Manifestações orais da doença cárie em pacientes odontopediátricos com Transtorno do Espectro Autista: revisão integrativa da literatura

Autistic Spectrum Disorder (ASD) is a complex neurodevelopmental disorder, characterized by impaired language and social interactions. Therefore, these patients present greater risks to oral health, as they tend not to be able to perform proper hygiene. The objective of this study was to identify the oral health condition and the occurrence of caries in children and adolescents with Autistic Spectrum Disorder. An integrative literature review was carried out in the electronic databases PubMed, LILACS and Scielo, using the following descriptors in Portuguese and their corresponding ones in English: dental caries OR dental caries OR decayed tooth AND autism spectrum disorder or Autism. Inclusion and exclusion criteria followed the PRISMA-ScR strategy. 43 articles were found, 5 of which were included in this review. A deficit in hygiene and food selectivity was noticed, which can have consequences in the oral cavity according to the cariogenic level of these foods, gingival alteration and molar-incisor hypomineralization (MIH). It was concluded, therefore, that given the multifactorial cause of caries disease and the various factors that can affect a patient with ASD, these, together, can cause a predisposition to the involvement of the caries lesion. Related factors are food selectivity, poor hygiene, behavioral changes and hypersensitivity. Furthermore, the studies showed that the medication and salivary composition acting on the protective buffering effect did not demonstrate a significant negative effect on the oral cavity of these patients.O Transtorno do Espectro Autista (TEA) é um transtorno complexo de neurodesenvolvimento, caracterizado por deficiência na linguagem e interações sociais. Sendo assim, esses pacientes apresentam maiores riscos à saúde oral, pois os mesmos tendem a não conseguir realizar a higienização de maneira adequada. O objetivo desse trabalho foi identificar a condição de saúde bucal e a ocorrência da doença cárie em crianças e adolescentes com Transtorno do Espectro Autista. Foi realizada uma revisão integrativa de literatura nas bases de dados eletrônicas PubMed, LILACS e Scielo, utilizando os seguintes descritores em português e seus correspondentes em inglês: cárie dentária OU cárie dental OU dente cariado AND transtorno do espectro autista ou Autismo. Os critérios de inclusão e exclusão seguiram a estratégia PRISMA-ScR. Foram encontrados 43 artigos, sendo 5 incluídos nessa revisão. Percebeu-se um déficit na higienização e seletividade alimentar, que pode apresentar consequências na cavidade oral de acordo com o nível cariogênico desses alimentos, alteração gengival e hipomineralização molar-incisivo (HMI). Concluiu-se, portanto que diante da causa multifatorial da doença cárie e dos diversos fatores que podem afetar um paciente com TEA, esses, em conjunto podem causar uma predisposição ao acometimento da lesão de cárie. Os fatores relacionados são seletividade alimentar, déficit na higienização, alterações comportamentais e hipersensibilidade. Ademais, os estudos mostraram que a medicação e composição salivar atuando no efeito tampão de proteção não demonstraram efeito negativo significativo na cavidade oral desses pacientes

Endobronchial myxoma: Case report

INTRODUCTION: Pulmonary myxoma is an extremely rare benign neoplasm. It is mostly parenchymal but may occasionally occur within the tracheobronchial tree. There are very few reports of endobronchial myxoma. CASE REPORT: We describe a case of endobronchial myxoma in a 40-year-old female patient with a history of asthma and repeated right-sided pneumonia. Thoracic computed tomography (CT) showed medium lobe atelectasis. Fiber optic bronchoscopy revealed a polypoid, well-circumscribed tumor, causing total obstruction of the medium lobe bronchus. Biopsy of the mass was non-diagnostic. Further study included a positron emission tomography (PET) which demonstrated low metabolic activity of the tumor and no evidence of neoplasia in other location. The patient was submitted to a medium lobectomy and microscopic examination of the tumor revealed myxoid stroma with lobulated pattern, elongated and stellate cells, compatible with myxoma. CONCLUSION: Pulmonary myxoma is extraordinary rare and endobronchial location is very few reported in medical literature

