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Adrenal Castleman's disease is rare. One case of left adrenal Castleman's disease, who underwent retroperitoneal laparoscopic left adrenal gland and tumor resection. The postoperative pathological diagnosis was adrenal Castleman's disease (transparent vascular type), and no tumor recurrence was found after 2 years of follow-up.
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Objective To investigate the refracture and risk factors after percutaneous vertebroplasty (PVP) in the patients with hormone induced osteoporotic thoracolumbar vertebral fracture.Methods A total of 646 patients with osteoporotic thoracolumbar vertebral fractures in 425 Central Hospital of PLA from April 2010 to July 2015 were selected and divided into the primary osteoporotic thoracolumbar vertebral fractures(n=542) and hormone-induced osteoporotic thoracolumbar vertebral fractures(n=104) according to the fracture types.The incidence rate of refracture was compared between the two types of patients.The patients with hormone induced osteoporotic thoracolumbar fractures were divided into the fracture group and non-fracture group according to the refracture occurrence situation.The clinical data of the two groups were performed the univariate and multivariate Logistic regression analysis.Results There were 542 cases of primary osteoporosis,102 cases had refracture with the incidence rate of 18.82％,104 cases had hormone induced osteoporosis and 53 cases had refracture with the incidence rate of 50.96％.BMI,bone mineral density,bone cement leakage,preoperative vertebral fissure change and proportion of unreceiving anti-osteoporosis treatment had statistical difference between the fracture group and non-fracture group (P＜0.05).Bone mineral density,bone cement leakage,preoperative vertebral fissure change and no anti-osteoporosis treatment were the independent risk factors for refracture after PVP operation in the patients with steroid-induced thoracolumbar vertebral fracture (P＜0.05).Conclusion The patients with hormone induced osteoporotic thoracolumbar vertebral fracture have higher risk of refracture.Bone mineral density,bone cement leakage,preoperative vertebral fissure change,whether accepting anti-osteoporosis treatment are the major risk factors of refracture.
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Objective To investigate the refracture and risk factors after percutaneous vertebroplasty (PVP) in the patients with hormone induced osteoporotic thoracolumbar vertebral fracture.Methods A total of 646 patients with osteoporotic thoracolumbar vertebral fractures in 425 Central Hospital of PLA from April 2010 to July 2015 were selected and divided into the primary osteoporotic thoracolumbar vertebral fractures(n=542) and hormone-induced osteoporotic thoracolumbar vertebral fractures(n=104) according to the fracture types.The incidence rate of refracture was compared between the two types of patients.The patients with hormone induced osteoporotic thoracolumbar fractures were divided into the fracture group and non-fracture group according to the refracture occurrence situation.The clinical data of the two groups were performed the univariate and multivariate Logistic regression analysis.Results There were 542 cases of primary osteoporosis,102 cases had refracture with the incidence rate of 18.82％,104 cases had hormone induced osteoporosis and 53 cases had refracture with the incidence rate of 50.96％.BMI,bone mineral density,bone cement leakage,preoperative vertebral fissure change and proportion of unreceiving anti-osteoporosis treatment had statistical difference between the fracture group and non-fracture group (P＜0.05).Bone mineral density,bone cement leakage,preoperative vertebral fissure change and no anti-osteoporosis treatment were the independent risk factors for refracture after PVP operation in the patients with steroid-induced thoracolumbar vertebral fracture (P＜0.05).Conclusion The patients with hormone induced osteoporotic thoracolumbar vertebral fracture have higher risk of refracture.Bone mineral density,bone cement leakage,preoperative vertebral fissure change,whether accepting anti-osteoporosis treatment are the major risk factors of refracture.
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Due to lack of the practical technique to measure the biomechanical properties of the ocular cornea in vivo, clinical ophthalmologists have some difficulties in understanding the deformation mechanism of the cornea under the action of physiological intraocular pressures. Using Young's theory analysis of the corneal deformation during applanation tonometry, the relation between the elasticity moduli of the cornea and the applanated corneal area and the measured and true intraocular pressures can be obtained. A new applanation technique has been developed for measuring the biomechanical properties of the ocular cornea tissue in vivo, which can simultaneously acquire the data of the applanation area and displacement of the corneal deformation as well as the exerted applanation force on the cornea. Experimental results on a rabbit's eyeball demonstrated that the present technique could be used to measure the elasticity moduli and creep properties of the ocular cornea nondestructively in vivo.
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Animals , Rabbits , Biomechanical Phenomena , Cornea , Elastic Modulus , Intraocular Pressure , Muscles , Tonometry, OcularABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of Nrf2 gene knockdown on hirsutanols A-induced cytotoxicity in cancer cells.</p><p><b>METHODS</b>The changes in the cell viability following treatment with different concentrations of hirsutanols A was detected by MTT assay, and the generation of reactive oxygen species (ROS) was assayed using flow cytometry. AnnexinV-FITC apoptosis kit was used to detect the cell apoptosis. Nrf2 protein expression in HepG2 and SW480 cells transfected with the siRNA targeting Nrf2 was analyzed with Western blotting.</p><p><b>RESULTS</b>At the concentrations of 1.25, 2.5, 5, 10, 20 and 40 µmol/L, hirsutanols A obviously inhibited the cell proliferation of human liver cancer HepG2 and colon cancer SW480 cells in a concentration-dependent manner. The levels of hydrogen peroxide increased rapidly after hirsutanols A treatment in both HepG2 (30 µmol/L) and SW480 (15 µmol/L) cells. Hirsutanols A also induced apoptosis of the two cells. Pretreatment with 5 mmol/L NAC totally inhibited apoptosis and ROS accumulation in the two cells induced by hirsutanols A. Transfection of HepG2 and SW480 cells with the siRNA caused a significant reduction in Nrf2 protein expression, which resulted in an increased sensitivity of the cells to hirsutanols A.</p><p><b>CONCLUSION</b>Hirsutanols A can induce apoptosis in HepG2 and SW480 cells by promoting ROS production and up-regulating Nrf2 expression. Nrf2 knockdown by siRNA can increase the sensitivity of the cancer cells to hirsutanols A in vitro.</p>
Subject(s)
Humans , Apoptosis , Cell Line, Tumor , Cell Proliferation , Colonic Neoplasms , Metabolism , Pathology , Gene Expression Regulation, Neoplastic , Gene Knockdown Techniques , Liver Neoplasms , Metabolism , Pathology , NF-E2-Related Factor 2 , Genetics , RNA, Small Interfering , Reactive Oxygen Species , Metabolism , Sesquiterpenes , PharmacologyABSTRACT
Objective To observe the relationship between cerebral border zone infarction and cerebral artery stenosis or occlusion.Methods 45 patients admitted to our hospital in 2002 were studied retrospectively.They were diagnosied as acute cerebral border zone infarction and classified into anterior border infartion,posterior border infartion and internal border infartion by diffusion weighted MR imaging(DWI). The stenosis or occlusion of cerebral arteries was evaluated by magnetic resonance angiography(MRA) or transcranial doppler(TCD) examinations.Results Cerebral artery stenosis or occlusion was founded in 32 patients(71.1%).The lesions were most located in middle cerebral artery(47.6%),next in internal carotid artery(31%), relatively seldom in anterior cerebral artery and posterior cerebral artery(11.9%). No difference of artery abnormity was found between the patients with single border infarction and the patients with mutiple border infarction.But middle cerebral artery stenosis was more frequently seen in the patients with internal border infartion( P