Extensão universitária e enfrentamento ao capacitismo em tempos de pademia

A extensão universitária é o espaço, por excelência, em que os problemas sociais ganham maior visibilidade dentro das Instituições de Ensino Superior. A Política Nacional de Extensão Universitária aponta a importância das trocas com as comunidades para problematizar a produção e a reprodução dos conhecimentos instituídos na academia. A temática das deficiências e do capacitismo explicita um problema social importante da sociedade, que precisa ser ampliado nas formações acadêmicas. Corpos que desviam ao padrão de funcionalidade tida como normal são inferiorizados e desvalorizados. Defendemos que a deficiência deve ser percebida principalmente como questão social e política, e não somente como questão individual e biológica

Extensão universitária e enfrentamento ao capacitismo em tempos de pademia

A extensão universitária é o espaço, por excelência, em que os problemas sociais ganham maior visibilidade dentro das Instituições de Ensino Superior. A Política Nacional de Extensão Universitária aponta a importância das trocas com as comunidades para problematizar a produção e a reprodução dos conhecimentos instituídos na academia. A temática das deficiências e do capacitismo explicita um problema social importante da sociedade, que precisa ser ampliado nas formações acadêmicas. Corpos que desviam ao padrão de funcionalidade tida como normal são inferiorizados e desvalorizados. Defendemos que a deficiência deve ser percebida principalmente como questão social e política, e não somente como questão individual e biológica

Inhibition of PDE5 restores depressed baroreflex sensitivity in renovascular hypertensive rats

Renal artery stenosis is frequently associated with resistant hypertension, which is defined as failure to normalize blood pressure (BP) even when combined drugs are used. Inhibition of PDE5 by sildenafil has been shown to increase endothelial function and decrease blood pressure in experimental models. However, no available study evaluated the baroreflex sensitivity nor autonomic balance in renovascular hypertensive rats treated with sildenafil. In a translational medicine perspective, our hypothesis is that sildenafil could improve autonomic imbalance and baroreflex sensitivity, contributing to lower blood pressure. Renovascular hypertensive 2-kidney-1-clip (2K1C) and sham rats were treated with sildenafil (45 mg/Kg/day) during 7 days. At the end of treatment, BP and heart rate (HR) were recorded in conscious rats after a 24-hour-recovery period. Spontaneous and drug-induced baroreflex sensitivity and autonomic tone were evaluated; in addition, lipid peroxidation was measured in plasma samples. Treatment was efficient in increasing both spontaneous and induced baroreflex sensitivity in treated hypertensive animals. Inhibition of PDE5 was also capable of ameliorating autonomic imbalance in 2K1C rats and decreasing systemic oxidative stress. Taken together, these beneficial effects resulted in significant reductions in BP without affecting HR. We suggest that sildenafil could be considered as a promising alternative to treat resistant hypertension

A DISINTEGRIN AND METALLOPROTEASE 17 IN THE CARDIOVASCULAR AND CENTRAL NERVOUS SYSTEMS

ADAM17 is a metalloprotease and disintegrin that lodges in the plasmatic membrane of several cell types and is able to cleave a wide variety of cell surface proteins. It is somatically expressed in mammalian organisms and its proteolytic action influences several physiological and pathological processes. This review focuses on the structure of ADAM17, its signaling in the cardiovascular system and its participation in certain disorders involving the heart, blood vessels and neural regulation of autonomic and cardiovascular modulation

Targeted next-generation sequencing of glandular odontogenic cyst: a preliminary study

Glandular odontogenic cyst (GOC) is an uncommon developmental cyst. Its molecular pathogenesis is unclear, and deep sequencing may help identify causative low-frequency variants in tumors. We investigated in GOC mutations in 50 genes commonly altered in human cancers. Study Design Targeted next-generation sequencing was used to interrogate a panel of approximately 2800 mutations in GOC. Results Six missense single nucleotide variations (SNVs) were reported. Three SNVs (TP53 rs1042522, KDR rs1870377, and KIT rs3822214) are listed as “common single-nucleotide polymorphisms” at the UCSC Genome Browser. The other SNVs (PIK3CA p.Glu689Lys, PIK3CA p.Ala708Thr, and TP53 p.Leu289Phe) are predicted to have deleterious or damaging effects on proteins, but they showed very low frequency in our samples and could not be further validated by orthogonal methods. Conclusions No pathogenic SNV was detected in this cohort of GOCs. Further studies with larger gene panels or whole exome sequencing are needed to find the genetic basis of GOC1245490494CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE MINAS GERAIS - FAPEMIGSem informaçãoSem informaçã

Glial Cells Are Involved in ANG-II-Induced Vasopressin Release and Sodium Intake in Awake Rats

It is known that circulating angiotensin II (ANG-II) acts on the circumventricular organs (CVOs), which partially lack a normal blood-brain barrier, to stimulate pressor responses, vasopressin (AVP), and oxytocin (OT) secretion, as well as sodium and water intake. Although ANG-II type 1 receptors (AT1R) are expressed in neurons and astrocytes, the involvement of CVOs glial cells in the neuroendocrine, cardiovascular and behavioral responses induced by central ANG II remains to be further elucidated. To address this question, we performed a set of experiments combining in vitro studies in primary hypothalamic astrocyte cells (HACc) and in vivo intracerebroventricular (icv) microinjections into the lateral ventricle of awake rats. Our results showed that ANG-II decreased glutamate uptake in HACc. In addition, in vivo studies showed that fluorocitrate (FCt), a reversible glial inhibitor, increased OT secretion and mean arterial pressure (MAP) and decreased breathing at rest. Furthermore, previous FCt decreased AVP secretion and sodium intake induced by central ANG-II. Together, our findings support that CVOs glial cells are important in mediating neuroendocrine and cardiorespiratory functions, as well as central ANG-II-induced AVP release and salt-intake behavior in awake rats. In the light of our in vitro studies, we propose that these mechanisms are, at least in part, by ANG-II-induced astrocyte mediate reduction in glutamate extracellular clearance