Two types of tetragonal zirconia polycrystals (TZP), a ceria-stabilized TZP/Al2O3 nanocomposite (CZA) and a conventional yttria-stabilized TZP (Y-TZP), were sandblasted with 70-μm alumina and 125-μm SiC powders, then partially annealed at 500-1200℃ for five minutes. Monoclinic ZrO2 content was determined by X-ray diffractometry and Raman spectroscopy. Biaxial flexure test was conducted on the specimens before and after the treatments. Monoclinic ZrO2 content and biaxial flexure strength increased after sandblasting, but decreased after heat treatment. However, in both cases, the strength of CZA was higher than that of Y-TZP. Raman spectroscopy showed that a compressive stress field was introduced on the sample surface after sandblasting. It was concluded that sandblasting induced tetragonal-to-monoclinic phase transformation and that the volume expansion associated with such a phase transformation gave rise to an increase in compressive stress on the surface of CZA. With the occurrence of such a strengthening mechanism in the microstructure, it was concluded that CZA was more susceptible to stress-induced transformation than Y-TZP.

A ceramic hip‐joint femoral head, made of a zirconia‐toughened alumina‐matrix material with the addition of small amounts of mixed oxides, has been evaluated with respect to environmental surface degradation in a moist environment. Microscopic insight into environmental surface degradation could be obtained according to Raman and fluorescence microprobe spectroscopies. By adopting an optimized confocal configuration for the optical probe, spectroscopic assessments could be performed in very shallow volumes, thus minimizing the effect on the spectra of sub‐surface portions of the material. Two main phenomena have been envisaged: (i) transformation of zirconia dispersoids from tetragonal to monoclinic polymorph, induced by aging periods at 121°C (0.1 MPa) in a vapor environment (in addition to a fraction of a monoclinic polymorph ≅20 vol% present in the as‐received femoral head); (ii) evolution of the (equilibrium) residual stress field stored within the joint surface from a tensile field in the as‐received material to a slightly compressive stress field after several hours of aging in a moist atmosphere. Exposures in vapor >50 h brought the joint surface into an increasingly tensile stress state. This residual stress field on the material surface may hinder the long‐term wear resistance of the load‐bearing femoral head, especially in the presence of microscopic impingements by microseparation contact and third‐body wear.

Study design: We investigated microRNA (miRNA) expression after spinal cord injury (SCI) in mice. Objectives: The recent discovery of miRNAs suggests a novel regulatory control over gene expression during plant and animal development. MiRNAs are short noncoding RNAs that suppress the translation of target genes by binding to their mRNAs, and play a central role in gene regulation in health and disease. The purpose of this study was to examine miRNA expression after SCI. Setting: Department of Orthopaedic Surgery, Graduate School of Biomedical Sciences, Hiroshima University. Methods: We examined the expression of miRNA (miR)-223 and miR-124a in a mouse model at 6 h, 12 h, 1 day, 3 days and 7 days after SCI using quantitative PCR. The miRNA expression was confirmed by in situ hybridization. Results: Quantitative PCR revealed two peaks of miR-223 expression at 6 and 12 h and 3 days after SCI. MiR-124a expression decreased significantly from 1 day to 7 days after SCI. In situ hybridization demonstrated the presence of miR-223 around the injured site. However, miR-124a, which was present in the normal spinal cord, was not observed at the injured site. Conclusion: Our results indicate a time-dependent expression pattern of miR-223 and miR-124a in a mouse model of SCI. In this study, the time course of miRNA-223 expression may be related to inflammatory responses after SCI, and the time course of decreased miR-124a expression may reflect cell death.

Chitin nanofibers were prepared from dry chitin powder by nanofibrillation using a Star Burst instrument employing a highpressure water jet system. FE-SEM micrographs showed that the nanofibers became thinner as the number of Star Burst passes increased. Fibrillation in an acidic condition made the chitin fibers thinner than those in a neutral condition. The transmittance spectra of chitin nanofiber/acrylic resin composites led us to the same conclusion. In addition, chitin nanofibers prepared by treatment consisting of five Star Burst passes in the neutral condition were thinner than the previously reported nanofibers. X-ray diffraction profiles showed that the Star Burst system did not damage the chitin nanofibers and did not reduce their crystallinity.

The IP-CHA spacer contributed to high bone fusion rates of the spacers and hinges of the laminae, and there were no complications associated with their use. Cervical laminoplasty with the IP-CHA spacers is a safe and simple method that yields sufficient fixation strength and provides sufficient bone bonding within a short period of time after operation.

