Welcome to Planet Texas 2050

The Medium writes about Planet Texas 2050 and the goals of the grand challege in an article published May 31, 2018.Office of the VP for Researc

From stormy seas to the doldrums: The challenges of navigating towards an ecologically coherent marine protected area network through England's Marine Conservation Zone process

There is an on-going process to establish Marine Conservation Zones (MCZs) in England, to form part of a coherent and representative network of marine protected areas under national and EU legislation. From 2009 to 2011, the MCZ process included strong participatory elements. Four regional multi-sector stakeholder groups developed MCZ recommendations collaboratively, in line with ecological guidance provided by the Government's nature conservation advisers. This guidance was based on Government policy principles, including that MCZs should be designated based on 'best available evidence'. This paper analyses the multi-dimensional conflicts that emerged within the stakeholder group in south-west England, which were magnified by uncertainty about future MCZ management. In September 2011, after working through these conflicts through trade-offs and negotiations, the stakeholder groups jointly recommended 127 MCZs to Government. The process subsequently shifted to a top-down approach, with further stakeholder engagement limited to bilateral consultation. There was a concurrent shift in policy, from a broad-scale network-level focus towards single-feature conservation. A lengthy series of evidence reviews concluded that the existing evidence at the time was insufficient to progress with the designation of most sites, marking a clear departure from the policy principle of proceeding with the designation of a representative network based on 'best available evidence', and effectively undermining the work carried out by stakeholder groups. Though MCZ designation was originally timetabled for 2012, in November 2013 just 27 of the recommended 127 MCZs were designated in a first tranche. At the time, no clear timetable was in place for subsequent tranches

Marine spatial planning in reality: introduction to case studies and discussion of findings

This paper explores the realities of marine spatial planning (MSP'ing), drawing on 12 case studies around Europe, employing a structured qualitative empirical approach. The findings indicate that (1) MSP'ing is often focused on achieving specific sectoral objectives, related to nationally important strategic priorities, and might better be termed 'strategic sectoral planning'. (2) MSP'ing processes tend to be complex, fragmented and emergent on an ad hoc basis, rather than cyclical, adaptive and prescribed on an a priori basis. (3) Top-down processes tend to dominate, more participative platforms tending to be 'disconnected by design' from executive decision-making. (4) Blue growth is the dominant overall priority, often aligned with strategic sectoral priorities, despite growing indications that the target for Good Environmental Status (GES) by 2020 is unlikely to be met. This is consistent with growing concerns about the tensions between the Marine Strategy Framework Directive and the Directive Establishing a Framework for Maritime Spatial Planning. It is concluded that the realities of how MSP'ing is working contrast with widely recognised concepts and ideals as to how MSP'ing should work, as integrated-use MSP'ing based on political expedience and blue growth priorities is diverging from and potentially competing with ecosystem-based MSP'ing, including marine protected area networks, based on GES priorities. It is argued that a more empirical approach should be taken to MSP'ing research, whereby conceptual approaches which integrate sustainable blue growth and GES co-evolve with marine spatial planning practices through critical analyses of whether the realities of MSP'ing are consistent with these concepts

Estudo do efeito neuroprotetor da mirtazapina e imipramina e sua relação com a expressão gênica de proteínas apoptóticas

Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências Biológicas. Programa de Pós-Graduação em Neurociências.Neste estudo foram investigados a ação neuroprotetora dos antidepressivos mirtazapina e imipramina e os efeitos destes compostos sobre a expressão gênica de proteínas anti- e pró-apoptóticas em células de neuroblastoma humano (SH-5YSY). Mirtazapina e imipramina mostraram baixa citotoxicidade sobre neuroblastoma humano e nas concentrações de 1-10 ?M aumentaram a viabilidade celular. As células de neuroblastoma humano foram pré-tratadas com mirtazapina e imipramina e depois incubadas na presença de tapsigargina ou peróxido de hidrogênio (H2O2). O pré-tratamento com mirtazapina e imipramina protegeu as células de neuroblastoma da citotoxicidade induzida pelo peróxido de hidrogênio. As células foram incubadas com mirtazapina e imipramina e a expressão gênica (RNAm) das proteínas envolvidas na sobrevivência (Bcl-2) e na morte celular (Bax, Bad e p53) foram determinadas por transcrição reversa e reação em cadeia da polimerase quantititiva (qRT-PCR). A mirtazapina reduziu e a imipramina não afetou a expressão gênica da proteína Bcl-2. A expressão gênica das proteínas Bax e p53 foi bastante reduzida pela mirtazapina e imipramina. A mirtazapina e a imipramina (2 ?M) aumentaram a razão Bcl-2/Bax e Blc-2/p53, indicando um efeito positivo na sobrevivência celular. Os resultados sugerem que o efeito neuroprotetor da mirtazapina e da imipramina envolve a redução da expressão gênica das proteínas pró-apoptóticas Bax e p53.In this study we investigated the neuroprotective effect of mirtazapine and imipramine and how these compounds affect the gene expression of anti-apoptotic and pro-apoptotic proteins in human neuroblastoma cells SH-SY5Y. Mirtazapine and imipramine showed low cytotoxicity on neuroblastoma cells and at concentrations of 1-10 ìM they increased the cell viability. Human neuroblastoma cells were pre-treated with mirtazapine and imipramine and then incubated with thapsigargin or hydrogen peroxide (H2O2). The pre-treatment with mirtazapine and imipramine protected the cells against H2O2-induced cell death. Cells were incubated with mirtazapine and imipramine and gene expression (mRNA) was determined for anti-apoptotic (Bcl-2) and pro-apoptotic proteins (Bax, Bad and p53) through qRT-PCR. Mirtazapine reduced and imipramine did not affect the expression level of the anti-apoptotic protein Bcl-2. The expression of Bax and p53 were strongly reduced by mirtazapine and imipramine. Both antidepressants increased the expression ratio of Bcl-2/Bax and Bcl-2/p53. These data suggest that the neuroprotective effect of mirtazapine and imipramine might be due the downregulation of pro-apoptotic Bax and p53 expression

Efeito neuroprotetor do pramipexol, agonista de receptores dopaminérgicos D2/D3, nos modelos de esclerose múltipla e de depressão

