Objective To study the relationship between ATP level changes detected by hepatic 31P MRS with the pathologic changes of liver in rabbits and to investigate the diagnostic value of ATP level changes in acute hepatic radiation injury. Methods A total of 30 rabbits received different radiation doses ( ranging from 5,10,20 Gy) to establish acute hepatic injury models. Blood hepatic function tests, 31P MRS and pathological examinations were carried out 24 h after irradiation The degree of injury was evaluated according to hepatocyte pathology. Ten healthy rabbits served as controls. The MR examination was performed on a 1.5 T imager using a 1H-31P surface coil with 2D chemical shift imaging technique. The relative quantities of phosphomonoesters (PME), phosphodiesters (PDE), inorganic phosphate (Pi) and adenosine triphosphate (ATP) were measured. Analysis of variance was used to compare the results of 31P MRS and histopathology under various acute hepatic radiation injuries, and SNK was used further to conduct comparison between each other if there was significant difference. Results The ATP relative quantification in control( n= 10), mild ( n = 12), moderate ( n = 11 ), and severe ( n = 7 ) injury groups according to pathological grading were 1.83 ± 0. 33, 1.58 ± 0. 25, 1.32 ± 0. 07 and 1.02 ± 0. 18, with significant differences among them (F =22. 878 ,P ＜0. 01 ), and it decreased progressively with the increased degree of injury. The PDE index showed no significant trend for the evaluation of hepatic radiation injury. The area under the peak of β-ATP decreased with the increased severity of radiation injury. Conclusions The relative quantification of hepatic ATP levels can reflect the pathological severity of acute hepatic radiation injury. The decreasing hepatic ATP levels may be used as biomarker of acute liver injury following radiation.

Objective To investigate the effect and mechanisms of factor fibroblast growth factor inducible 14(Fn14)in the high glucose induced-cardiomyocyte hypertrophy. Method To observe the expression of collagenⅠ, connective tissue growth factor ( CTGF ) , transforming growth factor-β1 ( TGF-β1 ) , and Fn14 in high glucose induced-cardiomyocyte hypertrophy. Fn14 expressions was down-regulated by siRNA interference technique, and then the expressions of collagen Ⅰ, CTGF, and TGF-β1 were observed, and the mechanism was also explored. Results The expression of collagen I, CTGF and TGF-β1 was significantly up-regulated after high glucose induced-cardiomyocyte hypertrophy for 72 h. At the same time, the expression of Fn14 was increased after 72 h-treatment, and reached the peak at concentration of 30 mmol/L high glucose. High glucose could not up-regulated the expression of collagenⅠ, CTGF, and TGF-β1 after siFn14 interference, while the same result was observed in the expression of p-JNK. Conclusion The expressions of collagenⅠ, CTGF, TGF-β1, and Fn14 in cardiomyocyte of neonatal rats were induced by high glucose. While Fn14 expression was inhibited, the expressions of collagenⅠ, CTGF, and TGF-β1 were down-regulated, which seems to be involved with p-JNK signaling pathway.

BACKGROUND: It is a hotspot that calcium phosphate and calcium sulphate as the main ingredients are combined with one or more other materials to improve or increase the performance of bone tissue engineering scaffolds. OBJECTIVE: To introduce the research advance of these two kinds of scaffolds in bone tissue engineering. METHODS: The articles related to the bone tissue engineering published during January 2000 to June 2015 were retrieved from CNKI and PubMed databases by computer. The key words were “bone tissue engineering, scaffold, calcium phosphate, calcium sulphate, vascularization” in Chinese and English, respectively. ESULTS AND CONCLUSION: Calcium phosphate and calcium sulfate are characterized as having good biocompatibility, biodegradability, osteoconductivity and complete bone substitutability. However, single use of calcium phosphate or calcium sulfate scaffold has certain disadvantages, both of which are difficult to ful y meet the requirements of the bone defect repair. Improvement can be acquired in the mechanical strength, injectability and biodegradability, as wel as drug-loading and pro-angiogenesis of the scaffold in combination with other materials. In the basal and clinical research, we should explore and develop ideal scaffolds in on the basis of therapeutic aim. However, most of the scaffold studies are stil at the extracorporeal and animal experiment stage, and the comparative studies on composite scaffolds and optimal proportion of those composite scaffolds stil need to be further investigated.

BACKGROUND:There are many postmenopausal women taking hormone, which leads to much loss of bone mass, further inducing fragility fractures. The studies on the hormone exposure combined with ovariectomy-induced osteoporotic model are still immature, and the related molecular mechanism remains unclear. OBJECTIVE: To establish the rat osteoporotic model induced by ovariectomy combined with glucocorticoid exposure and to explore the underlying molecular mechanism. METHODS: Thirty 3-month-old female Sprague-Dawley rats were randomly divided into blank control, sham and model groups (n=10 per group). The rats in the blank control group received no intervention; rats in the sham group were clipped off a little of coeliac adipose tissue; the model rats received bilateral ovariectomy and 4-week administration of glucocorticoid. RESULTS AND CONCLUSION:At 4 weeks after modeling, compared with blank control and sham groups, the model group showed significantly lower bone mineral density of the femur, number of bone trabeculae and bone volume/total volume, and significantly wider bone trabecular spacing. Additionally, the model group revealed the damaged bone trabecular structure and thiner cortical bone. The expression level of Runx2 was downregulated whereas both collagen type 1α1 and peroxisome proliferators activated receptor γ mRNA were upregulated in the model group. These findings suggest that ovariectomized rats exposed to glucocorticoid rapidly develop femur osteoporosis, maybe by downregulating the expression of Runx2, as well as upregualting collagen type 1α1 and peroxisome proliferators activatedreceptor γ mRNA.