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Objective To investigate the correlation between Kruppel-like transcription factor 6 (KLF6) and gastric cancer.Methods By using immunohistochemistry (IHC) and reverse transcription PCR,the expression of KLF6 protein and mRNA in human gastric carcinoma specimens and adjacent tissues from 73 patients were examined.Results The KLF6 protein expression rates were 39.7 ％ (29/73) and 90.41％(66/73) in 73 cases of gastric cancer and adjacent tissues,The KLF6 protein expression was significantly lower in human gastric carcinomas than the adjacent tissues by chi-square test (P ＜ 0.01).The KLF6 expression rates were 25.0 ％ (10/40),57.6 ％ (19/33) in poorly and well differentiated cancer.The difference between the two groups was significant (P ＜ 0.01).The optical density ratio of KLF6 mRNA were 0.1586±0.1071 and 0.8899±0.0638 in the gastric cancer and cancer adjacent tissue respectively,the difference between the two groups was significant (P ＜ 0.01).Conclusion KLF6 expression is low in gastric carcinoma,and moreover,KLF6 expression is significantly lower in poorly differentiated cancers than the well differentiated gastric cancers,there are negative correlation between KLF6 and gastric cancer,therefore KLF6 could be a useful marker for gastric cancer.
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It has been revealed that the major mechanism of KLF6 is to upregulate p21 in an p53-independent manner leading to inhibition of cell proliferation. Lacking of KLF6 activity or its abnormal expression may be related to multiple tumors'development and prognosis such as prostate cancer, liver cancer, gastric cancer and other tumors. Furthermore, KLF6 may become a novel candidate for molecular target therapy.
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Objective To investigate the therapeutic effects and mechanisms of propofol on acute necrotizing pancreatitis (SAP) in rats.Methods 54 male Sprague-Dawley rats were randomized into three groups with 18 rats in each group:sham-operation group,ANP group,propofol-treatod group.After ANP models were induced,propofol(10 mg·kg~(-1)· h~(-1)) were injected by dorsal vein of penis in the propofoltreated group.The rats in all groups were sacrificed at 3,6,12 hours after induction of the model.The serum amylase,lipase,nitric oxide (NO),TNF-a,superoxide dismutase (SOD),IL-6 were detected;the histopathological score of pancreatic tissue were evaluated.Results At 6 h,the levels of serum amylase in sham-operation group,ANP group,propofol-treatod group were(1743± 370) U/L,(7745± 1030) U/L and (5529± 874) U/L;the levels of serum lipase were(274.9± 36.1)U/L,(1672± 262)U/L and(1219± 207 )U/L;the levels of serum TNF-a were (1.110± 0.276)mg/L,(3.191± 0.279)mg/L and (2.361±0.281 )mg/L;the levels of serum IL-6 were (102.6±28.5)ng/L,(334.1±34.0)ng/L and (268.6±29.8)ng/L;the levels of serum NO were (42.2±18.1)μmol/L,(120.7±22.3)μmol/L and(73.6±19.3)μmol/L;the levels of serum SOD were(120.6± 20.1)U/ml,(54.1± 15.3)U/ml and(85.7± 17,1)U/ml;the histopathological scores were 0.333± 0.408,4.417± 0.665 and 3.500±0.707.The serum levels of amylase,lipase,NO,TNF-a,IL-6 and the histopathological score of pancreas in ANP group were significantly higher than those in sham-operation group group(P＜0.05 ),while the serum levels of SOD were significantly lower(P＜0.05).The serum levels of amylase,lipase,NO,TNF-a,IL-6 and the histopathological score of pancreas in propofol-treated group were significantly lower than those in the ANP group(P＜0.05),while the serum levels of SOD were significantly higher(P＜0.05).Conclusions Propofol could decrease the levels of serum amylase and lipase,reduce pancreatic tissue damage,and had therapeutic effects on ANP in rats.
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0.05 . In combined test, the combined OR= 3.164 , OR = 3.209 and its 95% confidence interval was in 1.390 ～ 7.200 and 1.747 ～ 5.900 , respectively. CONCLUSION: The case fatality rates in combination group were significantly lower than those in single somatostain group. The efficacy of combination group was superior to that of single somatostain group.
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AIM:To investigate whether propofol can alter the pulmonary inflammation induced by severe acute pancreatitis(SAP)in rats during its early period.METHODS:Seventy-two adult male Sprague-Dawley(SD)rats were randomly divided into nine groups with 8 animals in each group:sham group,SAP 30,60,120,360 min groups and propofol treatment 30,60,120,360 min groups.The preparation of SAP were induced by retrograde injection of 5% sodium taurocholate into the pancreatic duct of rats.And the treatment groups received propofol with doses of 150 ?g?kg-1?min-1 injected continually immediately in vena caudalis after the preparation of ASP were made.Rats were sacrificed at different time points,and the level of AMY and LIP,the wet dry weight ratio(W/D)of pulmonary and pancreatic tissue,the pathological change of pulmonary and pancreatic tissue were examined.RESULTS:Water content and pathological score of pulmonary tissue were decreased significantly within 360 minutes after reproduction of SAP were received propofol(both P0.05).CONCLUSION:propofol can alleviate pulmonary inflammation induced by severe acute pancreatitis in its early period.But propofol can not alleviate the injury of pancreatitis tissue.
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Objective To study the relationship between lymph node micrometastasis and clinicopathological parameters. Methods Immunohistochemical method was adopted to detect CK19,CK20 and CD44v6 in 509 lymph nodes from 53 cases of gastric cancer, in which, conventional pathological diagnosis showed no lymph node metastasis. Results Micrometastasis was found in 47 lymph nodes (9.2%) of 21cases ( 39.6 %). The incidence of micrometastasis was correlated with the depth of invasion, and the incidence of micrometastasis in PT 3 and PT 4 patients was more than that in PT 1 and PT 2 patients(P
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AIM: To investigate p16 gene alterations in gastric carcinoma. METHODS: 36 fresh tumor specimens taken from gastric cancer patients were analyzed for p16 gene deletion and mutation by polymerase chain reaction (PCR) and DNA sequencing. RESULTS: Homozygous deletion of exon 1 and exon 3 was observed in 2 cases and 3 cases of diffuse carcinoma, respectively. The frequency of homozygous deletion was 13.89%. No p16 gene point mutation was detected. CONCLUSION: The deletion of p16 genes may be related to gastric carcinogenesis.