Usability of Ultrasonic Frequency Testing for Rapid Generation of High and Very High Cycle Fatigue Data.

Ultrasonic fatigue testing is an increasingly used method to study the high cycle fatigue (HCF) and very high cycle fatigue (VHCF) properties of materials. Specimens are cycled at an ultrasonic frequency, which leads to a drastic reduction of testing times. This work focused on summarising the current understanding, based on literature data and original work, whether and how fatigue properties measured with ultrasonic and conventional equipment are comparable. Aluminium alloys are not strain-rate sensitive. A weaker influence of air humidity at ultrasonic frequencies may lead to prolonged lifetimes in some alloys, and tests in high humidity or distilled water can better approximate environmental conditions at low frequencies. High-strength steels are insensitive to the cycling frequency. Strain rate sensitivity of ferrite causes prolonged lifetimes in those steels that show crack initiation in the ferritic phase. Austenitic stainless steels are less prone to frequency effects. Fatigue properties of titanium alloys and nickel alloys are insensitive to testing frequency. Limited data for magnesium alloys and graphite suggest no frequency influence. Ultrasonic fatigue tests of a glass fibre-reinforced polymer delivered comparable lifetimes to servo-hydraulic tests, suggesting that high-frequency testing is, in principle, applicable to fibre-reinforced polymer composites. The use of equipment with closed-loop control of vibration amplitude and resonance frequency is strongly advised since this guarantees high accuracy and reproducibility of ultrasonic tests. Pulsed loading and appropriate cooling serve to avoid specimen heating.

Bisphosphonate treatment of type I diabetic mice prevents early bone loss but accentuates suppression of bone formation.

Type I (T1) diabetes is an autoimmune and metabolic disease associated with bone loss. Previous studies demonstrate that T1-diabetes decreases osteoblast activity and viability. Bisphosphonate therapy, commonly used to treat osteoporosis, is demonstrated to inhibit osteoclast activity as well as osteoblast apoptosis. Therefore, we examined the effect of weekly alendronate treatments on T1-diabetes induced osteoblast apoptosis and bone loss. Bone TUNEL assays identified that alendronate therapy prevents the diabetes-induced osteoblast death observed during early stages of diabetes development. Consistent with this, alendronate treatment for 40 days was able to prevent diabetes-induced trabecular bone loss. Alendronate was also able to reduce marrow adiposity in both control diabetic mice compared to untreated mice. Mechanical testing indicated that 40 days of alendronate treatment increased bone stiffness but decreased the work required for fracture in T1-diabetic and alendronate treated mice. Of concern at this later time point, bone formation rate and osteoblast markers, which were already decreased in diabetic mice, were further suppressed in alendronate-treated diabetic mice. Taken together, our results suggest that short-term alendronate treatment can prevent T1-diabetes-induced bone loss in mice, possibly in part by inhibiting diabetes onset associated osteoblast death, while longer treatment enhanced bone density but at the cost of further suppressing bone formation in diabetic mice.

The effects of damage accumulation on the tensile strength and toughness of compact bovine bone.

Damage accumulation in compact bovine femur subjected to uniaxial tensile loading was examined by strong light illumination effects of microcracking. Imaging was done using a high-speed camera capturing image at 200 to 1500FPS. The tensile tests were performed in a multipurpose tensile testing system with cross-head speeds ranging from 0.5 to 10mm/min which leads to strain rates of 0.0001 to 0.0012s(-1) (physiologically relevant to walking and running Hansen et al., 2008). The post-failure images were then examined in a scanning electron microscopy (SEM) and effects of microstructure, strain rate, and orientation were evaluated. Correlation of the high-speed images with stress-strain curves indicated that optically visible microcracks were most likely initiated at yielding, and the specimens with dispersed microcracks exhibited a higher energy-absorption capacity compared to the specimens with coalesced local cracks. It was found that damage accumulation negatively correlates to strain rate and that transverse specimens exhibited a different failure pattern compared to the longitudinal specimens. Strain hardening and softening were found in the longitudinal and transverse specimens respectively. The microcracking in the transverse specimens instantly increased to peak after yielding compared to the gradual growth until failure in the longitudinal specimens. The average Young's modulus (21.5GPa) and ultimate stress (93.5MPa) of the specimens loaded in the longitudinal direction were more than twice that of the specimens (10.9GPa and 36.2MPa respectively) loaded in the transverse direction. The current technique has shown potential in relating damage accumulation real time in bone samples subjected to tensile loading condition. This information will be helpful in relating the role of micro damage accumulation in initiating failure and/or remodeling in bone.

