Analysis of Biofilm Adhesion on CAD/CAM Lithium Disilicates Under Different Types of Intraoral Polishing.

PURPOSE: To evaluate the adhesion of Streptococcus mutans (S. mutans) on lithium disilicate ceramics, submitted to different intraoral polishing protocols, and the degree of surface smoothness obtained. MATERIALS AND METHODS: Fifty lithium disilicate specimens were divided into 5 groups (n=10): G1-Glaze Group (positive control); G2-Glaze Group + Wear + Glaze; G3-Wear Group (negative control); G4-Ceramisté Wear Group; G5-Optrafine Wear Group. Surface roughness (Ra - µm) was evaluated and the surface characteristics were assessed using a scanning electron microscope (SEM); to assess S. mutans biofilm, the number of cultured cells was evaluated by counting colony-forming units (CFU/mL). The data underwent one-way ANOVA followed by Tukey's test (P⟨.05). RESULTS: There was a significant difference in the surface roughness of all groups compared with G3. There was no significant difference between the G4 and G5 groups that received polishing. G1 group had the lowest mean roughness values. There was a difference in Log values (CFU/mL) between the G3 group and the groups that received glaze (G1 and G2). The G3 group had the highest adhesion of S. mutans (4.53 Log). CONCLUSION: The most effective polishing protocol after wear is glazing, presenting the lowest roughness and CFU/mL values.

Macrophage migration inhibitory factor promotes eosinophil accumulation and tissue remodeling in eosinophilic esophagitis.

Macrophage migration inhibitory factor (MIF) is involved in eosinophil biology and in type 2 inflammation, contributing to allergic and helminthic diseases. We hypothesized that MIF participates in the pathogenesis of eosinophilic esophagitis (EoE), an allergic condition characterized by esophageal eosinophilic inflammation. MIF is highly expressed in esophageal mucosa of patients with EoE, compared with gastro-esophageal reflux disease and control patients, where it co-localizes predominantly with eosinophils. In vitro, recombinant MIF promotes human eosinophil chemotaxis, while MIF antagonist and CXCR4 antagonist, AMD3100, revert this effect. In a model of EoE induced by ovalbumin, Mif-deficient mice have reduced inflammation and collagen deposition compared with wild-type (WT) mice. Importantly, treatment of WT mice with anti-MIF or with AMD3100 during the challenge phase prevents accumulation of eosinophils and tissue remodeling. Conversely, recombinant MIF promoted tissue eosinophil inflammation in allergic mice. Together, these results implicate MIF in the pathogenesis of esophageal inflammation and suggest that targeting MIF might represent a novel therapy for EoE.

Morphometric evaluation of nitric oxide synthase isoforms and their cytokine regulators predict pulmonary dysfunction and survival in systemic sclerosis.

Because histopathological changes in the lungs of patients with systemic sclerosis (SSc) are consistent with alveolar and vessel cell damage, we presume that this interaction can be characterized by analyzing the expression of proteins regulating nitric oxide (NO) and plasminogen activator inhibitor-1 (PAI-1) synthesis. To validate the importance of alveolar-vascular interactions and to explore the quantitative relationship between these factors and other clinical data, we studied these markers in 23 cases of SSc nonspecific interstitial pneumonia (SSc-NSIP). We used immunohistochemistry and morphometry to evaluate the amount of cells in alveolar septa and vessels staining for NO synthase (NOS) and PAI-1, and the outcomes of our study were cellular and fibrotic NSIP, pulmonary function tests, and survival time until death. General linear model analysis demonstrated that staining for septal inducible NOS (iNOS) related significantly to staining of septal cells for interleukin (IL)-4 and to septal IL-13. In univariate analysis, higher levels of septal and vascular cells staining for iNOS were associated with a smaller percentage of septal and vascular cells expressing fibroblast growth factor and myofibroblast proliferation, respectively. Multivariate Cox model analysis demonstrated that, after controlling for SSc-NSIP histological patterns, just three variables were significantly associated with survival time: septal iNOS (P=0.04), septal IL-13 (P=0.03), and septal basic fibroblast growth factor (bFGF; P=0.02). Augmented NOS, IL-13, and bFGF in SSc-NSIP histological patterns suggest a possible functional role for iNOS in SSc. In addition, the extent of iNOS, PAI-1, and IL-4 staining in alveolar septa and vessels provides a possible independent diagnostic measure for the degree of pulmonary dysfunction and fibrosis with an impact on the survival of patients with SSc.