EFEITOS DO TREINAMENTO DE FORÇA SOBRE A FUNÇÃO PANCREÁTICA E A SENSIBILIDADE TECIDUAL À INSULINA EM RATOS

Estudos tm demonstrado que o exerccio aerbio promove elevao na sensibilidade tecidual insulina (SI) e na tolerncia glicose (TG), porm a anlise de tais variveis aps treinamento de fora (TF) tem sido pouco explorada. Assim, o objetivo deste estudo foi avaliar os efeitos do TF sobre a TG e SI em ratos. Foram estudados 20 ratos Wistar, pareados por peso e aleatoriamente distribudos em 2 grupos: G1 Sham e G2 TF. Todos os animais foram submetidos a 3 dias de adaptao e, subsequentemente, treinados com cargas progressivas por 3 vezes por semana, durante 8 semanas numa escada de madeira. Para avaliar SI e TG foram realizadas coletas de sangue e avaliada a cintica da glicemia pelo teste de tolerncia insulina (% de decaimento da curva; B) e o teste de tolerncia glicose (rea sob a curva; AC), antes da adaptao e aps o 24 dia de treinamento. A anlise estatstica foi realizada pelo teste t de Student pareado e no-pareado, sendo o p 0,05. Apenas G2 mostrou significativo aumento no B aps treinamento, sendo que o delta do B entre os grupos mostrou diferenas significativas (p 0,05), com maiores valores no G2. Em contraste, AC no apresentou alterao significativa entre os grupos nem entre os deltas (p 0,05). O TF promoveu benefcios adaptativos na sensibilidade tecidual insulina, sugerindo que o TF pode ser um recurso interessante durante programas de fisioterapia cardiovascular em doenas crnicas

The Combination of Gefitinib With ATRA and ATO Induces Myeloid Differentiation in Acute Promyelocytic Leukemia Resistant Cells

In approximately 15% of patients with acute myeloid leukemia (AML), total and phosphorylated EGFR proteins have been reported to be increased compared to healthy CD34(+) samples. However, it is unclear if this subset of patients would benefit from EGFR signaling pharmacological inhibition. Pre-clinical studies on AML cells provided evidence on the pro-differentiation benefits of EGFR inhibitors when combined with ATRA or ATO in vitro. Despite the success of ATRA and ATO in the treatment of patients with acute promyelocytic leukemia (APL), therapy-associated resistance is observed in 5-10% of the cases, pointing to a clear need for new therapeutic strategies for those patients. In this context, the functional role of EGFR tyrosine-kinase inhibitors has never been evaluated in APL. Here, we investigated the EGFR pathway in primary samples along with functional in vitro and in vivo studies using several APL models. We observed that total and phosphorylated EGFR (Tyr992) was expressed in 28% and 19% of blast cells from APL patients, respectively, but not in healthy CD34(+) samples. Interestingly, the expression of the EGF was lower in APL plasma samples than in healthy controls. The EGFR ligand AREG was detected in 29% of APL patients at diagnosis, but not in control samples. In vitro, treatment with the EGFR inhibitor gefitinib (ZD1839) reduced cell proliferation and survival of NB4 (ATRA-sensitive) and NB4-R2 (ATRA-resistant) cells. Moreover, the combination of gefitinib with ATRA and ATO promoted myeloid cell differentiation in ATRA- and ATO-resistant APL cells. In vivo, the combination of gefitinib and ATRA prolonged survival compared to gefitinib- or vehicle-treated leukemic mice in a syngeneic transplantation model, while the gain in survival did not reach statistical difference compared to treatment with ATRA alone. Our results suggest that gefitinib is a potential adjuvant agent that can mitigate ATRA and ATO resistance in APL cells. Therefore, our data indicate that repurposing FDA-approved tyrosine-kinase inhibitors could provide new perspectives into combination therapy to overcome drug resistance in APL patients

