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1.
Chinese Journal of Postgraduates of Medicine ; (36): 436-439, 2018.
Article in Chinese | WPRIM | ID: wpr-700240

ABSTRACT

Objective To investigate the correlation between serum hepcidin level and iron, mineral metabolism in maintenance hemodialysis (MHD) patients. Methods Seventy-five MHD patients were selected. The serum hepcidin, serum iron and mineral metabolism indexes were detected by enzyme-linked immunosorbent double antibody sandwich method, and their correlation was analyzed. Results The level of serum hepcidin in 75 MHD patients was 87- 264 μg/L. The patients were divided into 3 groups according to serum hepcidin level. In group A, the serum hepcidin level of 26 cases was<120 μg/L; in group B, the serum hepcidin level of 24 cases was 120- 200 μg/L; in group C, the serum hepcidin level of 25 cases was>200 μg/L. There were no significant differences in age, gender, albumin and serum calcium among 3 groups (P > 0.05). The levels of ferritin, transferrin saturation (TS), serum phosphorus and parathyroid hormone (PTH) increased in the 3 groups as the hepcidin level increased, while hemoglobin, serum iron, total iron binding capacity (TIBC), and 25 hydroxy vitamin D decreased significantly, and there were statistical differences (P<0.05). The Pearson correlation analysis result showed that serum hepcidin was positively correlated with ferritin, PTH, serum phosphorus (r = 0.862, 0.536 and 0.320; P<0.01); and serum hepcidin was negative correlation with serum iron, TIBC, hemoglobin, 25 hydroxy vitamin D (r=-0.358,-0.270,-0.284 and-0.614; P<0.01); but there was no correlation between serum hepcidin and albumin and serum calcium (r=0.018 and-0.005, P>0.05). Conclusions The serum hepcidin level in MHD patients is closely related to iron and mineral metabolism.

2.
Chinese Journal of Tissue Engineering Research ; (53): 9041-9044, 2009.
Article in Chinese | WPRIM | ID: wpr-405288

ABSTRACT

BACKGROUND:Under different induction conditions,bone marrow mesenchymal stem cells can differentiate into the mesodermal tissues such as osteoblasts,chondroblasts,muscle cells,adipocytes and so on.OBJECTIVE:To verify the effect on repairing the rabbit articular cartilage injury using bone marrow mesenchymal stern cells (MSCs)induced by tissue engineering method.DESIGN,TIME AND SETTING:Randomized controlled animal experiment was performed in the Clinical Center Laboratory of Shenyang Medical College between May 2005 and December 2007.MATERIALS:Twenty health New Zealand rabbits,irrespective of genders,aged 2-3 months,were used.METHODS:①Rabbit bone marrow MSCs were cultured in vitro,experiment group was cultured for one week withdexamethasone,basic fibroblast growth factor and vitamin C,then for additional 3 weeks with transforming growth factor-β instead of basic fibroblast growth factor;calls without inductors served as controls;②Twenty rabbits were used to establish knee articular cartilage defect models,which were then divided into three groups at random. Experiment group (n=5) was transplanted with the induced bone marrow MSCs;control group with the non-induced cells;blank control group with saline. At 2,4,6,8 weeks postoperation,two rabbits in the experiment group were killed,while one animal in control group and blank control group was killed for the index determination.MAIN OUTCOME MEASURES:①Cell morphology. ②Alkaline phosphatase activities.③General observation. ④X-ray observation.⑤Histological observation.RESULTS:①The morphology of the induced bone marrow MSCs was changed,from long fusiform to polygon,which was similar to cartilage calls-like morphology.②After the bone marrow MSCs were induced for 4 weeks,the alkaline phosphatase activities were obviously enhanced(P<0.05).③Eight weeks after transplantation,the specimens in the experiment group exhibited smooth surface and unclear outlines with surrounding cartilage;X-ray results showed joint space broadened,subchondral bone sack was improved;histological slices observation revealed similarity with normal chondrocytes.CONCLUSION:Autologous MSCs transplantation can repair articular cartilage injury.

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