BackgroundBreast cancer is a heterogeneous disease associated with different patient prognosis and responses to therapy. Vitamin D has been emerging as a potential treatment for cancer, as it has been demonstrated that it modulates proliferation, apoptosis, invasion and metastasis, among others. It acts mostly through the Vitamin D receptor (VDR) and the synthesis and degradation of this hormone are regulated by the enzymes CYP27B1 and CYP24A1, respectively. We aimed to study the expression of these three proteins by immunohistochemistry in a series of breast lesions.MethodsWe have used a cohort comprising normal breast, benign mammary lesions, carcinomas in situ and invasive carcinomas and assessed the expression of the VDR, CYP27B1 and CYP24A1 by immunohistochemistry.ResultsThe results that we have obtained show that all proteins are expressed in the various breast tissues, although at different amounts. The VDR was frequently expressed in benign lesions (93.5%) and its levels of expression were diminished in invasive tumours (56.2%). Additionally, the VDR was strongly associated with the oestrogen receptor positivity in breast carcinomas. CYP27B1 expression is slightly lower in invasive carcinomas (44.6%) than in benign lesions (55.8%). In contrast, CYP24A1 expression was augmented in carcinomas (56.0% in in situ and 53.7% in invasive carcinomas) when compared with that in benign lesions (19.0%).ConclusionsFrom this study, we conclude that there is a deregulation of the Vitamin D signalling and metabolic pathways in breast cancer, favouring tumour progression. Thus, during mammary malignant transformation, tumour cells lose their ability to synthesize the active form of Vitamin D and respond to VDR-mediated Vitamin D effects, while increasing their ability to degrade this hormone.

There is increasing evidence that hypercholesterolemia during midlife may represent a predictor of subsequent mild cognitive impairments and dementia decades later. However, the exact mechanism underlying this phenomenon remains unknown since plasmatic cholesterol is not able to cross the blood-brain barrier. In the present study, we evaluated the hypothesis that cognitive impairments triggered by hypercholesterolemia during aging may be related to brain oxidative stress and altered brain acetylcholinesterase (AChE) activity. We also performed a neuropathological investigation in order to analyze whether the cognitive impairments may be associated with stroke-related features. To address these questions we used three- and fourteen-month-old low-density lipoprotein receptor-deficient mice (LDLr-/-). The current findings provide new evidence that aged LDLr-/- mice, exposed to over three-fold cholesterol levels from early life, show working, spatial reference, and procedural memory impairments, without alterations in motor function. Antioxidant imbalance and oxidative damage were evidenced by a marked increase in lipid peroxidation (thiobarbituric acid reactive substances levels) and glutathione metabolism (increase in glutathione levels, glutathione reductase, and glutathione peroxidase activities) together with a significant increase in the AChE activity in the prefrontal cortex of aged hypercholesterolemic LDLr-/- mice. Notably, hypercholesterolemia was not related to brain infarcts and neurodegeneration in mice, independent of their age. These observations provide new evidence that hypercholesterolemia during aging triggers cognitive impairments on different types of learning and memory, accompanied by antioxidant imbalance, oxidative damage, and alterations of cholinergic signaling in brain areas associated with learning and memory processes, particularly in the prefrontal cortex.

Odontogenic tumors (OTs) are lesions that develop exclusively on maxillary bones, and form a heterogeneous group. They vary from hamartomatous lesions to benign and malign tumors. Although they are rarely observed in dentistry clinics, it is extremely important for the dentist to be aware of them. The aim of this study was to investigate the incidence of odontogenic tumors diagnosed in the population of Florianópo-lis, Santa Catarina, Brazil. Cases of odontogenic tumors were selected from the anatomopathological diagnostic services at Federal University of Santa Catarina from 1998 to 2011. Clinical data on these cases were collected from biopsy reports and patient files. Seventy-eight cases of odontogenic tumors were surveyed. Of these diagnoses, 51% were keratocystic odontogenic tumors (KCOTs); the remaining cases were mainly ameloblastomas and odontomas. The most frequently observed lesion in this retrospective study was KCOT (more than half of cases). Thus, this study shows that modifying the classification of the OTs altered the frequency of the lesions, possibly making KCOT the most common lesion observed in diagnostic services worldwide.

PURPOSE: Sleeve gastrectomy (SG) removes substantial part of the gastric mucosa, which produces ghrelin. This reduction is expected to force other organs, such as the duodenum, to compensate by increasing the number of ghrelin-producing cells. The purpose of this study was to evaluate whether this response occurs. METHODS: Twelve adult male, Wistar rats underwent SG and were reoperated 30 or 60 days after the initial surgery. During the second surgery, a segment of the duodenum was resected to count ghrelin cells using immunohistochemistry. In six animals, SG was not performed, and the duodenal segment served as a control for ghrelin cell counts. The ghrelin cell index (GCI), which is the number of ghrelin cells divided by the number of villi in each segment, was measured and used in statistical analysis by one-way analysis of variance (ANOVA). RESULTS: There were increases in the absolute numbers of cells 30 and 60 days after SG, but statistical analysis by ANOVA showed no significant difference between the groups. CONCLUSION: A compensatory increase in the number of duodenal immunopositive ghrelin cells did not occur as a response to sleeve gastrectomy.

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