Objective:To construct the Helicobacter pylori infected C57BL/6 mice model to observe the activation of NOD1/NF-κB signaling pathways in the gastric tissues,and study its roles in inflammatory response during Hp infection.Methods:6-8 week-old C57BL/6 mice were randomly divided into two groups,the Hp infection group and the control group,and mice were given by gavage every 48 h for five times with Hp or PBS,respectively.All the animals were sacrificed at different time point and the gastric tissue were stained with hematoxylin-eosin( HE);The mRNA expression of NOD1 and RIP2 in gastric tissues were examined by RT-PCR;Levels of IFN-βand IP-10 in mice serum were assessed by ELISA;Nuclear translocation of p65 in gastric tissue was detected by Western blot.Results:Hp infection elicits an inflammatory cell response,glands in gastric tissue were reduced or atrophic,as compared with that in the control group.The levels of IP-10 and IFN-βincreased in the model group, and peaked at 16 weeks after Hp infection.Hp infection increased the mRNA expression of NOD1 and the p65 content in nuclear between 24-120 h(P<0.05),and the highest level at 48 h,subsequently the expression levels were began to decrease.The mRNA expression level of RIP2 was up-regulated after Hp was administrated, peaked at 48 h and declined after 72 h.However, the expression levels would rise again at 120 h.Conclusion: Hp infection can activate the NOD1/NF-κB signaling pathways and induce the production of IFN-βand IP-10 in gastrics of mice.

Medicine, Chinese Traditional

OBJECTIVE To investigate genes associated with aminoglycosides modification enzymes(AMEs) in Pseudomonas aeruginosa(PAE) isolated from ICU patients.METHODS Drug-reisistant genes encoding AMEs such as aac(3)-Ⅰ,aac(3)-Ⅱ,aac(6′)-Ⅰ,aac(6′)-Ⅱ,ant(3″)-Ⅰ and ant(2″)-Ⅰ were detected by polymerase chain reaction(PCR)(amplification) in 21 PAE isolates.RESULTS The positive rates of aac(3)-Ⅱ,aac(6′)-Ⅰ,aac(6′)-Ⅱ,ant(3″)-Ⅰ,ant(2″)-Ⅰ and aac(3)-Ⅰ genes were positive in 19.0%,23.8%,9.5%,4.8%,19.0% and 0% of 21 isolates,respectively. Drug-resistant genes encoding AMEs were detected positively in 42.8% of 21 isolates.(CONCLUSIONS) AMEs genes are present in high percentage of PAE isolated from ICU patients.

dialysis.

Purpose:To investigate the prevention and treatment protocol for Af after resection of esophageal and car- dia carcinoma.Methods:Analyses for clinical materials of 1527 patients underwent resection for esophageal and cardiac carcinoma.Results:There were Af 23 cases.Age older than 60 years,abnormal ECG or/and pulmonary function before operation,gastro-esophageal anastomosis above the aortic arch and histological staging Ⅲ～Ⅳ were risk factors for AF.Fa- tal AF was rarely seen.In our 23 cases after treatment in time AF disappeared.Conclusions:Further recognition for post- operative AF and management of perioperative period complication,may reduce the danger of postoperative AF.

Objective To investigate the effects and mechanisms of immunosuppressants on in- duction of apoptosis of peripheral T lymphocytes.Methods T lymphocytes were derived from healthy donors and activated by super antigen SEB.The rest or activated T lymphocytes were incubated with immunosuppressants such as myophenolate mofetil (MMF),cyclosporine A (CsA),FK506,azathio- prine (Aza),sirolimus (SRL),prednisone (Pred),and daclizumab (Dac,anti-CD25mAb),alone or combined,for 3 days.The incidence of apoptosis was determined by the methods of confocal microsco- py,flow cytometer,DNA-ladder fragmentation electrophoresis,and reverse transcription-polymerase chain reaction (RT-PCR) gene amplification profiles.The quantitive assay of IL-2 and Fas in the cul- ture medium was also performed using the enzyme linked immunosorbent assay kit.Results Apoptosis in rest T lymphocytes was just induced by Pred among various immunosuppressants.MMF,Aza,and Pred promoted apoptosis in activated T lymphocytes (P＜0.05,P＜0.01),but it was blocked by CsA,FK506,SRL,and Dac (P＜0.01).After adding two or three kinds of immunosuppressants, the incidence of apoptosis in activated T lymphocytes was apparently lower than in control group (P＜0.01).The expression of Fas and IL-2 by activated T lymphocytes was inhibited by FK506 and CsA (P＜0.05).Conclusion MMF,Aza,and Pred may induce apoptosis of activated T lymphocytes via the signal pathway of Fas/Fasl.CsA and FK506 could inhibit the apoptosis of activated T lymphocytes by blocking the production of IL-2.Also,SRL and Dac can block the apoptosis of activated T lympho- cyte by interfering with the effect of IL-2 on T lymphocytes activation process.

