The employment experiences of graduates with disabilities in South Africa : challenges and resilience

A submitted thesis of Masters of Art in Social and Psychological Research, University of the Witwatersrand, Faculty of Humanities, School of Human and Community Development, 2017The career trajectory for persons with disabilities (PWDs) has largely been associated with decline and stagnation. Resilience and positive attributes have not been investigated related to graduates with disabilities (GWDs) successfully entering, adjusting to and further developing within the work environment. The aim of this study was to report on challenges, resilience and positive attributes amongst GWDs as a positive contributing factor to employment practices as well as policy. A participant sample of 6 employed GWDs (working age 26-45; 4 males and 2 females; 3 Black, 2 White and 1 Coloured) were individually interviewed. The participants’ disabilities consisted mainly of physical, hearing and visual impairments. The data was analysed using thematic and discourse analysis. Results show that despite the negative experiences encountered within the social and work environment, participants demonstrated resilience within their narratives and decision-making processes. A self-developed conceptual model of resilience and positive attributes was thus proposed to track this resilience. However, the resilience observed amongst participants did not fully reflect the existing definitions and theoretical frameworks around resilience. Critically re-examining these existing definitions and the theoretical framework showed new meanings can be derived with implications for policy and intervention. The fact that the majority of participants did not show awareness of or ownership of their resilience shows a missing key element – that they are not only making use of it, but they also do not even appear to realise its importance.MT201

AMPLIANDO A DISCUSSÃO SOBRE ECOLOGIA NEOTROPICAL

In face of the Brazilian megadiversity, the contribution of Brazilian researchers to the conception of new hypotheses and theories in ecology can still be considered as shy, and this may be one of the main reasons why we have advanced less than we potentially could. In consequence of this reality, the 1st Symposium on Ecological Theory (I SET) took place at the Federal University of Minas Gerais in 2004, aiming to stimulate the concept of new theories by  Brazilian ecologists. In 2006, the 2 nd Symposium on Ecological Theory (II SET) took place at the Federal University of Rio de Janeiro, organized by the Pos Graduation Program in Ecology (PPGE/UFRJ), aiming to give continuity to the fist event, through the discussion of various hypotheses and theories that compose the mosaic of traditional ecology, with emphasis on tropical systems. This article presents a historical perspective of this event and the themes discussed during the event written in a resumed form.Frente à megadiversidade brasileira, pode-se qualificar como ainda tímida a contribuição de pesquisadores do país na geração de novas hipóteses e teorias ecológicas, o que talvez seja uma das principais razões pela qual tenhamos avançado menos do que potencialmente poderíamos. Em face a esta realidade, o I Simpósio de Ecologia Teórica (I SET) foi realizado em 2004, na Universidade Federal de Minas Gerais, com o intuito de incentivar o avanço dos ecólogos brasileiros na elaboração de novas teorias. Em 2006, o Programa de Pós-Graduação em Ecologia da Universidade Federal do Rio de Janeiro (PPGE/UFRJ) organizou o II Simpósio de Ecologia Teórica (II SET) com o objetivo de dar continuidade ao primeiro evento através da discussão das diversas hipóteses e teorias que compõem o mosaico da ecologia tradicional, com enfoque nos sistemas tropicais. Este manuscrito faz um breve apanhado do evento e apresenta resumidamente os demais artigos que constam desta publicação e que foram base para as palestras e mesas redondas

