Affecting factors of nylon monofilament induced focal cerebral ischemia in rats

AIM: To study factors affecting the stability of nylon monofilament for intraluminal middle cerebral artery occlusion in rats.METHODS:Successful rates and infarct volume of ischemic model were compared by polyvinyl alcohol (PVA) coated and silicon coated nylon monofilament intraluminal occlusion of middle cerebral artery under condition of ligation and without ligation of peterygopalatine artery.RESULTS:The successful rates were 60% and 53% in two groups under condition of ligation of peterygopalatine artery, and 20% and 27% in other two groups under condition of without ligation of peterygopalatine artery respectively. The intracranial length of nylon monofilament were about 7 mm in successful model and 4 mm in failure model. Animals in the PVA coated nylon monofilament group showed neurological dificit signs earlier, and had a significantly larger infarct volume at 12 hours of ischemia than those in the silicon coated group.CONCLUSIONS:The ligation of peterygopalatine artery is critical in the success of making this kind of ischemic model. The appropriate position of nylon monofilament entering crania and the good expansibility of PVA play an important role in occlusion of blood flow. Because of the relatively lower successful rate, a new substitute with unique quality, proper hardness and better elasticity needs to be explored in the future.     

Effects of panax notoginseng saponins on malondialdehyde content of the brain following brain injury in rabbits

AIM: To study the protective effect of panax notoginseng saponins (PNS) on brain in experimental brain injury. RESULTS:The MDA in the brain tissue following brain injury significantly increased, which related to the degree of brain edema; PNS dramatically decreased MDA in the brain tissue following brain injury and can alleviate the neuron ultrastructures damage.CONCLUSION:The inhibition of injury induced MDA increasing in the brain tissue by PNS may contribute to its overall neuroprotective action.     

Early-onset type 1 diabetes causes brain injury and mitochondrial dysfunction

AIM:To explore the main risk factors of diabetic encephalopathy and to investigate the changes of mitochondria in early-onset type 1 diabetes. METHODS:Single dose of streptozotocin was injected through the femoral vein to establish type 1 diabetes model in rats. The levels of glucose, triglyceride and cholesterol in plasma, cerebrospinal fluid and cerebral cortex were measured. Oxidative and antioxidative status was evaluated by determining the levels of malondialdehyde and glutathione in the isolated mitochondria of cerebral cortex. Furthermore, the level of active AMP-activated protein kinase(AMPK) in the isolated mitochondria was detected by Western blotting. Degenerative neurons were identified by Fluo-Jade-C staining in serial brain sections. Autophagy-lysosome was observed under electron microscope. RESULTS:The main risk factor in the development of diabetic encephalopathy was hyperglucemia, which increased the Fluo-Jade-C positive neurons in the cerebral cortex of diabetic rats. The content of malondialdehyde was increased and glutathione was decreased in diabetic rats compared with the control animals. The activity of AMPK was lower in diabetic brain than that in normal brain. Aggregated autophagysome and mitochondria enveloped by autophagy-lysosome were observed in pyramidal cells of cerebral cortex in diabetic rats. CONCLUSION:Persistent hyperglycemia and mitochondrial dysfunction contribute to the diabetic encephalopathy at an early stage in type 1 diabetes, indicating that the mechanism may be partly related to the oxidative stress and activation of autophagy.     

Biotech crops: technologies, achievements and prospects

During the past decade the development and adoption of transgenic technology has progressed rapidly. In 2007, biotech crops were grown by 12 million farmers in 23 countries covering 114.3 million hectares. This progress can be attributed to developments in molecular genetics, plant transformation and regeneration techniques and a better understanding of the underlying processes involved in DNA recombination. While almost every significant crop species has been successfully transformed, in many species the development of rapid, highly efficient, and routine transformation systems is still in progress. The commonly-used methods along with some promising alternative methods of plant transformation are described here. Achievements and future prospect in the areas of developing biotic and abiotic stress-tolerant crop varieties and progress in incorporating nutritional and other useful qualities into plants are also discussed in this paper.     

The function of GAP-43 on the recovery of brain injury

Neuronal growth associated protein (GAP-43) is a membrane bound phosphoprotein found in the axonal growth cones of sprouting central nervous system axons. It is neuron specific and is proposed to play a critical role in growth cone function during development of the nervous system or the regenerative recovery from axon injury. The injury leads to the transfection of fibroblasts with the GAP-43 gene, which result in increasing GAP-43 expression. GAP-43 is expressed at high levels during the course of recovery of brain injury. GAP-43 acts with calmodulin and G protein to regulate metabolic responses that initates axonal growth. It is important to reestablish neuronal structure and axonal sprouting. The level of GAP-43 returns to basal level once sprouting has finished. So more and more researchers attach importance to the study of GAP-43, which will improve the level of treatment with brain injury.     

基因打靶技术的研究进展

基因打靶技术是通过外源基因与受体细胞染色体基因组上的序列之间发生同源重组,将外源基因整合到某一特定位点上,从而实现外源基因的定点整合、修饰和改造受体细胞遗传特性的技术。作者简要介绍基因打靶技术的基本原理、产生、筛选策略及该技术的应用等研究进展。     

Propofol inhibits activation of p38 MAPK in rat brain tissues with LPS-induced brain injury

AIM: To investigate the effects of propofol on lipopolysaccharide (LPS)-induced activation of p38 mitogen-activated protein kinase (p38 MAPK) and inducible nitric oxide synthase (iNOS) in brain tissues of rats. METHODS: Sprague-Dawley rats of both sexes were randomly divided into 3 groups (n=24 each): control group, LPS group and LPS+propofol group. The models of LPS-induced brain injury were established by injecting LPS (1 mg/kg) via left internal carotid artery in LPS group. Propofol (100 mg/kg) was given intraperitoneally immediately after the LPS was given in LPS+propofol group. The same volume of normal saline was given to the rats in control group. The rats were decapitated 6 h, 24 h, 48 h and 72 h after administration. The brains were immediately isolated to detect the water content, activation of p38 MAPK and the exepression of iNOS protein. Meanwhile, the pathological changes were observed under light microscope. RESULTS: The water content of the brain was higher in LPS group than that in control group. The protein levels of phosphorylated p38 MAPK(p-p38 MAPK) and iNOS in LPS group increased 6 h after LPS administration, reached the peak at 24 h, and still higher than those in control group at 48 h and 72 h (P<0.05). The levels of those indexes were all lower in LPS+propofol group at various time points than those in corresponding LPS group (P<0.05). The pathological changes were slighter than those in LPS group. The water content of the brain was positively correlated with the levels of p-p38 MAPK and iNOS (r=0.603, r=0.727,P<0.05). CONCLUSION: Propofol attenuates LPS-induced brain injury by inhibiting the activation of p38 MAPK and down-regulating iNOS expression.