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Endothelial progenitor cells (EPCs) improve survival and reduce organ failure in cecal ligation and puncture-induced sepsis; however, expanded EPCs may represent an even better approach for vascular repair. To date, no study has compared the effects of non-expanded EPCs (EPC-NEXP) with those of expanded EPCs (EPC-EXP) and mesenchymal stromal cells of human (MSC-HUMAN) and mouse (MSC-MICE) origin in experimental sepsis. One day after cecal ligation and puncture sepsis induction, BALB/c mice were randomized to receive saline, EPC-EXP, EPC-NEXP, MSC-HUMAN or MSC-MICE (1 × 10 5 ) intravenously. EPC-EXP, EPC-NEXP, MSC-HUMAN, and MSC-MICE displayed differences in phenotypic characterization. On days 1 and 3, cecal ligation and puncture mice showed decreased survival rate, and increased elastance, diffuse alveolar damage, and levels of interleukin (IL)-1β, IL-6, IL-10, tumor necrosis factor-α, vascular endothelial growth factor, and platelet-derived growth factor in lung tissue. EPC-EXP and MSC-HUMAN had reduced elastance, diffuse alveolar damage, and platelet-derived growth factor compared to no-cell treatment. Tumor necrosis factor-α levels decreased in the EPC-EXP, MSC-HUMAN, and MSC-MICE groups. IL-1β levels decreased in the EPC-EXP group, while IL-10 decreased in the MSC-MICE. IL-6 levels decreased both in the EPC-EXP and MSC-MICE groups. Vascular endothelial growth factor levels were reduced regardless of therapy. In conclusion, EPC-EXP and MSC-HUMAN yielded better lung function and reduced histologic damage in septic mice.

We hypothesized whether propofol or active propofol component (2,6‐diisopropylphenol [DIPPH] and lipid excipient [LIP‐EXC]) separately may alter inflammatory mediators expressed by macrophages and neutrophils in lean and obese rats. Male Wistar rats (n = 10) were randomly assigned to receive a standard (lean) or obesity‐inducing diet (obese) for 12 weeks. Animals were euthanized, and alveolar macrophages and neutrophils from lean and obese animals were exposed to propofol (50 µM), active propofol component (50 µM, 2,6‐DIPPH), and lipid excipient (soybean oil, purified egg phospholipid, and glycerol) for 1 h. The primary outcome was IL‐6 expression after propofol and its components exposure by alveolar macrophages extracted from bronchoalveolar lavage fluid. The secondary outcomes were the production of mediators released by macrophages from adipose tissue, and neutrophils from lung and adipose tissues, and neutrophil migration. IL‐6 increased after the exposure to both propofol (median [interquartile range] 4.14[1.95–5.20]; p = .04) and its active component (2,6‐DIPPH) (4.09[1.67–5.91]; p = .04) in alveolar macrophages from obese animals. However, only 2,6‐DIPPH increased IL‐10 expression (7.59[6.28–12.95]; p = .001) in adipose tissue‐derived macrophages. Additionally, 2,6‐DIPPH increased C‐X‐C chemokine receptor 2 and 4 (CXCR2 and CXCR4, respectively) in lung (10.08[8.23–29.01]; p = .02; 1.55[1.49–3.43]; p = .02) and adipose tissues (8.78[4.15–11.57]; p = .03; 2.86[2.17–3.71]; p = .01), as well as improved lung‐derived neutrophil migration (28.00[−3.42 to 45.07]; p = .001). In obesity, the active component of propofol affected both the M1 and M2 markers as well as neutrophils in both alveolar and adipose tissue cells, suggesting that lipid excipient may hinder the effects of active propofol. In obesity, the active component of propofol affected M1 and M2 alveolar macrophages from adipose tissue differently. In neutrophils from lung and adipose tissue, only the active propofol component increased chemokine receptors, suggesting that lipid excipient may hinder the effects of active propofol.

Asthma is characterized by chronic lung inflammation and airway hyperresponsiveness. Despite recent advances in the understanding of its pathophysiology, asthma remains a major public health problem and, at present, there are no effective interventions capable of reversing airway remodeling. Mesenchymal stromal cell (MSC)-based therapy mitigates lung inflammation in experimental allergic asthma; however, its ability to reduce airway remodeling is limited. We aimed to investigate whether pre-treatment with eicosapentaenoic acid (EPA) potentiates the therapeutic properties of MSCs in experimental allergic asthma. Seventy-two C57BL/6 mice were used. House dust mite (HDM) extract was intranasally administered to induce severe allergic asthma in mice. Unstimulated or EPA-stimulated MSCs were administered intratracheally 24 h after final HDM challenge. Lung mechanics, histology, protein levels of biomarkers, and cellularity in bronchoalveolar lavage fluid (BALF), thymus, lymph nodes, and bone marrow were analyzed. Furthermore, the effects of EPA on lipid body formation and secretion of resolvin-D (RvD ), prostaglandin E (PGE ), interleukin (IL)-10, and transforming growth factor (TGF)-β1 by MSCs were evaluated . EPA-stimulated MSCs, compared to unstimulated MSCs, yielded greater therapeutic effects by further reducing bronchoconstriction, alveolar collapse, total cell counts (in BALF, bone marrow, and lymph nodes), and collagen fiber content in airways, while increasing IL-10 levels in BALF and M2 macrophage counts in lungs. In conclusion, EPA potentiated MSC-based therapy in experimental allergic asthma, leading to increased secretion of pro-resolution and anti-inflammatory mediators (RvD , PGE , IL-10, and TGF-β), modulation of macrophages toward an anti-inflammatory phenotype, and reduction in the remodeling process. Taken together, these modifications may explain the greater improvement in lung mechanics obtained. This may be a promising novel strategy to potentiate MSCs effects.

