Letteratura scientifica selezionata sul tema "Skeletal Adaptation"

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Articoli di riviste sul tema "Skeletal Adaptation"

1

Hibbitt, Catherine. "Using Skeleton Typograms to Explore Comparative Anatomy". American Biology Teacher 82, n. 2 (1 febbraio 2020): 120–22. http://dx.doi.org/10.1525/abt.2020.82.2.120.

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A highlight activity of the author's comparative anatomy class, this skeletal typogram activity challenges students to take their understanding of the skeletal system's components beyond mere memorization of bone names and locations. Each student creates a poster of a vertebrate skeleton, using the letters of the bone names to depict the actual bone shape and location. Animals are chosen by the teacher to represent a wide variety of evolutionary adaptations (swimming, flying, grazing, hunting, etc.). Students are then asked to compare the different typograms through analysis of contrasting skeletal evolutionary adaptations. The infographic nature of the project helps students understand the power of visual information, allowing for creative cross-disciplinary work. Through developing and comparing typograms, students deepen their understanding of how skeletal form fits function and the role of adaptation in vertebrate evolution.
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2

Turner, Charles H. "Skeletal Adaptation to Mechanical Loading". Clinical Reviews in Bone and Mineral Metabolism 5, n. 4 (dicembre 2007): 181–94. http://dx.doi.org/10.1007/s12018-008-9010-x.

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3

Röckl, Katja S. C., Michael F. Hirshman, Josef Brandauer, Nobuharu Fujii, Lee A. Witters e Laurie J. Goodyear. "Skeletal Muscle Adaptation to Exercise Training". Diabetes 56, n. 8 (18 maggio 2007): 2062–69. http://dx.doi.org/10.2337/db07-0255.

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4

Mcleod, Kenneth J., Clinton T. Rubin, Mark W. Otter e Yi-Xian Qin. "Skeletal Cell Stresses and Bone Adaptation". American Journal of the Medical Sciences 316, n. 3 (settembre 1998): 176–83. http://dx.doi.org/10.1016/s0002-9629(15)40398-2.

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5

Wang, Y., e J. M. Winters. "Predictive model for skeletal muscle adaptation". Journal of Biomechanics 39 (gennaio 2006): S43. http://dx.doi.org/10.1016/s0021-9290(06)83047-2.

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6

Burton, H. W., B. M. Carlson e J. A. Faulkner. "Microcirculatory Adaptation to Skeletal Muscle Transplantation". Annual Review of Physiology 49, n. 1 (marzo 1987): 439–51. http://dx.doi.org/10.1146/annurev.ph.49.030187.002255.

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7

Carter, Dennis R., e Tracy E. Orr. "Skeletal development and bone functional adaptation". Journal of Bone and Mineral Research 7, S2 (dicembre 1992): S389—S395. http://dx.doi.org/10.1002/jbmr.5650071405.

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8

Warden, Stuart J. "Extreme Skeletal Adaptation to Mechanical Loading". Journal of Orthopaedic & Sports Physical Therapy 40, n. 3 (marzo 2010): 188. http://dx.doi.org/10.2519/jospt.2010.0404.

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9

McLEOD, KENNETH J., CLINTON T. RUBIN, MARK W. OTTER e YI-XIAN QIN. "Skeletal Cell Stresses and Bone Adaptation". American Journal of the Medical Sciences 316, n. 3 (settembre 1998): 176–83. http://dx.doi.org/10.1097/00000441-199809000-00005.

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10

Yuan, Chong-Xi, Qiang Ji, Qing-Jin Meng, Alan R. Tabrum e Zhe-Xi Luo. "Earliest Evolution of Multituberculate Mammals Revealed by a New Jurassic Fossil". Science 341, n. 6147 (15 agosto 2013): 779–83. http://dx.doi.org/10.1126/science.1237970.

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Multituberculates were successful herbivorous mammals and were more diverse and numerically abundant than any other mammal groups in Mesozoic ecosystems. The clade also developed diverse locomotor adaptations in the Cretaceous and Paleogene. We report a new fossil skeleton from the Late Jurassic of China that belongs to the basalmost multituberculate family. Dental features of this new Jurassic multituberculate show omnivorous adaptation, and its well-preserved skeleton sheds light on ancestral skeletal features of all multituberculates, especially the highly mobile joints of the ankle, crucial for later evolutionary success of multituberculates in the Cretaceous and Paleogene.
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Più fonti

Tesi sul tema "Skeletal Adaptation"

1

Ellman, Rachel. "Skeletal adaptation to reduced mechanical loading". Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/107612.

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Abstract (sommario):
Thesis: Ph. D. in Medical Engineering and Bioastronautics, Harvard-MIT Program in Health Sciences and Technology, 2014.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 126-139).
Bone adapts its mass and architecture in response to its mechanical environment. Yet control of this process by mechanical cues is poorly understood, particularly for unloading. Defining the fundamental mechano-regulation of bone adaptation is critical for the better understanding and mitigation of bone loss in astronauts as well as clinical conditions such as spinal cord injury, stroke, muscular dystrophy, and bed rest. The overall goal of this work was to study skeletal adaptation to varying amounts of reduced loading to help delineate the relationship between mechanical stimuli and skeletal adaptation. We first examined the relative contribution of muscle and gravitational forces to the maintenance of skeletal health in mice, using botulinum toxin (BTX) to induce muscle paralysis and hindlimb unloading to eliminate external loading on the hindlimbs, alone and in combination. BTX led to greater bone loss than hindlimb unloading, while the combination of interventions led to the most detrimental effects overall, suggesting that both muscle and gravitational forces play a role in skeletal maintenance, with greater contributions from muscle forces. We then characterized skeletal adaptation to controlled reductions in mechanical loading of varying degrees employing a novel model that enables long-term exposure of mice to partial weightbearing (PWB). We found that declines in bone mass and architecture were linearly related to the degree of unloading. Even mice bearing 70% of their body weight exhibited significant bone loss, suggesting that the gravity of the moon (0.16 G) and Mars (0.38 G) will not be sufficient to prevent bone loss on future exploration missions. Finally, since bone remodeling is highly site-specific, we used gait analysis and inverse dynamics to determine the mechanical environment during PWB, and then developed a finite element model of the tibia to resolve the local strain-related stimulus proposed to drive changes in bone mass. We found modest correlations between cortical bone architecture at different PWB levels and strain energy density. Altogether this work provides a critical foundation and rationale for future studies that incorporate detailed quantification of the mechanical stimuli and longitudinal changes in bone architecture to further advance our understanding of the skeletal response to reduced loading.
by Rachel Ellman.
Ph. D. in Medical Engineering and Bioastronautics
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2