Finite element analysis of ramming in Ovis canadensis.

The energy produced during the ramming of bighorn sheep (Ovis canadensis) would be expected to result in undesirable stresses in their frontal skull, which in turn would cause brain injury; yet, this animal seems to suffer no ill effects. In general, horn is made of an α-keratin sheath covering a bone. Despite volumes of data on the ramming behavior of Ovis canadensis, the extent to which structural components of horn and horn-associated structure or tissue absorb the impact energy generated by the ramming event is still unknown. This study investigates the hypothesis that there is a mechanical relationship present among the ramming event, the structural constituents of the horn, and the horn-associated structure. The three-dimensional complex structure of the bighorn sheep horn was successfully constructed and modeled using a computed tomography (CT) scan and finite element (FE) method, respectively. Three different three-dimensional quasi-static models, including a horn model with trabecular bone, a horn model with compact bone that instead of trabecular bone, and a horn model with trabecular bone as well as frontal sinuses, were studied. FE simulations were used to compare distributions of principal stress in the horn and the frontal sinuses and the strain energy under quasi-static loading conditions. It was noticed that strain energy due to elastic deformation of the complex structure of horn modeled with trabecular bone and with trabecular bone and frontal sinus was different. In addition, trabecular bone in the horn distributes the stresses over a larger volume, suggesting a mechanical link between the structural constituents and the ramming event. This phenomenon was elucidated through the principal stress distribution in the structure. This study will help designers in choosing appropriate material combinations for the successful design of protective structures against a similar impact.

CCAAT/enhancer binding protein ß-deficiency enhances type 1 diabetic bone phenotype by increasing marrow adiposity and bone resorption.

Bone loss in type 1 diabetes is accompanied by increased marrow fat, which could directly reduce osteoblast activity or result from altered bone marrow mesenchymal cell lineage selection (adipocyte vs. osteoblast). CCAAT/enhancer binding protein beta (C/EBPß) is an important regulator of both adipocyte and osteoblast differentiation. C/EBPß-null mice have delayed bone formation and defective lipid accumulation in brown adipose tissue. To examine the balance of C/EBPß functions in the diabetic context, we induced type 1 diabetes in C/EBPß-null (knockout, KO) mice. We found that C/EBPß deficiency actually enhanced the diabetic bone phenotype. While KO mice had reduced peripheral fat mass compared with wild-type mice, they had 5-fold more marrow adipocytes than diabetic wild-type mice. The enhanced marrow adiposity may be attributed to compensation by C/EBPδ, peroxisome proliferator-activated receptor-γ2, and C/EBPα. Concurrently, we observed reduced bone density. Relative to genotype controls, trabecular bone volume fraction loss was escalated in diabetic KO mice (-48%) compared with changes in diabetic wild-type mice (-22%). Despite greater bone loss, osteoblast markers were not further suppressed in diabetic KO mice. Instead, osteoclast markers were increased in the KO diabetic mice. Thus, C/EBPß deficiency increases diabetes-induced bone marrow (not peripheral) adipose depot mass, and promotes additional bone loss through stimulating bone resorption. C/EBPß-deficiency also reduced bone stiffness and diabetes exacerbated this (two-way ANOVA P < 0.02). We conclude that C/EBPß alone is not responsible for the bone vs. fat phenotype switch observed in T1 diabetes and that suppression of CEBPß levels may further bone loss and decrease bone stiffness by increasing bone resorption.