AIM: To observe the effects of D-galactose on the lumber vertebra body and investigate the reasons. METHODS: 12 rats at age of 6 months were divided into two groups, control group and D-galactose group (n=6 in each). The control group were administered saline solution sc, and the D-galactose group were administered 5% D-galactose solution sc at dose of 100 mg?kg -1. After 3 month, the rats were killed by exsanguination from heart. The fourth lumber vertebra was taken and immerged in formalin. The testicle were taken and immerged in formalin at the same time. The blood serum was collected by centrifugating the collected blood after resting for a while, and it was preserved in refrigeratory at the degree of - 70 ℃.The vertebra body were embedded in plastic and sliced up after being dehydrated step by step with different concentration ethanol. The slices were analyzed under the image analysis apparatus. The testicle were made into paraffin slices and observed under the common microscope. The concentration of serum testosterone and luteinizing hormone were measured by radio-immunity assay. RESULTS: The lumber vertebra body in D-galactose group appeared osteoporosis. The serum testosterone hormone concentrations of D-galactose rats were significantly decreased. And the microstructure of testicle present aging change, but no change of serum LH concentration was observed. CONCLUTION: D-galactose can cause the osteoporosis in male rats, which may be related to affect the function of thalamus-pituitary-testicle axis, decrease the content of testosterone of D-galactose.

Objective To examine the early effects of prostaglandin E 2 (PGE 2 ) on cancellous bone in 20-month aged male rats. Methods PGE 2 was given to the aged rats for 10 and 30 days at dose of 3 mg?kg -1 d -1 respectively, while designing intact aged male rats as controls. After twice in vivo fluorochrome labeling, undecalcified longitudinal sections were subjected to analysis of bone histomorphometry. Results After 10 days treatment, osteoblast surface 〔(12.3?7.6)%〕 and osteoid surface 〔(20.4?7.2)%〕 were markedly increased than that of controls 〔(1.6?0.7)% and (4.3?1.7)%, P

AIM: To investigate the effects of D-galactose on ultrastructure of rats' hypothalamic arcuate nucleus.METHODS: 12 rats at age of 6 months were divided into two groups at random,the control and D-galactose group.Rats of control group were treated with saline solution by sc,and rats of D-galactose group were treated with D-galactose by sc at dose of 100(mg?kg~(-1)). Three months later the rats were killed by exsanguinating from heart.After being infused into the left ventricle with 2%-(2.5)% polyformaldehyde at the dose of 50(mg?kg~(-1)),the brains were taken and immerged in(2.5)% polyformaldehyde,then the arcuate nucleus was taken according to the atlas of brain,the tissues taken were made into ultrathin sections to be observed under electron microscope.RESULTS: comparing to rats in control group,neurons of the arcuate nucleus of rats in D-galactose group appeared aging,the number of organelle in plasma decreased,but the number of lipochromesome in plasma increased significantly,and the size of neurons decreased also.Furthermore the apoptosis neuron was observed,the chromosome of which congregated around the nucleus' membrane,the typical aging neuron was also observed,the neuraxon of which was atrophying.But there were no obvious changes observed in neurons of the arcuate nucleus of rats in control group,plenty of organelles were observed under electron microscope clearly.CONCLUSION:D-galactose can cause neurons of rats' arcuate nucleus aging,the neurons appeared atrophying and apoptosis.

Objective To explore the related causes and management of the death cases (following) orthotopic heart transplantation (OHT). Methods The data of the death cases (14 cases) were studied retrospectively.Results Fourteen cases died among the total 54 cases of OHT from Aug. 1995 to Dec. 2004 in our hospital. Eight cases died within 1 month and 1 case subject to combined heart-kidney transplantation died on the 38th day, and the other 5 cases died during the period from 17 weeks to 4 years. The death cases died of acute right ventricular failure (4 cases), lung infection (5 cases, including 3 cases associated with fungus infection), acute rejection (4 cases), acute renal failure (4 cases), arrhythmia (4 cases), adult respiratory distress syndrome (2 cases) and diabetes (2 (cases)). The death of 8 cases was related with several causes.Conclusion Various causes should be (responsible) for the results. In order to decrease the mortality rate, the recipients should be selected with low pulmonary vascular resistance and less preoperative complications. It is very important to discover and manage complications in time perioperatively.

