PubMed · 14384825
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G O BAUMRUCKER. 1954. Another ureterosigmoidostomy modification.. https://pubmed.ncbi.nlm.nih.gov/14384825/
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The epithelial sodium channel (ENaC) controls colonic sodium absorption. So far, investigation of ENaC was limited by an unexplained lack of steroid-dependent ENaC expression in cultured intestinal cells, which we aimed to resolve. HT-29/B6 cells constitutively expressed the alpha-ENaC subunit, while beta- and gamma-ENaC subunits could not be detected due to deficient basal as well as corticosteroid-induced transcription. This was due to a lack of expression of both activating and inhibiting isoforms of glucocorticoid receptor (GR-alpha, -beta) and mineralocorticoid receptor. Stable transfection of GR-alpha restored intestine-specific glucocorticoid upregulation of beta- and gamma-ENaC in HT-29/B6 cells, which was followed by intact targeting of ENaC channels to the apical cell membrane and dose-dependent induction of electrogenic sodium absorption. In conclusion, ENaC deficiency is due to a lack of steroid receptors and not the consequence of a crypt-like phenotype of cultured intestinal cells. By stable GR transfection we obtained a model, in which ENaC regulation can be studied.
The mechanisms of how DNA mutations are fixed within the human gastrointestinal tract and how they spread are poorly understood and are hotly debated. It has been well documented that human colonic crypts are clonal units; one epithelial stem cell within the crypt becoming dominant and taking over the crypts' entire stem cell population--so called monoclonal conversion. Studies have revealed that crypts can exist as families and develop into patches. The questions have been how do such patches in the human colon develop? Does this have implications on how DNA mutations spread? We have previously shown that mitochondrial DNA (mtDNA) mutations, which result in the deficiency of cytochrome c oxidase, are established within a single colonic crypt stem cell, resulting in a crypt with a mixed phenotype. Over time that mutated stem cell can take over the entire stem cell population resulting in a wholly-mutated crypt. We have furthered this research by showing that entirely cytochrome c oxidase-deficient crypts are able to divide by a process called crypt fission, to form two cytochrome c oxidase-deficient daughter crypts, each sharing the exact parental mtDNA mutation. Furthermore, patches of these crypts also possess a founder mtDNA mutation suggesting that fission repeats itself to form patches, which increase in size with age. Here, we hypothesize that this can be expanded into other areas of the gastrointestinal tract, especially the stomach, where there is a paucity of data regarding clonality and the spread of DNA mutations. We ask if these mutated crypts expand at a different rate to wild type ones. We also discuss the implications for the spread of potential carcinogenic mutations within the gut.
BACKGROUND: Lower gastrointestinal bleeding is a frequent cause of hospitalization, but diagnostic methods for this condition are not fully established. Transabdominal ultrasound is a widely accepted diagnostic tool in bowel diseases. AIM: To evaluate the usefulness of transabdominal ultrasound for lower gastrointestinal bleeding. METHODS: We reviewed the medical records of consecutive patients who underwent transabdominal ultrasound as the first diagnostic procedure for acute haematochezia during the period June 1999 to June 2004. The study group comprised 111 patients and all underwent colonoscopy thereafter. Detection and diagnosis of lower gastrointestinal bleeding by ultrasonographic examination were evaluated by comparing the ultrasound diagnosis with the colonoscopic findings and final diagnosis. RESULTS: The bleeding site was localized by colonoscopy in 90 of the 111 patients (81%). The bleeding site was localized by ultrasound in 59 of the 90 patients (66%). When the bleeding site was in the rectum, ultrasonographic detectability was 30% (10/33); ultrasonographic detectability was 82-100% when the bleeding site was elsewhere. Rectal bleeding and diverticular bleeding were difficult to diagnose by ultrasound, but for the other diseases, diagnosis by ultrasonographic examination was possible in 91-100% of cases. CONCLUSIONS: Ultrasonographic examination may be an effective screening method for lower gastrointestinal bleeding.