Helicobacter pylori infection and changes of cell gap junction of gastric epithelial cells in patients with gastric cancer and precancerous lesion / 中南大学学报(医学版)

OBJECTIVE@#To observe the changes of cell gap junction ultrastructure of gastric epithelial cells in patients with gastric cancer(GC) and precancerous lesion(PL),and to investigate the relation between these changes and H.pylori infection.@*METHODS@#Seventy patients with GC, 88 with PL, and 33 with chronic superfial gastritis (CSG) were studied. H.pylori was detected by rapid urease test,basic fuchsin stain and 14C-urea breath test. The CagA gene of H.pylori was determined by polymerase chain reaction(PCR).The cell gap junction ultrastructure was observed under transmission electronic microscope.@*RESULTS@#Length of junction/unit perimeter of gastric epithelial cells in patients with PL was smaller than that in CSG patients, and the smallest width of the intercellular space was bigger than that in CSG patients. The number of cell junction, the number of junction/unit perimeter, and the length of junction/unit perimeter in patients with GC were all smaller than those in patients with CSG or PL, and its smallest width of the intercellular space was bigger than that in patients with CSG. In patients with GC, the number of cell junction, the number of junction/unit perimeter and the length of junction/unit perimeter in CagA+ H.pylori group were smaller than those in CagA(-) H.pylori group, and its smallest width of the intercellular space was bigger than that in CagA(-) H.pylori group. In PL patients, the intercellular space decreased, and the length of cell junction of gastric epithelial cells became bigger after H.pylori eradication. The length of junction/unit perimeter in patients of H.pylori eradication was bigger than that in patients without eradication, and the smallest width of the intercellular space was smaller than that in patients without eradication.@*CONCLUSION@#The changes of cell gap junction of gastric epithelial cells in patients with GC and PL are associated with H.pylori infection especially CagA+ H.pylori infection. Eradication of H.pylori can promote the formation of cell junction.

Expressions of connexin 32 and connexin 43 in patients with gastric precancerous lesion after eradication of Helicobacter pylori / 中南大学学报(医学版)

OBJECTIVE@#To observe the change in expressions of connexin 32 and connexin 43 after the eradication of Helicobacter pylori (H.pylori) in patients with gastric precancerous lesion.@*METHODS@#The expressions of connexin 32 and connexin 43 in gastric mucosa specimens biopsy under endoscopy were detected by immunohistochemistry. The expressions of connexin 32 and connexin 43 were detected before and after the eradication of H.pylori in 88 patients with gastric precancerous lesion, and in 33 patients with chronic superficial gastritis (CSG).@*RESULTS@#The positive expression rates and the expressional intensity of connexin 32 and connexin 43 in patients with gastric precancerous lesions (51.1% and 54.5%) were lower than those in patients with CSG (100% and 93.9%, P 0.05).@*CONCLUSION@#The expressions of connexin 32 and connexin 43 in patients with gastric precancerous lesions are low, and the eradication of H.pylori can upregulate their expressions.

Effect of CagA(+) helicobacter pylori strain on the expression of connexin 43 and cell proliferation in BGC-823 cells / 中南大学学报(医学版)

