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Percebe-se cada vez mais urgente a necessidade de se trabalhar nas escolas assuntos considerados polêmicos como: homossexualidade, homofobia, machismo e racismo. É fundamental a discussão desses temas para assim, despertar nos educandos uma consciência crítica diante dessas reflexões. Conforme esses aspectos, o objetivo geral desse estudo foi analisar como a escola pesquisada lida com as temáticas: homossexualidade, homofobia, machismo e racismo no âmbito escolar. Foi realizada uma pesquisa qualitativa com método bibliográfico baseado em Brasil (1997), Drummontt (1980), Nogueira (1985), Parolin (2007) e Pinar (2016), entre outros. Também foi realizada uma pesquisa de campo em uma escola da rede municipal de Teresina-PI. Os sujeitos da pesquisa foram dois professores e uma coordenadora pedagógica. A coleta dos dados foi feita através de uma entrevista semiestruturada em que foi permitida a gravação da conversa e, posteriormente, a observação de suas práticas em sala de aula. O estudo nos permitiu um conhecimento mais amplo acerca dos temas: homossexualidade, homofobia, machismo e racismo tão presentes em nossa sociedade e mostrou que a escola pesquisada de fato trabalha esses assuntos tendo como base central o respeito perante as diferenças. Os professores estão preparados para orientar sobre dilemas polêmicos rompendo de forma segura a lacuna do silêncio que contribuía para o desenvolvimento da discriminação, apresentando informações esclarecedoras sobre o diferente, não só para o mundo escolar em que estão inseridos, mas a toda sociedade que o cercam. A educação tem que ser a ferramenta principal para combater o preconceito e romper de vez com a homofobia, o racismo e o machismo que permeiam a sociedade brasileira e o mundo. Contudo, é necessário destacar a importância da cumplicidade da família x escola x aluno nesse processo de aprendizagem.

Introduction: Several studies have suggested that diet, especially the one enriched in microbiota-fermented fibers or fat, regulates behavior. The underlying mechanisms are currently unknown. We previously reported that certain macronutrients (fermentable fiber and protein) regulate energy homeostasis via the activation of intestinal gluconeogenesis (IGN), which generates a neural signal to the brain. We hypothesized that these nutriments might control behavior using the same gut-brain circuit. Methods: Wild-type and IGN-deficient mice were fed chow or diets enriched in protein or fiber. Changes in their behavior were assessed using suited tests. Hippocampal neurogenesis, extracellular levels of serotonin, and protein expression levels were assessed by immunofluorescence, in vivo dialysis, and Western blotting, respectively. IGN was rescued by infusing glucose into the portal vein of IGN-deficient mice. Results: We show here that both fiber- and protein-enriched diets exert beneficial actions on anxiety-like and depressive-like behaviors. These benefits do not occur in mice lacking IGN. Consistently, IGN-deficient mice display hallmarks of depressive-like disorders, including decreased hippocampal neurogenesis, basal hyperactivity, and deregulation of the hypothalamic-pituitary-adrenal axis, which are associated with increased expression of the precursor of corticotropin-releasing hormone in the hypothalamus and decreased expression of the glucocorticoid receptor in the hippocampus. These neurobiological alterations are corrected by portal glucose infusion mimicking IGN. Conclusion: IGN translates nutritional information, allowing the brain to finely coordinate energy metabolism and behavior.

Tamoxifen is a selective estrogen receptor modulator used to activate the CREERT2 recombinase, allowing tissue-specific and temporal control of the somatic mutagenesis to generate transgenic mice. Studies integrating development and metabolism require a genetic modification induced by a neonatal tamoxifen administration. Here, we investigate the effects of a neonatal tamoxifen administration on energy homeostasis in adult male and female C57BL/6J mice. C57BL/6J male and female mouse pups received a single injection of tamoxifen 1 day after birth (NTT) and were fed a high-fat/high-sucrose diet at 6 weeks of age. We measured weight, body composition, glucose and insulin tolerance, basal metabolism, and tibia length and weight in adult mice. The neonatal tamoxifen administration exerted long-term, sex-dependent effects on energy homeostasis. NTT female mice became overweight and developed impaired glucose control in comparison to vehicle-treated littermates. NTT females exhibited 60% increased fat mass, increased food intake, decreased physical activity and energy expenditure, impaired glucose and insulin tolerance, and fasting hyperglycemia and hyperinsulinemia. In contrast, NTT male mice exhibited a modest amelioration of glucose and insulin tolerance and long-term decreased lean mass linked to decreased bone weight. These results suggest that the neonatal tamoxifen administration exerted a marked and sex-dependent influence on adult energy homeostasis and bone weight and must therefore be used with caution for the development of transgenic mouse models regarding studies on energy homeostasis and bone biology.