Tese (doutorado) - Universidade Federal de Santa Catarina, Centro de Ciências Biológicas, Programa de Pós-Graduação em Neurociências, Florianópolis, 2016.As doenças de Parkinson, de Alzheimer e esclerose múltipla (EM), bem como os transtornos de humor, como a depressão, apresentam componentes inflamatórios. As células do sistema imune possuem 5 receptores que respondem ao neurotransmissor dopamina, os quais modulam diferentemente a inflamação. Assim, é esperado que o pramipexol (PPX), um agonista de receptores dopaminérgicos (D2/D3), tenha efeito imunomodulatório. Para testar essa hipótese foram utilizados dois modelos que causam neuroinflamação: a) a encefalomielite autoimune experimental (EAE), modelo de esclerose múltipla e b) a administração periférica de lipopolissacarídeo (LPS), modelo de transtorno depressivo maior. A EAE foi induzida em camundongos C57BL/6 através da administração do peptídeo 35-55 da glicoproteína de mielina oligodendroglial e o PPX (0,1 e 1 mg/kg/dia) foi administrado pela via intraperitoneal por 40 dias. A dose de 1 mg/kg inibiu completamente o surgimento dos sinais motores induzidos pela EAE, além de prevenir a desmielinização na medula espinhal. Além disso, o PPX teve um forte efeito anti-inflamatório, confirmado através da redução da infiltração de células inflamatórias, da ativação astroglial na medula espinhal, e da redução nos níveis de IL-17 nos linfonodos. Além disto, o PPX reverteu várias alterações induzidas pela EAE na medula espinhal e no estriado, incluindo a redução nos níveis de a-sinucleína, o aumento nos níveis de parkina, alteração na enzima glutationa peroxidase e a produção de espécies reativas de oxigênio. Em conjunto os dados sugerem que o PPX deve ser estudado como um possível agente farmacológico para tratar a EM. No modelo de depressão induzida por inflamação periférica através da injeção de LPS em camundongos Swiss, o PPX (1 mg/kg), foi administrado por 7 dias por via intraperitoneal. Uma hora após a última aplicação de PPX, injetou-se LPS (0,1 mg/kg) via intraperitoneal, 24 h depois foi dado início aos testes comportamentais. O LPS induziu comportamento tipo-depressivo no teste do nado forçado e no splash test, sem alterar a locomoção no teste do campo aberto. Também foi observado o aumento de Interleucina-1ß e adutos de 3-nitrotirosina no hipocampo dos animais tratados com LPS. Todos estes parâmetros foram revertidos pelo PPX, indicando que o PPX é capaz diminuir os eventos inflamatórios que podem estar associados ao comportamento tipo-depressivo. Os antagonistas de receptores dopaminérgicos, haloperidol e sulpirida, não reverteram o efeito tipo-antidepressivo do PPX, indicando que a atuação do PPX parece não ser mediada por estes receptores. Em conjunto, os dados sugerem que o PPX é capaz de causar uma forte diminuição em processos inflamatórios, tanto no modelo de EAE como no modelo de depressão, o que pode ser o mecanismo responsável por sua ação. Porém, mais estudos são necessários para confirmar esta hipótese.Abstract : Neurologic diseases as Parkinson's, Alzheimer's and multiple sclerosis (MS) as well as mood disorders, like major depression, present inflammatory components. Immune cells express 5 different dopamine receptors, which are known to modulate inflammation. In this context, it is expected that pramipexole (PPX), a dopamine D2/D3 receptor agonist, would have an immunomodulatory effect. To evaluate this hypothesis two neuroinflammatory disease models were used, the experimental autoimmune encephalomyelitis (EAE), a mice model of MS, and the peripheral administration of lipopolysaccharide (LPS), a mice model of major depression disorder (MDD). EAE was induced in C57Bl/6 mice by the injection of the 35-55 peptide of myelin oligodendroglial glycoprotein. PPX (0.1 and 1 mg/kg) was administered by intraperitoneal route for 40 days. The dose of 1 mg/kg of PPX completely abolished motor impairment induced by EAE, and prevented medular demyelination. Besides, PPX had a marked anti-inflammatory effect, which was observed by reduction of inflammatory cells infiltration, astroglyal activation, and by decreasing IL-17 levels in lymph nodes. Besides, PPX reversed several alterations in the spinal cord and striatum induced by EAE, inclunding reduction in a-synuclein levels, enhancement of parkin levels, alteration in glutathione peroxidase activity and reactive oxygen species production. Together, these results suggest that PPX can be studied as a potential drug for MS treatment. In the MDD model induced by peripheral inflammation induced with the bacterial lipopolysacchired (LPS) administration in Swiss mice, PPX (1 mg/kg) was administered for 7 days by intraperitoneal route. One hour after the last PPX injection, LPS (0.1 mg/kg) was administered intraperitoneally, and 24 h later behavioral analysis were performed. LPS induced depressive-like behavior in the forced swimming test and splash test, without locomotor alterations in the open field test. It was also observed enhancement of Interleukin-1ß and 3-nitrotyrosin protein adducts in mice hippocampus of LPS treated animals. PPX reversed all these alterations, indicating that PPX can prevent the inflammatory events related to the depressive-like behavior. Interestingly, the dopamine receptor antagonists, haloperidol and sulpiride, did not reverse the PPX antidepressant-like effect in the forced swimming test, indicating that PPX effect seems to be unrelated by these receptors. Together, these results suggest that PPX present a marked antiinflammatory action, in both EAE and LPS models, suggesting that this could be the mechanism of action of PPX. Nevertheless, further studies are required to confirm this hypothesis

Financial Frictions, the Phillips Curve and Monetary Policy

How does the presence of financial frictions alter the Phillips curve and the conduct of optimal monetary policy? I investigate this question in a tractable small-scale New Keynesian DSGE model with a financial accelerator. The accelerator amplifies shocks, decreases the slope of the Phillips curve and renders forward-looking behavior more relevant for current macroeconomic dynamics. I show analytically that these three factors imply an inflationary bias of discretionary monetary policy relative to the standard model and a stabilization bias relative to commitment policy. A conservative central banker who places a larger weight on inflation stabilization than society is able to reduce both biases and closely mimics the optimal policy under commitment. The required degree of inflation conservatism increases in the degree to which financial frictions are present