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1.
An Pediatr (Engl Ed) ; 2024 Jun 20.
Article in English | MEDLINE | ID: mdl-38906802

ABSTRACT

In this article we present a protocol for the use of the low-FODMAP diet in paediatric patients and review of the current evidence on its efficacy. These short-chain carbohydrates, which can be fermented by the intestinal microbiota, are found in a wide variety of foods, mainly of plant origin. The low-FODMAP diet is a therapeutic tool used for the management of gastrointestinal disorders such as irritable bowel syndrome. The sources we used were PubMed, Web of Science, Google Scholar and institutional websites. Following consumption of FODMAP-rich foods, a series of end products are generated that are not absorbed, giving rise to symptoms. Before starting a low-FODMAP diet, it is important to carry out a diagnostic evaluation including any applicable tests. Treatment is structured in 3 phases: elimination, reintroduction and personalization phase. In the first phase, FODMAP-rich foods are eliminated for 2-3 weeks. In the second phase, lasting 8 weeks, FODMAP-rich foods are gradually reintroduced. The last phase consists in customizing the diet according to individual tolerance. This article details which foods contain FODMAPs and possible substitutes. In addition, specific food diary/intake tracking and educational materials are provided in a series of appendices to facilitate adherence to the diet. Although most studies have been conducted in adults, there is also some evidence on the beneficial effects in the paediatric age group, with a reduction of symptoms, especially in patients with functional gastrointestinal disorders. Nevertheless, more research is required on the subject.

2.
J Endod ; 47(3): 424-435, 2021 Mar.
Article in English | MEDLINE | ID: mdl-33359532

ABSTRACT

INTRODUCTION: Melatonin is an endogenous neurohormone with well-reported anti-inflammatory and antioxidant properties, but the direct biological and immunomodulatory effects of melatonin on human dental pulp stem cells (hDPSCs) has not been fully elucidated. The aim of this study was to evaluate the influence of melatonin on the cytocompatibility, proliferation, cell migration, odontogenic differentiation, mineralized nodule formation, and immunomodulatory properties of hDPSCs. METHODS: To address the melatonin biological effects on hDPSCs, the cytocompatibility, proliferation, cell migration, odontogenic differentiation, mineralized nodule formation, and immunomodulatory properties of hDPSCs after melatonin treatment were evaluated. The statistical differences were evaluated using 1-way analysis of variance with the Tukey multiple comparison test. RESULTS: We found that melatonin did not alter hDPSC immunophenotype or cell viability, even at the highest concentrations used. However, using intermediate melatonin concentrations (10-300 µmol/L), a significantly higher proliferation rate (P < .05 and P < .01) and migration of hDPSCs (P < .01) were observed. Importantly, melatonin treatment (100 µmol/L) significantly increased the secretion of the anti-inflammatory cytokine transforming growth factor beta (P < .05 and P < .01) and provoked a more robust antiproliferative effect on mitogen-stimulated T cells (P < .05). Finally, and unlike previous results found with mesenchymal stem cells from other sources, melatonin fails to induce or accelerate the spontaneous osteogenic differentiation of hDPSCs. CONCLUSIONS: Together, these findings provide key data on the bioactivity of melatonin and its effects on hPDSC biological and immunomodulatory properties.


Subject(s)
Melatonin , Mesenchymal Stem Cells , Cell Differentiation , Cell Proliferation , Cells, Cultured , Dental Pulp , Humans , Melatonin/pharmacology , Osteogenesis , Stem Cells , Transforming Growth Factor beta
3.
PLoS One ; 6(2): e16955, 2011 Feb 09.
Article in English | MEDLINE | ID: mdl-21347393

ABSTRACT

Telomere length and telomerase activity are important factors in the pathobiology of human diseases. Age-related diseases and premature aging syndromes are characterized by short telomeres, which can compromise cell viability, whereas tumour cells can prevent telomere loss by aberrantly upregulating telomerase. The zebrafish (Danio rerio) offers multiple experimental manipulation advantages over other vertebrate models and, therefore, it has been recently considered as a potential model for aging, cancer, and regeneration studies. However, it has only partially been exploited to shed light on these fundamental biological processes. The aim of this study was, therefore, to investigate telomere length and telomerase expression and activity in different strains of zebrafish obtained from different stock centres to determine whether they undergo any changes during aging and regeneration. We found that although both telomerase expression and telomere length increased from embryo to adulthood stages, they drastically declined in aged fish despite telomerase activity was detected in different tissues of old fish. In addition, we observed a weaker upregulation of telomerase expression in regenerating fins of old fish, which well correlates with their impaired regeneration capacity. Strikingly, telomeres were elongated or maintained during the fin regeneration process at all ages and after repeated amputations, likely to support high cell proliferation rates. We conclude that the expression of telomerase and telomere length are closely related during the entire life cycle of the fish and that these two parameters can be used as biomarkers of aging in zebrafish. Our results also reveal a direct relationship between the expression of telomerase, telomere length and the efficiency of tissue regeneration.


Subject(s)
Aging/genetics , Regeneration/genetics , Telomerase/metabolism , Telomere/genetics , Zebrafish Proteins/metabolism , Zebrafish/genetics , Zebrafish/physiology , Animals , Biomarkers/metabolism , Female , Gene Expression Regulation, Developmental , Humans , NF-kappa B/metabolism , Promoter Regions, Genetic , Proto-Oncogene Proteins c-myc/metabolism , Telomerase/genetics , Telomere Shortening , Zebrafish/growth & development , Zebrafish/metabolism , Zebrafish Proteins/genetics
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