Objective To explore the experience of long-term outcomes of orthotopic heart transplantation. Methods From Aug. 1995 to Dec. 2004, 40 patients with end-stage dilatation cardiomyopathy, 36 males and 4 females, aged 13～60 years underwent orthotopic heart transplantation (OHT) , 39 standard styles and 1 total style. Results 40 cases were all successful treated. The survival time is from 8 to 112 months with heart function of 0-I degree. All cases are in good quality of live and enjoy normal entertainments and work. Pulmonary infection and cardiac arrhythmia are the most common complications but they did not degrade the result after proper treatments. Conclusion Heart transplantation is an effective treatment for patients with end-stage heart diseases. Appropriate selections of recipients with low pulmonary vascular resistance, satisfactory myocardial preservation are the key points to success. The precautions and prompt treatments to the postoperative complications are guarantee for the ultimate results of heart transplantations.

Objective To identify the role of FOXC2 in the invasion and migration of colorectal cancer cells .Methods Stable cell lines expressing FOXC2(SW480/FOXC2) or vector (SW480/pBabe) were established using retroviral infection method .The morphology alterations of SW480 cells were observed using a microscope .Western blot analysis and immunofluorescence staining assays were performed to detect the expression of E‐cadherin ,Vimentin and N‐cadherin .The invasive and migratory abilities of colorectal cancer cells evaluated using Transwell invasion chamber experiment detection .Results The morphology of SW480 cells was significantly changed after overexpression .From the original shape typical of epithelial cells became spindle shaped growth , similar to the morphology of fibroblasts .Western blot analysis and immunofluorescence staining displayed that overexpression of FOXC2 led to significant downregulation of the epithelial marker E‐cadherin ,but upregulation of the mesenchymal markers Vimen‐tin and N‐cadherin .Transwell assay reveals that overexpression of FOXC2 strongly enhanced the migratory and invasive ability of SW480 cells .Conclusion FOXC2 induces epithelial‐mesenchymal transition and promotes the invasive ability of colorectal cancer cells .

BACKGROUND: Since chronic liver disorders are associated with bone loss commonly, it is very significant to probe into the prevention of such bone loss for the treatment of osteoporosis.OBJECTIVE: To study the mechanism of glycyrrhizic acid on prevention and treatment of bone loss induced by liver fibrosis in mice.DESIGN: Randomized and controlled study in which the experimental animals were taken as the objects.SETTING: Experimental animal center, central experimental room and pharmacological research room of a universityMATERIALS: The experiment was performed from January to September 2001. Forty common-grade PCR mice of either sex were employed, weighted varied from 20 to 22 g, provided by Experimental Animal Center of the Institution. According to mass-equivalence principle, 4 groups were randomized, named as control, model group, the treatment with colchicine group(CL group) and the treatment of glycyrrhizic acid group(GA group-) with 10 mice in each group.METHODS: Except the control group, in the model group, CL group and GA group, the subcutaneous injection with 400 g/L carbon tetrachloride prepared with peanut oil was given for 5 weeks to induce liver fibrosis in mice. Afterward, the treatment was applied with carbon-tetrachloride peanut-oil solution 10 mL/kg, colchicum autumnale solution 0. 1 g/kg and glycyrrhizic acid solution 0. 1 mg/kg successively. At the end of the experiment, the eyeball was extirpated for blood collection. The serum was separated to assay the various relevant biochemical indexes of liver injury, observe the changes in liver pathological tissues and measure bone calcium(Ca2+) content of femur and the contents of other bone trace elements as well as bone oxyproline hydroxyproline (Hyp).Effects of glycyrrhizic acid on the contents of bone trace elements in mice of every group.RESULTS: The levels of serum aspartate aminotransferase(AST) and alanine aminotransferase(ALT) in CL group and GA group were lower than those in the model group( P < 0. 01 ). The level of albumin and ratio between albumin and globulin in the model group were lower than those in CL group and GA group( P < 0.01, P < 0.05) . The content of bone calcium in CL group and GA group were lower than that in the control group ( P < 0. 05),but that was higher than the model group( P < 0.05) . The unit contents of copper(Cu2+ ), magnesium(Mg2+) and zinc(Zn2+) in the right femur of the model group were all higher than the control group ( P < 0.01 ), but the contents of those in GA group were not indicated significant differences compared with the control group ( P > 0.05 ). The liver pathological changes of mice in GA group were obviously milder compared with the model group ( P < 0.01 ) and it was shown with VG staining the severity of hyperplasia of liver collagenous fibers was remarkably milder compared with the model group( P < 0.01).CONCLUSION: The extractive solution of glycyrrhizic acid induces medical metabolic enzyme in the liver, enhances detoxification of liver, protects liver to maintain protein metabolic level and maintains the normal metabolism of bone to promote bone Ca2+ and balance between oxyproline hydroxyproline (Hyp) and trace elements of bone so as to prevent and treat bone loss.

