AIM:To observe the histopathological changes of vascular calcificated rats following intervention with alendronate,further more,to verify the therapeutic action of alendronate on angiosteosis.METHODS:Thirty Sprague Dawley rats were divided into the normal,Vitamin D3 and alendronate groups by random number table after feeding for 1 week.Rats in the Vitamin D3 and alendronate groups were lavaged with 250 000 U/(kg ?d) Vitamin D3 or iso-capacity of sodium chloride at 0,24,and 48 hours after model preparation.From the fourth day,rats in the alendronate group were treated with 0.9 mg/(kg ?d) alendronate.All rats were sacrificed at the end of 6 weeks,removed aorta and aortic arch.The pathological change was analyzed by hematoxylin-eosin staining.In addition,calcium contents of blood vessel were measured.Von Kossa staining,Image-Pro Plus 6.0 image analysis software were used to determine the ratio of calcified plaque,and detected the content of blood fat.RESULTS:There had calcified plaque in the vessel wall of aortic arch in the alendronate group,but the number was obvious smaller than and the necrosis area was significantly lower than that of the Vitamin D3 group.The calcium contents of blood vessel,ratio of calcificated area,as well as the concentration of total cholesterol was decreased compared with the Vitamin D3 group(P

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 study the antitumor e ff ects of losartan in EAC mice. METHODS: The inhibitory rates of t umor growth and the ratio of extending viability were observed in EAC mice in th ree groups given losartan, 5-FU and NS, respectively. RESULTS: Comparing with the control groups, the inhibition to tumor growth was 46.3 % in losartan ( 12.5 mg?kg -1 ) group. But losartan did not lengthen life time in EAC mice. The inhibition to tumor growth was was 31.5 % in 5-F U (5 mg?kg -1 ) group. CONCLUSION: Losartan can inhibit the tumor growth of EAC, but not lengthen life time of the animals.

OBJECTIVE:To study the effect of Yupingfeng(YPF)extract on Ca,P,Mg and hydroxyproline of bone in model rats with osteoporosis induced by cyclophosphamide(CP)and to discuss the preventive and therapeutic effect of YPF ext-ract on CP-induced osteoporosis.METHODS:A total of 40 rats were randomly divided into four groups:control group,CP group,YPF extract group,and calci?m carbonate + Vit D group.The rats were sacrificed at 15 days of experiment,and the levels of Mg,Ca,P and hydroxyproline of left femoral bone were determined.RESULTS:Compared with control group,levels of different index with CP group was significantly decreased;compared with CP group,levels of Ca,Mg,P and hydroxyproline of bone in rats treated with YPF extract were significantly increased.CONCLUSION:CP may induce decrease of levels of Ca,Mg,P and hydroxyproline of bone,however,on which YPF extract has preventive and therapeutic effect.

Dermatitis and eczema are allergic relapsing inflammatory skin disorders. The precise mechanisms still are unclear. Experimental animal models are indispensable tools to study the pathogenic mechanisms and test novel therapy. A considerable number of mouse models have been proposed and used to study specific aspects of the disease. This paper summarizes the currently available animal models.

Objective To observe the changes of morphology and biochemical parameters in rats with D-galactose-induced skin ageing. Methods Twenty-six female and male rats were randomly divided into 2 groups. D-galactose group rats were injected subcutaneously with 120 mg?kg-1?d-1 of D-galactose everyday, whereas the control group with normal saline. The rats were sacrificed on days 100. The ageing-related biochemical parameters were detected in the blood and skin, and the cutaneous histopathology was observed. Epidermal thickness and area of elastic fibers were determined quantitatively with imaging analysis system. Results Epidermal thickness and content of elastic fibers were significantly lower in D-galactose group than those in the control group. The loose arrangement of collagen and elastic fibers was evident in D-galactose group. These features of the rats in D-galactose group were similar to those in the ageing skin of human beings. Compared with the control group, the levels of hydroxyproline decreased and malondialdehyde (MDA) increased in the skin of the D-galactose group. The activity of glutathione peroxidase (GSH-PX) and catalase (CAT) in the whole blood and that of superoxide dismutase (SOD) in erythrocytes were remarkably reduced in the D-galactose group as compared to the control group. Conclusions The rat models with skin ageing are established by subcutaneous injection of 120 mg?kg-1?d-1 of D-galactose once daily for 100 days. The changes of morphologic and biochemical parameters in these models are analogous to those in human skin ageing.

Humans ; Neoplasm Recurrence, Local ; prevention & control ; Pelvis ; pathology ; Postoperative Period ; Rectal Neoplasms ; pathology ; surgery

Humans ; Neoadjuvant Therapy ; Stomach Neoplasms ; therapy

This study examined the effects of arsenic trioxide on apoptosis and interleukin4 release in T cells of asthmatic patients in vitro and investigated the role of Bcl2 in the active mechanism. Tcells were isolated from asthmatic patients (n=21) and healthy controls (n=20), and then treated with arsenic trioxide and dexamethasone. Cell apoptosis was measured using fluorescence microscopy, flow cytometry and a cytochrome c ELISA kit. Interleukin4 levels in the serum and in supernatants from T cells were quantified by ELISA. Flow cytometric analysis and immunofluorescence studies were performed to determine Bcl 2 expression. Tcells of the asthmatic patients (I.e. without treatment) exhibited decelerated spontaneous apoptosis after 24 h incubation in vitro when compared to T cells of the healthy controls. With dexamethasone treatment, an increase in apoptosis of Tcells was not significantly different between both groups, irrespective of the method used. Arsenic trioxide treatment, however, significantly increased the apoptosis of T cells of the asthmatic group and showed a slight effect on the control group. In asthmatic patients, elevated levels of interleukin 4 and upregulated Bcl 2 expression were detected. Moreover, in vitro, T cells of asthmatic patients spontaneously released more interleukin4 and exhibited more Bcl 2 expression than T cells from the control group. Arsenic trioxide treatment significantly decreased interleukin4 release and downregulated Bcl 2 expression in asthmatic patients, while it only slightly affected healthy controls. Dexamethasone treatment decreased interleukin4 release in both groups examined. It did not significantly influence Bcl2 expression. These results suggest that arsenic trioxide induces T cell apoptosis and decreases interleukin4 release in T cells of asthmatic patients in vitro and that downregulation of Bcl2 expression may be an important mechanism.

AIM To study the possible mechanism of the treatment of arsenic trioxide on asthma. METHODS T cells isolated from 21 asthmatic patients and 20 healthy controls were treated with arsenic trioxide (0.1 mg·L-1) or dexamethasone (5 mg·L-1),in vitro, for 24 h. Interleukin-4 (IL-4) levels in supernatants from T cells were quantified with ELISA. Cell apoptosis was measured by using fluorescence microscopy, flow cytometry and cytochrome c ELISA kit. RESULTS T cells of asthmatic patients spontaneously released more IL-4 than that of healthy controls. Arsenic trioxide significantly decreased IL-4 release of T cells from asthmatic patients, which was more obvious compared with healthy controls. Dexamethasone decreased IL-4 release in both groups. Apoptosis percentage and cytochrome c content in cytoplasm of T cells from asthmatic patients were lower than those from healthy controls. Arsenic trioxide significantly increased the apoptosis percentage and cytochrome c content in cytoplasm of T cells in the asthmatic group, and had slighter effects on that in healthy controls. Dexamathasone increased the apoptosis percentage and cytochrome c content of T cells in both groups. CONCLUSION The mechanism of the treatment of arsenic trioxide on asthma involves the induction of T cell apoptosis and decrease of IL-4 release in asthmatic patients.