Beta-catenin can function as an oncogene when it is translocated to the nucleus, binds to T-cell factor (TCF) or lymphoid enhance factor and transactivate its target gene. The mechanism responsible for the activation of Wnt signaling pathway in the Cytotoxin-associated antigen A (CagA) Helicobacter pylori (H. pylori)-infected gastric carcinoma has not been elucidated. We hypothesize that whether interaction of MUC1 with beta-catenin modulates the Wnt signaling and its target gene cyclinD1 in CagA H. pylori-infected gastric carcinoma. The result demonstrate that binding of MUC1 CT with Protein Kinase C delta (PKC delta), tyrosine phosphorylation of MUC1 CT, and CagA are strongly associated with the interaction of MUC1 with beta-catenin in CagA H. pylori-infected gastric carcinoma. A statistically significant difference (chi(2) = 24.49; P< 0.001) was found when the binding of MUC1 CT and beta-catenin was compared to subcellular localization of beta-catenin. We also observed significant statistical correlation (chi(2) = 14.885; P < 0.001) between the cyclinD1 overexpression and the subcellular localization of beta-catenin. The overexpression of cyclinD1 was significantly higher (chi(2) = 13.785; P < 0.002) in advanced gastric carcinoma with CagA H. pylori infection. In addition cyclinD1 overexpression was significantly higher (chi(2) = 37.267; P < 0.001) with the interaction of MUC1 CT with beta-catenin in advanced gastric cancer. These findings indicate that MUC1 CT plays a role in the intracellular signaling through its interaction with beta-catenin and upregulate the Wnt target gene cyclinD1 in CagA H. pylori-infected gastric carcinoma.
In addition to routine water flushing, the routine prophylactic use of pancreatic enzyme-sodium bicarbonate suspension (pH 7.5) prevents occlusion of feeding tubes.
Particle Induced X-ray Emission (PIXE) technique has been used to determine the trace elements present in fourteen representative human gallstone samples collected from eastern region (Orissa) and thirteen representative samples collected from southern region (Chennai) of India. PIXE irradiation of the samples has been carried out by using the 3 MV tandem type horizontal pelletron accelerator facility at Institute of Physics, Bhubaneswar with proton beam of energy 3 MeV. In the present investigation, twenty one trace elements like S , Cl , K , Ca , Ti , V , Cr , Mn , Fe , Ni , Cu , Zn , As , Se , Br , Rb , Sr , Y , Zr , Mo and Pb have been estimated in all the three types of gallstones viz. cholesterol stone, mixed stone and pigment stone. While sulphur in cholesterol stones in the eastern region was less than that of the southern region, sulphur was present as a minor element in the pigment stones of both the regions. Less concentration of copper in the gallstones from eastern region is another interesting observation. The lower values of copper in the patients of eastern region may be due to different types of food habits. The concentrations of all the elements in the southern region pigment stones have higher values than that of the eastern region. Moreover, the concentrations of Fe and Mo in cholesterol stone and pigment stone samples in southern region have also higher values than in eastern region. The current PIXE study is of its first kind in this eastern region of India.
Tropical and alcoholic forms of chronic pancreatitis differ in their clinical, aetiological and epidemiological features. We compared the radiological appearances of pancreatic calculi seen on plain roentgenogram of the abdomen of 89 patients with tropical calcific pancreatitis (TCP) and 32 patients with alcoholic calcific pancreatitis (ACP) seen in Madras, Southern India. While TCP was characterized by the frequent occurrence of large, discrete, dense calculi, patients with ACP had typically small, speckled calculi with irregular, hazy margins. The calculi in TCP resembled those described for hereditary pancreatitis. This is the first report comparing the radiological appearances of TCP and ACP patients seen at the same centre.
CONCLUSION:We report concordance between ATP7B mutation and WD phenotype within each family with > 1 member affected with WD. Homozygous ATP7B mutation was present in 3 of the 4 families studied. Our report supports allelic dominance as a determinant of WD phenotype. However, in one family with compound heterozygous mutation, there was a similar WD phenotype which suggests that there may be other factors determining the phenotype.
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