AIM:To investigate the effect of miRNA-181a inhibition on the proliferation, migration and cell cycle of the human multiple myeloma cell line RPMI 8226.METHODS:Real-time PCR was used to detect miRNA-181a expression in serum samples from multiple myeloma or healthy subjects .After transfection with miRNA-181a inhibitor, the cell viability was examined by CCK-8 assay and colony formation assay .The cell migration ability was analyzed by wound healing assay .The cell cycle was detected by flow cytometry .Moreover , the protein level of cyclin D 1 and the phosphoryla-tion of PI3K and Akt were determined by Western blot .RESULTS:The expression of miRNA-181a was significantly in-creased in the serum from multiple myeloma patients as compared with healthy group .Inhibition of miRNA-181a expression by transfection with miRNA-181a inhibitor remarkably decreased the cell viability , migratory ability, the population of G0/G1 phase and cyclin D1 protein expression in the RPMI8226 cells.However, the population of S phase and the phosphory-lation of PI3K and Akt were reduced .CONCLUSION:Down-regulation of miRNA-181a inhibits the viability and migra-tory ability in the RPMI8226 cells via inhibition of cell cycle and PI 3K/Akt signaling pathway .

Aged ; Aged, 80 and over ; Anthracosis ; blood ; Erythrocyte Indices ; Erythrocytes ; Hemoglobinometry ; Humans ; Middle Aged

Adult ; Ammonia ; poisoning ; Female ; Humans ; Microscopy, Electron ; Poisoning ; complications ; Respiratory Function Tests ; Respiratory System ; drug effects ; pathology ; ultrastructure ; Time Factors

OBJECTIVE To investigate the existence of genes for beta-lactam antibiotic resistance and for aminoglycosides modification enzymes(AMEs) in Pseudomonas aeruginosa(PAE) isolates from ICU patients and analyze the homology among strains.METHODS ?-Lactamase genes including TEM,SHV,OXA-10,PER,VEB,GES,CARB,IMP,VIM,SPM,GIM,DHA,FOX,MOX and oprD2,were detected by PCR amplication in 21 PAE isolates.The genes for AMES including aac(3)-Ⅰ,aac(3)-Ⅱ,aac(6′)-Ⅰ,aac(6′)-Ⅱ,ant(3″)-Ⅰ and ant(2″)-Ⅰwere determined by PCR amplification as well.RESULTS Among 21 isolates 21(100%),2(9.5%),1(4.8%),2(9.5%)and 4(19.0%) were positive for TEM,SHV,GES,CARB and VIM genes,respectively.The deletion of oprD2 gene was found in 14 out of 21 strains.Other ?-lactamase genes were absent in all isolates.As for AME genes,aac(3)-Ⅱ,aac(6″)-Ⅰ,aac(6)-Ⅱ,ant(3″)-Ⅰ,ant(2″)-Ⅰ and aac(3)-Ⅰgenes were present in 19.0%,23.8%,9.5%,4.8%,and 19.0% of 21 isolates,However,aac(3)-Ⅰ gene was no position in any isolates.CONCLUSIONS P.aeruginosa carries various beta-lactamase and AME genes in ICU patients.Genetic cluster analysis suggested that clonal propagation result in nosocomial infection of PAE.