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1.
Curr Mol Med ; 13(7): 1110-21, 2013 Aug.
Article in English | MEDLINE | ID: mdl-23170831

ABSTRACT

Inflammatory bowel disease (IBD) is a group of inflammatory disorders in the small and large intestines. Several studies have proved that persistent and disregulated host/microbial interactions are required for the development of IBD. It is well known that chronic IBD is strongly associated with an increased risk of developing colorectal cancer by 0.5-1% annually, 8-10 years after the initial diagnosis. To detect the tiny dysplasia or early stage of cancer in chronic IBD patients, a tremendous amount of effort is currently directed for improving colonoscopic technology and noninvasive serological marker development. However, there is only a limited amount of data available to understand the exact mechanism of how long term chronic colitis is connected to the development of colorectal tumors. Recently, our group has identified significantly increased expression of chitinase 3-like 1 (CHI3L1) molecule in non-dysplastic mucosa from patients with IBD and remote dysplasia/cancer, compared to patients with IBD without dysplasia or healthy controls. CHI3L1 seems to contribute to the proliferation, migration, and neoplastic progression of colonic epithelial cells (CECs) under inflammatory conditions. Furthermore, the TLR4-mediated intracellular signaling cascade is likely to interact with CHI3L1 signaling in CECs. In this review article, we have concisely summarized the cellular and molecular mechanisms underlining the development of IBD and colitis-associated cancer, with particular focus on the TLR4- and CHI3L1-signaling pathways in CECs.


Subject(s)
Adipokines/genetics , Colonic Neoplasms/genetics , Inflammatory Bowel Diseases/genetics , Lectins/genetics , Toll-Like Receptor 4/genetics , Adipokines/metabolism , Carcinogenesis , Cell Movement/genetics , Cell Proliferation , Chitinase-3-Like Protein 1 , Colitis/etiology , Colitis/genetics , Colitis/pathology , Colonic Neoplasms/complications , Colonic Neoplasms/pathology , Epithelial Cells/metabolism , Epithelial Cells/pathology , Humans , Inflammatory Bowel Diseases/complications , Inflammatory Bowel Diseases/pathology , Lectins/metabolism , Signal Transduction , Toll-Like Receptor 4/metabolism
2.
J Pediatr ; 86(5): 759-65, 1975 May.
Article in English | MEDLINE | ID: mdl-1169293

ABSTRACT

To determine the risk of infection created by catheterization of the umbilical vein per se, 75 jaundiced, but otherwise healthy, newborn infants subjected to exchange transfusion were studied. Twenty-three were given antibiotics because of premature rupture of membranes. Fifty-three percent of the umbilici were contaminated before the insertion of the catheter, even after a very careful cleansing procedure. Sixty-two percent of the catheters were colonized upon removal. Bacteria were isolated from 44.9% of blood specimens drawn via the catheter at the onset of ET, but only in 14% of blood specimens drawn in the same way at the end of the procedure. Seven newborn infants (10%) were found to be bacteremic 4-6 after ET; four of these infants were not treated and were able to eliminate the bacteremia. Systemic antibiotic therapy did not reduce the overall prevalence of colonization of cord and catheter of positive blood cultures pre- and postexchanges transfusion or the rate of bacteremia.


Subject(s)
Catheterization/adverse effects , Exchange Transfusion, Whole Blood/adverse effects , Infant, Newborn, Diseases/etiology , Jaundice, Neonatal/therapy , Sepsis/etiology , Umbilical Veins , Erythroblastosis, Fetal/therapy , Female , Glucosephosphate Dehydrogenase Deficiency/therapy , Humans , Infant, Newborn , Infant, Premature, Diseases/etiology , Pregnancy , Risk , Umbilical Veins/microbiology
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