Tissue repair after injury in adult mammals, usually results in scarring and loss of function in contrast to lower vertebrates such as the newt and zebrafish that regenerate. Understanding the regulatory processes that guide the outcome of tissue repair is therefore a concerning challenge for regenerative medicine. In multiple regenerative animal species, the nerve dependence of regeneration is well established, but the nature of the innervation required for tissue regeneration remains largely undefined. Using our model of induced adipose tissue regeneration in adult mice, we demonstrate here that nociceptive nerves promote regeneration and their removal impairs tissue regeneration. We also show that blocking the receptor for the nociceptive neuropeptide calcitonin gene-related peptide (CGRP) inhibits regeneration, whereas CGRP administration induces regeneration. These findings reveal that peptidergic nociceptive neurons are required for adult mice tissue regeneration.

O objetivo do artigo é o estudo das criptomoedas, em especial a Bitcoin, como mecanismo de planejamento tributário. O uso da criptografia garante a segurança e anonimato das transações com as criptomoedas. Diante do crescente uso das criptomoedas, começaram a ocorrer questionamentos sobre negócios jurídicos realizados com a Bitcoin, em especial na seara da tributação. Sendo assim, questiona-se se as criptomoedas podem ser utilizadas como planejamento tributário. A metodologia adotada foi a qualitativa, com leitura de artigos científicos, análise da regulamentação normativa no âmbito do direito brasileiro. Ao final conclui-se que as criptomoedas podem ser utilizadas como planejamento tributário.

Objective: The respective contributions to endogenous glucose production (EGP) of the liver, kidney and intestine vary during fasting. We previously reported that the deficiency in either hepatic or intestinal gluconeogenesis modulates the repartition of EGP via glucagon secretion (humoral factor) and gut–brain–liver axis (neural factor), respectively. Considering renal gluconeogenesis reportedly accounted for approximately 50% of EGP during fasting, we examined whether a reduction in renal gluconeogenesis could promote alterations in the repartition of EGP in this situation. Methods: We studied mice whose glucose-6-phosphatase (G6Pase) catalytic subunit (G6PC) is specifically knocked down in the kidneys (K-G6pc-/- mice) during fasting. We also examined the additional effects of intestinal G6pc deletion, renal denervation and vitamin D administration on the altered glucose metabolism in K-G6pc-/- mice. Results: Compared with WT mice, K-G6pc-/- mice exhibited (1) lower glycemia, (2) enhanced intestinal but not hepatic G6Pase activity, (3) enhanced hepatic glucokinase (GK encoded by Gck) activity, (4) increased hepatic glucose-6-phosphate and (5) hepatic glycogen spared from exhaustion during fasting. Increased hepatic Gck expression in the post-absorptive state could be dependent on the enhancement of insulin signal (AKT phosphorylation) in K-G6pc-/- mice. In contrast, the increase in hepatic GK activity was not observed in mice with both kidney- and intestine-knockout (KI-G6pc-/- mice). Hepatic Gck gene expression and hepatic AKT phosphorylation were reduced in KI-G6pc-/- mice. Renal denervation by capsaicin did not induce any effect on glucose metabolism in K-G6pc-/- mice. Plasma level of 1,25 (OH)2 D3, an active form of vitamin D, was decreased in K-G6pc-/- mice. Interestingly, the administration of 1,25 (OH)2 D3 prevented the enhancement of intestinal gluconeogenesis and hepatic GK activity and blocked the accumulation of hepatic glycogen otherwise observed in K-G6pc-/- mice during fasting. Conclusions: A diminution in renal gluconeogenesis that is accompanied by a decrease in blood vitamin D promotes a novel repartition of EGP among glucose producing organs during fasting, featured by increased intestinal gluconeogenesis that leads to sparing glycogen stores in the liver. Our data suggest a possible involvement of a crosstalk between the kidneys and intestine (via the vitamin D system) and the intestine and liver (via a neural gut-brain axis), which might take place in the situations of deficient renal glucose production, such as chronic kidney disease. Keywords: Endogenous glucose production, Gluconeogenesis, Hypoglycemia, Glycogen, Chronic kidney disease, Vitamin D