Proton magnetic resonance spectroscopy of the frontal, cingulate and perirolandic cortices and its relationship to skin conductance in patients with schizophrenia

The aim of the present study was to determine whether specific subgroups of schizophrenic patients, grouped according to electrodermal characteristics, show differences in the N-acetylaspartate/creatine plus choline (NAA / (Cr + Cho)) ratios in the frontal, cingulate and perirolandic cortices. Skin conductance levels (SCL) and skin conductance responses to auditory stimulation were measured in 38 patients with schizophrenia and in the same number of matched healthy volunteers (control). All subjects were submitted to multivoxel proton magnetic resonance spectroscopic imaging. When compared to the control group, patients presented significantly lower NAA / (Cr + Cho) ratios in the right dorsolateral prefrontal cortex (schizophrenia = 0.95 ± 0.03; control = 1.12 ± 0.04) and in the right (schizophrenia = 0.88 ± 0.02; control = 0.94 ± 0.03) and left (schizophrenia = 0.84 ± 0.03; control = 0.94 ± 0.03) cingulates. These ratios did not differ between electrodermally responsive and non-responsive patients. When patients were divided into two groups: lower SCL (less than the mean SCL of the control group minus two standard deviations) and normal SCL (similar to the control group), the subgroup with a lower level of SCL showed a lower NAA / (Cr + Cho) ratio in the left cingulate (0.78 ± 0.05) than the controls (0.95 ± 0.02, P < 0.05) and the subgroup with normal SCL (0.88 ± 0.03, P < 0.05). There was a negative correlation between the NAA / (Cr + Cho) ratio in the left cingulate of patients with schizophrenia and the duration of the disease and years under medication. These data suggest the existence of a schizophrenic subgroup characterized by low SCL that could be a consequence of the lower neuronal viability observed in the left cingulate of these patients.CNPqFAPES

The receptor AT1 appears to be important for the maintenance of bone mass and AT2 receptor function in periodontal bone loss appears to be regulated by AT1 receptor

A large number of experimental studies has demonstrated that angiotensin II (Ang II) is involved in key events of the inflammatory process. This study aimed to evaluate the role of Ang II type 1 (AT1) and Ang II type 2 (AT2) receptors on periodontitis. Methods: Experimental periodontitis was induced by placing a 5.0 nylon thread ligature around the second upper left molar of AT1 mice, no-ligature or ligature (AT1-NL and AT1-L), AT2 (AT2-NL or AT2-L) and wild type (WT-NL or L). Alveolar bone loss was scanned using Micro-CT. Cytokines, peptides and enzymes were analyzed from gingival tissues by Elisa and RT-PCR. Results: The blockade of AT1 receptor resulted in bone loss, even in healthy animals. Ang II receptor blockades did not prevent linear bone loss. Ang II and Ang 1-7 levels were significantly increased in the AT2-L (p < 0.01) group compared to AT2-NL and AT1-L. The genic expression of the Mas receptor was significantly increased in WT-L and AT2-L compared to (WT-NL and AT2-NL, respectively) and in AT1-L. Conclusions: Our data suggest that the receptor AT1 appears to be important for the maintenance of bone mass. AT2 receptor molecular function in periodontitis appears to be regulated by AT1

AT1 and AT2 receptor knockout changed osteonectin and bone density in mice in periodontal inflammation experimental model

