1.SERO-DIAGNOSIS OF HELICOBACTER PYLORI INFECTION
Microbiology 1992;0(04):-
Sera from 80 patients suffering from gastritis and/or digestive ulcer were examined for IgG, IgA and IgM to Helicobacter pylori by enzyme-linked immunosorbent assay (ELISA). Anti-H. pylori IgG and IgA in serum could be used for diagnosis of H. pylori infection, but the former had good sensitivity (92.0%) and the latter had a great specificity (94.4%). Serum anti-H, pylori IgM level was not associated with H. pylori infection. There were no remarkable relationship between H. pylori infection degree arid levels of anti-H, pylori IgG IgA. The positive percentage of anti-H, pylori IgG of health population deceased after 50 years old but the anti-H, pylori IgA increased.
2.Advance of the diagnosis and treatment of breast cancer
Chinese Journal of General Surgery 1994;0(05):-
Objective To introduce the advance of the diagnosis and tretment of breast cancer(BC). Methods Reveiwing the recently world reference regarding to the diagnosis and treatment of BC was done for making an advancing paper of BC. Results The NF ?B and telomerase may be a new target of anti cancer of breast. The ECT, fiberoptic mammaroductoscopy, examine of micrometastase of BC, immuno cell chemical examine were progressing in the diagnosis of BC. The advance of the treatiment of BC included breast conservative surgery, lymphatic mapping and sentinel node biopsy, biochemical response modifier, new adjuvant chemotherapy, TAM and 1,25 (OH) 2D 3 treatmen. Conclusions The idea and mould of the diagnosis and treatment of BC have advanced obviously.
3.The effect of exogenous estrogen and tamoxifen on murine experimental precancerous breast disease
Chinese Journal of General Surgery 2001;16(2):110-112
Objectiver To establish murine breast precancerous model and evaluate the effect of exogenous estrogen and tamoxifen. Method 50 female Wistar rats were divided into contol group (n=12), the other 38 received low dose carcinogen (DMBA) by gastrogavage, and then divided into DMBA group (common diet,n=8); DMBA+DES group(DES added chow,n=15); and DMBA+TAM group (TAM added chow,n=15). 3 months later, the status of breast hyperplasia, AgNOR and DNA content were measured. Results All indexs in control group and DMBA+TAM group were normal.However,in DMBA group and DMBA+DES group,the breast hyperplasia rate was 75%, 93.3%, AgNOR was 3.71±0.76, 5.60±0.42, DNA was 88.59±7.17, 137.75±3.13 respectively.Compared with control group and DMBA+TAM group, the differences of indexes in DMBA and in DMBA+DES group were significant (P<0.01). Conclusion Low dosage DMBA administered by gastrogavage established breast precancerous model. Exogenous estrogen promotes the development of breast precancerous disease induced by DMBA, while TAM suppresses the canceration.
4.The effects of CD151 on the expression of phosphoinositide 3-kinase and the proliferation of human umbilical vein endothelial cells in vitro
Zhenzhong ZHENG ; Zhenxiang LIU
Journal of Chinese Physician 2001;0(05):-
Objective To investigate the effects of CD151 on the expression of phosphoinositide 3-kinase(PI3K) and the proliferation of human umbilical vein endothelial cells(HUVEC) in vitro.Methods The plasmid p-AAV-CD151 was constructed and transfected into HUVEC.The proliferation activity of HUVEC was measured by MTT colorimetric assay.The expressions of CD151 and PI3K were tested by Western Blot.Results After transfection with p-AAV-CD151,the expressions of CD151 and PI3K were significantly increased compared with those of non-transfected group and p-AAV-GFP transfected group(P
5.Changes of oxygen metabolism and neutrophil cellular rheological characteristics in canine with respiratory distress syndrom induced with oleic acid
Changming WANG ; Zhenxiang ZHANG
Chinese Journal of Anesthesiology 1994;0(04):-
To observe the alterations of oxygen delivery/consumpation, the deformability and adherence of neutrophil in canine with respiratory distress syndrom(RDS), Method:The 15 selected healthy mongrel dogs were randomly allocated to receiving intravenous oleic acid 0.06 ml. kg~(-1) (test group, n= 8)or equivalent volume of saline (control group, n=7) respectively following anesthesia induction. The hemodynamics was monitored with Swan-Ganz catheter technique, the neutrophils were collected from arterial blood with centrifugal way to measure the deformability and adherence at 1st, 2nd, 4th and 6th hour after the administration of oleic acid separately. The pulmonary pathological examination underwent at 6th hour after the administration. Result: The pathological findings of test group were compatible with the RDS pathological characteristics. One hour after the administration, the deformability decreased significantly and the adheranee increased markedly (P
6.Study on the mechanism of pyrrolidine dithiocarbamate down-regulating matrix metalloproteinase-9 expression
Chinese Pharmacological Bulletin 1987;0(01):-
Aim To study the effects of pyrrolidine dithiocarbamate(PDTC) on matrix metalloproteinase-9(MMP-9) expression in alveolar macrophages(AM) induced by TNF-?,and then to explore it's signal pathway.Methods AM were collected from bronchoalveolar lavage fluid in patients with chronic obstructive pulmonary disease.AM were pretreated with PDTC and then stimulated by TNF-? or IL-1.MMP-9 mRNA expression was detected by semi-quantitative reverse transcription-polymerase chain reaction and MMP-9 protein expression was detected by Western blot.Phospho-I?B? protein levels induced by TNF-? or IL-1 were detected by Western blot.NF-?B activity was detected by electrophoretic mobility shift assay.Results Both the mRNA and protein levels of MMP-9 induced by TNF-? in AM were significantly elevated in a dose dependent manner(P0.05).PDTC had distinct effect of inhibiting the activation of NF-?B induced by TNF-? or IL-1 in a dose-dependent manner(P0.05).Conclusions NF-?B plays an important role in MMP-9 expression induced by TNF-? in AM;PDTC can down-regulate MMP-9 expression induced by TNF? in AM possibly through preventing the degradation of I?B? via ubiquitylation-proteasome proteolytic pathway.
