Progress of the conversion reaction of Mn3O4 particles as a function of the depth of discharge.

A comprehensive investigation of the morphological and interfacial changes of Mn3O4 particles at different lithiation stages was performed in order to improve our understanding of the mechanism of the irreversible conversion reaction of Mn3O4. The micronization of Mn3O4 into a Mn-Li2O nanocomposite microstructure and the formation of a solid electrolyte interphase (SEI) on the Mn3O4 surface were carefully observed and characterized by combining high-resolution transmission electron microscopy (HRTEM), X-ray photoelectron spectroscopy (XPS), and in situ X-ray absorption fine structure (XAFS) measurements. Accumulation of a thin SEI film of 2-5 nm thickness on the surfaces of the Mn3O4 particles due to their catalytic decomposition was observed at a depth of discharge (DOD) of 0%.

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.

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.

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.

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.