Objective To investigate the effects of cadmium on bone loss in ovariectomized rats. Methods Female Sprague-Dawley rats, aged 6 months, were divided to 5 groups, i.e. sham operation group (sh) , control group (ovariectomy 0 mg/L Cd), low dose group (ovariectomy+50 mg/L Cd), medium dose group (ovariectomy+100 mg/L Cd), high dose group (ovariectomy+200 mg/L Cd). Cadmium was administrated via drinking water. After 24- week exposure, the following indices were measured, bone mineral density (BMD) at the femurs necks, serum estradiol, urinary and blood cadmium, urinary ? 2-MG, bone calcium and cadmium, and calcium contents in feces and urine. Results Estradiol and BMD significantly declined in the ovariectomized rats. Cadmium administration aggravated the declines of BMD in a dose-effect pattern. Urinary ? 2-MG, the excretions of calcium in feces and urine were significantly higher in cadmium-exposed groups in a dose-effects pattern. And bone calcium was also significantly lower in the group exposed to 200 mg/L cadmium than in the control group. Conclusion It is indicated that cadmium could increase bone loss and decrease BMD in ovariectomized rats by increasing the excretions of calcium in feces and urine.

Objective To investigate the clinical and pathological features of patients co-infected with hepatitis B virus(HBV)and hepatitis C virus(HCV)and to study the underlying interaction between HBV and HCV in these patients.Methods The liver biopsy and sera samples of 226 patients with chronic hepatitis were collected.Real-time fluorescent quantitative polymerase chain reaction were used tO measure HBV DNA and HCV RNA,respectively.Enzyme-linked immunosorbent assay (ELISA)was utilized to detect HBV serological marker and anti-HCV antibody.Liver biopsy examination was performed through needle aspiration.HBsAg and HBcAg in liver tissue were detected by immunohistochemistry,while HBV DNA and HCV RNA were detected by in situ hybridization.Results Sixty two point five percent patients co-infected with HBV and HCV suffered from severe hepatitis,while the rates of those infected with HBV or HCV alone were 27.1%and 30.6%,respectively(X2=14.70,P＜0.01).The serum alanine aminotransferase,aspartate aminotransferase, total bilirubin.direct bilirubin and albumin levels of patients infected with HBV alone were higher than those of patients co-infected with HBV and HCV or those infected with HCV alone,which showed statistically significant difference(X2=8.52.P＜0.05).The HBsAg titers in serum samples and in liver tissue samples were inconsistent in both co-infected patients and HCV mono infected patients (X2=15.60,P＜0.01).The HBV DNA positive rate of co-infected patients was 12.5%,which was lower than that of patients infected with HBV alone(87.7%,X2=17.66,P＜0.01).Meanwhile,the HCV RNA positive rate of patients co-infected with HBV and HCV was 75.0%,which was lower than that of patients infected with HCV alone(80.6%).However,the difference was not statistically significant(P＞0.05).Conclusion Co-infection with HBV and HCV may induce severer liver injury than HBV infection or HCV infection alone.

Objective To explore the diagnosis value of cystatin C(Cyst-C) level on the renal function early impairment of Henoch-Schonlein purpura(HSP).Methods The selected serum creatinine(SCr) normal 45 sufferers,with measured their urine routine analysis,and the same time did serum Cyst-C.Compared with 30 healthy children of serum Cyst-C.Results The levels of serum Cyst-C in HSP were definitely higher than those in healthy group,and the differences were together with its signifincance(P

OBJECTIVETo study the relationship between the protection of Ginsenoside(GS) for spinal cells and nitric oxide (NO).

METHODSpinal cells were cultured in vitro, the model of peripheral nerve was established by scarifying the cells, and NO was measured by Griess method.

RESULTNO in injury group was high than that in noninjury group and NO in group cultured by GS was less than that in group cultured by common medium.

CONCLUSIONNO increases when peripheral nerve is injuried, and the protective effect of GS on spinal cells may be through inhibiting NO release.

Animals ; Cells, Cultured ; Fetus ; Ginsenosides ; isolation & purification ; pharmacology ; Motor Neurons ; cytology ; drug effects ; metabolism ; Neurons, Afferent ; cytology ; drug effects ; metabolism ; Neuroprotective Agents ; pharmacology ; Nitric Oxide ; metabolism ; Panax ; chemistry ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; cytology ; metabolism