Lnk is an intracellular adaptor protein reported as a negative regulator of proliferation in c-Kit positive, Sca-1 positive, lineage marker-negative (KSL) bone marrow cells. The KSL fraction in mouse bone marrow is believed to represent a population of hematopoietic and endothelial progenitor cells (EPCs). We report here that, in vitro, Lnk 2/2 KSL cells form more EPC colonies than Lnk 1/1 KSL cells and show higher expression levels of endothelial marker genes, including CD105, CD144, Tie-1, and Tie2, than their wild-type counterparts. In vivo, the administration of Lnk 1/1 KSL cells to a mouse spinal cord injury model promoted angiogenesis, astrogliosis, axon growth, and functional recovery following injury, with Lnk 2/2 KSL being significantly more effective in inducing and promoting these regenerative events. At day 3 following injury, large vessels could be observed in spinal cords treated with KSL cells, and reactive astrocytes were found to have migrated along these large vessels. We could further show that the enhancement of astrogliosis appears to be caused in conjunction with the acceleration of angiogenesis. These findings suggest that Lnk deletion reinforces the commitment of KSL cells to EPCs, promoting subsequent repair of injured spinal cord through the acceleration of angiogenesis and astrogliosis. STEM CELLS 2010;28:365-375 Disclosure of potential conflicts of interest is found at the end of this article.

Interactions between endothelial and neural stem cells are believed to play a critical role in the kinetics of neural stem cells in the central nervous system. Here we demonstrate that endothelial progenitor cells promote the repair of injured spinal cord through the induction of Notch-dependent astrogliosis and vascular regulation. The transplantation of Jagged1(+/+) endothelial progenitor cells, but not Jagged1(-/-) endothelial progenitor cells, increased the number of reactive astrocytes during the acute phase, and improved functional recovery following spinal cord injury. Expression of the Notch effector Hes5 was upregulated in the injured spinal cord after Jagged1(+/+) endothelial progenitor cell transplantation. Furthermore, we found that the Notch ligand Delta-like-1 was highly expressed in Jagged1(-/-) endothelial progenitor cells. Transplantation of Delta-like-1, as well as Jagged1-overexpressing 3T3 cells, revealed that only Jagged1-overexpressing 3T3 stromal cells enhanced astrogliosis following spinal cord injury. In addition, Jagged1(+/+) endothelial progenitor cells exhibited not only dramatic pro-angiogenic effects, but also morphologically abnormal vessel stabilization, compared with Jagged1(-/-)endothelial progenitor cells in injured spinal cord. Thus, transplanted endothelial progenitor cells promote astrogliosis, vascular regulation, and spinal cord regeneration through activation of Jagged1-Notch signaling.

Introduction The number of cases of osteoporotic vertebral compression fracture (OVCF) with intravertebral cleft (IVC) with delayed neurologic deficit (DND) is increasing as the population ages. However, the cause of DND is poorly understood, and no definitive treatment of the disease has been established. The purpose of this study was to clarify the radiographic parameters contributing to the occurrence of DND, and to evaluate the efficacy and safety of percutaneous vertebroplasty for this pathology. Methods Percutaneous vertebroplasty was prospectively performed for 244 patients with OVCF with IVC; 30 had DND and 214 did not. Radiographic parameters of local kyphotic angle, percent spinal canal compromise and intravertebral instability were investigated for correlations to DND. Procedural outcomes were evaluated using visual analog scale (VAS), Oswestry Disability Index (ODI), and modified Frankel grades. Results Before vertebroplasty, no substantial difference in local kyphotic angle was seen between OVCF with IVC with and without DND, but percent spinal canal compromise and intravertebral instability were greater in OVCF with IVC with DND (P \ 0.001). After vertebroplasty, 25 of 30 cases (84 %) of OVCF with IVC with DND achieved clinically meaningful improvement (CMI), but 5 (17 %) did not. Patients with CMI showed substantial improvements in intravertebral instability (P \ 0.001), and no change in local kyphotic angle or percent spinal canal compromise. In five patients without CMI, four showed an initial improvement, but subsequent vertebral fracture adjacent to the treated vertebra caused neurologic re-deterioration. One patient with percent spinal canal compromise 54.9 % and intravertebral instability 4°achieved no neurologic improvement following vertebroplasty. No serious complications or adverse events related to the procedure were encountered. ConclusionsIntravertebral instability is the dominant cause of DND. Percutaneous vertebroplasty appears effective and safe in the treatment of OVCF with IVC with DND. Patients with less intravertebral instability and severe spinal canal compromise could be candidates for conventional surgical treatment.