Eliman, Rachel. "Skeletal adaptation to reduced mechanical loading". Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/95861.

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Abstract (sommario):
Thesis: Ph. D., Harvard-MIT Program in Health Sciences and Technology, 2014.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 126-139).
Bone adapts its mass and architecture in response to its mechanical environment. Yet control of this process by mechanical cues is poorly understood, particularly for unloading. Defining the fundamental mechanoregulation of bone adaptation is critical for the better understanding and mitigation of bone loss in astronauts as well as clinical conditions such as spinal cord injury, stroke, muscular dystrophy, and bed rest. The overall goal of this work was to study skeletal adaptation to varying amounts of reduced loading to help delineate the relationship between mechanical stimuli and skeletal adaptation. We first examined the relative contribution of muscle and gravitational forces to the maintenance of skeletal health in mice, using botulinum toxin (BTX) to induce muscle paralysis and hindlimb unloading to eliminate external loading on the hindlimbs, alone and in combination. BTX led to greater bone loss than hindlimb unloading, while the combination of interventions led to the most detrimental effects overall, suggesting that both muscle and gravitational forces play a role in skeletal maintenance, with greater contributions from muscle forces. We then characterized skeletal adaptation to controlled reductions in mechanical loading of varying degrees employing a novel model that enables long-term exposure of mice to partial weightbearing (PWB). We found that declines in bone mass and architecture were linearly related to the degree of unloading. Even mice bearing 70% of their body weight exhibited significant bone loss, suggesting that the gravity of the moon (0.16 G) and Mars (0.38 G) will not be sufficient to prevent bone loss on future exploration missions. Finally, since bone remodeling is highly site-specific, we used gait analysis and inverse dynamics to determine the mechanical environment during PWB, and then developed a finite element model of the tibia to resolve the local strain-related stimulus proposed to drive changes in bone mass. We found modest correlations between cortical bone architecture at different PWB levels and strain energy density. Altogether this work provides a critical foundation and rationale for future studies that incorporate detailed quantification of the mechanical stimuli and longitudinal changes in bone architecture to further advance our understanding of the skeletal response to reduced loading.
by Rachel Eliman.
Ph. D.
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3

Kohn, Tertius A. "Characteristics and adaptation of skeletal muscle to endurance exercise". Thesis, Stellenbosch : University of Stellenbosch, 2011. http://hdl.handle.net/10019.1/16517.

