The role of bone morphogenetic protein 2 in SMA-directed angiogenesis during distraction osteogenesis

Bone is one of the few organs capable of regeneration after a substantial injury. As the bone heals itself after trauma, the coupling of angiogenesis to osteogenesis is crucial for the restoration of the skeletal tissue. In prior studies we have shown that Bone Morphogenetic Protein 2 (BMP2), a potent agonist for skeletal formation is expressed by vessels making it a prime candidate that links the morphogenesis of the two tissues. To investigate the role of BMP2 in the coordination of vessel and bone formation, we used a tamoxifen inducible Smooth Muscle Actin (SMA) promoter that conditionally expresses Cre recombinases crossed with a BMP2 floxed mouse in order to conditionally delete the BMP2 gene in smooth muscle actin (SMA) expressing cells. Using the mouse femur as our model for bone regeneration, we performed a surgical technique called distraction osteogenesis (DO) where an osteotomy is created followed by distraction or a gradual separation of the two pieces of bone. This primarily promotes intramembranous ossification at the osteotomy site by mechanical stimulation. Tamoxifen treatment started at day 6 and continued throughout the experiment. At post-operative days 3, 7, 12, 17, 24, and 31, we analyzed the bone and vessel formation by plain X-ray, micro-computed tomography (µCT) and vascular contrast enhanced µCT, and quantitative polymerase chain reaction (qPCR) of selective genes. We assessed both the femur and surrounding tissue to obtain qualitative and quantitative assessments for skeletal and vascular formation. Our results demonstrated that the deletion of BMP2 in vascular tissue resulted in a reduction of angiogenesis in vivo followed by a decrease in skeletal tissue development

Least Squares Regression Estimations Based on Censored Data with Measurement Errors

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Setup Cost Reduction in the Lumpy Demand Production Quantity Model with Discounting

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Strong solutions of the compressible nematic liquid crystal flow

We study strong solutions of the simplified Ericksen-Leslie system modeling compressible nematic liquid crystal flows in a domain $\Omega \subset\mathbb R^3$. We first prove the local existence of unique strong solutions provided that the initial data $\rho_0, u_0, d_0$are sufficiently regular and satisfy a natural compatibility condition. The initial density function $\rho_0$ may vanish on an open subset (i.e., an initial vacuum may exist). We then prove a criterion for possible breakdown of such a local strong solution at finite time in terms of blow up of the quantities $\|\rho\|_{L^\infty_tL^\infty_x}$ and $\|\nabla d\|_{L^3_tL^\infty_x}$