Proton affinities of amino group functionalizing 2D and 3D boron compounds

We report quantum-chemical computations of Proton Affinities (PA) of icosahedral amino boranes, carboranes and Co-containing metallacarboranes with arelative error of ~ 2% - when experimental data available- by means of the B3LYP and BP86 functionals. Use of larger basis sets for simple systems such as NH3, CH3NH2, and borazine (B3H6N3) reduces theerr or to ~ 0.5 % indicating the validity of these functionals for these computations and prediction of PA for unavailable experimental data on amino-derived (car)boranes and metalla(car)boranes. The computed PA show that, from an electronic structure point of view, when substituting an exo H atom by an NH2 group in B12H12(2-), CB11H12(-), (ortho, meta, para)-C2B10H12, and the metalla carborane [3-Co(1,2-C2B9H11)2](-)=COSAN the most similar system to be compared with is the anion NH2-BH3(-) – computed PA(B3LYP/cc-pVTZ) = 1505 kJ·mol-1 – rather than methylamine CH3NH2 or borazine, the two latter with experimental PA of 900 and 803 kJ·mol-1 respectively. The largest PA for a given isomer correspond, following this order, to: 1-NH2-B12H11(2-), (-)BH3NH2 , 12-NH2-CB11H11(-), cisoid8-NH2-COSAN, transoid 9-NH2-COSAN, 9-NH2-1,2-C2B10H11, 9-NH2-1,7-C2B10H11, and 2-NH2-1,12-C2B10H11. The rule for larger PA applies for isomers with the NH2 groups farthest aways from (non-metal) carborane C(cage) atoms. Pyramidalization energy computation shows an enhanced facility for planarization of the amino group in cisoid 8-NH2-COSAN as compared to cisoid 1-NH2-COSAN

Up-regulation of the anti-inflammatory adipokine adiponectin in acute liver failure in mice

BACKGROUND/AIMS: Recent reports suggest that the adipose tissue and adipokines are potent modulators of inflammation. However, there is only scarce knowledge on the functional role and regulation of endogenous adiponectin in non-fat tissues such as the liver under conditions of acute inflammation. METHODS: In the present study, we investigated adiponectin expression in healthy murine liver tissue and under inflammatory conditions in vivo. RESULTS: Adiponectin mRNA was readily detectable in healthy liver tissue and further increased in ConA-mediated acute liver failure. Adiponectin protein expression was mainly found in hepatic endothelial cells. In vitro adiponectin mRNA expression was detectable in several cell types, including primary hepatic sinusoidal endothelial cells, stellate cells, and macrophages. Mice pretreated with adiponectin before ConA administration developed reduced hepatic injury as shown by decreased release of transaminases and reduced hepatocellular apoptotis. Of note, TNF-alpha levels were not affected by adiponectin, whereas IL-10 production was increased. Neutralisation of IL-10 diminished the protective effect of adiponectin. CONCLUSIONS: Adiponectin expression is up-regulated in ConA-mediated acute liver failure. Therefore, adiponectin might play a role in the control and limitation of inflammation in the liver. Moreover, our data suggest a role for IL-10 in adiponectin-mediated hepatoprotection

Inhibition of soluble epoxide hydrolase modulates inflammation and autophagy in obese adipose tissue and liver. Role for omega-3 epoxides

Soluble epoxide hydrolase (sEH) is an emerging therapeutic target in a number of diseases that have inflammation as a common underlying cause. sEH limits tissue levels of cytochrome P450 (CYP) epoxides derived from omega-6 and omega-3 polyunsaturated fatty acids (PUFA) by converting these antiinflammatory mediators into their less active diols. Here, we explored the metabolic effects of a sEH inhibitor (t-TUCB) in fat-1 mice with transgenic expression of an omega-3 desaturase capable of enriching tissues with endogenous omega-3 PUFA. These mice exhibited increased CYP1A1, CYP2E1, and CYP2U1 expression and abundant levels of the omega-3-derived epoxides 17,18-epoxyeicosatetraenoic acid (17,18-EEQ) and 19,20-epoxydocosapentaenoic (19,20-EDP) in insulin-sensitive tissues, especially liver, as determined by LC-ESI-MS/MS. In obese fat-1 mice, t-TUCB raised hepatic 17,18-EEQ and 19,20-EDP levels and reinforced the omega-3-dependent reduction observed in tissue inflammation and lipid peroxidation. t-TUCB also produced a more intense antisteatotic action in obese fat-1 mice, as revealed by magnetic resonance spectroscopy. Notably, t-TUCB skewed macrophage polarization toward an antiinflammatory M2 phenotype and expanded the interscapular brown adipose tissue volume. Moreover, t-TUCB restored hepatic levels of Atg12-Atg5 and LC3-II conjugates and reduced p62 expression, indicating up-regulation of hepatic autophagy. t-TUCB consistently reduced endoplasmic reticulum stress demonstrated by the attenuation of IRE-1α and eIF2α phosphorylation. These actions were recapitulated in vitro in palmitate-primed hepatocytes and adipocytes incubated with 19,20-EDP or 17,18-EEQ. Relatively similar but less pronounced actions were observed with the omega-6 epoxide, 14,15-EET, and nonoxidized DHA. Together, these findings identify omega-3 epoxides as important regulators of inflammation and autophagy in insulin-sensitive tissues and postulate sEH as a druggable target in metabolic diseases