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Abstract (sommario):
Thesis (PhD)--University of Stellenbosch, 2005.
ENGLISH ABSTRACT: Skeletal muscle adapts to stimuli by modifying structural and metabolic protein expression. Furthermore, a muscle group may vary within itself to accommodate specialisation in regions. Structural and metabolic characteristics of an individual are regulated partly by genotype, but contraction duration and intensity may play a greater role in muscle phenotype. The aims of this dissertation were to investigate: structural and metabolic regionalisation in a muscle group, possible relationships between training volume and intensity and hybrid fibres, muscle characteristics of athletes from two different ethnic groups, and muscle adaptation in already well-trained athletes subjected to high intensity interval training. Myosin heavy chain (MHC) isoform content and citrate synthase (CS) activities were measured in the Quadriceps femoris (QF) muscle of 18 female rats. Muscle was divided into superficial, middle and deep, distal, central and proximal parts. MHC IIb and IIx were more abundant in superficial regions (P < 0.05) with low CS activities compared to deeper parts. Isoform content varied along the length of deep regions. This study showed that the QF has regional specialisation. Therefore, standardisation of sampling site is important. Hybrid fibre proportions in muscle biopsies of 12 middle distance runners and 12 non-runners were investigated. MHC IIa/IIx correlated with training volume/week in runners (r = -0.66, P < 0.05) and MHC IIa/IIx correlated with exercise hours/week in non-runners (r = -0.72, P < 0.01). Average preferred racing distance (PRDA) correlated better with MHC IIa/IIx in runners (r = -0.85, P < 0.001). MHC IIa/IIx may therefore be more closely related to exercise intensity than previously thought. Fibre type characteristics and performance markers were investigated in 13 Xhosa and 13 Caucasian distance runners, matched for performance, training volume and PRDA. Xhosa runners had less MHC I and more MHC IIa fibres in muscle biopsies than Caucasian runners (P < 0.05). Xhosa runners had lower plasma lactate at 80% peak treadmill speed (PTS) (P < 0.05), but higher lactate dehydrogenase (LDH) (P < 0.01) and phosphofructokinase (P = 0.07) activities in homogenate muscle samples. LDH activities in MHC I (P = 0.05) and IIa (P < 0.05) fibre pools were higher in Xhosa runners. Xhosa athletes may thus have a genetic advantage or they may have adapted to running at a higher intensity. Six weeks of individually standardised high intensity interval treadmill training (HIIT) were investigated in 15 well-trained runners. PTS increased after HIIT (P < 0.01), while maximum oxygen consumption (VO2max) only showed a tendency to have increased as a result of HIIT (P = 0.06). Sub-maximal tests showed lower plasma lactate at 64% PTS (P = 0.06), with lower heart rates at workloads from 64% to 80% PTS (P < 0.01) after HIIT. No changes were observed for cross-sectional area, capillary supply and enzyme activities in homogenates muscle samples. LDH activity showed a trend (P = 0.06) to have increased in MHC IIa pools after HIIT. Higher HIIT speed was related to decreases in MHC I fibres, but increases in MHC IIa/IIx fibres (r = -0.70 and r = 0.68, respectively, P < 0.05). Therefore, HIIT may alter muscle fibre composition in well-trained runners, with a concomitant improvement in performance markers.
AFRIKAANSE OPSOMMING: Skeletspier kan adapteer deur strukturele en metaboliese protein ekspressie te verander as gevolg van stimulante. ‘n Spiergroep kan ook intern verskil om spesialisering in spierdele toe te laat. Strukturele en metaboliese karaktereienskappe van ‘n individu word deels gereguleer deur gene, maar kontraksie tydperk en intensiteit mag ‘n groter rol speel in spierfenotipe. Die doelwitte van hierdie tesis was om ondersoek in te stel in: strukturele en metaboliese eienskappe in spiergroepstreke, moontlike verhoudings tussen oefeningsvolume of intensiteit en baster vesels, spier eienskappe in atlete van twee etniese groepe, en spier adaptasie in goed geoefende atlete blootgestel aan hoë intensiteit interval oefening. Miosien swaar ketting (MSK) isovorm inhoud en sitraat sintase (SS) aktiwiteite is gemeet in die Quadriceps femoris (QF) spier van 18 wyfie rotte. Spiere was opgedeel in oppervlakkig, middel en diep, asook distaal, sentraal en proksimale dele. MSK IIb en IIx was meer oorvloedig in oppervlakkige dele (P < 0.05) met lae SS aktiwiteite in vergelyking met dieper dele. Isovorm inhoud het ook verskil oor die lengte van diep dele. Dus bevat die QF gespesialiseerde streke en is die area van monsterneming belangrik. Baster vesel proporsies is ondersoek in spiermonsters van 12 middel afstand hardlopers en 12 niehardlopers. MSK IIa/IIx van hardlopers het met oefeningsvolume/week gekorreleer (r = -0.66, P < 0.05), asook MSK IIa/IIx van nie-hardlopers met oefeningsure/week (r = -0.72, P < 0.01). Gemiddelde voorkeur wedloop afstand (VWAG) het beter met MSK IIa/IIx gekorreleer in hardlopers (r = -0.85, P < 0.001). MSK IIa/IIx mag dus meer verwant wees aan oefeningsintensiteit. Veseltipe eienskappe en prestasie merkers was ondersoek in 13 Xhosa en 13 Caucasian langafstand atlete, geëweknie vir prestasie, oefeningsvolume en VMAG. Xhosa hardlopers het minder tipe I en meer tipe IIA vesels in hul spiermonsters gehad as die Caucasian hardlopers (P < 0.05). Xhosa hardlopers het laer plasma laktaat by 80% van hul maksimale trapmeul spoed (MTS) (P < 0.05), maar hoër laktaat dihidrogenase (LDH) (P < 0.01) en fosfofruktokinase (P = 0.07) aktiwiteite in homogene spiermonsters gehad. LDH aktiwiteite in MSK I (P = 0.05) en IIa (P < 0.05) veselbondels was hoër in Xhosa hardlopers. Xhosa atlete mag dus ‘n genetiese voorsprong geniet, of hulle het geadapteer om by hoër intensiteite te hardloop. Ses weke van geïndividualiseerde gestandardiseerde hoë intensiteit interval trapmeul oefening (HIIT) was ondersoek in 15 goed geoefende hardlopers. MTS het verhoog na HIIT (P < 0.01), en maksimale surrstof verbruik (VO2max) het ‘n neiging getoon om te verhoog het na HIIT (P = 0.07). Submaksimale toetse het laer plasma laktaat by 64% MTS getoon (P = 0.06), met laer harttempos by werkladings 64% tot 80% MTS (P < 0.01). Geen veranderings was gemerk vir deursnit area, kapillêre toevoer en ensiem aktiwiteite in homogene spiermonsters nie. LDH aktiwiteit het ‘n neiging getoon om te verhoog het (P = 0.06) in MSK IIa veselbondels na HIIT. Hoër HIIT snelhede was verwant aan ‘n daling in MSK I vesels, maar ‘n verhoging in MSK IIa/IIx vesels (r = -0.70 en r = 0.68, respektiwelik, P < 0.05). HIIT mag dus spier veseltipe verander in goed geoefende hardlopers, met gevolglike verbetering in prestasie merkers.
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4

Beckitt, Timothy. "Skeletal muscle adaptation following a supervised exercise programme for claudication". Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539766.

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5

Wiebe, Peter N., e res cand@acu edu au. "Effects of Different Loading Intensities on Skeletal Adaptation to Exercise in Prepubertal Girls". Australian Catholic University. School of Exercise Science, 2004. http://dlibrary.acu.edu.au/digitaltheses/public/adt-acuvp62.29082005.

