THE ROLE OF PEAK LOAD MAGNITUDE AND LOADING HISTORY ON BONE ADAPTATION IN HUMAN FOREARM

2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S82
Author(s):  
M-Y Wang ◽  
G Salem
2020 ◽  
Vol 68 (4) ◽  
Author(s):  
Jingchun Lyu ◽  
Novaf Özgün ◽  
David J. Kondziela ◽  
Roland Bennewitz

AbstractFriction of textiles on the human forearm is an important factor in comfort sensations of garments. We built an experiment to measure friction for textiles sliding on the forearm under loading conditions which are characteristic for wearing shirts or jackets. The hair coverage of the participants’ forearm was quantified by image analysis of photographs of the arm in the region of contact. Friction results for five standard textiles suggest to treat hair coverage in two classes. Sweating after physical activity leads to an increase of friction by factors of 2 to 5 for participants with less hairy forearms, while an increase by a factor of 1 to 1.7 only was found for participants with more hairy forearms. We introduce a method of wetting the forearm of study participants in a controlled way with water, which results in similar friction as for the sweating forearm after physical activity. The method allows for efficient studies of the role of skin moisture for friction including varying hair coverage of the skin.


1997 ◽  
Vol 92 (2) ◽  
pp. 123-131 ◽  
Author(s):  
Masanari Shiramoto ◽  
Tsutomu Imaizumi ◽  
Yoshitaka Hirooka ◽  
Toyonari Endo ◽  
Takashi Namba ◽  
...  

1. It has been shown in animals that substance P as well as acetylcholine releases endothelium-derived nitric oxide and evokes vasodilatation and that ATP-induced vasodilatation is partially mediated by nitric oxide. The aim of this study was to examine whether vasodilator effects of substance P and ATP are mediated by nitric oxide in humans. 2. In healthy volunteers (n = 35), we measured forearm blood flow by a strain-gauge plethysmograph while infusing graded doses of acetylcholine, substance P, ATP or sodium nitroprusside into the brachial artery before and after infusion of NG-monomethyl-l-arginine (4 or 8 μmol/min for 5 min). In addition, we measured forearm blood flow while infusing substance P before and during infusion of l-arginine (10 mg/min, simultaneously), or before and 1 h after oral administration of indomethacin (75 mg). 3. Acetylcholine, substance P, ATP or sodium nitroprusside increased forearm blood flow in a dose-dependent manner. NG-Monomethyl-l-arginine decreased basal forearm blood flow and inhibited acetylcholine-induced vasodilatation but did not affect substance P-, ATP-, or sodium nitroprusside-induced vasodilatation. Neither supplementation of l-arginine nor pretreatment with indomethacin affected substance P-induced vasodilatation. 4. Our results suggest that, in the human forearm vessels, substance P-induced vasodilatation may not be mediated by either nitric oxide or prostaglandins and that ATP-induced vasodilatation may also not be mediated by nitric oxide.


2006 ◽  
Vol 3 (2) ◽  
pp. 10-16 ◽  
Author(s):  
Jan G Hazenberg ◽  
Thomas C Lee ◽  
David Taylor
Keyword(s):  

2003 ◽  
Vol 284 (2) ◽  
pp. H711-H718 ◽  
Author(s):  
H. M. Omar Farouque ◽  
Ian T. Meredith

The extent to which ATP-sensitive K+ channels contribute to reactive hyperemia in humans is unresolved. We examined the role of ATP-sensitive K+channels in regulating reactive hyperemia induced by 5 min of forearm ischemia. Thirty-one healthy subjects had forearm blood flow measured with venous occlusion plethysmography. Reactive hyperemia could be reproducibly induced ( n = 9). The contribution of vascular ATP-sensitive K+ channels to reactive hyperemia was determined by measuring forearm blood flow before and during brachial artery infusion of glibenclamide, an ATP-sensitive K+ channel inhibitor ( n = 12). To document ATP-sensitive K+ channel inhibition with glibenclamide, coinfusion with diazoxide, an ATP-sensitive K+ channel opener, was undertaken ( n = 10). Glibenclamide did not significantly alter resting forearm blood flow or the initial and sustained phases of reactive hyperemia. However, glibenclamide attenuated the hyperemic response induced by diazoxide. These data suggest that ATP-sensitive K+ channels do not play an important role in controlling forearm reactive hyperemia and that other mechanisms are active in this adaptive response.


2014 ◽  
Vol 624 ◽  
pp. 502-509 ◽  
Author(s):  
Ismael Basilio ◽  
Roberto Fedele ◽  
Paulo B. Lourenço ◽  
Gabriele Milani

In this contribution, original limit analysis numerical results are presented dealing with some reinforced masonry arches tested at the University of Minho-UMinho, PT. Twelve in-scale circular masonry arches were considered, reinforced in various ways at the intrados or at the extrados. GFRP reinforcements were applied either on undamaged or on previously damaged elements, in order to assess the role of external reinforcements even in repairing interventions. The experimental results were critically discussed at the light of limit analysis predictions, based on a 3D FE heterogeneous upper bound approach. Satisfactory agreement was found between experimental evidences and the numerical results, in terms of failure mechanisms and peak load.


2002 ◽  
Vol 124 (3) ◽  
pp. 322-327 ◽  
Author(s):  
S. Ramtani ◽  
M. Zidi

In this work an extension of the adaptive-elasticity theory is proposed in order to include the contribution of bone microdamage as a stimulus. Some aspects of damaged-bone tissue adaptation, brought about by a change of the daily loading history, are investigated. In particular, under the assumption of a small strain approximation and isothermal conditions, the solution of the remodeling rate equation for steady homogeneous stress is discussed and the damage effect upon the remodeling time constant is shown. The result is both theoretical and numerical, based on a recent theory of internal damaged-bone remodeling (Ramtani, S., and Zidi, M., 1999, “Damaged-Bone Remodeling Theory: Thermodynamical Approach,” Mechanics Research Communications, Vol. 26, pp. 701–708. Ramtani, S., and Zidi, M., 2001, “A Theoretical Model of the Effect of Continum Damage on a Bone Adaption Model,” Journal of Biomechanics, Vol. 34, pp. 471–479) and motivated by the works of Cowin, S. C., and Hegedus, D. M., 1976, “Bone Remodeling I: Theory and Adaptive Elasticity,” Journal of Elasticity, Vol. 6, pp. 471–479 and Hegedus, D. H., and Cowin, S. C., 1976, “Bone Remodeling II: Small Strain Adaptive Elasticity,” Journal of Elasticity, Vol. 6, pp. 337–352.


Energy ◽  
2012 ◽  
Vol 48 (1) ◽  
pp. 108-117 ◽  
Author(s):  
Marko Ban ◽  
Goran Krajačić ◽  
Marino Grozdek ◽  
Tonko Ćurko ◽  
Neven Duić

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