Circulating miRNAs as biomarkers in cardiovascular diseases.

Cardiovascular diseases (CVDs) have shown a high prevalence every year, presenting arterial hypertension as prime factor for their development, also driven by population growth, the aging of population and epidemiologic changes in disease. One of the main challenges in the study of CVD is the identification of reliable biomarkers that can be used in clinical practice and, in this context, microRNAs (miRNAs) have attracted much attention recently. MiRNAs are small non-coding RNAs, identified as post-transcriptional regulators of the expression of several genes both in physiologic and pathologic conditions. They have been studied as possible biomarkers, since they are highly expressed in the vascular system and are crucial modulators for the differentiation, contraction, migration and apoptosis of vascular cells, so modifications in their expression can cause several vascular alterations. Thus, this review aimed to compile the main studies regarding the role of miRNAs in the development of cardiac diseases, their potential applicability in the diagnosis, prognosis and treatment of these disorders. It was possible to verify that alterations in miRNAs expression are present in almost all cardiovascular diseases, such as the development of cardiac hypertrophy, coronary heart disease, heart failure and other conditions. Furthermore, growing evidence indicates that circulating miRNAs may become a potential tool for rapid and easy tests, since they are detected in peripheral blood, also allowing new therapeutic possibilities.

Fracture Resistance of Endodontically Treated Maxillary Premolars Restored With Different Methods.

PURPOSE:: The purpose of this in vitro study was to evaluate the resistance and patterns of fracture of endodontically treated maxillary premolars (ETPs) restored with different methods. METHODS AND MATERIALS:: Mesio-occluso-distal cavities were prepared in 50 extracted caries-free human maxillary premolars after endodontic treatment. The teeth were divided into five groups (n=10), according to the restorative method. G1: intact teeth (control group); G2: conventional composite resin; G3: conventional composite resin with a horizontal glass fiber post inserted between buccal and palatal walls; G4: bulk-fill flowable and bulk-fill restorative composites; and G5: ceramic inlay. For direct restorations, Filtek Z350 XT, Filtek Bulk Fill Flowable Restorative, and Filtek Bulk Fill Posterior Restorative were used. Indirect restorations were fabricated from a pressable lithium disilicate glass-ceramic (IPS e-max Press) and adhesively cemented (RelyX Ultimate). All specimens were subjected to thermocycling (5°C to 55°C/5000 cycles) and additionally submitted to cyclic loading 50,000 times in an Electro-Mechanical Fatigue Machine. Next, the specimens were subjected to a compressive load at a crosshead speed of 1 mm/min until fracture. The fractured specimens were analyzed to determine the fracture pattern using a stereomicroscope, and then representative specimens were carbon coated to allow for the studying of the fracture surface under scanning electron microscopy. One-way analysis of variance (ANOVA) was used to compare fracture resistance of the groups. The results of fracture patterns were submitted to the Fisher exact test (α=0.05). RESULTS:: All specimens survived fatigue. Mean (standard deviation) failure loads (N) for groups were as follows: G1: 949.6 (331.5); G2: 999.6 (352.5); G3: 934.5 (233.6); G4: 771.0 (147.4); and G5: 856.7 (237.5). The lowest fracture resistance was recorded for G4, and the highest ones were recorded for G2, followed by that of G1 and G3. One-way ANOVA did not reveal significant differences between groups ( p>0.05). The highest repairable fracture rates were observed in G1 (100%) and G3 (80%). CONCLUSIONS:: ETPs restored with conventional composite resin with or without horizontal fiber post, bulk-fill composite, and ceramic inlay showed fracture resistance similar to that of sound teeth. Conventional composite resin restorations exhibited the highest prevalence of unrepairable fractures, and the insertion of a horizontal fiber post decreased this prevalence. Intact teeth showed 100% of repairable fractures. It is difficult to extrapolate the results directly to a clinical situation due to the limitations of this study.

Mice with Deletion of Neuromedin B Receptor Exhibit Decreased Oral Glucose-Stimulated Insulin Release.

Neuromedin B (NB) and gastrin-releasing peptide (GRP) are bombesin-like peptides, found in the gastrointestinal tube and pancreas, among other tissues. Consistent data proposed that GRP stimulates insulin secretion, acting directly in pancreatic cells or in the release of gastrointestinal hormones that are incretins. However, the role of NB remains unclear. We examined the glucose homeostasis in mice with deletion of NB receptor (NBR-KO). Female NBR-KO exhibited similar fasting basal glucose with lower insulinemia (48.4%) and lower homeostasis model assessment of insulin resistance index (50.5%) than wild type (WT). Additionally, they were more tolerant to oral glucose, demonstrated by a decrease in the area under the glucose curve (18%). In addition, 15 min after an oral glucose load, female and male NBR-KO showed lower insulin serum levels (45.6 and 26.8%, respectively) than WT, even though blood glucose rose to similar levels in both groups. Single injection of NB, one hour before the oral glucose administration, tended to induce higher serum insulin in WT (28.9%, p=0.3), however the same did not occur in NBR-KO. They showed no changes in fasting insulin content in pancreatic islets by immunohistochemistry, however, the fasting serum levels of glucagon-like peptide, a potent incretin, exhibited a strong trend to reduction (40%, p=0.07). Collectively, mice with deletion of NB receptor have lower insulinemia, especially in response to oral glucose, and females also exhibited a better glucose tolerance, suggesting the involvement of NB and its receptor in regulation of insulin secretion induced by incretins, and also, in insulin sensitivity.