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Abstract (sommario):
This study involved a 28-week school-based exercise trial of single-leg drop-landing exercise with 42 girls (Tanner stage 1; 6-10 yr old) randomly assigned to control (C), low-drop (LD) or high-drop(HD) exercise groups. The latter two groups performed single-leg drop-landings (3 sessions.wk-1 and 50 landings.session-1) from 14cm and 28cm, respectively using the non-dominant leg. Single-leg peak ground-reaction impact forces (PGRIF) in a sub-sample ranged between 2.5 – 4.4 x body-weight (BW). No differences (p>0.05) among groups at baseline for age, stature, lean tissue mass (LTM - DXA - Lunar 3.6-DPX), leisure time physical activity or average daily calcium intake were detected. No significant within group changes for between leg differences from baseline to post-training and no significant differences among groups at baseline, or in magnitude of change for any of the dominant or non-dominant (loaded) leg bone mineral content (BMC g) measures determined by DXA – loaded leg total - 19.06, 25.5, 25.46 [p=.156], femoral neck - 0.14, 0.11, 0.15 [p=.959], greater trochanter - 0.37, 0.06, 0.26 [p=.733], mid femoral shaft - 3.87, 3.87, 3.42 [p=.677] for the C, LD and HD groups, respectively, after adjusting for the covariates baseline body and fat mass, and change in LTM (ANCOVA) were observed. Similarly, following ANCOVA adjustments no significant differences for changes in calcaneal speed of sound and broadband ultrasound attenuation (CUBA Clinical), DXA derived changes in femoral neck (-0.009, 0.033, -0.009; p=.189) and total MFS (0.029, 0.041, 0.053; p=.447) volumetric BMD (g.cm-3), or MFS cortical volumetric BMD, the latter derived by a new technique combining MRI and DXA were identified. TBBMC changed by 79.6g-C, 100.2g-LD and 91.9g-HD (p=.339). Combining data from both exercise groups to increase statistical power produced similar results. No significant within group changes for between leg differences from baseline to post-training and no significant differences among groups at baseline, or in magnitude of change for any of the dominant or non-dominant (loaded) leg bone geometrical (area cm2) determined by MRI using ANALYZE® software of proximal - 22.18, 12.91, 19.86 [p=.248], mid - 19.83, 15.91, 19.64 [p=.233], or distal - 14.78, 16.07, 13.35 [p=.792], slice cortical area for the C, LD and HD groups, respectively, after adjusting for the covariates baseline body and fat mass, and change in LTM (ANCOVA) were detected. Similarly there were no significant biomechanical cross sectional moment of inertia (CSMI cm4) changes determined by Scion Image® (Frederick, Maryland: Version-Beta 3B) and a custom macro program of proximal - 896, 815, 649 [p=.415], mid - 1054, 806, 1087 [p=.471], or distal - 1197, 1079, 966 [p=.606], slice CSMI for the C, LD and HD groups, respectively after adjusting for the same covariates. In contrast to some recent reports, our findings suggest that strictly controlled uni-modal; uni-directional single-leg drop-landing exercises involving low-moderate peak ground-reaction impact forces are not osteogenic in the developing prepubertal female skeleton.
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Hirschberg, Jens. "Simulations of mechanical adaptation and their relationship to stress bearing in skeletal tissue". University of Western Australia. School of Anatomy and Human Biology, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0095.

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Abstract (sommario):
[Truncated abstract] In this work a computer simulation program, similar to a finite element program, is used to study the relationship between skeletal tissue structure and function. Though other factors affect the shape of bone (e.g., genetics, hormones, blood supply), the skeleton adapts its shape mainly in response to the mechanical environment to which it is exposed throughout life. The specific relationship between the mechanical environment and the mechanical adaptation response of the skeleton is reviewed. Theories of mechanical adaptation are applied to the sites of tendon attachment to bone (entheses), the adaptation of generalised trabecular bone (i.e., Wolff’s Law of trabecular architecture), sesamoid bones that are often found where a tendon wraps around a bony pulley, and the internal trabecular structure of a whole bony sesamoid such as the patella. The relative importance of compression rather than tension in bone adaptation theories is still not fully understood. Some mechanical adaptation theories suggest that an overwhelming tensile stress at a skeletal location does not stimulate bone deposition, but would instead lead to bone resorption. The skeletal locations studied in this work were chosen because they have been proposed to be in tension. Computer simulations involving models are an ideal method to analyse the mechanical environment of a skeletal location. They are able to determine the mechanical stresses at, and the stress patterns around, complex biological situations. This study uses a two dimensional computer simulation program, Fast Lagrangian Analysis of Continua (Flac), to analyse the stress at the skeletal locations, and to test theories of mechanical adaptation over time by simulating physiological adaptation. The initial purpose of this study is to examine the stress in the skeletal tissue in generalised trabeculae, anatomical sites where a tendon wraps around a bony pulley, in the trabecular networks that fill the patella, and at tendon attachments. A secondary purpose, that follows directly from the first, is to relate the results of these initial stress analyses to existing and hypothetical skeletal tissue remodelling theories, to suggest how the complex skeletal structures might be generated solely in response to their mechanical environment. The term “remodelling” is used throughout this work to refer to mechanical adaptation of bone, usually at a surface of bone, rather than the internal regeneration of osteons (Haversion systems)
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Chen, Ting. "LKB1 Regulation of High-Fat Diet-induced Adaptation in Mouse Skeletal Muscle". BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6682.