Leishmaniasis is a zoonotic disease of major public health and veterinary importance, affecting 88 countries with up to 2 million cases per year. This review emphasizes the animal reservoirs and spreading of visceral leishmaniasis (VL) in urban areas, particularly in two Brazilian metropolitan areas, namely São Luis and Belo Horizonte, where the disease has become endemic in the past few years. Urbanization of visceral leishmaniasis in Brazil during the last decades has created favorable epidemiological conditions for maintenance of the disease, with dense human populations sharing a tropical environment with abundant populations of the mammalian reservoir and the invertebrate vector, facilitating transmission of the disease.

This study aimed to evaluate the association between substance use during pregnancy (SUDP) and dental caries considering the Tooth Development Hypothesis and the Behavioral Hypothesis . This is a Brazilian cohort study conducted on 865 children (12–36 months). Exposure to SUDP was the latent variable and consisted of the use of alcohol, tobacco, and illicit drugs. The dependent variable was the number of dental caries lesions according to the Nyvad criteria. Structural equation modeling was used for analysis, estimating the standardized coefficient (SC) in two models: traditional (1) and with bias-corrected bootstrap estimates (2). The models were adjusted for socioeconomic status (SES), child’s age, maternal age, symptoms of minor psychiatric disorders, sugar consumption, feeding, developmental defects of enamel, and gingival bleeding on brushing (GBoB) (α = 5%). SUDP did not affect dental caries. SES (SC model1 =0.168, p  = 0.037; SC model2 =0.134, p  = 0.056), GBoB (SC model1 =0.407, p  < 0.001; SC model2 =0.297, p  < 0.001), child’s age (SC model1 =0.087, p  = 0.003; SC model2 =0.087, p  = 0.005), and sugar consumption (SC model1 =0.167, p  = 0.021; SC model2 =0.167, p  = 0.048) had a direct effect on the outcome. Child’s age exerted a specific indirect effect mediated by GBoB (SC model1 =0.048, p  = 0.017; SC model2 =0.048, p  = 0.034). SUDP did not increase the risk of dental caries considering the Tooth Development Hypothesis and the Behavioral Hypothesis , suggesting that child-directed oral health care and tooth development may be similar between mothers exposed and not exposed to SUDP.

This study aimed to evaluate the maximum compressive strength, the modulus of elasticity, pH variation, ionic release, radiopacity and biological response of an experimental endodontic repair cement based on 45S5 Bioglass®. An in vitro and in vivo study with an experimental endodontic repair cement containing 45S5 bioactive glass was conducted. There were three endodontic repair cement groups: 45S5 bioactive glass-based (BioG), zinc oxide-based (ZnO), and mineral trioxide aggregate (MTA). In vitro tests were used to evaluate their physicochemical properties: compressive strength, modulus of elasticity, radiopacity, pH variation, and the ionic release of Ca+ and PO4. An animal model was used to evaluate the bone tissue response to endodontic repair cement. Statistical analysis included the unpaired t-test, one-way ANOVA and Tukey’s test. BioG showed the lowest compressive strength and ZnO showed the highest radiopacity among the groups, respectively (p < 0.05). There were no significant differences in the modulus of elasticity among the groups. BioG and MTA maintained an alkaline pH during the 7 days of evaluation, both at pH 4 and in a pH 7 buffered solutions. PO4 was elevated in BioG, peaking at 7 days (p < 0.05). Histological analysis showed less intense inflammatory reactions and new bone formation in MTA. BioG showed inflammatory reactions that decreased over time. These findings suggest that the BioG experimental cement had good physicochemical characteristics and biocompatibility required for bioactive endodontic repair cement.

Longitudinal studies evaluating the relationship between UPF consumption and the incidence of Metabolic Syndrome (MetS) and its components are still scarce. This study aimed to evaluate the effect of UPF consumption on the incidence of MetS and its components in adults. A prospective study was conducted with 896 participants from the 1978/79 Ribeirão Preto cohort, São Paulo, Brazil. UPF consumption was evaluated in %kcal and %g at ages 23–25 years. Incidence of MetS and its components were estimated at ages 37–39 years, according to the Joint Interim Statement criteria. Poisson regression was used to assess associations, and interactions with sex were investigated. UPF consumption had no association with MetS (%kcal Adjusted PR: 1.00; 95% CI: 0.99–1.01; %g Adjusted PR: 1.00; 95% CI: 0.99–1.01). However, women with higher UPF consumption, in %kcal and %g, had a higher risk of abdominal obesity (%kcal: p = 0.030; %g: p = 0.003); and women with higher UPF consumption, in %g, had a higher risk of low HDL-cholesterol (p = 0.041). For the other components of MetS, no significant associations were observed in either sex. These findings suggest evidence of no association between UPF consumption and MetS; however, consumption of UPF was associated with increased WC and low HDL-c, but only in women.