Morphometric evaluation of nitric oxide synthase isoforms and their cytokine regulators predict pulmonary dysfunction and survival in systemic sclerosis

Because histopathological changes in the lungs of patients with systemic sclerosis (SSc) are consistent with alveolar and vessel cell damage, we presume that this interaction can be characterized by analyzing the expression of proteins regulating nitric oxide (NO) and plasminogen activator inhibitor-1 (PAI-1) synthesis. To validate the importance of alveolar-vascular interactions and to explore the quantitative relationship between these factors and other clinical data, we studied these markers in 23 cases of SSc nonspecific interstitial pneumonia (SSc-NSIP). We used immunohistochemistry and morphometry to evaluate the amount of cells in alveolar septa and vessels staining for NO synthase (NOS) and PAI-1, and the outcomes of our study were cellular and fibrotic NSIP, pulmonary function tests, and survival time until death. General linear model analysis demonstrated that staining for septal inducible NOS (iNOS) related significantly to staining of septal cells for interleukin (IL)-4 and to septal IL-13. In univariate analysis, higher levels of septal and vascular cells staining for iNOS were associated with a smaller percentage of septal and vascular cells expressing fibroblast growth factor and myofibroblast proliferation, respectively. Multivariate Cox model analysis demonstrated that, after controlling for SSc-NSIP histological patterns, just three variables were significantly associated with survival time: septal iNOS (P=0.04), septal IL-13 (P=0.03), and septal basic fibroblast growth factor (bFGF; P=0.02). Augmented NOS, IL-13, and bFGF in SSc-NSIP histological patterns suggest a possible functional role for iNOS in SSc. In addition, the extent of iNOS, PAI-1, and IL-4 staining in alveolar septa and vessels provides a possible independent diagnostic measure for the degree of pulmonary dysfunction and fibrosis with an impact on the survival of patients with SSc.

Resistance exercise: a non-pharmacological strategy to minimize or reverse sleep deprivation-induced muscle atrophy.

Sleep is important for maintenance of skeletal muscle health. Sleep debt can induce muscle atrophy by increasing glucocorticoids and decreasing testosterone, growth hormone and insulin-like growth factor-I. These hormonal alterations result in a highly proteolytic environment characterized by decreased protein synthesis and increased degradation. Given that sleep deprivation is increasingly prevalent in modern society, strategies to minimize or reverse its adverse effects need to be investigated. Resistance exercise has been suggested as an intervention that would benefit the muscle health. The practice of this type of exercise can increase the concentration of testosterone, growth hormone and insulin-like growth factor I and stimulate the protein synthesis through a key signaling molecule, mammalian target of rapamycin. Thus, we hypothesized that resistance exercise is an important non-pharmacological strategy to counteract deleterious effects of sleep debt on skeletal muscle.

Chronic exercise promotes alterations in the neuroendocrine profile of elderly people.

