High-resolution MRI vessel wall imaging: spatial and temporal patterns of reversible cerebral vasoconstriction syndrome and central nervous system vasculitis.

BACKGROUND AND PURPOSE: High-resolution MR imaging is an emerging tool for evaluating intracranial artery disease. It has an advantage of defining vessel wall characteristics of intracranial vascular diseases. We investigated high-resolution MR imaging arterial wall characteristics of CNS vasculitis and reversible cerebral vasoconstriction syndrome to determine wall pattern changes during a follow-up period. MATERIALS AND METHODS: We retrospectively reviewed 3T-high-resolution MR imaging vessel wall studies performed on 26 patients with a confirmed diagnosis of CNS vasculitis and reversible cerebral vasoconstriction syndrome during a follow-up period. Vessel wall imaging protocol included black-blood contrast-enhanced T1-weighted sequences with fat suppression and a saturation band, and time-of-flight MRA of the circle of Willis. Vessel wall characteristics including enhancement, wall thickening, and lumen narrowing were collected. RESULTS: Thirteen patients with CNS vasculitis and 13 patients with reversible cerebral vasoconstriction syndrome were included. In the CNS vasculitis group, 9 patients showed smooth, concentric wall enhancement and thickening; 3 patients had smooth, eccentric wall enhancement and thickening; and 1 patient was without wall enhancement and thickening. Six of 13 patients had follow-up imaging; 4 patients showed stable smooth, concentric enhancement and thickening; and 2 patients had resoluton of initial imaging findings. In the reversible cerebral vasoconstriction syndrome group, 10 patients showed diffuse, uniform wall thickening with negligible-to-mild enhancement. Nine patients had follow-up imaging, with 8 patients showing complete resolution of the initial findings. CONCLUSIONS: Postgadolinium 3T-high-resolution MR imaging appears to be a feasible tool in differentiating vessel wall patterns of CNS vasculitis and reversible cerebral vasoconstriction syndrome changes during a follow-up period.

Diagnostic yield of colonoscopy for constipation as the sole indication.

AIM: There is controversy over whether constipation as the only symptom should be an indication for routine diagnostic colonoscopy. The study was carried out to assess the prevalence of abnormal pathology on colonoscopy and to assess the risk factors for colonic neoplasia in patients with constipation but without 'high risk symptoms'. METHOD: A cross-sectional, single-centre study was conducted on individuals who underwent colonoscopy for constipation as the sole indication between 2005 and 2008. Standardized endoscopic and pathology reports were reviewed. Univariable and multivariable analyses were performed. RESULTS: A total of 786 patients (595 women, 75.7%; mean age, 57.4±13.5 years) underwent diagnostic colonoscopy for constipation. Forty-three (5.5%) had polyps, of whom 19 (2.4%) had hyperplastic polyps and 19 (2.4%) adenomas. No cancers were found. In patients with adenoma, the detection rate was 2.9% for patients below age 40 years and 1.7% for patients below age 50 years. Older age was associated with a polyp in both univariate and multivariate analysis. Gender, ethnicity and smoking were not associated with polyp or adenoma. CONCLUSION: Colonoscopy for patients with constipation as the sole indication had a lower yield of neoplastic lesions than that for patients undergoing routine screening colonoscopy. Colonoscopy in constipation may only be warranted in patients who are over 50 years of age.

Mutated in colorectal cancer, a putative tumor suppressor for serrated colorectal cancer, selectively represses beta-catenin-dependent transcription.

Mutated in colorectal cancer (MCC) was originally identified as a candidate gene for familial adenomatous polyposis (FAP) but further study identified adenomatous polyposis coli (APC) as responsible for FAP and the physiologic/pathologic roles of MCC remained poorly understood. Recently, MCC promoter methylation was discovered as a frequent early event in a distinct subset of precursor lesions and colorectal cancer (CRC) associated with the serrated CRC pathway. Here we provide the first evidence of the biological significance of MCC loss in CRC and the molecular pathways involved. We show MCC expression is dramatically decreased in many CRC cell lines and the distinct subset of sporadic CRC characterized by the CpG island methylator phenotype and BRAF(V600E) mutation due to promoter methylation as reported previously. Importantly, we find MCC interacts with beta-catenin and that reexpression of MCC in CRC cells specifically inhibits Wnt signaling, beta-catenin/T-cell factor/lymphoid-enhancer factor-dependent transcription and cellular proliferation even in the presence of oncogenic mutant APC. We also show that MCC is localized in the nucleus and identify two functional nuclear localization signals. Taken together, MCC is a nuclear, beta-catenin-interacting protein that can act as a potential tumor suppressor in the serrated CRC pathway by inhibiting Wnt/beta-catenin signal transduction.