Objective To observe the effect of bone repair and evaluate its esthetic outcome with heterogeneous acellular dermal matrix cover the alveolar cleft bone grafting area in the alveolar cleft operation.Methods In 67 cases,unilateral cleft palate,were treated by alveolar cleft conventional surgical method.Cancellous iliac bone grafting were control group,heterogeneous acellular dermal matrix cover the alveolar cleft bone grafting area were treatment group.Radiographs was taken at 1 st,3 rd,6 th,12 th,18 th,24 th month postoperatively to observe the bone regeneration alveolar cleft zone.Results The alveolar cleft graft area new bone formation with Ⅰ,Ⅱ,Ⅲ,Ⅳ grade after 6 months in control group was 15,11,9,6 cases and in treatment group was 13,9,3,1 case.The graft survival rate and success rate (97.8％,84.3％) of treatment group were higher than that of control group (84.5％,63.7％),the difference was statistically significant (P ＜ 0.05).Conclusion The successful rate of operation could be warranted,by the joint application of autogenous iliac bone grafts and heterogeneous acellular dermal matrix in the alveolar cleft operation.

Objective To investigate the effects of different dosage of atorvastation on inflammatory factors in patients with unstable angina(UAP)post PCI.Methods 116 patients with their coming order were randomly divided into two groups.The observation group of 56 cases with the dosage of 20mg/d,and the control group of 60 cases with the common dosage of 10mg/d.Blood samples were examined at the day of the operation preoperatively,24 h after PCI,4W,12W after administration.Results(1)The consistency of hs-CRP and cTnI of patients after PCI were more higher than that before PCI(P

Objective To study the toxic effect of glufosinate-ammonium on the liver. Methods SD rats aged 6 weeks with weight of 140-160 g were randomly divided into four groups, 20 (10 males and 10 females) in each group. The rats were treated for three months by gavaging different doses of glufosinate-ammonium (0, 100, 250, 500 mg/kg bw) for the experimental group and 2% Tween-80 solution for the control group. All the rats were weighted once a week. The activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) in the serum were determined at the end of the study. Liver weight was measured and liver index was calculated. Pathological examination was performed. Results Treated with high-dose of glufosinate-ammonium, a retarded growth of rats was seen, the activity of ALT, AST and ALP increased significantly in both male and female rats, the liver index increased significantly and pathological changes of the liver were also observed compared with the control. No significant changes were found in the rats treated with moderate and low dose compared with the control. Conclusion Glufosinate-ammonium may produce a toxic effect on the liver of rat when the exposed dose is more than 500 mg/kg.

Objective To investigate the effects of nerve growth factor (NGF) on the expression of 67-kDa laminin receptor (67LR) in human bile duct carcinoma QBC939 cells, and study the possible mechanism of perineural invasion and metastasis of bile duct carcinoma. Methods ( 1 ) The expression of a high-affinity receptor for NGF, TrkA, was detected by immunofluorescence staining. ( 2 ) QBC393 cells were pretreated by β-NGF at different concentrations ( 1, 10, 100,200 μg/L), and then the mRNA and protein expressions of 67LR were examined by Real-Time PCR and Western blot assay. QBC939 cells were divided into control group and β-NGF (1, 10, 100,200 μg/L) groups. (3) The ideal concentration of β-NGF was selected according to the results of previous tests, and then the mRNA and protein expressions of 67LR were re-examined by adding specific TrkA inhibitor K252a at different concentrations ( 100,200,300 nmol/L). QBC939 cells were divided into control group, β-NGF 100 μg/L group and K252a ( 100,200,300 nmol/L) groups. All data were analyzed by one-way analysis of variance or LSD-test. Results (1) A strong expression of TrkA was detected in the membrane of QBC939 cells. (2) The mRNA and protein expressions of 67LR in QBC939 cells were 0.35 ± 0.06 and 0. 32 ± 0.05 in the control group, 0.38 ±0.14 and 0.50 ±0.09 in the β-NGF 1 μg/L group, 0.62 ±0.14 and 0. 69 ±0. 13 in β-NGF 10 μg/L group, 0.90 ± 0.08 and 0.93 ± 0.07 in the β-NGF 100 μg/L group, and 0. 70 ± 0. 10 and 0. 76 ±0.07 in the β-NGF 200 μg/L group, there were significant differences among the five groups (F = 22. 4, 14. 6,P ＜0.05). The mRNA and protein expressions of 67LR in the β-NGF 100 μg/L group were significantly higher than those in the control group ( t = 19. 0, 21.0, P ＜ 0. 05 ). (3) The mRNA and protein expressions of 67LR in the QBC939 cells were 0.35 ±0.10 and 0.41 ±0.10 in the control group, 0. 88 ±0. 14 and 0.84 ±0.10 in the β-NGF 100 μg/L group, 0.80±0.08 and 0.76 ±0.04 in the K252a 100 nmol/L group, 0.67 ±0.12 and 0.61 ± 0.09 in the K252a 200 nmol/L group, and 0. 43 ± 0.07 and 0. 50 ± 0. 12 in the K252a 300 nmol/L group, there were significant differences among the five groups ( F = 14. 1, 8. 9, P ＜ 0.05 ). There were no significant differences in the mRNA and protein expressions of 67LR between the K252a 300 nmol/L group and the control group (t =1.02, 0. 85, P＞0.05). Conclusion In bile duct carcinoma cells, NGF enhances the expression of 67LR by combining with TrkA, which might be the mechanism of NGF mediating perineural invasion of bile duct carcinoma.