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Abstract (sommario):
Ad libitum high-fat diet (HFD)-induced obesity leads to insulin resistance in skeletal muscle, altered gene expression, and altered growth signaling, all of which contributes to pathological changes in metabolism. Liver kinase B1 (LKB1) is an important metabolism regulator. The purpose of this dissertation was to understand how knocking out LKB1 influences HFD induced adaptations in mouse skeletal muscle. To do so, control and skeletal muscle LKB1 knock-out (LKB1-KO) mice were put on either standard diet (STD) or HFD for 1 week or 14 weeks, or put on the HFD for 14 weeks and then switched to STD for 1 week (switched diet). The major differences in adaptation in the LKB1-KO mice include: 1) lower fasting blood glucose levels but impaired glucose tolerance compared to WT mice (although conflicting results are generated if the data is not normalized to fasting blood glucose levels), 2) altered expression of 16 HFD-induced genes, and 3) decreased muscle weight. The lower fasting blood glucose in LKB1-KO mice was likely due to elevated serum insulin levels, and the impaired glucose tolerance was associated with decreased phosphorylation of TBC1D1, an important regulator of insulin stimulated glucose uptake. 16 potential important target genes (metabolism, mitochondrial, cytoskeleton, cell cycle, cell-cell interactions, enzyme, ion channel) were identified in the context of HFD feeding and LKB1-KO. These genes were quantified by RT-PCR and grouped according to changes in their patterns of expression among the different groups. Among several other interesting changes in gene expression, the muscle growth-related protein, Ky was not affected by short-term HFD, but increased after long-term HFD, and did not decrease after switched diet, showing that its expression may be an important long-term adaptation to HFD. LKB1-KO promoted anabolic signaling through increasing t-eIF2α and eIF4E expression, and promoted protein degradation through increasing protein ubiquitination. Because the degradation is the main effect and lead to muscle weight decrease. The effect of HFD and/or LKB1-KO on the LKB1-AMPK system was also determined. The results showed that knocking-out LKB1 decreased AMPK activity, decreased nuclear distribution for AMPK α2 and increased AMPK α1 expression. Long-term HFD increased t-AMPK expression in LKB1-KO mice, decreased the cytoplasm p-AMPK and nuclear p/t-AMPK ratio in CON mice. Together the findings of this dissertation demonstrated HFD induced glucose/insulin tolerance, while LKB1-KO had a controversial effect on glucose/insulin sensitivity. Both HFD and LKB1-KO affect AMPK expression and cellular location, while LKB1-KO also affects AMPK activity. LKB1-KO promoted protein degradation through ubiquitination in skeletal muscle.
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Isaacs, Ashwin Wayne. "Muscle damage and adaptation in response to plyometric jumping". Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/20384.

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Abstract (sommario):
Thesis (MSc)--Stellenbosch University, 2012.
ENGLISH ABSTRACT: The aim of the study was to investigate skeletal muscle changes induced by an acute bout of plyometric exercise before and after plyometric training. The study consisted of an acute study and training intervention study. The acute study, investigated whether direct evidence of ultrastructural damage and identification of indirect factors were more evident in subjects presenting with rhabdomyolysis. Moreover the training intervention study investigated whether plyometric training would protect the muscle from ultrastructural damage and rhabdomyolysis. During the acute intervention, twenty six healthy untrained individuals completed an acute bout of plyometric exercise (10 x 10 squat-jumps, 1 min rest). After, thirteen subjects continued with the training intervention. Eight of these subjects completed 8 weeks of plyometric jump training, while five subjects were instructed to rest from physical activity for 8 weeks. Seven days after the final training session the training and rest group repeated a second acute bout of plyometric exercise. Acute Study: Creatine kinase (CK) activity increased significantly following the single bout of plyometric exercise in all subjects (baseline: 129 to day 4: 5348 U/l). This was accompanied by an increase in perceived pain, C-reactive protein (CRP) a marker of inflammation as well as white blood cells (WBCs). Electron micrographs of muscle biopsies taken 3 days post exercise showed evidence of ultrasructural damage and membrane damage was apparent by immunofluorescence by the loss of dystrophin staining. A stretch of the c-terminus of titin was observed by immunogold, and western blot analysis indicated an increase in calpain-3 autolysis. Based on individual CK responses (CK range: 153-71,024 U/L at 4days after exercise) the twenty six subjects were divided into two groups, namely the high (n=10) and low responders (n=16). Training intervention: Following training the trained group did not experience: a rise of CK activity (110.0 U/l), perceived pain, CRP, WBCs, Z-line streaming, a stretch of titin or calpain-3 activation; while in the control group only two subjects presented with Z-line streaming. The results indicate that high responders have a more pronounced inflammatory response compared to low responders after eccentric exercise, therefore more WBCs and more specifically neutrophils are recruited to damaged areas resulting in greater membrane damage by respiratory burst in high responders. This damage can be limited with training by remodelling sarcomeric proteins via calpain activation resulting in the stable assembly of proteins in the sarcomere preventing the release of proteins.
AFRIKAANSE OPSOMMING: Die doel van die studie was om skeletspier veranderinge wat teweeggebring is deur voor en na afloop van akute pleometriese oefening, te ondersoek. Die studie bestaan uit ‘n akute intervensie en ‘n oefeningsintervensie gedeelte. Die akute intervensie het ondersoek ingestel na die direkte bewyse van ultrastrukturele skade en identifikasie van indirekte faktore meer sigbaar is in proefpersone wat met rhabdomiolose presenteer. Meerso het die oefningsintervensie die moontlikheid dat pleometriese oefening die spier van ultrastrukturele skade en rhabdomiolose beskerm, ondersoek. Tydens die akute intervensie is 26 gesonde ongeoefende individue die akute pleometriese oefeningsessie (10 x 10 hurkspronge, 1 min rus) voltooi. Hierna het 13 proefpersone voortgegaan met die oefeningsintervensie. Agt van hierdie proefpersone het agt weke pleometriese sprongsessie oefeninge voltooi, terwyl vyf proefpersone gevra is om vir 8 weke geen oefeninge te doen nie. Sewe dae na afloop van die finale oefeningssessie het die oefening en kontrole groep in ‘n tweede herhaalde akute pleometriese oefeningsessie deelgeneem. Akute intervensie: kreatienkinase (KK) aktiwiteit het betekenisvol verhoog na die enkel pleometriese oefeningsessie in all proefpersone (basislyn: 129 tot op dag vier: 5348 U/l). Hierdie is vergesel met ‘n toename in die persepsie van pyn, c-reaktiewe proteïen (CRP) ‘n merker van inflammasie sowel as witbloedselle (WBS). Elektronmikrograwe van spierbiopsies wat geneem is drie dae na afloop van die oefeninge, het tekens van ultrastrukturele skade en membraanskade getoon wat ook deur immunofluoresensie duidelik warneembaar was deur die verlies van distrofienverkleuring. ‘n Verrekking van die c-terminus van titin is ook waargeneem deur middel van immunogold. Westernblot analyse het ‘n toename in calpain-3 outolise getoon. Gegrond op individuele KK response (KK grense: 153-71,024 U/L na vier dae post oefening) is 26 proefpersone verdeel in twee groepe naamlik ‘n hoë (n=10) en lae responders (n=16). Oefeningintervensie:: Na oefening het die geoefende groep nie ‘n toename in KK aktiwiteit getoon nie (KK aktiwiteit (110.0 U/l)), pynervaring, CRP, WBS, Z-lynstroming, ‘n strekking van titin of calpain-3 aktivering; terwyl in die kontrole groep daar slegs twee proefpersone met Z-lynstroming geïdentifiseer is. Die resultate wyse daarop dat hoë responders ‘n meer uitgesproke inflammatoriese reaksie toon vergeleke met die lae responders na afloop van essentriese oefening. Daar word dus meer WBS en spesifiek meer neutrofiele na beskadigde areas gelokaliseer wat in grootter membraanskade deur respiratoriese inspanning in die hoë responders. Hierdie skade kan beperk word deur oefening waardeur hermodulering van sarkomeriese proteïene via calpain aktivering tot stabiele rangskiking van proteïene in die sarcomere lei en daardeur proteïen vrystelling verhinder.
The NRF for financial assistance
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9

