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The growth, changes in shape, topography and relation to the peritoneum of the descending colon were assessed on the basis of material taken from 178 foetuses of both sexes, aged from 72 to 236 days of pregnancy. The statistical analysis method demonstrated that the descending colon growth process occurs about a month earlier in female foetuses as compared to male ones. From the statistical point of view, the longitudinal growth of the descending colon significantly slows down in the 7th and 8th months of pregnancy, while the width of this part of the large intestine increases sharply towards the end of the foetal development period. The statistically important process of the descending colon rising over the surface of the left kidney and adrenal gland was noticed in male foetuses. This occurs approximately one month earlier in female foetuses as compared to males. The ascent of this part of the colon is accompanied by a change in its shape from straight, to curved and, finally, to wavy in the oldest age group of male foetuses. The changes in relation to the peritoneum are manifest in a gradual change in the position of this section of the intestine from the intraperitoneal, where more than 40% of the cases examined had a fully movable mesentery, to the extraperitoneal, with 14% of foetuses having a mesentery in the 8th month of pregnancy.
This review describes the structure of the adenomatous polyposis coli (APC) gene with expressed proteins and their possible tissue interactions. The functions of APC in animals and humans are discussed. The mutational spectrum with clinical impact on colon pathology and gynaecological pathology similarities are presented, along with a discussion of a highly sensitive molecular biology test.
Retinoid resistance has limited the clinical application of retinoids as differentiation-inducing and apoptosis-inducing drugs. This study was designed to investigate whether celecoxib, a selective COX-2 inhibitor, has effects on retinoid sensitivity in human colon cancer cell lines, and to determine the possible mechanism of said effects. Cell viability was measured using the MTT assay. Apoptosis was detected via Annexin-V/PI staining and the flow cytometry assay. PGE2 production was measured with the ELISA assay. The expression of RARβ was assayed via western blotting. The results showed that celecoxib enhanced the inhibitory effect of ATRA in both COX-2 high-expressing HT-29 and COX-2 low-expressing SW480 cell lines. Further study showed the ATRA and celecoxib combination induced greater apoptosis, but that the addition of PGE2 did not affect the enhanced growth-inhibitory and apoptosis-inducing effects of the combination. Moreover, NS398 (another selective COX-2 inhibitor) did not affect the inhibitory effects of ATRA in the two cell lines. Western blotting showed that the expression of RARβ in HT-29 cell lines was increased by celecoxib, but not by NS398, and that the addition of PGE2 did not affect the celecoxib-induced expression of the retinoic acid receptor beta. In conclusion, celecoxib increased the expression of RARβ and the level of cellular ATRA sensitivity through COX-2-independent mechanisms. This finding may provide a potential strategy for combination therapy.
This study reports on changes in CART-like immunoreactive (CART-LI) nerve structures in the porcine descending colon during chemically driven inflammation and after axotomy. The distribution pattern of CART-LI nerve structures was studied using doublelabeling immunofluorescence technique in the circular muscle layer, myenteric (MP), outer submucous (OSP) and inner submucous plexuses (ISP) and also in the mucosal layer of the porcine descending colon in physiological conditions as well as under pathological factors. In the control animals, CART-LI perikarya have been shown to constitute 5.11% ± 0.64, 4.03% ± 1.17 and 0.05% ± 0.04 in MP, OSP and ISP, respectively. Changes in CART-immunoreactivity depended on the pathological factor and the part of the enteric nervous system (ENS) studied. Numbers of CART-LI perikarya amounted to 2.77% ± 0.64, 2.60% ± 0.36 and 0.26% ± 0.19 during chemically-induced colitis and 3.04% ± 0.88, 2.46% ± 0.8 and 0.43% ± 0.09 after axotomy in MP, OSP and ISP, respectively. Both studied pathological processes also caused an increase in the number of CART-LI nerve fibers in the circular muscle as well as in the mucosal layer.
Free fatty acids (FFAs) are not only an important source of energy but they also play key roles in regulating various physiological responses. FFAs including short-chain fatty acids (SCFAs) have recently been demonstrated to act as ligands of several G-protein-coupled receptors (GPCRs) (FFA1, FFA2, FFA3, GPR84 and GPR120). FFA1 and GPR120 are activated by medium- and long chain fatty acids. GPR84 is activated by mediam-chain, but not long chain FFAs. On the other hand, FFA2 and FFA3 are both activated by SCFAs. Tissue distribution studies have indicated that FFA2 and FFA3 function as chemical sensors in the colon. For the involvement of SCFAs in the regulation of colonic motility, propionate and butyrate concentration- -dependently induced phasic and tonic contractions in rat colonic circular muscle. The responses were not observed in mucosal free preparation. Thus, FFA2 and FFA3 are important molecular devices to monitor the chemical composition in colonic lumen. For the local function of SCFAs, it should be stressed that individual SCFA has different mode of actions on colonic smooth muscles. These different effects may be due to the relative contribution of FFA2 and FFA3 on the control of intestinal muscle activity. In this article, we have reviewed the expression and functions of these molecules, especially FFA2 and FFA3 on the regulation of colonic motility.
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This review was designed to show the role of expression of cyclooxygenase (COX)-1 and COX-2 in the cancerogenesis of esophagus, stomach and colon. Unlike COX-1, which is expressed in the normal esophageo-gastro-colonic mucosa, COX-2 was found to be expressed mainly in the pre-cancer changes in the mucosa including Barrett's esophagus, Helicobacter pylori (H. pylori)-induced gastritis and inflammatory changes in colonic mucosa. In Barrett's esophagus, prostaglandins (PGs) derived from upregulated COX-2 contribute to the progression of low-grade to high-grade dysplasia and finally to cancer. In chronic gastritis induced by chronic H. pylori infection, overexpression of COX-2 is probably induced by inflammatory cytokines, growth factors, especially gastrin and reactive oxygen species leading to mutagenesis and subsequent metaplasia, dysplasia and cancer formation. The imbalance between cell proliferation and apoptosis caused mainly by products of COX-2 leads to cancerogenesis. Similarly, in colorectal cancer the overexpression of COX-2, possibly induced by the action of growth promoting factors including progastrin and gastrin and overexpression of survivin contribute to the colorectal cancerogenesis that could be, at least in part, amended by the treatment with specific COX-2 inhibitors. We conclude that: 1) COX-2-derived PGs play a key role in the tumorogenesis in the gastrointestinal tract; 2) The tumor-promoting effect of PGs may be attributed to their ability to stimulate cell proliferation and migration, to inhibit the apoptosis and to increase angiogenesis and invasiveness; 3) In accordance to the proposed major role of COX-2 in cancerogenesis, selective COX-2 inhibitors have been shown in numerous studies to exhibit strong chemopreventive effect on the development of gastrointestinal cancers.
Patients with colorectal carcinoma showed statistically significant lower values of transferrin saturation, total iron binding capacity and serum iron level as compared with control group, while the level of ferritin and the size of labile iron pool in carci­noma patients were higher, although this difference was not statistically significant. Our observations are in favour of the hypothesis which suggests that changes in iron metabolism restrict iron availability for tumour cells and as consequence, slow their growth.
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