Studies using isolated rat fundus strip preparation demonstrated that l-stephanine ( l-STP ) , l-roemerine ( 1-REM ), l-stepholidine (l-SPD), 1-tetrahydropalmatine ( l-THP ) and dl-tetrahydrode-berine ( THB ) possessed 5-HT blockade properties. 1-STP ( 16, 25 ?M ) produced competitve antagonism against 5-HT receptor on rat fundus, while higher concentration ( 50 ?M ) suggested a non-competi tive inhibition, with pA2' and2' values equal to 5.8 and 4.2 respectively. 1-REM was found to be a non-competitive antagonIst ( pD' 2 = 4.5). 1-SPD, 1-THP and THB cuased a parallel shift to the right of 5-HT concentration response curve without any significant changes in their maximum response, indicating that they were competitive antagonists of 5-HT receptor. The antagonistic potencies of 1-SPD, l-THP and THB were expressed as pA2 values: 6.2,5.2 and 5.0.

HIV envelope glycoprotein transmembrane subunit gp41 plays a major role in the fusion of viral and target cell membranes. The extracellular region of gp41 consists of N-terminal fusion peptide and downstream N- and C-heptad repeat (NHR and CHR) regions. The peptidesderived from the NHR and CHR regions, designated N- and C-peptides, respectively, have potent inhibitory activity on the HIV mediated cell fusion. C-peptide T-20 has just got the approval of U.S. FDA, which became the first success of one new class anti-HIV agents, named HIV-fusion inhibitors. However, a relatively long peptide such as T-20 suffers from several limitations including proteolytic sensitivity, large dosage, therefore it is unable to produced by gene engineering. Alternately, shorter peptidic fusion inhibitors and active peptides suitable for gene engineering are pursued. In the recent years, this kind of peptide modifications are hot spots in HIV research field and contribute a lot to the inhibitory mechanism of N- and C-peptide.

Grant administration in hospitals is one of the important tasks for administrators of scientific research, and all leaders should also pay enough attention to it and regard it as a strategic assignment of hospital development. In this paper, we found out the key points in different phases of scientific researches through quality analysis of grants and the whole procedure of research, and put forward the keystone administration. We also discussed a new model of subject construction, thesis and achievements administration leaded by grant administration, which should basically and greatly raise the level of scientific research in the hospital.

Objective To investigate the gene variation and the dependability and to evaluate the possible tumor suppressor genes on chromosome 9 in the development and progression of EC. Methods LOH was detected in normal esophageal mucosa, high-grade squamous dysplasia and esophageal squamous cell carcinoma by microdissection, polymerase chain reaction, denaturing polyacrylamide gel eleetrophoresis and silver nitrate staining technology. The changes of LOH at six microsatellite markers and the relationship between LOH rate were analyzed. Results In the informative cases, total frequency of LOH was 17.2 % in high-grade squamous dysplasia and 24.9 % in esophageal squamous cell carcinoma. In high grade squamous dysplasia and squamous cell carcinoma, LOH was detected at marker D9S162 (20.8 %, 36.7 %), D9S171 (33.3 %, 36 %), D9S753(34.8 %, 46.2 %), D9S1748(4.2 %, 13.8 %), D9S242(14.3 %, 21.2 %), D9S43(0, 0). The frequency of LOH showed significant difference among the six microsatellite markers (X2=17.26, P< 0.005; X2=22.66,P<0.005). Conclusion The progression from normal squamous epithelium to high-grade Squamous dysplasia and subsequently to squamous cell carcinoma of the esophagus is associated with accumulation of chromosomal change. The situs of D9S171, D9S162, D9S242, D9S753 exist higher LOH and all exceed 20 %. Possible tumor suppressor genes at or near D9S171, D9S162, D9S242, D9S753 may be related to the progression of esophageal squamous cell carcinoma.

The training of 24-hour resident physicians is the key link of standard training for resident physi-cians.The question of how to improve the quality of residency training is an important task.The article summarized practices in standardized training process for 24-hour resident doctors and argued the construction of the monitoring and examining system for the purpose of promoting the training.

Objective To study the possible relationship between mitochondrial DNA point mutations and hereditary ataxia (HA). Methods Polymerase chain reaction (PCR), restriction fragment length polymophism (RFLP) were performed to search A3243G, T8993G or T8993C point mutations in the amplified mitochondrial DNA of extract human perpheral white blood cells of 26 patients with HA and 35 normal controls. Results No point mutations of mitochondrial DNA A3243G, T8993G or T8993C were found in HA group and control group.Conclusion mitochondrial DNA A3243G, T8993G and T8993C mutations are not likely to be genetic factors of hereditary ataxia.