Owino, Dorcas Vivian Apiyo. "Evaluation of role of paracrine/autocrine IGF-1 system in skeletal muscle adaptation". Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406510.

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10

Varley, I. "Association of genotype with bone metabolism, skeletal adaptation and stress fracture injury occurrence". Thesis, Nottingham Trent University, 2014. http://irep.ntu.ac.uk/id/eprint/223/.

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Abstract (sommario):
Positive changes in bone metabolism, structural characteristics, size and mass are commonly associated with weight-bearing exercise. Despite this, negative effects of exercise on bone phenotypes, such as stress fracture injuries have been reported. Little is known about the extent of the genetic mediation of changes in bone characteristics, stress fracture injury and bone resorption in response to exercise. Accordingly, this thesis investigated: the genotype dependent changes in bone phenotypes in academy footballers before and after an increase in training volume; genetic associations with stress fracture injury in elite athletes and a preliminary investigation into genetic associations with bone resorption following 120 min of treadmill running. The tibial bone characteristics of 80, full-time academy footballers was determined using pQCT before and after 12 weeks of increased volume football training. Genetic associations with baseline, post increased training and change in bone characteristics were then determined. Secondly, radiologically confirmed stress fracture history was reported in 518 elite athletes, forming the Stress Fracture Elite Athlete (SFEA) cohort. Genetic associations were analysed for the whole group, and were also sub-stratified. Finally, recreationally active healthy male participants (n=42) performed a 120 min run at 70% O2max. Genetic associations with bone resorption at baseline, immediately, 24, 48 and 72 hours post run were investigated. SNPs in the proximity of genes in P2X7R and the RANK/RANKL/OPG signalling and Wnt signalling pathways were associated with bone phenotypes before and following 12 weeks of increased volume football training (P<0.05). SNPs in close proximity to SOST, P2X7R, RANK, RANKL, OPG, Bradykinin and VDR genes were associated with stress fracture injury in the whole cohort and in various sub-classifications of elite athletes (P<0.05). No associations were shown in bone resorption prior to, immediately following or in the 3 days following 120 min of treadmill running. The data suggest a role for specific genes and SNPs in bone phenotypic changes as a result of exercise training and in the susceptibility to stress fracture injury. The association of SNPs in P2X7R and the RANK/RANKL/OPG signalling and Wnt signalling pathways with bone phenotypes and stress fracture injury susceptibility highlights their role in the maintenance of bone health, and offers potential targets for therapeutic interventions.
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Libri sul tema "Skeletal Adaptation"

1

Ruff, Christopher B., a cura di. Skeletal Variation and Adaptation in Europeans. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781118628430.

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MacPherson, Laura Lynn. Adaptations of skeletal muscle pyruvate dehydrogenase kinase in response to food-restriction in mitochondrial subpopulations. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2007.

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3

Mechanobiology: Osteoarthritis and Skeletal Regeneration, and Osteoporosis and Bone Functional Adaptation. Diane Pub Co, 2000.

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4

Ruff, Christopher B. Skeletal Variation and Adaptation in Europeans: Upper Paleolithic to the Twentieth Century. Wiley & Sons, Incorporated, John, 2017.

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Skeletal Variation and Adaptation in Europeans: Upper Paleolithic to the Twentieth Century. Wiley-Blackwell, 2018.

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Ruff, Christopher B. Skeletal Variation and Adaptation in Europeans: Upper Paleolithic to the Twentieth Century. Wiley & Sons, Incorporated, John, 2017.

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7

Adaptation of skeletal muscle to spaceflight: COSMOS Rhesus project, COSMOS 2044 and 2229 : final report. [Washington, DC: National Aeronautics and Space Administration, 1994.

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8

(Editor), Neil Spurway, e Henning Wackerhage (Editor), a cura di. Genetics and Molecular Biology of Muscle Adaptation (Advances in Sport and Exercise Science). Churchill Livingstone, 2006.

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9

Skeletal muscle and hepatic enzyme adaptation to physical training under beta-adrenergic blockade in the rat. 1985.

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Skeletal muscle and hepatic enzyme adaptation to physical training under beta-adrenergic blockade in the rat. 1987.

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Capitoli di libri sul tema "Skeletal Adaptation"

1

Ruff, Christopher B. "Quantifying Skeletal Robusticity". In Skeletal Variation and Adaptation in Europeans, 39–47. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118628430.ch3.

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Ruff, Christopher B. "Introduction". In Skeletal Variation and Adaptation in Europeans, 1–13. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118628430.ch1.

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Ruff, Christopher B., e Heather Garvin. "Iberia". In Skeletal Variation and Adaptation in Europeans, 281–314. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118628430.ch10.