OBJECTIVE@#To determine the effect of CagA(+) Helicobacter pylori(H.pylori)strain and anti-H.pylori drugs on the expression of connexin 43(Cx43) and cell proliferation of BGC-823 cells in vitro,and to investigate the relation between the changes of Cx43 expression, cell proliferation of BGC-823 cells and CagA(+)H.pylori.@*METHODS@#BGC-823 cells were co-cultured with CagA(+) H.pylori strain(NCTC J99) or CagA(-) H.pylori strain(NCTC 12908)at bacteria/cells ratio of 20:1,100:1 and 500:1 for 24 hours and 48 hours respectively. anti-H.pylori drugs was given in the group co-cultured at bacteria/cells ratio of 100:1 after 16 hours. In the control group, BGC-823 cells were cultured for 24 hours and 48 hours respectively,but without H.pylori or antij H.pylori drugs. Immunocytochemical SABC method and the image analysis of the computer were applied to detect the changes of Cx43 expression in BGC-823 cells. The cell proliferation was examined by methyl tetrazolium (MTT) method.@*RESULTS@#(1)The expression of Cx43 in the control group after cultivation for 48 hours was higher than that for 24 hours (P0.05). Cx43 expression in the groups co-cultured with CagA(-) H.pylori strain at the ratio of 100:1 and 500:1 was lower than that in the control group, and Cx43 expression at the ratio of 500:1 was lower than that at the ratio of 20:1 for 24 hours and 48 hours. Cx43 expression increased after the intervention with anti-H.pylori drugs for 48 hours. (2) In the groups co-cultured with CagA(+)H.pylori strain, the optical density value of MTT indicated that the cell proliferation at the bacteria/cells ratio of 100:1 was higher than that in the control group, but no significant difference was found in other two groups co-cultured for 24 hours. After co-culturing for 48 hours, the cell proliferation at the bacteria/cells ratio of 20:1 and 100:1 was significantly accelerated, while the cell proliferation at 500:1 was inhibited. In the groups co-cultured with CagA(-) H.pylori strain,there was no change in the cell proliferation. Intervention with anti-H.pylori drugs could suppress the cell proliferation.@*CONCLUSION@#CagA(+) H.pylori can down-regulate the expression of Cx43 in BGC-823 cells,which is related to the reaction time and the density of H.pylori. Low density of CagA(+)H.pylori suspensions can accelerate the proliferation of BGC-823 cells, while high density can suppress the cell proliferation. The CagA(-) H.pylori has no effect on the cell proliferation. Intervention with anti-H.pylori drugs can up-regulate the expression of Cx43,and suppress the cell proliferation of BGC-823 cells.

Effect of various uses of propofol on the upper gastrointestinal endoscopy / 中南大学学报(医学版)

OBJECTIVE@#To investigate the efficacy and security of different uses of propofol on the sedation during the upper gastrointestinal endoscopic procedures.@*METHODS@#Four hundred patients who underwent gastroscopy received midazolam and propofol as sedation. Patients were divided to 4 groups with different intervals between midazolam and propofol: Group A and D with the interval of 30 seconds to 1 minute, Group B and C with 3 to 5 minute interval. All patients were premedicated with midazolam and propofol at 16 approximately 25 mg/10s (Group A and B) and 6 approximately 7 mg/10s (Group C and D).@*RESULTS@#The doses of propofol of Group A,B,C, and D were (111.90+/-22.43),(102.20+/-15.99),(73.05+/-13.08) and (80.90+/-17.36)mg respectively, with significant difference(P<0.01). The time of return to consciousness decreased markedly in Group C and D [(9+/-1), (10+/-2)min ], and that of Group A and B was [(14+/-5), (13+/-3)min ]. There was significant difference between Group C, D and Group A, B(P<0.01).@*CONCLUSION@#The dose of propofol and the time of return to consciousness depend on the rate of administration and the interval between midazolam and propofol. Appropriate rate and interval can produce safer and more effective sedation for the upper gastrointestinal endoscopic procedure.

Antibiotic resistance of Helicobacter pylori / 中南大学学报(医学版)

OBJECTIVE@#To examine the infection and bacteria resistance of Helicobacter pylori (H.pylori) to clarithromycin and furazolidone,to determine whether the antibiotic resistance is primary or secondary, and to decide if a new H.pylori infection plays a role in eradication failures.@*METHODS@#Twenty one H.pylori had been isolated from human biopsy specimens, and antimicrobial susceptibility testing was performed. DNA fingerprints were generated using random amplification polymorphic DNA (RAPD) to determine the identity of H.pylori before and after the eradication therapy.@*RESULTS@#Eight bacteria resisted against clarithromycin, and one against furazolidone, with the resistant rates 38.1% and 4.8% respectively. The number of primary antibiotic resistance, secondary resistance and new infection was 1 for each.@*CONCLUSION@#Resistance to clarithromycin is more common compared with that to furazolidone. Development of primary and secondary resistance to clarithromycin occurs as a rule in eradication failures. New H.pylori infection plays a role in eradication failures.