Understanding the Stability of LiNi0.5Mn0.5O2 as a Co-Free Positive Electrode.

To understand the stability of Co-free positive electrode materials, LiNi0.5Mn0.5O2 was synthesized with different amounts of lithium added during calcination. The valence states of the Ni and Mn transition metals of the prepared samples were determined through accurate stoichiometry analyses (via inductively coupled plasma optical emission spectrometry), magnetic moment measurements (via superconducting quantum interference device magnetometry), and element valence analyses (via X-ray spectroscopy in combination with Ar ion etching for depth profiling). Unexpectedly, the Ni and Mn transition metals in the interior and on the surface of the LiNi0.5Mn0.5O2 particles show different electrochemical properties. This clarifies the open questions on the Li deintercalation mechanism in LiNi0.5Mn0.5O2.

Three dimensional finite element analysis of the pediatric lumbar spine. Part II: biomechanical change as the initiating factor for pediatric isthmic spondylolisthesis at the growth plate.

A non-linear 3-dimensional finite element pediatric lumbar spine model with vertebral growth plate and apophyseal bony ring was developed. Lumbar spondylolysis was simulated in the model. The Von Mises stresses in the structures surrounding the vertebral growth plate, including apophyseal bony ring and osseous endplate were calculated in various loading modes. Instantaneous axis of rotation (IAR) path from flexion to extension was also analyzed. The results were compared with those of the intact model and the literature. The IAR path was at the posterior disc-endplate space of the lower vertebra in the intact spine, and moved cranially towards the upper-posterior disc space in the lytic spine. This was in agreement with in vivo radiological data by Sakamaki et al. [19]. During various loading modes, stresses in the spondylolytic pediatric model were higher than that of the intact model; ranging from 1.1 to 6.0 times, with the highest value in extension at the growth plate. In conclusion, FE models indicate that stress concentrations in the lytic model increase at the growth plate which may lead to physis stress fracture leading to spondylolisthesis.

Three-dimensional finite element analysis of the pediatric lumbar spine. Part I: pathomechanism of apophyseal bony ring fracture.

The purpose of this study was to (1) develop a three-dimensional, nonlinear pediatric lumbar spine finite element model (FEM), and (2) identify the mechanical reasons for the posterior apophyseal bony ring fracture in the pediatric patients. The pediatric spine FE model was created from an experimentally validated three-dimensional adult lumbar spine FEM. The size of the FEM was reduced to 96% taking into account of the ratio of the sitting height of an average 14-years-old children to that of an adult. The pediatric spine was created with anatomically specific features like the growth plate and the apophyseal bony ring. For the stress analyses, a 10-N m moment was applied in all the six directions of motion for the lumbar spine. A preload of 351 N was applied which corresponds to the mean body weight of the 14-years-old group. The stresses at the apophyseal bony ring, growth plate and endplate were calculated. The results indicate that the structures surrounding the growth plate including apophyseal bony ring and osseous endplate were highly stressed, as compared to other structures. Furthermore, posterior structures in extension were in compression whereas in flexion they were in tension, with magnitude of stresses higher in extension than in flexion. Over time, the higher compression stresses along with tension stresses in flexion may contribute to the apophyseal ring fracture (fatigue phenomena).

Cyclooxygenase-2 inhibitor delays fracture healing in rats.

BACKGROUND: Cyclooxigenase-2 (COX-2) inhibitors have been reported to delay fracture healing. To investigate the major inhibitory period of COX-2 inhibitors in fracture healing, we administrated etodolac, a COX-2-specific inhibitor, to a rat fracture model by altering the period of administration from early to late. METHOD: After closed fractures had been created at the middle of the femoral shafts in 12-week-old Wister rats, a standardized dose of etodolac was administrated in three ways: group I received it for 3 weeks, group II for just the first week after operation, and group III for just the third (final) week. Group IV was the vehicle control group. Bone maturation was estimated by radiographic scoring system, and mechanically by a three-point bending test. RESULTS AND INTERPRETATION: In both the radiographic and mechanical studies, groups I and II showed lower scores than group IV, indicating that even a short period of administration of a COX-2-specific inhibitor in the early phase of fracture healing creates a risk of delayed healing. blacksquare, square, filled.

Cyclooxygenase-2 inhibitor inhibits the fracture healing.

We investigated the effects of cyclooxigenase-2 (cox-2) on fracture healing. After closed non-displaced fractures were created at the middle of both femoral shafts in 12-week-old Wister rats, a cox-2 specific inhibitor, etodolac (20 mg/day; intra-peritoneal) was administered every day for three weeks (E group). Bone union and callus formation were evaluated by weekly radiographs. Three weeks after surgery, the mechanical strength of the fractured femur was evaluated by a three-point-bending test. These results were compared with those of a vehicle control group (V group). The fracture healing score on radiographs in the E group three weeks after the surgery was 3.3 +/- 0.9, and in the V group it was 5.8 +/- 1.5, indicating that fracture healing was significantly poorer in the E than the V group (p < 0.05). From the three point bending test, the ultimate strength and stiffness of etodolac-treated fractured femurs were shown to be significantly lower than those in vehicle control group (p < 0.05). Mechanically, femurs of etodolac treated rats were weaker than those of control rats. Thus, it was concluded that etodolac, a cox-2 specific inhibitor, inhibited fracture healing.