Aging and physical inactivity are 2 factors that favour the development of cardiovascular disease, metabolic syndrome, obesity, and diabetes. In contrast, adopting a habitual moderate exercise routine may be a nonpharmacological treatment alternative for neuroendocrine aging disorders. We aimed to assess the effects of moderate exercise training on the metabolic profiles of elderly people with sedentary lifestyles. Fourteen sedentary, healthy, elderly male volunteers participated in a moderate training regimen for 60 min/day, 3 days/week for 24 weeks at a work rate equivalent to their ventilatory aerobic threshold. The environment was maintained at a temperature of 23±2°C, with a humidity of 60±5%. Blood samples for analysis were collected at 3 intervals: at baseline (1 week before training began), and 3 and 6 months after training. The training promoted increased aerobic capacity (relative VO(2), and time and velocity to VO(2)max; (p<0.05)) and reduced serum α-MSH (p<0.05) after 3 months of training when compared with the baseline data. In addition, serum thyroid hormone (T3 and T4) was reduced after 6 months of training compared with baseline levels. Our results demonstrate that a moderate exercise training protocol improves the metabolic profile of older people, and metabolic adaptation is dependent on time.

Sleep and muscle recovery: endocrinological and molecular basis for a new and promising hypothesis.

Sleep is essential for the cellular, organic and systemic functions of an organism, with its absence being potentially harmful to health and changing feeding behavior, glucose regulation, blood pressure, cognitive processes and some hormonal axes. Among the hormonal changes, there is an increase in cortisol (humans) and corticosterone (rats) secretion, and a reduction in testosterone and Insulin-like Growth Factor 1, favoring the establishment of a highly proteolytic environment. Consequently, we hypothesized that sleep debt decreases the activity of protein synthesis pathways and increases the activity of degradation pathways, favoring the loss of muscle mass and thus hindering muscle recovery after damage induced by exercise, injuries and certain conditions associated with muscle atrophy, such as sarcopenia and cachexia.

Chronic lead poisoning in an adult battery worker.

BACKGROUND: Lead poisoning is a common environmental health hazard in developing countries. Incidences of lead poisoning are seen in all age groups, especially in adults working in lead-based industries, where many still remain unaware of the adverse effects of exposure to unusually high levels of lead. METHODS: We report the case of an adult battery worker, who initially received symptomatic treatment because of clinical misdiagnosis. Later, he was treated with appropriate chelators, which helped to decrease blood lead levels drastically. However, being unable to change his occupation, he continues to be exposed to potentially lethal doses of lead. CONCLUSIONS: A key role for health agencies, besides providing opportunities for diagnosis and therapy, should be to increase public awareness about this widespread environmental hazard through education, documentation and communication.

Expression of lymphocyte-endothelial receptor-ligand pairs, alpha4beta7/MAdCAM-1 and OX40/OX40 ligand in the colon and jejunum of patients with inflammatory bowel disease.

BACKGROUND: The interaction between leucocytes and vascular endothelial cells is essential for leucocyte migration into inflammatory sites. AIMS: To study the local expression of the pairs of complementary molecules, alpha4beta7/mucosal addressin cell adhesion molecule (MAdCAM-1) and OX40/OX40 ligand in the lamina propria of the colon and jejunum of patients with inflammatory bowel disease. METHODS: Ten patients with active ulcerative colitis (UC), nine with active Crohn's disease (CD), and seven irritable bowel syndrome (IBS) controls were submitted to endoscopic and peroral jejunal biopsies. Specimens were immunostained by indirect alkaline phosphatase using antibodies against CD3, intercellular adhesion molecule (ICAM) 1, alpha4beta7, MAdCAM-1, and OX40. An OX40-mouse-IgG fusion protein was used to detect OX40 ligand on frozen sections. Immunohistological analysis was carried out by optical microscopy using a computer assisted image analyser. RESULTS: Colonic lamina propria of patients with CD and UC showed increased density of CD3+, alpha4beta7+, and OX40+ cells compared with IBS controls. ICAM-1, MAdCAM-1, and OX40 ligand positive vessels were also increased compared with IBS controls. No significant difference was found in the density of any of these cells in the jejunal mucosa of patients compared with IBS controls. CONCLUSIONS: The expression of MAdCAM-1 and OX40 ligand on gut endothelial and OX40+ cells is increased in sites of mucosal inflammation in patients with inflammatory bowel disease. No evidence was found for increased lamina propria T cells or increased vascular adhesion molecule expression in the proximal intestine of patients with distal inflammatory bowel disease.