BACKGROUND:Disequilibrium of proportion of adipogenesis and osteogenesis from bone marrow mesenchymal stem cells (BMSCs)is associated with many bone diseases.However,it has been demonstrated that Wnt signaling pathway could play an important role in regulation of BMSC differentiation.OBJECTIVE:To investigate the different gene expression profiles and to find the target gene on Wnt signaling pathway of the BMSCs,after being induced to osteoblasts and adipocytes respectively using Wnt signaling pathway PCR array.METHODS:The third-passage BMSCs,after being induced to osteoblasts and adipocytes respectively for 7 days.The total mRNA of MSCs was extracted by Trizol.BMSC morphology was observed following osteogenic and adipogenic induction under an inverted microscope.Gene array was detected by rat Wnt signaling pathway PCR array.Non-induction group served as controls.The ratio of increase/reduction gene of osteoblasts and adipocytes was calculated.RESULTS AND CONCLUSION:Under an inverted microscope,BMSCs with high homogenicity were obtained following passage 3.BMSCs differentiated into osteoblasts following osteogenic induction,and into adipocytes following adipogenic induction.Compared with non-induction group,fifteen genes(Dkk1,kremen,FZD1,FZD7,et al.)were expressed up-regulated(ratio ＞ 2)and 16(sFrp 5,β-catenin,Dvl3,Tcf7,et al.)genes down-regulated(ratio ＜ 0.5)when the third-passage BMSCs were induced to adipocytes.Six genes(Dkk1,kremen,β-catenin,Wnt11,et al.)were expressed up-regulated and 15 genes(sFrp5,sFRP4,Fzd1,et al.)down-regulated when BMSCs being induced to osteoblasts.Above-mentioned results suggested that Wnt signaling pathway plays an important role in the osteoblast and adipocyte differentiation from BMSCs.

AIM To study the dose dependent effects on osteoporosis induced by retinoic acid(RA) and to analysis the metabolic characteristics of bone. METHODS Three dosages of retinoic acid were given to the mice for 2 weeks while the body weight(BW) were measured once a week. At the end, femoral dry weight, Bone hydroxyproline, calcium content, Phosphor, Magnesium, Zinc, Manganese and Sulphonium of femora were measured. RESULTS Compared with normal control mice, three dosages of retinoic acid can induce the decrease of femoral dry weight and the short transverse diameter of femoral, Bone hydroxyproline content decreased remarkably, and so did the bone mineral. The Bone HOP and Bone Ca content was coincident with the femoral dry weight, but the lessening of Bone P, Bone Mg, Bone Zn and Bone Mn became inverse ratio with the femoral dry weight, particularly that of the Bone Zn. CONCLUSION Three dosages of retinoic acid in mice can induce osteoporosis with the lessening of bone mass, which characteristics were the losing of Bone HOP and the Bone Ca content in geometric proportion. The levels of Bone P, Bone Mg, and Bone Zn had lost remarkably in the early time, the Bone Zn may play importance function in osteoporosis model induced by retinoic acid.