Pervasive gaps in Amazonian ecological research

Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear un derstanding of how ecological communities respond to environmental change across time and space.3,4 While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes,5–7 vast areas of the tropics remain understudied.8–11 In the American tropics, Amazonia stands out as the world’s most diverse rainforest and the primary source of Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepre sented in biodiversity databases.13–15 To worsen this situation, human-induced modifications16,17 may elim inate pieces of the Amazon’s biodiversity puzzle before we can use them to understand how ecological com munities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple or ganism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region’s vulnerability to environmental change. 15%–18% of the most ne glected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lostinfo:eu-repo/semantics/publishedVersio

Pervasive gaps in Amazonian ecological research

Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear understanding of how ecological communities respond to environmental change across time and space.3,4 While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes,5,6,7 vast areas of the tropics remain understudied.8,9,10,11 In the American tropics, Amazonia stands out as the world's most diverse rainforest and the primary source of Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepresented in biodiversity databases.13,14,15 To worsen this situation, human-induced modifications16,17 may eliminate pieces of the Amazon's biodiversity puzzle before we can use them to understand how ecological communities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple organism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region's vulnerability to environmental change. 15%–18% of the most neglected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lost

Obesity does not Lead to Imbalance Between Myocardial Phospholamban Phosphorylation and Dephosphorylation

Background: The activation of the beta-adrenergic system promotes G protein stimulation that, via cyclic adenosine monophosphate (cAMP), alters the structure of protein kinase A (PKA) and leads to phospholamban (PLB) phosphorylation. This protein participates in the system that controls intracellular calcium in muscle cells, and it is the primary regulator of sarcoplasmic reticulum calcium pump activity. In obesity, the beta-adrenergic system is activated by the influence of increased leptin, therefore, resulting in higher myocardial phospholamban phosphorylation via cAMP-PKA. Objective: To investigate the involvement of proteins which regulate the degree of PLB phosphorylation due to beta-adrenergic activation in obesity. In the present study, we hypothesized that there is an imbalance between phospholamban phosphorylation and dephosphorylation, with prevalence of protein phosphorylation. Methods: Male Wistar rats were randomly distributed into two groups: control (n = 14), fed with normocaloric diet; and obese (n = 13), fed with a cycle of four unsaturated high-fat diets. Obesity was determined by the adiposity index, and protein expressions of phosphatase 1 (PP-1), PKA, PLB, phosphorylated phospholamban at serine16 (PPLB-Ser16) were assessed by Western blot. Results: Obesity caused glucose intolerance, hyperinsulinemia, hypertriglyceridemia, hyperleptinemia and did not alter the protein expression of PKA, PP-1, PLB, PPLB-Ser16. Conclusion: Obesity does not promote an imbalance between myocardial PLB phosphorylation and dephosphorylation via beta-adrenergic system

Myocardial Dysfunction after Severe Food Restriction Is Linked to Changes in the Calcium-Handling Properties in Rats

Severe food restriction (FR) impairs cardiac performance, although the causative mechanisms remain elusive. Since proteins associated with calcium handling may contribute to cardiac dysfunction, this study aimed to evaluate whether severe FR results in alterations in the expression and activity of Ca2+-handling proteins that contribute to impaired myocardial performance. Male 60-day-old Wistar–Kyoto rats were fed a control or restricted diet (50% reduction in the food consumed by the control group) for 90 days. Body weight, body fat pads, adiposity index, as well as the weights of the soleus muscle and lung, were obtained. Cardiac remodeling was assessed by morphological measures. The myocardial contractile performance was analyzed in isolated papillary muscles during the administration of extracellular Ca2+ and in the absence or presence of a sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) specific blocker. The expression of Ca2+-handling regulatory proteins was analyzed via Western Blot. Severe FR resulted in a 50% decrease in body weight and adiposity measures. Cardiac morphometry was substantially altered, as heart weights were nearly twofold lower in FR rats. Papillary muscles isolated from FR hearts displayed mechanical dysfunction, including decreased developed tension and reduced contractility and relaxation. The administration of a SERCA2a blocker led to further decrements in contractile function in FR hearts, suggesting impaired SERCA2a activity. Moreover, the FR rats presented a lower expression of L-type Ca2+ channels. Therefore, myocardial dysfunction induced by severe food restriction is associated with changes in the calcium-handling properties in rats