7.Construction and expression of maspin/pEFIRES-N expression vector
Journal of Third Military Medical University 2003;0(22):-
Objective To construct the expression vector maspin/pEFIRES-N so as to study maspin gene on the inhibition of the growth,invasion,and metastasis in hepatocellular carcinoma.Methods The full lenth of maspin gene was cloned and ligated to the expression vector pEFIRES-N digested by EcoRⅠ+XbaⅠ by T4 DNA ligase.The recombinant vector maspin/pEFIRES-N was stably transfected into hepatocellular carcinoma MHCC-97 cell line,and the expressive changes of maspin gene were detected.Results The recombinant plasmid was amplified in the E.coli.JM109.After the identification and sequencing,the reconstructive plasmid was confirmed containing the correct and full nucleotide sequence of maspin gene and the mRNA and protein level of maspin gene were up-regulated in hepatocellular carcinoma MHCC-97 cells.The proliferation and invasion of MHCC-97 cells was inhibited.Conclusion The expression vector maspin/pEFIRES-N was constructed successfully and could be expressed in eukaryotic cells.
8.Data and analysis of the cancer genome atlas
Chinese Journal of Clinical Oncology 2014;(5):349-353
Multiple chromosomal aberrations, nucleotide substitutions, and epigenetic modifications may occur in human cancer cells, which drive malignant transformation. The Cancer Genome Atlas (TCGA) project aims to promote large-scale multi-dimensional analysis of these molecular characteristics in human cancer and rapidly provide data to researchers. In this study, we introduce four flow paths of the production of TCGA data, the collections of various cancer types, the data category and level, and the standardized pipeline of data analysis, as well as several existing data analytical tools. We used ovarian cancer as an example to introduce the application of the TCGA data in the analyses of mutation, copy number, analysis, and expression. We summarized the important findings of glioblasto-ma by TCGA teams.
9.Postoperative Nosocomial Infection in Esophageal Cancer Patients:Investigation and Analysis
Chinese Journal of Nosocomiology 2006;0(02):-
OBJECTIVE To investigate the risk factors of postoperative nosocomial infection in esophageal cancer patients,and to provide evidences for controlling nosocomial infection.METHODS The data of 466 cases with esophageal cancer,from Jan 2002 to Dec 2005,were studied retrospectively.RESULTS The nosocomial infection rate of patients with esophageal cancer was 21.03%.The main locations of infection were operation incision,lower respiratory tract and thorax.The nosocomial infection rate had increasing trend as lengthening the hospitalization duration.CONCLUSIONS The nosocomial infection with esophageal cancer is related to age,hospitalization duration and postoperative time.To take measures for infective factors,for example,intraoperative aseptic operation,postoperative drainage tube unblocked and rational use of antibiotics,is important to control and decrease the nosocomial infection.
10.Advances of the Research on Mechanisms of Breast Cancer Escaping from Host Immune Surveillance
Chinese Journal of Bases and Clinics in General Surgery 2004;0(01):-
Objective To review the mechanisms of breast cancer escaping from host immune surveillance. Methods The current literatures on the mechanisms of breast cancer cells escaping from host immune surveillance were reviewed in the following aspects: alterations of MHC-Ⅰmolecule phenotype, deficiency of costimulatory molecules, apoptosis of T-lymphocytes induced by breast cancer cells presenting Fas ligand (FasL) and TNF-related apoptosis-inducing ligand (TRAIL) and host immune tolerance induced by tumor cells. Results Loss of classical antigen-presenting human leukocyte antigen (HLA) class-Ⅰmolecules, expression of non-classical HLA class-ⅠmoleculesHLA-G, loss of costimulatory molecule B7, apoptosis of T-lymphocytes induced by tumor cells presenting FasL and TRAIL and antigen-inducing host immune tolerance were related to breast cancer escaping from immune surveillance. Conclusion Breast cancer cells escape from host immune surveillance by altering MHC-Ⅰmolecules, lacking of costimulatory molecules, inducing of apoptosis of T cells and host immune tolerance. But the factors resulting in breast cancer escaping from host immune surveillance are not yet clear and should be further studied.