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.

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 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.

Aim To investigate the effect of tanshinol on bone mineral density and microstructure of proximal tibias in rats with bone loss induced by glucocorticoid. Methods Sixty 7-month-old female SPF SD rats were randomly divided into 6 groups with 1 0 rats per group:control group(saline:5 ml·kg -1 ·d -1 ),glucocorti-coid group (prednisone acetate:6 mg·kg -1 ·d -1 ), glucocorticoid +low dose of tanshinol group(1 2.5 mg ·kg -1 ·d -1 ),glucocorticoid +medium dose of tan-shinol group (25 mg·kg -1 ·d -1 ),glucocorticoid +high dose of tanshinol group (50 mg·kg -1 ·d -1 ), glucocorticoid +(positive control drug)calcitriol group (0.045 μg · kg -1 · d -1 ).Rats were gavaged with prednisone acetate continuously for 1 4 weeks to estab-lish the bone loss model.Meanwhile,tanshinol and calcitriol were orally administered to the rats which were treated with prednisone acetate for intervention. At the end of the experiment,the left proximal tibias were collected for Micro-CT scanning and three-dimen-sional reconstruction of cortical and trabecular bone re-
spectively to observe the changes of bone microstruc-ture and test related parameters.Results Bone min-eral density was decreased and bone microstructure was destroyed in proximal tibias of rats after treatment with glucocorticoid.Both tanshinol (25 mg·kg -1 ·d -1 ) and calcitriol(0.045 μg·kg -1 ·d -1 )could increase bone mineral density and improve bone microstructure in proximal tibias without significant differences be-tween each other.Tanshinol (50 mg · kg -1 · d -1 ) could improve bone microstructure to some extent,but it had no significant effect on bone mineral density. Tanshinol(1 2.5 mg·kg -1 ·d -1 )had no significant effect on bone mineral density or microstructure.Con-clusion Oral administration of tanshinol (25 mg · kg -1 ·d -1 )to the rats treated with glucocorticoid can increase bone mineral density and improve bone micro-structure in proximal tibias.

AIM: To investigate the protective effect of 6% Hydroxyethyl Starch(HES,200/(0.5)) on the brain of hemorrhagic-shocked rats.METHODS: Sprague-Dawley rats were randomly divided into sham operation group(group A),hemorrhagic shocked group(group B),whole blood return group(group C),HES at 2x shed blood volume(SBV) group(group D),HES at 1x SBV plus 1/2 SBV group(group E).Hemorrhagic Shock was induced by intermittently withdrawing blood from an iliac catheter.Except group A and B,the other groups were resuscitated with different liquids and lasted 30 min after 1h for shock.The extent of brain edema and inflammatory cells infiltrating was observed by Hematoxylin-Eosin staining,and the expression of nuclear factor kappa-B(NF-?B) in the rat brain and translocation of nucleus were detected using immunohistochemistry and Western blot method.RESULTS: Except the sham group,there were brain edema and inflammatory cells infiltrating in the other groups,which was more obvious in group C and D.The expression of NF-?B in the rat brain was significantly increased in group B and other groups as compared with those in group A(P

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.

AIM: To study the cerebra damaged by long-term administration of prednisone,and investigate the preventive effects of compound danqi (CD) in rats. METHODS: 40 SD rats were randomly divided into 5 groups with 8 rats each group. Group 1 was control (NS group),other groups were oral gavages prednisone ( 2.7 mg?kg -1 ?d -1 ) first,and then plus vehicle (GC group),or plus CD at dose of 2.5 , 5.0 or 10.0 g?kg -1 ?d -1 ,respectively,once a day for 12 weeks. At the experimental endpoint,animals were drawn blood from right ventricle under anesthesia. The left half cerebrum was milled in 10% homogenate to test the content of mono-amine oxidase (MAO),superoxide dismutase (SOD) and acetylcholinesterase (AchE). The right half cerebrum was for histological observation. RESULTS: The concentration of SOD and AchE decreased,yet MAO increased significantly in GC group. Moreover,histopathology showed that the structure of cerebrum cortex became thinner and hippocampi was in disorder. Dropsical and necrotic nerve cells were found. Yet CD could prevent the changes of nerve centre in prednisone tats. CONCLUTION: Cerebra damage occurs in four-month-old male Sprague-Dawley rats after prednisone-treated for 12 weeks. The treatment of CD in different dose can prevent the damage.