume
MRI
Reduction of total lung capacity in obese men: comparison of total intrathoracic and gas volumes
Article
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
oai:uobrep.openrepository.com:10547/5947642020-04-23T07:34:19Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Kim, Sangkyu
author
Bi, Xiuhua
author
Czarny-Ratajczak, Malwina
author
Dai, Jianliang
author
Welsh, David A.
author
Myers, Leann
author
Welsch, Michael A.
author
Cherry, Katie E
author
Arnold, Jonathan
author
Poon, Leonard W.
author
Jazwinski, S. Michal
department
Tulane University Health Sciences Center
2016-01-25T10:41:51Z
2012-04
Kim, S. et al (2012) 'Telomere maintenance genes SIRT1 and XRCC6 impact age-related decline in telomere length but only SIRT1 is associated with human longevity'. Biogerontology 13 (2):119-31
1573-6768
21972126
10.1007/s10522-011-9360-5
http://hdl.handle.net/10547/594764
Biogerontology
PMC3272146
Leukocyte telomere length is widely considered a biomarker of human age and in many studies indicative of health or disease. We have obtained quantitative estimates of telomere length from blood leukocytes in a population sample, confirming results of previous studies that telomere length significantly decreases with age. Telomere length was also positively associated with several measures of healthy aging, but this relationship was dependent on age. We screened two genes known to be involved in telomere maintenance for association with the age-related decline in telomere length observed in our population to identify candidate longevity-associated genes. A single-nucleotide polymorphism located in the SIRT1 gene and another in the 3' flanking region of XRCC6 had significant effects on telomere length. At each bi-allelic locus, the minor variant was associated with longer telomeres, though the mode of inheritance fitting best differed between the two genes. No statistical interaction was detected for telomere length between the SIRT1 and XRCC6 variants or between these polymorphisms and age. The SIRT1 locus was significantly associated with longevity (P < 0.003). The frequency of the minor allele was higher in long-lived cases than in young controls, which coincides with the protective role of the minor variant for telomere length. In contrast, the XRCC6 variant was not associated with longevity. Furthermore, it did not affect the association of SIRT1 with exceptional survival. The association of the same variant of SIRT1 with longevity was near significant (P < 0.07) in a second population. These results suggest a potential role of SIRT1 in linking telomere length and longevity. Given the differences between this gene and XRCC6, they point to the distinct impact that alternate pathways of telomere maintenance may have on aging and exceptional survival.
en
Archived with thanks to Biogerontology
telomeres
age
ageing
Telomere maintenance genes SIRT1 and XRCC6 impact age-related decline in telomere length but only SIRT1 is associated with human longevity
Article
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
oai:uobrep.openrepository.com:10547/5947702020-04-23T08:42:06Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Credeur, Daniel P.
author
Mariappan, Nithya
author
Francis, Joseph
author
Thomas, David
author
Moraes, Denzil
author
Welsch, Michael A.
department
University of Missouri
2016-01-25T11:22:08Z
2012-11
Credeur, D.P. et al (2012) 'Vasoreactivity before and after handgrip training in chronic heart failure patients'. Atherosclerosis 225 (1):154-9
1879-1484
23010159
10.1016/j.atherosclerosis.2012.08.013
http://hdl.handle.net/10547/594770
Atherosclerosis
The purpose of this study was to investigate the vasodilatory and vasoconstrictor responses of the brachial artery in patients with chronic heart failure (CHF) and controls (CON) before and after a period of training and detraining.
en
Archived with thanks to Atherosclerosis
vasoreactivity
handgrip
chronic heart failure
Vasoreactivity before and after handgrip training in chronic heart failure patients
Article
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oai:uobrep.openrepository.com:10547/5947672020-04-23T07:34:19Zcom_10547_132196col_10547_132226
University of Bedfordshire Repository
author
Thomas, E. Louise
author
Parkinson, James R.
author
Frost, Gary S.
author
Goldstone, Anthony P.
author
Doré, Caroline J.
author
McCarthy, John
author
Collins, Adam L.
author
Fitzpatrick, Julie
author
Durighel, Giuliana
author
Taylor-Robinson, Simon D.
author
Bell, Jimmy D.
department
Imperial College London
2016-01-25T11:01:22Z
2012-01
Thomas, E.L. et al (2012) 'The missing risk: MRI and MRS phenotyping of abdominal adiposity and ectopic fat' Obesity 20 (1):76-87
1930-739X
21660078
10.1038/oby.2011.142
http://hdl.handle.net/10547/594767
Obesity (Silver Spring, Md.)
Individual compartments of abdominal adiposity and lipid content within the liver and muscle are differentially associated with metabolic risk factors, obesity and insulin resistance. Subjects with greater intra-abdominal adipose tissue (IAAT) and hepatic fat than predicted by clinical indices of obesity may be at increased risk of metabolic diseases despite their "normal" size. There is a need for accurate quantification of these potentially hazardous depots and identification of novel subphenotypes that recognize individuals at potentially increased metabolic risk. We aimed to calculate a reference range for total and regional adipose tissue (AT) as well as ectopic fat in liver and muscle in healthy subjects. We studied the relationship between age, body-mass, BMI, waist circumference (WC), and the distribution of AT, using whole-body magnetic resonance imaging (MRI), in 477 white volunteers (243 male, 234 female). Furthermore, we used proton magnetic resonance spectroscopy (MRS) to determine intrahepatocellular (IHCL) and intramyocellular (IMCL) lipid content. The anthropometric variable which provided the strongest individual correlation for adiposity and ectopic fat stores was WC in men and BMI in women. In addition, we reveal a large variation in IAAT, abdominal subcutaneous AT (ASAT), and IHCL depots not fully predicted by clinically obtained measurements of obesity and the emergence of a previously unidentified subphenotype. Here, we demonstrate gender- and age-specific patterns of regional adiposity in a large UK-based cohort and identify anthropometric variables that best predict individual adiposity and ectopic fat stores. From these data we propose the thin-on-the-outside fat-on-the-inside (TOFI) as a subphenotype for individuals at increased metabolic risk.
en
Archived with thanks to Obesity (Silver Spring, Md.)
MRI
MRS
magnetic resonance imaging
intra-abdominal adipose tissue
hepatic fat
The missing risk: MRI and MRS phenotyping of abdominal adiposity and ectopic fat.
Article
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