BackgroundThe benefits of breast feeding may be associated with better formation of eating habits beyond childhood. This study was designed to verify the association between breast feeding and food consumption according to the degree of processing in four Brazilian birth cohorts.MethodsThe duration of exclusive, predominant and total breast feeding was evaluated. The analysis of the energy contribution of fresh or minimally processed foods (FMPF) and ultra-processed foods (UPF) in the diet was evaluated during childhood (13–36 months), adolescence (11–18 years) and adulthood (22, 23 and 30 years).ResultsThose who were predominantly breastfed for less than 4 months had a higher UPF consumption (β 3.14, 95% CI 0.82 to 5.47) and a lower FMPF consumption (β −3.47, 95% CI −5.91 to −1.02) at age 22 years in the 1993 cohort. Exclusive breast feeding (EBF) for less than 6 months was associated with increased UPF consumption (β 1.75, 95% CI 0.25 to 3.24) and reduced FMPF consumption (β −1.49, 95% CI −2.93 to −0.04) at age 11 years in the 2004 cohort. In this same cohort, total breast feeding for less than 12 months was associated with increased UPF consumption (β 1.12, 95% CI 0.24 to 2.19) and decreased FMPF consumption (β −1.13, 95% CI −2 .07 to −0.19). Children who did not receive EBF for 6 months showed an increase in the energy contribution of UPF (β 2.36, 95% CI 0.53 to 4.18) and a decrease in FMPF (β −2.33, 95% CI −4 .19 to −0.48) in the diet at 13–36 months in the 2010 cohort. In this cohort, children who were breastfed for less than 12 months in total had higher UPF consumption (β 2.16, 95% CI 0.81 to 3.51) and lower FMPF consumption (β −1.79, 95% CI −3.09 to −0.48).ConclusionExposure to breast feeding is associated with lower UPF consumption and higher FMPF consumption in childhood, adolescence and adulthood.

The use of lemongrass oil as food preservative present great potential, however it has high volatility and intense aroma, making them limited to be used as food additives. Microencapsulation processes become interesting alternatives to overcome these issues. This work investigated the influence of the partial replacement of gum arabic by modified starches on the microencapsulation of lemongrass oil as core material. Gum arabic and its combinations with modified starches: cassava and corn maltodextrins with different dextrose equivalent (DE) and octenyl succinic anhydride modified starch (OSA-starch) were studied. The emulsions were spray dried at controlled temperature of 170 °C. The evaluated parameters particles solubility, moisture content, and oil composition did not showed significant differences among the treatments. Replacement of gum arabic by maltodextrin DE20 and OSA-starch resulted in higher wetting times. Oil retention was increased (81.2%) when gum arabic was replaced by OSA-starch; the treatment without substitution, with only gum arabic had 67.5% of oil retention. Application of OSA-starch in association with gum arabic in microencapsulation by spray drying of lemongrass oil presented greater potential to be used due to its higher oil retention. Polymer blends should be assessed since they present advantages over individually applied polymers. Although maltodextrins show some differences compared to the treatment with only gum arabic, it may also be a viable alternative because of its lower cost.

Purpose. To evaluate the mineral ion loss of root dentine after treatment with 2% chlorhexidine solution (CHX) and to compare its yield and flexural strength (fs) after exposure to calcium hydroxide [Ca(OH)2]. Materials and Methods. Dentine bars (DB) were made from 90 roots of bovine incisors and randomized into three groups: GControl: distilled/deionized water (DDW), GNaOCl: 2.5% sodium hypochlorite + 17% EDTA, and GCHX: CHX + DDW. The release of phosphate (PO4) and calcium (Ca) ions was measured by spectrophotometry. The DB were exposed to Ca(OH)2 paste for 0, 30, 90, and 180 days. DB were subjected to the three-point bending test to obtain yield and fs values. The fracture patterns were evaluated (20x). Data were analyzed using Kruskal-Wallis and Dunn’s post hoc tests or one- and two-way ANOVA followed by Tukey’s post hoc test (α=0.05). Results. GCHX showed lower PO43- and Ca2+ ionic release than GNaOCl (p<0.001). For yield and fs, GCHX>GNaOCl in all periods (p<0.001), except for yield strength values on 90 days (p=0.791). A larger frequency of vertical fractures was observed in GNaOCl and that of oblique fractures in GCHX (p<0.05). Conclusions. CHX prevented PO43- and Ca2+ loss and showed a tendency to preserve the yield and fs of root dentine over time following exposure to Ca(OH)2 paste.