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Sládek, Vladimír, Margit Berner, Eliška Makajevová, Petr Velemínský, Martin Hora e Christopher B. Ruff. "Central Europe". In Skeletal Variation and Adaptation in Europeans, 315–54. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118628430.ch11.

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Niskanen, Markku, Heli Maijanen, Juho-Antti Junno, Sirpa Niinimäki, Anna-Kaisa Salmi, Rosa Vilkama, Tiina Väre, Kati Salo, Anna Kjellström e Petra Molnar. "Scandinavia and Finland". In Skeletal Variation and Adaptation in Europeans, 355–96. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118628430.ch12.

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Ruff, Christopher B., e Brigitte Holt. "The Balkans". In Skeletal Variation and Adaptation in Europeans, 397–418. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118628430.ch13.

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Ruff, Christopher B., Brigitte Holt, Markku Niskanen, Vladimir Sládek e Margit Berner. "Conclusions". In Skeletal Variation and Adaptation in Europeans, 419–26. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118628430.ch14.

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Niskanen, Markku, e Christopher B. Ruff. "Body Size and Shape Reconstruction". In Skeletal Variation and Adaptation in Europeans, 15–37. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118628430.ch2.

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Niskanen, Markku, Christopher B. Ruff, Brigitte Holt, Vladimir Sládek e Margit Berner. "Temporal and Geographic Variation in Body Size and Shape of Europeans from the Late Pleistocene to Recent Times". In Skeletal Variation and Adaptation in Europeans, 49–89. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118628430.ch4.

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Holt, Brigitte, Erin Whittey, Markku Niskanen, Vladimir Sládek, Margit Berner e Christopher B. Ruff. "Temporal and Geographic Variation in Robusticity". In Skeletal Variation and Adaptation in Europeans, 91–132. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118628430.ch5.

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Atti di convegni sul tema "Skeletal Adaptation"

1

Qin, Yi-Xian, Hoyan Lam e Murtaza Malbari. "The Effects of Loading Rate and Duration on Mitigation of Osteopenia by Dynamic Muscle Stimulation". In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206685.

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Abstract (sommario):
Musculoskeletal adaptations to aging and disuse environment have significant physiological effects on skeletal health, i.e., osteopenia and bone loss. Osteoporosis often occurs together with muscle loss. Such musculoskeletal complications cause severe physiologic changes and have been proposed the synergistic effects of muscle function and bone adaptation. The role of mechanobiology in the skeletal tissue may be closely related to load-induced transductive signals, e.g., bone fluid flow, which is proposed to be a critical mediator of bone and muscle adaptation. The skeletal muscle may serve as a muscle pump that may mediate bone mechanotransduction via modulation of intramedullary pressure. Muscular stimulation (MS) is proposed to be used to simultaneously treat both muscle and bone loss. Indeed, our recent data have demonstrated that high frequency, short duration stimulation can inhibit bone loss and muscle atrophy. Although 10 min dynamic loading can effectively attenuate bone loss, it cannot totally recover disuse osteopenia. The optimal parameters required for such treatment are unclear. Studies have separately investigated the optimal signal parameters for bone or muscle. Insertion of recovery periods during high frequency stimulations to extend the loading cycles have shown potential to reduce muscle atrophy by minimizing fatigue and mimicking physiologic contractions, and demonstrated enhancement of bone remodeling. The overall hypothesis for this study is that dynamic MS can enhance anabolic activity in bone, and inhibit bone loss in a functional disuse condition. Combined high frequency and sufficient loading cycle may be able to completely mitigate bone loss induced by disuse osteopenia.
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2

Qin, Yi-Xian, e Hoyan Lam. "Bone Formation and Inhibition of Bone Loss by Dynamic Muscle Stimulation With Altered Interstitial Fluid Pressure". In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176607.

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Abstract (sommario):
Tissue-level mechanisms and functions, including bone strain and muscle, are the potential key players in bone physiology and adaptation [1,2,3]. However, the mechanisms are not yet fully understood. Exercise such as muscle contraction appears to increase blood flow to the skeletal tissues, i.e., bone and muscle. These evidences imply that bone fluid flow induced by muscle dynamics may be an important role in regulating fluid flow through coupling of muscle and bone via microvascular system.
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3

Ali, Adiba, e Yi-Xian Qin. "Inhibition of Bone Loss and Muscle Atrophy by Dynamic Muscle Contractions With Rest Periods in a Functional Disuse Mouse Model". In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193066.

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Abstract (sommario):
Osteoporosis, induced by aging and long-term disuse, often occurs together with muscle loss. Musculoskeletal disuse causes severe physiologic changes and it has been proposed the synergistic effects of muscle function and bone adaptation. Bone fluid flow has been shown to be induced during mechanical loading, and is proposed to be a critical mediator of bone adaptation. The skeletal muscle may serve as a muscle pump that may mediate bone mechanotransduction via modulation of intramedullary pressure. Thus, muscular stimulation is proposed to be used to simultaneously treat both muscle and bone loss, but the optimal parameters required for such treatment is unclear. Studies have separately investigated the optimal signal parameters for bone or muscle. Insertion of recovery periods during high frequency stimulations have shown potential to reduce muscle atrophy by minimizing fatigue and mimicking physiologic contractions, and demonstrated enhancement of bone remodeling. Our preliminary research has indicated that dynamic muscle contractions within an optimal frequency range can significantly recover disuse induced bone loss. However, the optimal rest periods required to prevent muscle fatigue during stimulations are not clear. The overall objective of this study was to evaluate optimized dynamic muscle stimulations at relatively high frequency, e.g., 20 Hz, and to test the role of varying the rest duration on muscle mass and bone morphology in a functional hind limb disuse mouse model.
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Taylor, Rebecca E., Chunhua Zheng, Ryan P. Jackson, Joey C. Doll, Julia Chen, Katherine R. S. Holzbaur, Thor Besier e Ellen Kuhl. "Critical Loading During Serve: Modeling Stress-Induced Bone Growth in Performance Tennis Players". In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192005.

