A ambientalização curricular de programas de Educação Física em universidades federais do Brasil

ResumoO objetivo do artigo foi analisar evidências de ambientalização curricular em programas de educação física no contexto do ensino superior brasileiro. De acordo com esse objetivo, o "corpus" de análise foi composto pelos planos de ensino de disciplinas que abordam questões ambientais em programas de educação física de Universidades Federais do Brasil. O "corpus" foi analisado a partir da Análise Textual Discursiva, metodologia que compreende: a) desmontagem dos textos (unitarização); b) estabelecimento de relações (categorização); c) captação de um novo emergente (metatexto original). As unidades de significado destacadas na etapa de unitarização foram organizadas em categorias pré-definidas a partir das características da Rede ACES para um estudo ambientalizado. A escolha desse referencial ("benchmark") se justifica por sua representatividade diante das produções científicas no campo ambiental, constituindo-se como significativo (con)texto social atual, trazendo em suas definições o resultado de embates históricos em torno da emergência/legitimação de elementos que constituem os atuais conceitos sobre o "ambiental". Esperar-se-ia, assim, que pelo menos os conceitos chaves de cada categoria fossem contemplados pelas propostas presentes em planos de ensino de disciplinas que propõem um diálogo entre o campo ambiental e o campo da educação física. No entanto, os resultados da pesquisa mostram uma realidade bem diferente, colocando em evidência as práticas esportivas e recreativas na natureza como foco quase que exclusivo das disciplinas que abordam questões ambientais em programas de educação física de Universidades Federais do Brasil. Nos argumentos conclusivos são apresentadas significativas evidências sobre as dimensões dos discursos ambientais que estão sendo incorporados pelos currículos de educação física no âmbito do ensino (superior), assim como novas/"alternativas" perspectivas que emergem nos encontros entre o campo ambiental e o campo da educação física

May Measurement Month 2018: a pragmatic global screening campaign to raise awareness of blood pressure by the International Society of Hypertension

Aims Raised blood pressure (BP) is the biggest contributor to mortality and disease burden worldwide and fewer than half of those with hypertension are aware of it. May Measurement Month (MMM) is a global campaign set up in 2017, to raise awareness of high BP and as a pragmatic solution to a lack of formal screening worldwide. The 2018 campaign was expanded, aiming to include more participants and countries. Methods and results Eighty-nine countries participated in MMM 2018. Volunteers (≥18 years) were recruited through opportunistic sampling at a variety of screening sites. Each participant had three BP measurements and completed a questionnaire on demographic, lifestyle, and environmental factors. Hypertension was defined as a systolic BP ≥140 mmHg or diastolic BP ≥90 mmHg, or taking antihypertensive medication. In total, 74.9% of screenees provided three BP readings. Multiple imputation using chained equations was used to impute missing readings. 1 504 963 individuals (mean age 45.3 years; 52.4% female) were screened. After multiple imputation, 502 079 (33.4%) individuals had hypertension, of whom 59.5% were aware of their diagnosis and 55.3% were taking antihypertensive medication. Of those on medication, 60.0% were controlled and of all hypertensives, 33.2% were controlled. We detected 224 285 individuals with untreated hypertension and 111 214 individuals with inadequately treated (systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg) hypertension. Conclusion May Measurement Month expanded significantly compared with 2017, including more participants in more countries. The campaign identified over 335 000 adults with untreated or inadequately treated hypertension. In the absence of systematic screening programmes, MMM was effective at raising awareness at least among these individuals at risk

Growth hormone stimulates the tyrosine kinase activity of JAK2 and induces tyrosine phosphorylation of insulin receptor substrates and Shc in rat tissues

