ABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression of Wnt and integrin pathways in colorectal laterally spreading tumors (LSTs) and their correlation with the different endoscopic subtypes of LSTs to better understand the special growth mechanism of LSTs.</p><p><b>METHODS</b>Fifty-two patients with colorectal LSTs were randomly selected from the cases diagnosed between January 1, 2010 and June 10, 2015 in our hospital, including 37 of nodular mixed type (LST-G-M), 60 of homogeneous type (LST-G-H), 5 of flat elevated type (LST-NG-FE), and 4 of pseudodepressed type (LST-NG-PD). The expression of β-catenin, phospho- GSK-3β, paxillin and ILK in 52 colorectal LSTs and 15 protruded adenomas (PAs) were investigated by immunohistochemical staining. The correlation of β-catenin, phospho-GSK-3β, paxillin and ILK expressions among the endoscopic subtypes of LSTs were analyzed.</p><p><b>RESULTS</b>β-catenin expression was significantly higher in LSTs than in Pas (P<0.05). β-catenin, phospho-GSK-3β, paxillin and ILK expressions were significantly higher in LST-NG-PD than in Pas (P<0.05). The expressions of β-catenin, phospho-GSK-3β and ILK expression were significantly correlated in LSTs (P<0.05) but not in PAs (P>0.05).</p><p><b>CONCLUSION</b>The macroscopic feature of LST-NG-PD may result from a special mechanism of development distinct from other endoscopic subtypes; ILK may play a role in regulating Wnt signaling in LSTs.</p>
ABSTRACT
OBJECTIVE@#To observe the therapeutic effect of Bacillus acidi lactici on Helicobacter Pylori (Hp) infectious gastritis in Balb/c mouse model so as to explore a possible non-antibiotic treatment for Hp.@*METHODS@#To establish a Balb/c mouse model with Hp infectious gastritis through inoculation of mankind Hp,32 Balb/c mice infected by Hp were randomly divided into 4 groups:Group 1(PPI trigeminy treatment group),Group 2 (Bacillus acidi lactici CL22 treatment group),Group 3 (Bacillus acidi lactici CL24 treatment group),and Group 4 (normal saline control group). Intragastric administration was given continuously for 10 days. Another 8 normal mice were chosen as Group 5(blank control group). All mice were killed after 4 weeks since last intragastric administration. Hp was detected by rapid urease test,Giemsa dying, and bacterial culture,and histopathologic changes in the gastric mucosa of mice were determined by H-E staining.@*RESULTS@#There were significant differences in pathohistologic scores in sinus ventriculi among the 5 groups (F = 7.932, P = 0.000). The scores in Group 1, Group 2, Group 3, and Group 5 were obviously lower than those in Group 4 (P 0.05). The pathohistologic score in Group 3 was obviously higher than that in Group 5 (P 0.05). There was significant difference in Hp eradication rates in sinus ventriculi among the 5 groups (chi2 = 16.923, P=0.002). The Hp eradication rates in Group 1 and 2 were obviously lower than those in Group 4 (P 0.05). There also were significant differences in Hp eradication rate in corpus ventriculi among the 5 groups (chi2 = 14.295, P=0.006). Of them, Group 1 and Group 2 were higher than Group 4 (P 0.05).@*CONCLUSION@#Bacillus acidi lactici strain CL22 can effectively inhibit and eradicate Hp in Balb/c mouse model with Hp infectious gastritis in vivo. The therapeutic effect of Bacillus acidi lactici strain CL22 is equal to PPI + antibiotics and could be another choice of nonjantibiotic treatment for Hp.