Objective To investigate the effects of human endostatin(hES)on ovarian cancer cells A2780 growth in vitro and in vivo and the possible mechanism.Methods The coding region for hES was amplified by PCR from human liver tissue and then subcloned into pcDNA3.1 vector.The growth rate of A2780 cells transfected with hES was observed.A2780 cells(1× 10~7/ml)were inoculated subcutaneously into 20 nude mice,and the mice were randomly divided into two groups:the hES-trans-fected group(group A,n=10)and the control group(group B,n=10).One month later,the size of subcutaneous tumor was measured,and the tumor inhibition rate was calculated.The specimens were stained with HE for the histological analysis.Cell apoptosis in ovarian neoplasm transplantation tissues was determined by flow cytometry.The expression of hES and Bcl-2 was detected by Western blot.Results The growth rate of the hES-transfected ovarian cancer cells A2780 was significantly decreased.In group A,growth of tumor in nude mice was significantly slowed as compared with group B(P<0.01),with the tumor inhibition rate being 74% in group A.The tumor necrosis was increased and the basophilia stain of nucleus decreased significantly in group A as compared with group B.The expression of hES was increased significantly,but that of Bcl-2 was decreased significantly in group A.Flow cytometry revealed that hES transfection could significantly incyease the apoptosis rate of tumor cells(P<0.05).Conclusion Transfection of hES could suppress the growth of ovarian cancer cells A2780 in vitro and in vivo,which may be related tO the promotion of apoptosis.

Adolescent ; Adult ; Female ; Finger Injuries ; surgery ; Humans ; Male ; Middle Aged ; Skin Transplantation ; Soft Tissue Injuries ; surgery ; Surgical Flaps ; Young Adult

TcpC is a homolog of the Toll/interleukin-1 receptor (TIR) domain and is secreted by uropathogenic E. coli strain CFT073. TcpC can bind to MyD88, hereby exerting inhibitory effects on macrophages. TcpC represents an important virulence factor that promotes bacterial survival and pathogenicity. TcpC plays a critical role in urinary tract infection, particularly in the pathogenesis of pyelonephritis. In this review,the progress and prospects in TcpC research are discussed.
Animals ; Escherichia coli ; pathogenicity ; Escherichia coli Proteins ; physiology ; Humans ; Mice ; Pyelonephritis ; microbiology ; Urinary Tract Infections ; microbiology ; Virulence Factors ; physiology

Objective To investigate the role of basophils in the imbalance of Th 1/Th2 response in mouse models of collagen-induced arthritis(CIA).Methods 4-6-weeks old C57/BL6 mice were immunized with collagen at multiple points on the back and foot twice (0 and 3 weeks) to establish a mouse model of collagen-induced arthritis.Blood samples were collected before the first immunization and 1, 3, 6 and 9 weeks after immunization , and cells from lymph nodes were collected.Flow cytometry and ELISA were employed to detect the levels of basophils and IL-4, and the joint swelling was scored.Results Mouse model of CIA was successful established .The ratio of IL-4/IFN-γof the CIA group was significantly lower than that in the mice before CIA modeling and the control group , indicating a Th2-dominant response .At the same time, the peripheral basophils counting and percentage of IL-4 positive basophils of the CIA group were significantly higher than those of the control group .While, the IL-4/IFN-γratio of the CIA group was significantly higher than that of the control group , indicating a Th1-dominant response .The peripheral basophils counting of the CIA group was slightly lower than that of the control group .Conclusion Basophils may participate in the development of CIA in mouse models through affecting the imbalance of Th 1/Th2 response.

Objective To explore the function of ERCC2/XPD polymorphisms in the repair of DNA damage induced by UVC. Methods Plas?mids stably expressing ERCC2/XPD rs13181 AA(Lys751)and ERCC2/XPD rs13181 CC(Gln751)were transfected into Chinese hamster ovary cells,and the stable ERCC2 transfected cell lines were obtained. MTT assay was used to compare the inhibitory rates of the transfected cells treated with UVC at different irradiation intensity. The DNA damage repair ability of the transfected cells treated with UVC for 1,3,6 and 24 h was detected by modified comet assay. Results Compared with UV5ERCC2(CC),UV5ERCC2(CC) was more sensitive to UVC with decreased cell viability. DNA damage level of UV5ERCC2(CC) cells was more serious than UV5ERCC2(CC). Conclusion DNA repair capacity of ERCC2/XPD rs13181A allelic is lower than its wild?type,suggesting that ERCC2/XPDpolymorphisms play a critical role in UVC?induced DNA damage repair.

AIM: In order to explore the pathogenesis of ulcerative colitis (UC), an experimental colitis in mouse was induced by the hapten dinitrochlorobenzene (DNCB), and the activity of leukocyte migration inhibitory factor (LMIF) was measured at the same time. METHODS: 67 BALB/c mice were randomly divided into control (60% ethanol) and DNCB groups. After they were sensitized by smearing 3.3% DNCB on the abdominal skin, they were challenged with DNCB at concentration of 0.1%, 0.2% and 0.4% respectively by instillation once a day. The weight, stool viscosity and hematochezia were observed and accumulated as disease active index (DAI) score. The pathological changes in colon tissue were judged macropathologically and by means of microscope. LMIF activity was determined by the absorbance (A) of migrated leukocytes. RESULTS: Compared to control group, the increases in DAI accumulate score, pathologic score, and LMIF activity in DNCB groups were observed. CONCLUSION: Mouse colitis was induced by DNCB, which was accompanied by an increase in LMIF activity. [