GH stimulates the tyrosine phosphorylation of various cellular polypeptides, including the GH receptor itself, in an early part of the intracellular response. Some of these phosphorylations are catalyzed by a GH receptor-associated kinase identified as JAK2, a member of the Janus family of tyrosine kinases. In cultured cells, GH stimulates the tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1), IRS-2, and Shc. This study investigated whether GH could cause the tyrosine phosphorylation of IRSs and Shc proteins in fasted rat tissues in vivo. GH was administered to fasted Wistar rats via a portal vein, and extracts of different tissues were immunoprecipitated with specific antibodies. GH increased the tyrosine phosphorylation of IRS-1, IRS-8, JAK2, and Shc proteins in the liver, heart, kidney, muscle, and adipose tissue of rats. The roles of these substrates as signaling molecules for GH were further demonstrated by the finding that GH stimulated the association of IRS-1/2 with phosphatidylinositol 3-kinase, Grb2, and phosphotyrosine phosphatase and of Shc with Grb2. The correlation between JAK2 tyrosyl phosphorylation and IRS-1 tyrosyl phosphorylation in response to GH together with the results of the in vitro tyrosine kinase assay are consistent with the hypothesis that JAK2 may mediate GH-induced phosphorylation of IRS-1.o TEXTO COMPLETO DESTE ARTIGO, ESTARÁ DISPONÍVEL À PARTIR DE AGOSTO DE 2015.1401556

G120K-PEG, a human GH antagonist, decreases GH signal transduction in the liver of mice

After receptor binding, growth hormone (GH) induces GH receptors (GHR) dimerization and JAK2 is activated after its association with a dimerized GHR, stimulating the tyrosyl phosphorylation of insulin receptor substrate-1 (IRS-1), IRS-2 and She proteins. G120K-PEG, a GH antagonist is produced by a mutation that blocks GH action by preventing the GHR dimerization. This study shows that the inhibitory effect of G120K-PEG was maximal with a GH:G120K-PEG ratio of 1:100, as no increase in JAK2 tyrosyl phosphorylation was observed with this dose of GH. When the dose of GH was increased and with a GH:G120K-PEG ratio of 1:10 some tyrosyl phosphorylation of JAK2 could be observed. Additionally, GH-induced IRS-1, IRS-2 and SHC tyrosyl phosphorylation was inhibited similar to50% at equimolar concentrations of the antagonist of GH and almost abolished with a GH:G120K-PEG ratio of 1:100. The results clearly show that G120K-PEG inhibits GH signal transduction in mouse liver. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.19241671657

United States Department of the Interior budget justifications by state: Arizona: FY 2002

8 pages (PDF version). File size: 70.645 KB. Other states' park operational summaries and funding documents can be found at http://home.nps.gov/applications/budgetweb/fy2002/sbtoc-main.ht

Regulation of cardiac JAK-2 in animal models of insulin resistance

Insulin induces phosphorylation and activation of JAK2 tyrosine, as well as its association with STAT1 and SHP2 in insulin-sensitive tissues of intact rats, thus demonstrating a new pathway in transduction of insulin signals. We investigated this pathway in hearts of rats in three situations of insulin resistance: 72 h of fasting, chronic treatment with dexamethasone, and acute treatment with epinephrine. The acute treatment with epinephrine showed no difference in insulin-induced JAK2 tyrosine phosphorylation or JAK2/STAT1 and JAK2/SHP2 association in comparison with the control. In fasted rats the JAK2 protein concentration decreased, accompanied by a decrease in the stoichiometry of the phosphorylation to 70 %, an increase in association of JAK2/STAT1 to 160%, and a decrease in JAK2/SHP2 association to 85%. In the dexamethasone-treated group, the JAK2 protein concentrations increased but the stoichiometry of its phosphorylation decreased to 20%, whereas the JAK2/STAT1 and JAK2/SHP2 associations changed by 70% and 170%, respectively, In fasting and dexamethasone-treated rats, therefore, insulin-induced JAK2 tyrosine phosphorylation decreases, and the JAK2 protein expression is differentially regulated such that the insulin-induced JAK2 association with SHP2 and STAT1 shows opposite interactions with the kinase.49650150