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Abstract (sommario):
On September 27, 2004 Andy Roddick hit the current world record 155 mph serve in his Davis Cup match against Belarus, which set him up with three match points against Vladimir Voltchkov. By that time, at 22 years of age, Roddick had broken his own speed record for the third time. In tennis, like in almost all other high performance sports, professional athletes tend to reach their peak performance at a much younger age than they used to several decades ago. Accordingly, athletes have to start full-time practice in their early childhood that strongly overlaps with the period of skeletal and muscular development. It is the responsibility of their coaches and physicians to design efficient training programs targeted at maximal performance and minimal risk of injury. Biomechanics can play a crucial role in supporting the design of these training strategies. By predicting the functional adaptation of bones and muscles, biomechanics simulation can help to explain and eventually prevent common forms of injuries caused by chronic overuse.
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Bonivtch, Amber Rath, Lynda F. Bonewald e Daniel P. Nicolella. "Tissue Strain Transduction and Amplification at the Osteocyte as a Result of Microstructural Changes in the Bone Matrix". In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176139.

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Abstract (sommario):
It is well known that bone adapts to changes in its mechanical environment and that this adaptation is controlled at the cellular level through the coordinated actions of osteoblasts, osteocytes, and osteoclasts. Osteocytes make up over 90% of all bone cells [1], and are hypothesized to be the mechanosensors in bone [2] that mediate the effects of bone loading through their extensive communication network. The application of force to the skeletal system produces several potential stimuli for osteocyte function including hydrostatic pressure, fluid flow-induced shear stress, and bone tissue strain. Previously, the basis used for studying the stimulatory effects of mechanical strain on bone cell biological responses in vitro has been the direct measurement of bone strain in humans during various physical activities [3,4]. The limitation of applying this strain magnitude data to cells in vitro, however, is that the in vivo strain gage measurements represent continuum measures of bone deformation. Clearly, at the spatial level of bone cells, cortical bone is not a continuum and microstructural inhomogeneities will result in inhomogeneous microstructural strain fields; local tissue strains will be magnified in association with microstructural features [5,6]. It is unclear as to how much of these magnified strains will be directly transmitted to the osteocyte itself. Additionally, if the osteocyte has the ability to alter its perilacunar environment [7], it is unknown what effect do these changes have on the strain that is transmitted to the osteocyte and cell process.
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Hu, M., J. Cheng, S. Ferreri, F. Serra-Hsu, W. Lin e Y. X. Qin. "Induced Intramedullary Pressure by Dynamic Hydraulic Stimulation and Its Potential in Attenuation of Bone Loss". In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-54015.

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Bone loss is a critical health problem of astronauts in long-term space missions. A growing number of evidence has pointed out bone fluid flow as a critical regulator in mechanotransductive signaling and bone adaptation. Intramedullary pressure (ImP) is a key mediator for bone fluid flow initiation and it influences the osteogenic signals within the skeleton. The potential ImP-induced bone fluid flow then triggers bone adaptation [1]. Previous in vivo study has demonstrated that ImP induced by oscillatory electrical stimulations can effectively mitigate disuse osteopenia in a frequency-dependent manner in a disuse rat model [2, 3]. In order to develop the translational potentials of ImP, a non-invasive intervention with direct fluid flow coupling is necessary to develop new treatments for microgravity-induced osteopenia/osteoporosis.
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Qin, Y. X., M. Hu, F. Serra-Hsu, J. Cheng, S. Ferreri, Y. Huang, Z. K. Zhang, L. Lin e D. Evangelista. "Local and Distant Intramedullary Pressure and Bone Strain by Dynamic Hydraulic Stimulation". In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-54017.

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Abstract (sommario):
Osteoporosis gives rise to fragile bones that have higher fracture risks due to diminished bone mass and altered bone microarchitecture [1]. Mechanical loading mediated bone adaptation has demonstrated promising potentials as a non-pharmacological alteration for both osteogenic response and attenuation of osteopenia [2]. Intramedullary pressure (ImP) has been proposed as a key factor for fluid flow initiation and mechanotransductive signal inductions in bone. It is also suggested that integration of strain signals over time allows low-level mechanical strain in the skeleton to trigger osteogenic activities. The potential bone fluid flow induced by strain and ImP mediates adaptive responses in the skeleton [3]. Previous in vivo studies using oscillatory electrical stimulations showed that dynamic muscle contractions can generate ImP and bone strain to mitigate disuse osteopenia in a frequency-dependent manner. To apply ImP alteration as a means for bone fluid flow regulation, it may be necessary to develop a new method that could couple external loading with internal bone fluid flow. In order to further study the direct effect of ImP on bone adaptation, it was hypothesized that external dynamic hydraulic stimulation (DHS) can generate ImP with minimal strain in a frequency-dependent manner. The aim of this study was to evaluate the immediate effects on local and distant ImP and bone strain induced by a novel, non-invasive dynamic external pressure stimulus in response to a range of loading frequencies.
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Klinder, Tobias, Hannes Wendland, Irina Wachter-Stehle, David Roundhill e Cristian Lorenz. "Adaptation of an articulated fetal skeleton model to three-dimensional fetal image data". In SPIE Medical Imaging, a cura di Sébastien Ourselin e Martin A. Styner. SPIE, 2015. http://dx.doi.org/10.1117/12.2081139.

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Rapporti di organizzazioni sul tema "Skeletal Adaptation"

1

Turner, Russel. Bone-97 Alcohol and Skeletal Adaptation to Mechanical Usage. Fort Belvoir, VA: Defense Technical Information Center, ottobre 2002. http://dx.doi.org/10.21236/ada415959.

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