Small-bowel involvement in systemic lupus erythematosus: a morphometric and immunohistochemical study.

BACKGROUND: We have investigated the intestinal mononuclear cell subpopulations in patients with systemic lupus erythematosus (SLE) and correlated these with the disease activity. METHODS: Eighteen female outpatients were studied; in 10 of them lupus activity was measured with the Lupus Activity Criteria Count and the SLE Disease Activity Index. Eight patients were in lupus remission. The control group consisted of 10 healthy volunteers. Peroral jejunal biopsy was performed in all individuals, at the angle of Treitz, using a Watson capsule, under X-ray control. Histologic studies analysed the villous to crypt ratio, lamina propria cells, and intraepithelial lymphocyte count. Immunohistochemical evaluation was carried out with the indirect immunoperoxidase technique, using monoclonal antibodies against CD3, CD4, CD8, D1, D7, D9, and M1. RESULTS: Lamina propria CD3+, CD8+, D7+, and M1+ cells from patients with SLE did not differ significantly from those of controls. CD4+ cells were decreased in all patients with SLE, especially in the clinically inactive patients. D1+ and D9+ cells were also decreased in all patients. CONCLUSION: The finding of quantitative abnormalities in the cell-mediated immunity of the intestinal mucosa may reflect systemic defects of the immune system in SLE.

Clinical patterns of diarrhea in AIDS. A retrospective study at the Federal University Hospital, Rio de Janeiro.

Three hundred and fifty two medical records of AIDS inpatients were analysed in a retrospective study to establish the frequency, clinical patterns and etiology of AIDS-related diarrhea. Diarrhea was observed in 58.8% of the patients, being a chronic symptom in 65.7%, and the first complaint in 24.6%. The most common cause of diarrhea was coccidea and the etiology remained unknown in 56.1% of the patients. Routine stool examination was the most sensitive method in the diagnosis of diarrhea. In countries with limited resources, the use of stool examinations seems to provide appropriate clinical management. The implementation of an objective protocol could improve the etiologic diagnosis of AIDS-related diarrhea without the burden of more complex and invasive technologies.

Phenotypic analysis of intestinal non-inflamed mucosa in Crohn's disease: evidence of mononuclear cell depletion in lamina propria.

OBJECTIVE: The objective of this study was to examine mononuclear cell subpopulations and evidence of cellular activation in unaffected jejunal mucosa in Crohn's disease. DESIGN: A cross-sectional study was performed in patients with Crohn's disease from the ambulatory unity of the University Hospital, UFRJ. METHODS: Mucosal samples from 20 patients with Crohn's colitis or ileitis were obtained by peroral jejunal biopsy. Patients with jejunal involvement or pregnant women were excluded from the study. Specimens were analysed histologically and by indirect immunoperoxidase method using anti-monoclonal antibodies to CD2, CD4, CD8, CD25, CD45RO, RFDR1, RFD1 and RFD7 by two 'blind' observers. Seven patients with non-inflammatory bowel disorders and two healthy volunteers were studied as controls. RESULTS: Lamina propria CD2-positive (CD2+) cells were reduced in Crohn's disease (P < 0.004) whether clinically active (P < 0.02) or clinically inactive (P < 0.008). CD4+ and CD8+ cells were also reduced in Crohn's disease (P < 0.003), whereas the CD4:CD8 ratio did not differ from that in controls. CD25+, CD45RO+ and HLA-DR+ cells were not significantly increased in patients with Crohn's disease. RFD7+ cells were decreased in Crohn's disease (P < 0.02), whereas RFD1+ cells were not significantly different from the control group. CONCLUSION: No evidence of cellular activation was found in the unaffected mucosa of Crohn's disease. The reduction in T-cell and macrophage-like cell numbers may result from cell migration to inflamed areas. It is also possible that this finding represents a primary defect which may have a role in the pathogenesis of Crohn's disease.