Objective To evaluate the clinical result of modified anterior decompression for the treatment of cervical myelopathy due to ossification of posterior longitudinal ligament(OPLL). Methods From April 1994 to October 2002, 42 cases of OPLL involving 134 cervical segments were operated using modified anterior decompression, among them there were 35 cases, 122 segments of the continuous type; 4 cases, 9 segments of the mixed type; 3 cases, 3 segments of the solitary type. The preoperative index of thickness (O-Index) ranged from 12.4%-78.8%, with an average of 43.2%. A slot was made in the vertebral body through anterior approach and bilateral border of the ossification was dissected from the posterior wall of vertebral body with burr-drill. Results The average follow-up was 3 years and 8 months ranging from 1 year and 6 months to 8 years. The recovery of neurologic function was evaluated according to JOA score: 28 cases with mild neurologic deficit (13-16 points) improved on average 74% postoperatively; 11 cases of the moderately damaged group (8-12 points) improved on 75%; 3 cases of the severely damaged group (

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.

This study sought to investigate the in vivo antiviral effect of amantadine (AM) and biphenyl dimethyl dicarboxylate (DDB) on hepatitis B virus (HBV) in HBV replication mice. HBV replication-competent plasmid was transferred into male BALB/c mice by using hydrodynamics-based in vivo transfection procedure to develop HBV replication mouse model. The model mice were matched by body weigh, age and serum levels of hepatitis B e antigen (HBeAg) and were divided into four groups: AM group, DDB group, AM+DDB group and NS group, with the last one as control, and the mice of each group were administered corresponding agent orally twice a day, in a medication course lasting 3 d. On the third day, the mice were sacrificed 4-6 h after the last oral intake. HBV DNA replication intermediates in liver were analyzed by Southern blot hybridization. The serum hepatitis B surface antigen (HBsAg) and HBeAg were detected by enzyme linked immunosorbent assay (ELISA). Compared to the animals in the control group, HBV DNA replication intermediates in liver and HBsAg and HBeAg in serum from the AM and AM plus DDB group of mice decreased, and there was no difference between these two groups of mice. The levels of HBV DNA intermediate from liver and the serum HBsAg and HBeAg between the control and DDB group, however, were not obviously different. In conclusion, the inhibition effect of AM on HBV was detected, but treatment with DDB for 3 days did not influence the viral replication and expression of HBV in the HBV replication mice.
Amantadine ; pharmacology ; Animals ; Antiviral Agents ; pharmacology ; DNA Replication ; DNA, Viral ; biosynthesis ; Dioxoles ; pharmacology ; Disease Models, Animal ; Hepatitis B ; virology ; Hepatitis B Surface Antigens ; blood ; Hepatitis B e Antigens ; blood ; Hepatitis B virus ; drug effects ; physiology ; Male ; Mice ; Mice, Inbred BALB C ; Plasmids ; Transfection ; Virus Replication ; drug effects

OBJECTIVETo study the antagonism of Zn-metallothionein (Zn-MT) to oxidative stress of rats with severe scalding after delayed resuscitation.

METHODS27 Wistar rats were randomly divided into three groups: normal control; burn with delayed fluid resuscitation group; and Zn-MT protected group. The rats were scalded with 30% total body surface area (TBSA) third degree burn. Four hours after injury, they were resuscitated, but Zn-MT (1 x 10(-5) mol/L) was given in the third group rats. 24 hours after they were scalded, blood was taken, RBCs were separated and labeled with electron spin resonance (ESR) spin label 3-maleimido-proxy l to detect membrane protein conformation. The serum was collected and added into the reaction system of xanthine, xanthine oxidase and ESR spin trap 5, 5-dimethylpyroline-N-oxide to assay the levels of superoxide dismutase (SOD) by ESR.

RESULTSThe ratios of strong solidity and weak solidity of RBC membrane proteins in the three groups were 0.352 +/- 0.043, 0.409 +/- 0.027, and 0.386 +/- 0.062 respectively, and the revolved times of membrane proteins were 1.300 +/- 0.210, 1.576 +/- 0.190 and 1.381 +/- 0.210 seconds respectively. Compared to the first group, the membrane protein conformation in the second group was changed remarkably, and the speed of membrane protein movement decreased significantly. However, those changes were alleviated obviously by Zn-MT. The SOD levels in serum of the three groups rats were 73.2% +/- 1.4%, 48.8% +/- 3.8% and 66.8% +/- 3.2% respectively. Compared to the normal control group, the SOD levels in serum of the second group decreased obviously. However, an excess of oxygen free radicals produced after injury could be scavenged by Zn-MT.

CONCLUSIONRBC membrane proteins of rats with severe scalding after delayed resuscitation were injured by oxygen free radicals produced after injury, and Zn-MT could alleviate this injury.

Animals ; Burns ; enzymology ; therapy ; Disease Models, Animal ; Erythrocyte Membrane ; drug effects ; metabolism ; Female ; Male ; Metallothionein ; pharmacology ; Protective Agents ; pharmacology ; Rats ; Rats, Wistar ; Reactive Oxygen Species ; metabolism ; Superoxide Dismutase ; metabolism ; Zinc ; pharmacology

As a potential vectored vaccine,Newcastle disease virus(NDV)has been subject to various studies for vaccine development,while relatively little research has outlined the immunomodulatory effect of the virus in antigen presentation.To elucidate the key inhibitory factor in regulating the interaction of infected dendritic cells(DCs)and T cells,DCs were pretreated with the NDV vaccine strain LaSota as an inhibitor and stimulated with lipopolysaccharide(LPS)for further detection by enzyme-linked immunosorbent assay(ELISA),flow cytometry,immunoblotting,and quantitative real-time polymerase chain reaction(qRT-PCR).The results revealed that NDV infection resulted in the inhibition of interleukin(IL)-12p40 in DCs through a p38 mitogen-activated protein kinase(MAPK)-dependent manner,thus inhibiting the synthesis of IL-12p70,leading to the reduction in T cell proliferation and the secretion of interferon-γ(IFN-γ),tumor necrosis factor-α(TNF-α),and IL-6 induced by DCs.Consequently,downregulated cytokines accelerated the infection and viral transmission from DCs to T cells.Furthermore,several other strains of NDV also exhibited inhibitory activity.The current study reveals that NDV can modulate the intensity of the innate?adaptive immune cell crosstalk critically toward viral invasion improvement,highlighting a novel mechanism of virus-induced immunosuppression and providing new perspectives on the improvement of NDV-vectored vaccine.