Elevated PVP in the early phase is strongly associated with poor patient survival attributable, at least in part, to small-for-size graft. Further elucidation of the pathogenesis behind this phenomenon and efforts to modify PVP will be key to improving results.
Aim: To investigate whether the perinatal and postnatal exposure of mice to bisphenol A (BPA) caused the development of obesity and/or hyperlipidemia. Methods: Pregnant mice were exposed to BPA in drinking water at concentrations of either 1 g/mL (LD group) or 10 g/mL (HD group) from gestation day 10 and throughout the lactating period. After weaning, the pups were allowed free access to drinking water containing the appropriate concentrations of BPA. The body weight, adipose tissue weight, and serum lipid levels were measured in the offspring at postnatal day 31.
If a narrow intercondylar notch contains a smaller anterior cruciate ligament, that may explain why people with narrow notches have a higher incidence of anterior cruciate ligament injuries. To investigate the significance of notch width measurement, we used 16 embalmed cadaveric knees. A positive mold of the entire anterior cruciate ligament, including its femoral and tibial insertions, was created with silicone rubber and plaster commonly used for dental molding. We had two hypotheses to test from this study. One was that the dimensions of the anterior cruciate ligament can be predicted by the notch width. The other was that the size of a person's anterior cruciate ligament can be predicted by a caliper measurement of the intercondylar notch. The width, sagittal length, and cross-sectional area of the midsubstance and the femoral and tibial insertions of the anterior cruciate ligament were measured. The notch width index, the ratio of notch width to width of the femoral condyle, showed a positive correlation only to the ratio of width to sagittal length of the tibial insertion. None of the parameters showed any differences between the knees with a notch width index less than or equal to 0.2 and those with a notch width index greater than 0.2. The knees with small notch width indexes did not have thinner anterior cruciate ligaments in them. These findings may not be applicable to knees obtained from other races, i.e., not Japanese.
To clarify the role of OPN in bone formation under mechanical stress, we examined the expression and the function of OPN in bone using an expansion force-induced osteogenesis model. Our results indicated that OPN expression was enhanced during the bone formation and that OPN would be one of the positive factors for the bone formation under mechanical stress.Introduction: Bone formation is known to be stimulated by mechanical stress; however, molecules involved in stress-dependent regulation of bone formation have not yet been fully characterized. Extracellular matrix proteins such as osteopontin (OPN) could play a role in mediation of the mechanical stress signal to osteoblasts. However, the function of OPN in bone formation under mechanical force is not known. Therefore, we examined the expression and the role of OPN in bone formation in vivo under tensile mechanical stress. Materials and Methods: Sagittal sutures of mice were subjected to expansion mechanical stress by setting orthodontic spring wires, and OPN expression during bone formation within the suture gap was examined. Results: Expansion of the sutures resulted in bone formation at the edges of the parietal bones within the sagittal suture. Immunohistochemical analysis revealed abundant accumulation of OPN protein in the matrix of newly formed bone on the inner edge of the parietal bone within the mechanically expanded sutures. Osteoblasts forming bone within the suture subjected to tensile stress also exhibited high levels of OPN protein expression. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis indicated that OPN mRNA expression was enhanced in wild-type calvariae subjected to expansion force compared with the control calvariae where dead spring wires were set without expansion stress. In addition, type I collagen mRNA was also expressed in the calvariae under the mechanical stimuli. To understand the function of OPN, sagittal sutures in OPN-deficient mice were subjected the expansion stress, and bone formation within the suture to fill the expanded gap was compared with that observed in wild-type mice. OPN deficiency reduced bone formation at the edge of the parietal bone in contact with the expanded suture gap. Conclusions: These observations revealed that OPN plays a pivotal role in bone formation under tensile mechanical stress.
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