This study evaluated the influence of relining fiber posts on the bond strength (BS) of resin cements in the root canal. Forty bovine teeth were divided in four groups (n = 10): G1 (ARC)-fiber post cemented with resin cement RelyX ARC; G2 (ARC+Z350)-relined fiber post cemented with RelyX ARC; G3 (U200)-fiber post cemented with self-adhesive cement RelyX U200; G4 (U200+Z350)-relined fiber post cemented with RelyX U200. The roots were sectioned in six 1.2-mm slices and the push-out test was performed. Data were analyzed by three-way analysis of variance (ANOVA), and Tukey's test (α = 0.05). For the conventional resin cement, there was no significant difference between groups G1-ARC (15.5 ± 3.8) and G2-ARC+Z350 (16.1 ± 4.5). For the self-adhesive cement, the results revealed higher BS values for relined posts G4-U200 + Z350 (19.9 ± 7.9) as compared to non-relined posts G3-U200 (14.4 ± 4.5). For both cements, in groups of relined posts, the apical and the cervical thirds presented similar BS. Relining enhances the performance of the self-adhesive resin cement, and the interaction between relining and root third influences the BS to the conventional resin cement.

Objective: Conduct a survey of scientific articles that aim the validation of instruments for children and adolescents with chronic disease. Results: Were found 16 articles that met the inclusion criteria. Method: Discussion:The construction of the summary of selected studies shows that the creation of an instrument in that theme is connected to a specific disease such as diabetes, sickle cell anemia and asthma.

Objectives To characterize an experimental model of pulmonary embolism by studying hemodynamics, lung mechanics and histopathologic derangements caused by pulmonary microembolism in pigs. To identify lung alterations after embolism that may be similar to those evidenced in pulmonary inflammatory conditions. Materials and methods Ten Large White pigs (weight 35-42 kg) were instrumented with arterial and pulmonary catheters, and pulmonary embolism was induced in five pigs by injection of polystyrene microspheres (diameter ~300 µM), in order to obtain a pulmonary mean arterial pressure of twice the baseline value. Five other animals injected with saline served as controls. Hemodynamic and respiratory data were collected and pressure x volume curves of the respiratory system were performed by a quasi-static low flow method. Animals were followed for 12 hours, and after death lung fragments were dissected and sent to pathology. Results Pulmonary embolism induced a significant reduction in stroke volume (71 ± 18 ml/min/bpm pre vs 36 ± 9 ml/min/bpm post, P < 0.05), an increase in pulmonary mean arterial pressure (27 ± 4 mmHg pre vs 39 ± 6 mmHg post, P < 0.05) and pulmonary vascular resistance (193 ± 122 mmHg/l/min pre vs 451 ± 149 mmHg/l/min post, P < 0.05). Respiratory dysfunction was evidenced by significant reductions in the PaO 2 /FiO 2 ratio (480 ± 50 pre vs 159 ± 55 post, P < 0.05), the dynamic lung compliance (27 ± 6 ml/cmH 2 O pre vs 19 ± 5 ml/cmH 2 O post, P < 0.05), the increase in dead space ventilation (20 ± 4 pre vs 47 ± 20 post, P < 0.05) and, the shift of pressure x volume curves to the right, with reduction in pulmonary hysteresis. Pathology depicted inflammatory neutrophil infiltrates, alveolar edema, collapse and hemorrhagic infarctions. Conclusion This model of embolism is associated with cardiovascular dysfunction, as well as respiratory injury characterized by a decrease in oxygenation, lung compliance and hysteresis. Pathology findings were similar to those verified in inflammatory pulmonary injury conditions. This model may be useful to study pathophysiology, as well as pharmacologic and ventilatory interventions useful to treat pulmonary embolism. P6 Hemodynamic and metabolic features of a porcine systemic low flow state model