BACKGROUND: The aim of this study was to evaluate the role of AT1 and AT2 receptors in a periodontal inflammation experimental model. METHODS: Periodontal inflammation was induced by LPS/Porphyromonas gingivalis. Maxillae, femur, and vertebra were scanned using Micro-CT. Maxillae were analyzed histopathologically, immunohistochemically, and by RT-PCR. RESULTS: The vertebra showed decreased BMD in AT1 H compared with WT H (p < 0.05). The femur showed increased Tb.Sp for AT1 H and AT2 H, p < 0.01 and p < 0.05, respectively. The Tb.N was decreased in the vertebra (WT H-AT1 H: p < 0.05; WT H-AT2 H: p < 0.05) and in the femur (WT H-AT1 H: p < 0.01; WT H-AT2 H: p < 0.05). AT1 PD increased linear bone loss (p < 0.05) and decreased osteoblast cells (p < 0.05). RANKL immunostaining was intense for AT1 PD and WT PD (p < 0.001). OPG was intense in the WT H, WT PD, and AT2 PD when compared to AT1 PD (p < 0.001). AT1 PD showed weak immunostaining for osteocalcin compared with WT H, WT PD, and AT2 PD (p < 0.001). AT1 H showed significantly stronger immunostaining for osteonectin in fibroblasts compared to AT2 H (p < 0.01). CONCLUSION: AT1 receptor knockout changed bone density, the quality and number of bone trabeculae, decreased the number of osteoblast cells, and increased osteonectin in fibroblasts

Prevalence and predictors of coronary artery disease in patients with a calcium score of zero

The absence of coronary calcification is associated with an excellent prognosis. However, a calcium score of zero does not exclude the presence of coronary artery disease (CAD) or the possibility of future cardiovascular events. Our aim was to study the prevalence and predictors of coronary artery disease in patients with a calcium score of zero. Prospective registry consisted of 3,012 consecutive patients that underwent cardiac CT (dual source CT). Stable patients referred for evaluation of possible CAD that had a calcium score of zero (n = 864) were selected for this analysis. The variables that were statistically significant were included in a multivariable logistic regression model. From 864 patients with a calcium score of zero, 107 (12.4 %) had coronary plaques on the contrast CT (10.8 %, n = 93 with nonobstructive CAD and 1.6 %, n = 14 with obstructive CAD). By logistic regression analysis, the independent predictors of CAD in this population were age >55 years [odds ratio (OR) 1.63 (1.05-2.52)], hypertension [OR 1.64 (1.05-2.56)] and dyslipidemia [OR 1.54 (1.00-2.36)]. In the presence of these 3 variables, the probability of having coronary plaques was 21 %. The absence of coronary artery calcification does not exclude the presence of coron

Diabetes as an independent predictor of high atherosclerotic burden assessed by coronary computed tomography angiography: The coronary artery disease equivalent revisited

(1) To study the prevalence and severity of coronary artery disease (CAD) in diabetic patients. (2) To provide a detailed characterization of the coronary atherosclerotic burden, including the localization, degree of stenosis and plaque composition by coronary computed tomography angiography (CCTA). Single center prospective registry including a total of 581 consecutive stable patients (April 2011-March 2012) undergoing CCTA (Dual-source CT) for the evaluation of suspected CAD without previous myocardial infarction or revascularization procedures. Different coronary plaque burden indexes and plaque type and distribution patterns were compared between patients with (n = 85) and without diabetes (n = 496). The prevalence of CAD (any plaque; 74.1 vs. 56 %; p = 0.002) and obstructive CAD (≥50 % stenosis; 31.8 vs. 10.3 %; p<0.001) were significantly higher in diabetic patients. The remaining coronary atherosclerotic burden indexes evaluated (plaque in LM-3v-2v with prox. LAD; SIS; SSS; CT-LeSc) were also significantly higher in diabetic patients. In the per segment analysis, diabetics had a higher percentage of segments with plaque in every vessel (2.6/13.1/7.5/10.5 % for diabetics vs. 1.4/7.1/3.3/4.4 % for nondiabetics for LM, LAD, LCx, RCA respectively; p<0.001 for all) and of both calcified (19.3 vs. 9.2 %, p<0.001) and noncalcified or mixed types (14.4 vs. 7.0 %; p<0.001); the ratio of proximal-to-distal relative plaque distribution (calculated as LM/proximal vs. mid/distal/branches) was lower for diabetics (0.75 vs. 1.04; p = 0.009). Diabetes was an independent predictor of CAD and was also associated with more advanced CAD, evaluated by indexes of coronary atherosclerotic burden. Diabetics had a significantly higher prevalence of plaques in every anatomical subset and for the different plaque composition. In this report, the relative geographic distribution of the plaques within each subgroup, favored a more mid-to-distal localization in the diabetic patients