ABSTRACT
The transcriptional repressor RE1 silencer transcription factor(NRSF/REST) is an important factor that restricts some neuronal traits in neurons.Since these traits are also present in pancreatic islet cells,NRSF-regulated genes involved in islet function are searched.A NRSE-like motif was analysed in human insulin promoter.The role of NRSE was evaluated by generating a model of insulin-secreting cells that firmly express NRSF.The presence of NRSF led to a decrease in activity of human insulin promoter by stable or transient transfection with human insulin-promoter luciferase.The predicted NRSE-like motif also confers NRSF-dependent transcriptional repression in the context of a surrogate gene promoter.Specific binding activity of NRSF/REST to the NRSE-like motif was confirmed by EMSA.Moreover,the binding activity is competed by consensus NRSE sequence.These data showed that human insulin promoter is regulated by the transcriptional repressor NRSF/REST via the NRSE-like motif.
ABSTRACT
The ophthalmological teaching of clinical laboratory and preventive medicine specialty should base on their own characteristics,and the teaching reform must be conducted form the four aspects of material,outline,practice and test to adapt to the demands of society development.
ABSTRACT
Objective To observe the early ultrastructural changes of the optic nerves after the brain impact injury. Methods Eighteen 15-week-old Wistar rats were used in the air-pressure brain impact injury examination. All of the rats underwent the procedures of right-parietal-bone fenestration after abdominal cavity anesthesia with 1% sodium pentolbarbital (45 mg/kg), and then they were divided randomly into 3 groups, i.e., mild injury group (8 rats) underwent with 7 kg of air pressure in distance of 11 cm; severe injury group (8 rats) with 7 kg of airpressure in distance of 8 cm; and control group (2 rats) underwent with the parietal-bone fenestration but without impact injury.The ultrastructural changes of the optic nerves were observed 1, 6, 24, and 72 hours after the injury by electron microscopy. Results The difference of ultrastructural changes of optic nerve was not obvious in wild injury group and the control group, and the lanthanum nitrate was only found in the blood vessels in optic nerve. The lanthanum nitrate entered the nerve stroma 1 hour after severe and increased as time goes on. Simultaneously, displayed dilatation of endoplasmic reticulum, cavitation and tumefaction of mitochondrion, vacuolation of nerve stroma, and vacuolation of some axis-cylinder were seen in the glial cells. Conclusion The brain impact injury may cause ultrastructural changes of the optic nerve and increase of permeability of blood vessels.