Sepsis, the body's response to infection, is associated with extremely high mortality rates. Why a protective mechanism turns into a deadly clinical picture is a matter of debate, and goes largely unexplained. In previous work we demonstrated that platelet-derived microparticles (MP) can induce endothelial and vascular smooth muscle cell apoptosis in septic patients through NADPH oxidasedependent superoxide release [1]. In this work we sought to create a model for ex vivo generation of septic-like MP and to identify the pathways responsible for MP free radical release and effects. Septic shock is a condition related to the generation of high amounts of thrombin, TNFα and nitrogen reactive species. Human platelets exposed to the NO donors diethylamine-NONOate (0.5 mM) and nitroprusside (2 mM) for 20 minutes generated MP similar to those found in the blood of septic shock patients. Flow cytometry and western blot analysis of those MP, like their septic counterparts, revealed exposure of the tetraspanin markers CD9, CD63, and CD81, but little phosphatidylserine. Such a membrane exposure, associated with their size, characterizes them as exosomes. Furthermore, we identified the Nox2 and p22phox NADPH oxidase subunits and the inducible isoform of NO synthase (NOS), but not the NOS I and III isoforms. On the other hand, platelets exposed to thrombin or TNFα released particles with clearly distinct characteristics, such as high phosphatidylserine and low tetraspanin. Like the septic MP, the MP obtained by NO exposure generated the superoxide radical and NO, as disclosed by lucigenin (5 µM) and coelenterazine (5 µM) chemiluminescence and by 4,5-diaminofluorescein (10 mM) and 2′,7′-dichlorofluorescein (10 mM) fluorescence. As expected, NOS inhibitors or NADPH oxidase inhibitors significantly reduced signals. In addition, endothelial cells exposed to this type of MP underwent apoptotic death, while control MP had negligible effects. NADPH oxidase as well as NOS inhibition significantly reduced apoptosis rates. Concomitant generation of NO and superoxide suggests biological effects of the highly reactive radical peroxynitrite. In fact, the peroxynitrite scavenger urate (1 mM) showed an additive effect on fluorescent signal inhibition, as well as on endothelial apoptosis rate reduction. We thus propose that platelet-derived exosomes may be another class of actors in the complex play known as 'vascular redox signaling'. In this sense, an exosome-based approach can provide novel tools for further understanding and even treating vascular dysfunction related to sepsis. Introduction The intestinal hypothesis of sepsis has been attributed to bacterial translocation (BT), and the aggravation of sepsis is related to the increased vascular permeability state that potentates the BT index. In this study we examined the BT index during sepsis with or without mesenteric lymph exclusion. Materials and methods Wistar rats (±200 g) were submitted to the BT process (E. coli R6 10 ml of 10 10 CFU/ml) and nonlethal sepsis (E. cloacae 89 2 ml ...

IntroductionKidney disease is a well-known and frequent complication of HIV infection. The aim of this study is to investigate novel biomarkers of kidney disease in HIV patients.MethodsThis is a cross-sectional study with HIV patients recruited in public health centres in Fortaleza city, Brazil, between January 2016 and March 2017. Three groups of HIV patients were included: I) those who have never received combined antiretroviral therapy (cART), II) those receiving cARTwithtenofovir/lamivudine/efavirenz or III) zidovudine/lamivudine/efavirenz. A group of 13 healthy subjects were the control group. The novel biomarkers investigated were: urinary and serum neutrophil gelatinase-associated lipocalin(uNGAL), urinary monocyte chemoattractant protein-1 (MCP-1) and urinary kidney injure molecule-1 (KIM-1), and the results were compared with the traditional biomarkers microalbuminuria and creatinine. Glomerular filtration rate (GFR) was estimated based on CKD-EPI equation.ResultsA total of 66 HIV patients were included, with mean age of 33±8 years, and 77% were male. The majority of the patients (63%) had undetectable viral load. Serum creatinine and GFR were similar in all groups. No HIV patient had GFR <60 mL/min and only two patients (3%) had microalbuminuria >30 mg/g-Cr).KIM-1 levels in patients using Tenofovir were higher than control group (1.25±0.6 vs 0.7±0.2 ng/mg-Cr, p<0.001).MCP-1 was significantly higher among HIV patients, and the highest values were found in those with no cART and high viral load. Urinary NGAL was also higher among HIV patients, but it only presented a tendency to significance (p=0.07). Regarding serum NGAL, no significant difference was observed between the groups (p=0.417). There was significant association between urinary NGAL andmicroalbuminuria (r=0.378, p=0.003) and MCP-1 (r=0.476, p<0.001) in all HIV patients. ConclusionHIV patients usingcART presents subclinical kidney disease detected through novel biomarkers. KIM-1 may serve as early marker of tenofovir nephrotoxicity, and MCP-1 appears to be related with higher viral load.