This study provides etiological data on the prevalence of UIAs in healthy asymptomatic Japanese adults, and may be useful in determining therapeutic managements for UIAs.

No abstract

Cerebral white matter lesions are ischemic symptoms caused mainly by microangiopathy; they are diagnosed by MRI because they show up as abnormalities in MRI images. Because patients with white matter lesions do not have any symptoms, MRI often detects the lesions for the first time. Generally, head MRI for the diagnosis and grading of cerebral white matter lesions is performed as an option during medical checkups in Japan. In this study, we develop a mathematical model for the prediction of white matter lesions using data from routine medical evaluations that do not include a head MRI. Linear discriminant analysis, logistic discrimination, Naive Bayes classifier, support vector machine, and random forest were investigated and evaluated by ten-fold cross-validation, using clinical data for 1,904 examinees (988 males and 916 females) from medical checkups that did include the head MRI. The logistic regression model was selected based on a comparison of accuracy and interpretability. The model variables consisted of age, gender, plaque score (PS), LDL, systolic blood pressure (SBP), and administration of antihypertensive medication (odds ratios: 2.99, 1.57, 1.18, 1.06, 1.12, and 1.52, respectively) and showed Areas Under the ROC Curve (AUC) 0.805, the model displayed sensitivity of 72.0%, and specificity 75.1% when the most appropriate cutoff value was used, 0.579 as given by the Youden Index. This model has shown to be useful to identify patients with a high-risk of cerebral white matter lesions, who can then be diagnosed with a head MRI examination in order to prevent dementia, cerebral infarction, and stroke.

No abstract

Alterations of the Wnt/beta-catenin signaling pathway are known to occur in mutations of the component genes such as APC, Axin, and beta-catenin, and play a pathogenetic role in tumorigenesis. Activated Wnt signaling stabilizes beta-catenin, which associates with T cell factor, resulting in transactivation of the downstream target genes including c-myc and cyclin D1. To investigate the involvement of Wnt/beta-catenin signaling pathway in thyroid tumorigenesis, we analyzed its activation and localization in 5 human thyroid cancer cell lines and 132 thyroid tumor tissue samples. Dislocalization of beta-catenin was observed in all cell lines. Constitutive activation of T cell factor in two of four thyroid cancer cell lines was observed using reporter gene assay. Furthermore, high expression levels of c-Myc and cyclin D1 were observed in cell lines that showed cytoplasmic or nuclear accumulation of beta-catenin. In 132 paraffin-embedded thyroid carcinoma tissue samples, cytoplasmic beta-catenin was immunohistochemically observed in 52 out of 78 (67%) papillary thyroid cancers, but only in 3 of 34 (9%) follicular adenomas and 5 of 20 (25%) follicular cancers. Cytoplasmic localization of beta-catenin significantly correlated with overexpression of cyclin D1 in papillary carcinomas. Our results suggest that aberrant activation of Wnt/beta-catenin signaling is strongly involved in thyroid tumorigenesis.