Small bowel enteroclysis with magnetic resonance imaging and computed tomography in patients with failed and uncertain passage of a patency capsule

<p>Abstract</p> <p>Background</p> <p>Video capsule enteroscopy (VCE) has revolutionized small bowel imaging, enabling visual examination of the mucosa of the entire small bowel, while MR enteroclysis (MRE) and CT enteroclysis (CTE) have largely replaced conventional barium enteroclysis. A new indication for MRE and CTE is the clinical suspicion of small bowel strictures, as indicated by delayed or non-delivery of a test capsule given before a VCE examination, to exclude stenosis. The aim of this study was to determine the clinical value of subsequent MRE and CTE in patients in whom a test capsule did not present itself in due time.</p> <p>Methods</p> <p>Seventy-five consecutive patients were identified with a delayed or unnoticed delivery of the test capsule. Seventy patients consented to participate and underwent MRE (44) or CTE (26). The medical records and imaging studies were retrospectively reviewed and symptoms, laboratory results and imaging findings recorded.</p> <p>Results</p> <p>Lesions compatible with Crohns disease were shown by MRE in 5 patients, by CTE in one and by VCE in four, one of whom had lesions on MRE. In patients without alarm symptoms and findings (weight loss, haematochezia, anaemia, nocturnal diarrheoa, ileus, fistula, abscess and abnormal blood tests) imaging studies did not unveil any such lesion. VCE's were performed in only 20 patients, mainly younger than 50 years of age, although no stenotic lesion was shown by MRE and CTE. In the remaining 50 patients no VCE or other endoscopic intervention was performed indicating that the referring physician was content with the diagnostic information from MRE or CTE.</p> <p>Conclusion</p> <p>The diagnostic value of MRE and CTE is sufficient for clinical management of most patients with suspected small bowel disease, and thus VCE may be omitted or at least postponed for later usage.</p

The Function of Hypoxia-Inducible Factor (HIF) Is Independent of the Endoplasmic Reticulum Protein OS-9

The protein “amplified in osteosarcoma-9” (OS-9) has been shown previously to interact with the prolyl hydroxylases PHD2 and PHD3. These enzymes initiate oxygen-dependent degradation of the α-subunit of hypoxia-inducible factor (HIF), a transcription factor that adapts cells to insufficient oxygen supply (hypoxia). A new model has been proposed where OS-9 triggers PHD dependent degradation of HIF-α. It was the aim of our study to define the molecular mode of action of OS-9 in the regulation of PHD and HIF activity. Although initial co-immunoprecipitation experiments confirmed physical interaction between OS-9 and PHD2, neither overexpression nor lentiviral inhibition of OS-9 expression affected HIF regulation. Subcellular localization experiments revealed a distinct reticular staining pattern for OS-9 while PHD2 was mainly localized in the cytoplasm. Further cell fractionation experiments and glycosylation tests indicated that OS-9 is a luminal ER protein. In vivo protein interaction analysis by fluorescence resonance energy transfer (FRET) showed no significant physical interaction of overexpressed PHD2-CFP and OS-9-YFP. We conclude that OS-9 plays no direct functional role in HIF degradation since physical interaction of OS-9 with oxygen sensing HIF prolyl hydroxylases cannot occur in vivo due to their different subcellular localization