ABSTRACT
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.
Subject(s)
Dental Polishing , Lithium , Biofilms , Ceramics , Dental Polishing/methods , Dental Porcelain , Materials Testing , Streptococcus mutans , Surface PropertiesABSTRACT
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.
Subject(s)
Eosinophilic Esophagitis/immunology , Eosinophils/immunology , Intramolecular Oxidoreductases/immunology , Macrophage Migration-Inhibitory Factors/immunology , Adolescent , Adult , Animals , Benzylamines , Cyclams , Eosinophilic Esophagitis/genetics , Eosinophilic Esophagitis/pathology , Eosinophilic Esophagitis/therapy , Eosinophils/pathology , Female , Heterocyclic Compounds/pharmacology , Humans , Intramolecular Oxidoreductases/genetics , Macrophage Migration-Inhibitory Factors/genetics , Male , Mice , Mice, Knockout , Middle Aged , Mucous Membrane/immunology , Mucous Membrane/pathology , Receptors, CXCR4/antagonists & inhibitors , Receptors, CXCR4/genetics , Receptors, CXCR4/immunologyABSTRACT
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.
Subject(s)
Jejunum/immunology , Jejunum/pathology , Lupus Erythematosus, Systemic/pathology , Adolescent , Adult , Biopsy , Female , Humans , Immunity, Mucosal , Immunohistochemistry , Intestinal Mucosa/immunology , Intestinal Mucosa/pathology , Leukocytes, Mononuclear , Lupus Erythematosus, Systemic/physiopathology , Middle Aged , Phenotype , Statistics, NonparametricABSTRACT
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.