Large emissions from floodplain trees close the Amazon methane budget

Wetlands are the largest global source of atmospheric methane (CH4), a potent greenhouse gas. However, methane emission inventories from the Amazon floodplain, the largest natural geographic source of CH4 in the tropics, consistently underestimate the atmospheric burden of CH4 determined via remote sensing and inversion modelling, pointing to a major gap in our understanding of the contribution of these ecosystems to CH4 emissions. Here we report CH4 fluxes from the stems of 2,357 individual Amazonian floodplain trees from 13 locations across the central Amazon basin. We find that escape of soil gas through wetland trees is the dominant source of regional CH4 emissions. Methane fluxes from Amazon tree stems were up to 200 times larger than emissions reported for temperate wet forests6 and tropical peat swamp forests, representing the largest non-ebullitive wetland fluxes observed. Emissions from trees had an average stable carbon isotope value (δ13C) of −66.2 ± 6.4 per mil, consistent with a soil biogenic origin. We estimate that floodplain trees emit 15.1 ± 1.8 to 21.2 ± 2.5 teragrams of CH4 a year, in addition to the 20.5 ± 5.3 teragrams a year emitted regionally from other sources. Furthermore, we provide a ‘top-down’ regional estimate of CH4 emissions of 42.7 ± 5.6 teragrams of CH4 a year for the Amazon basin, based on regular vertical lower-troposphere CH4 profiles covering the period 2010–2013. We find close agreement between our ‘top-down’ and combined ‘bottom-up’ estimates, indicating that large CH4 emissions from trees adapted to permanent or seasonal inundation can account for the emission source that is required to close the Amazon CH4 budget. Our findings demonstrate the importance of tree stem surfaces in mediating approximately half of all wetland CH4 emissions in the Amazon floodplain, a region that represents up to one-third of the global wetland CH4 source when trees are combined with other emission sources

Inflammatory macrophages reprogram to immunosuppression by reducing mitochondrial translation

Acute inflammation can either resolve through immunosuppression or persist, leading to chronic inflammation. These transitions are driven by distinct molecular and metabolic reprogramming of immune cells. The anti-diabetic drug Metformin inhibits acute and chronic inflammation through mechanisms still not fully understood. Here, we report that the anti-inflammatory and reactive-oxygen-species-inhibiting effects of Metformin depend on the expression of the plasticity factor ZEB1 in macrophages. Using mice lacking Zeb1 in their myeloid cells and human patient samples, we show that ZEB1 plays a dual role, being essential in both initiating and resolving inflammation by inducing macrophages to transition into an immunosuppressed state. ZEB1 mediates these diverging effects in inflammation and immunosuppression by modulating mitochondrial content through activation of autophagy and inhibition of mitochondrial protein translation. During the transition from inflammation to immunosuppression, Metformin mimics the metabolic reprogramming of myeloid cells induced by ZEB1. Mechanistically, in immunosuppression, ZEB1 inhibits amino acid uptake, leading to downregulation of mTORC1 signalling and a decrease in mitochondrial translation in macrophages. These results identify ZEB1 as a driver of myeloid cell metabolic plasticity, suggesting that targeting its expression and function could serve as a strategy to modulate dysregulated inflammation and immunosuppression.The study was conducted at IDIBAPS’ Centre de Recerca Biomèdica Cellex building, which was partly funded by the Cellex Foundation. The different parts of this study were independently funded by grants to AP from the Leo Foundation (LF-OC-19-000166), the Catalan Agency for Management of University and Research Grants (AGAUR) (2017-SGR-1174 and 2021-SGR-01328), and the Spanish State Research Agency (AEI) of the Ministry of Science and Innovation (MICINN) (PID2020-116338RB-I00) as part of MICINN’s National Scientific and Technical Research and Innovation 2021-2023 Plan, which is cofinanced by the European Regional Development Fund (ERDF) of the European Union Commission. AB is a recipient of a PhD scholarship from AGAUR (FI Program, 2021 FI_B 00514