Improved healing of critical-size femoral defect in osteoporosis rat models using 3D elastin/polycaprolactone/nHA scaffold in combination with mesenchymal stem cells.

Osteoporosis is a common bone disease that results in elevated risk of fracture, and delayed bone healing and impaired bone regeneration are implicated by this disease. In this study, Elastin/Polycaprolactone/nHA nanofibrous scaffold in combination with mesenchymal stem cells were used to regenerate bone defects. Cytotoxicity, cytocompatibility and cellular morphology were evaluated in vitro and observations revealed that an appropriate environment for cellular attachment, growth, migration, and proliferation is provided by this scaffold. At 3 months following ovariectomy (OVX), the rats were used as animal models with an induced critical size defect in the femur to evaluate the therapeutic potential of osteogenic differentiation of bone marrow mesenchymal stem cells (BM-MSCs) seeded on 3 dimension (3D) scaffolds. In this experimental study, 24 female Wistar rats were equally divided into three groups: Control, scaffold (non-seeded BM-MSC), and scaffold + cell (seeded BM-MSC) groups. 30 days after surgery, the right femur was removed, and underwent a stereological analysis and RNA extraction in order to examine the expression of Bmp-2 and Vegf genes. The results showed a significant increase in stereological parameters and expression of Bmp-2 and Vegf in scaffold and scaffold + cell groups compared to the control rats. The present study suggests that the use of the 3D Elastin/Polycaprolactone (PCL)/Nano hydroxyapatite (nHA) scaffold in combination with MSCs may improve the fracture regeneration and accelerates bone healing at the osteotomy site in rats.

Methamphetamine administration impairs behavior, memory and underlying signaling pathways in the hippocampus.

Methamphetamine (METH) is a strong psychostimulant drug which can essentially affect different brain regions. Hippocampus as one of main components of limbic system plays key roles in processing of short term, long term and spatial memory. Herein, we explored the changes in behavior, synaptic transmission and hippocampal volume along with gliosis following METH treatment. Besides, using genome-wide expression profiling, we applied a pathway-based approach to detect significantly dysregulated signaling pathways. In this regard, we found that METH administration interrupts spatial memory and long term potentiation (LTP). Additionally, stereological analysis revealed a significant alteration in hippocampal volume along with increased gliosis upon METH treatment. We also identified several signaling cascades chiefly related to synaptic transmission which were considerably interrupted in the hippocampus of METH-treated rats. Taken together, our data suggests a potential link between behavioral disruptions and dysregulated signaling pathways.