幼年豚鼠视网膜兴奋毒性损伤模型的建立

目的:观察谷氨酸钠不同给药时程对幼年豚鼠视网膜神经节细胞损伤的程度,以建立简便而稳定可靠的视网膜兴奋毒性损伤模型。方法:实验于2005-03/2006-06在泰山医学院动物实验中心和形态学实验室完成。①实验材料:45～50d(幼年)豚鼠35只,体质量280～320g,雌雄不拘;谷氨酸钠(上海伯奥生物科技有限公司生产),纯度99%,pH6.9～7.2,用生理盐水配成300g/L溶液。②实验分组:采用随机数字法将豚鼠分成2组,即正常对照组5只、谷氨酸钠组30只(谷氨酸钠组根据用药时间又分为4个亚组,即1d组5只、3d组6只、7d组9只,14d组10只)。③实验干预:谷氨酸钠组按3g/kg体质量腹腔注射谷氨酸钠,分别连续1,3,7和14d。④实验评估:给药后,再饲养10d后取材,观察视网膜神经节细胞数目和形态学的变化。结果:①各组豚鼠视网膜光镜观察结果:谷氨酸钠1d组视网膜神经节细胞未见明显形态学改变;3d组少数细胞发生皱缩;7d组视网膜神经节细胞损伤较为明显,多数神经节细胞发生核固缩;14d组动物半数死亡(5/10),视网膜神经节细胞损伤严重,明显脱失,残留细胞体积变小。②各组豚鼠视网膜神经节细胞密度:谷氨酸钠14d组、7d组视网膜神经节细胞密度与正常对照组比较差异均显著(P<0.01),谷氨酸钠3d组与正常对照组比较差别有统计学意义(P<0.05),谷氨酸钠1d组与正常对照组比较差异无显著性(P>0.05)。结论:谷氨酸钠对幼年豚鼠视网膜的毒性损伤与用药时程有关,按3g/kg体质量腹腔注射,1次/d,连续7d,能成功建立谷氨酸视网膜兴奋毒性豚鼠动物模型,且无一例死亡,损伤适中。     

Clinical and experimental vasogenic edema: in vivo sodium MR imaging. Work in progress

To investigate the sodium magnetic resonance (MR) imaging characteristics of acute vasogenic edema, an experimental canine model was developed. Vasogenic edema was produced in the hemisphere of the dogs by the intraarterial infusion of hypertonic mannitol (25%). This solution opens the blood-brain barrier, allowing the influx of water, electrolytes, and proteins into the brain. The main advantage of this model over the established "cold injury" model is the lack of associated brain necrosis. Two patients with chronic vasogenic edema secondary to well-circumscribed meningiomas also underwent MR imaging. The sodium signal was markedly elevated in both clinical and experimental studies of vasogenic edema fluid compared with signal in healthy brain tissue. Extracellular sodium associated with vasogenic edema displayed MR imaging characteristics similar to that of sodium in serum. There was a trend toward a shortened T2 in edema fluid secondary to the presence of serum macromolecules.     

Bone marrow patterns in aplastic anemia: observations with 1.5-T MR imaging

Six patients diagnosed as having aplastic anemia underwent magnetic resonance (MR) imaging. The bone marrow in the lumbar spine, pelvis, and proximal femora was examined in each case. One patient had a normal marrow signal intensity (SI) and pattern and was considered cured of disease. The other patients had varying numbers of focal low-SI areas interspersed with high-SI areas in the marrow of the spine. The pelves and proximal femora of all patients had diffuse high-SI marrow without focal abnormalities. Biopsy of a lumbar vertebral body in one patient demonstrated that the focal low-SI areas may have been islands of active hematopoietic cells scattered in otherwise fatty marrow. MR may prove to be a valuable, noninvasive method of following the response of patients with aplastic anemia to therapy; more investigation is necessary before this can be definitely concluded.     

Follistatin and activin A in extra-embryonic coelomic and amniotic fluids and maternal serum in early pregnancy

Follistatin is a specific binding protein which controls bioavailability of activins and inhibins which have an important role in fetal development. In the first trimester of pregnancy bioactive dimeric inhibins are found at high concentrations in the extra- embryonic coelomic fluid, but the distribution of follistatin and activins is not known. We have used recently developed immunoassays for follistatin, activin A and activin AB to determine their presence in the intrauterine compartments during early pregnancy. Follistatin was present in highest concentrations in the extra-embryonic coelomic fluid (11.72 +/- 1.70 ng/ml; median +/- SEM), with less in maternal serum (6.35 +/- 4.58) and lowest amounts in amniotic fluid (0.97 +/- 0.52). Follistatin concentrations in extra-embryonic coelomic fluid were highly correlated with both dimeric inhibin isoforms. Activin A was present in only barely detectable amounts in some samples of extra- embryonic coelomic fluid (41% of samples) and maternal serum (26%) and was undetectable in all amniotic fluid samples. Activin AB was undetectable in all compartments. The presence of follistatin in the amniotic and extra-embryonic coelomic fluids may regulate the availability of bioactive activins and inhibins which are released into the intrauterine compartments during the development of the fetus and placenta in early pregnancy.