RESUMO
Aim To study the effects of prenatal hy-poxia on the risk of fatty liver disease to search the drug targets .Methods Intrauterine hypoxia rats model was established .The bodies and livers of fetal rats of 21 days, and adult offspring rats of 5 months with and without anoxic treatment were all weighed .The liver index was calculated and the concentrations of renin-angiotensin system components in circulation system and livers of offspring rats were measured .Results The weight of the bodies , livers and index of liver weight to body weight ( liver index ) were significantly decreased in the PH group compared with the normal group.These differences disappeared in adulthood . However, the liver index of adult offsprings in the PH group after hypoxia stress for 7 days was significantly increased compared with that of adult offsprings in nor-mal group.There were no significant differences in the concentrations of AngⅠ, AngⅡ and ACE in plasma and livers between the two groups of fetal rats and the two groups of adult offspring rats separately .The con-centrations of AngⅡ in the livers of adult rats in PH group were significantly higher than those in normal group.The concentrations of AngⅠ in livers and the concentrations of AngⅡ in plasma and livers in the group treated with hypoxia stress for 7 days were signif-icantly higher than those without hypoxia stress .The concentrations of ACE in livers and the concentrations of AngⅡ in plasma and livers in PH adult offsprings were significantly higher than those of normal adult off-springs .Conclusion PH can induce the increase of RAS content in the livers of fetus and adult rats , RAS is more likely to be activated after hypoxia stimulation in the following adulthood .PH is a potential mecha-nism that mediates offspring susceptibility of fatty liver .
RESUMO
BACKGROUND:The reasons for spinal imbalance include spinal deformity, spinal degenerative disease osteoporotic vertebral compression fractures. We believe that the power factor (back muscle) plays a key role in spinal sagittal imbalance. OBJECTIVE:To analyze the reasons for spinal sagittal imbalance by observing clinical manifestations and therapeutic outcomes in patients with osteoporotic vertebral compression fractures. METHODS:A total of 41 patients with osteoporotic compression fractures combined with spinal sagittal imbalance were retrospectively analyzed from January 2012 to May 2013. Al patients were subjected to percutaneous bal oon vertebroplasty under local anesthesia. Before treatment, they received bone density, standing ful-spine lateral X-ray, CT and MR imaging with injured vertebrae as the center. Using standing ful-spine radiographs, the height of anterior border of the injured vertebrae, Cobb angle of kyphosis and improved angle, wedging angle of the injured vertebrae and improved angle were measured. The patients underwent weight loading test and walking test. Preoperative and postoperative data were compared. RESULTS AND CONCLUSION:The patients affected spinal sagittal imbalance symptoms, so the walking distance was significantly shorter than that postoperatively (P<0.05). Moreover, the time of weight loading test was significantly shorter than that postoperatively (P<0.05). In standing ful-spine radiographs, the average difference of Cobb angle was (10.01±0.76)°. The mean difference of vertebral wedging improvement was (4.84±0.40)° (P<0.05). Al patients were fol owed up. Low back pain and sagittal imbalance symptoms were relieved. No severe complications appeared after percutaneous bal oon vertebroplasty. Results indicated that patients with osteoporosis compression fractures can affect the symptoms of spinal sagittal imbalance, which is not only induced by wedging of the injured vertebra. In addition, after percutaneous bal oon vertebroplasty, imbalance symptoms are apparently improved, suggesting that back pain after spinal fracture limits back muscle strength and is an important cause for spinal sagittal imbalance.
RESUMO
Aim Toexaminethecombinedeffectsof 5-ALA and metformin on diabetes mellitus induced by streptozotocin( STZ) in mice, and to discuss the mech-anisminitially.Methods Thediabeticmiceinduced by intraperitoneal injection of STZ were treated with 5-ALA and/or metformin for 30 days. Physical signs, fasting blood glucose ( FBG ) , fasting plasma insulin ( FIns) , plasma leptin ( Lep) , glucose tolerance, and histological changes of liver and pancreas were as-sessed. Insulin resistance was evaluated by the homeo-stasismodelassessment(HOMA).Results There were more significant effects when 5-ALA combined with metformin than only using metformin on lowering FBG, FIns and Lep. And 5-ALA combined with met-formin could improve glucose tolerance and the insulin sensitivity. Microscopic analysis demonstrated that sig-nificant changes in pancreatic islet and characteristic feature of the vacuolization phenotype in liver was ob-served on diabetic mice, and use of 5-ALA could in-hibit shrinking pancreatic islet number and hepatic morphological changes, especially in combination with metformin.Conclusions Asynergisticeffectof5-ALA and metformin is observed. Combined therapy of 5-ALA and metformin can decrease FBG and improve glucose tolerance, insulin sensitivity and islet ? cells function and morphology.