Spinal cord injury (SCI) is a major cause of paralysis. Currently, there are no effective therapies to reverse this disabling condition. The presence of ependymal stem/progenitor cells (epSPCs) in the adult spinal cord suggests that endogenous stem cell-associated mechanisms might be exploited to repair spinal cord lesions. epSPC cells that proliferate after SCI are recruited by the injured zone, and can be modulated by innate and adaptive immune responses. Here we demonstrate that when epSPCs are cultured from rats with a SCI (ependymal stem/progenitor cells injury [epSPCi]), these cells proliferate 10 times faster in vitro than epSPC derived from control animals and display enhanced self renewal. Genetic profile analysis revealed an important influence of inflammation on signaling pathways in epSPCi after injury, including the upregulation of Jak/Stat and mitogen activated protein kinase pathways. Although neurospheres derived from either epSPCs or epSPCi differentiated efficiently to oligodendrocites and functional spinal motoneurons, a better yield of differentiated cells was consistently obtained from epSPCi cultures. Acute transplantation of undifferentiated epSPCi or the resulting oligodendrocyte precursor cells into a rat model of severe spinal cord contusion produced a significant recovery of motor activity 1 week after injury. These transplanted cells migrated long distances from the rostral and caudal regions of the transplant to the neurofilament-labeled axons in and around the lesion zone. Our findings demonstrate that modulation of endogenous epSPCs represents a viable cell-based strategy for restoring neuronal dysfunction in patients with spinal cord damage.

Here, we describe a 3-month-old XX male French Bulldog. The diagnosis was based on the clinical signs, gonadal histology and cytogenetic analysis. Additionally, the dog was confirmed to be Sry negative by semi-quantitative reverse transcription polymerase chain reaction (sqRT-PCR). Canine Sry-negative XX sex reversal is a disorder of gonadal development where individuals who have a female karyotype develop testes or ovotestes. To our knowledge, this case is the first XX male sex reversion described in a French Bulldog.

The utility of recombinant human bone morphogenetic protein-2 (rhBMP-2) in inducing bone formation in fractures of bone is well known. However, the influence of the mechanical environment on the actions of rhBMP-2 on fracture healing is not clear. An experimental model of fractures of the tibia in rabbits was developed and utilized to investigate the role of mechanical environment on rhBMP-2 action. A 1 mm osteotomy gap was stabilized by either a low- or high-stiffness fixator (LSF or HSF, respectively), and local treatment with rhBMP-2 in an absorbable collagen sponge (ACS) was evaluated. The results of the investigation were analysed by both histomorphometry and biomechanics. The LSF caused an increase in mineralized periosteal callus compared to HSF, the rhBMP-2 in ACS accelerated fracture healing only in the LSF group but not in the HSF group. The area of mineralized tissue in interfragmentary callus was determined by fixation stiffness and not by BMP treatment. rhBMP-2 caused higher bone resorption in the endosteal callus during the late stages of fracture healing, but these histological differences did not affect the mechanical properties. Biomechanical evaluation showed only differences at 3 weeks between LSF-rhBMP-2 and LSF-ACS. The bending and torsional properties were higher in the rhBMP-2/ACS group compared to ACS alone at 3 weeks.

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