177 research outputs found
The Landscape of Social Innovation in Canadian Universities: An Empirical Analysis
There has been global growth in the number of social innovation initiatives launched in the university sector over the last decade. These initiatives aim to address complex social problems and to promote institutional change. This surge is occurring without a well-developed empirical knowledge base. This article provides a comprehensive description and analysis of the landscape of social innovation initiatives in the Canadian university sector. Findings show that nearly half of Canadaâs 96 universities are associated with at least one initiative; many are interdisciplinary and emphasize collaborative problem-solving with sectors outside the university; and government agencies and charitable foundations are the most common funding sources. Findings suggest there is room for growth and for linking and clustering initiatives. The article concludes with directions for future research.
RĂSUMĂLa derniĂšre dĂ©cennie a Ă©tĂ© marquĂ©e par une croissance mondiale du nombre dâinitiatives dâinnovation sociale lancĂ©es dans le secteur universitaire. Ces initiatives visent Ă rĂ©soudre des problĂšmes sociaux complexes et Ă induire des changements institutionnels et systĂ©miques. Cette poussĂ©e de lâactivitĂ© dâinnovation sociale se produit sans une base de connaissances empiriques bien dĂ©veloppĂ©e. Nous y contribuons en fournissant une description et une analyse complĂštes de toutes les initiatives dâinnovation sociale auxquelles participe le secteur universitaire canadien, de leurs caractĂ©ristiques et du paysage quâelles constituent. RĂ©sultats notables: prĂšs de la moitiĂ© des 96 universitĂ©s canadiennes sont associĂ©es Ă au moins une initiative; de nombreuses initiatives sont interdisciplinaires et mettent lâaccent sur la rĂ©solution de problĂšmes en collaboration avec des secteurs extĂ©rieurs Ă lâuniversitĂ©; Les agences gouvernementales et les fondations caritatives sont les sources de financement les plus courantes. Les rĂ©sultats suggĂšrent: il existe un potentiel de croissance de lâinnovation sociale dans le secteur; il y a moins de liens internes et de regroupement dâinitiatives que ne le recommande la thĂ©orie de lâinnovation; lâaccent mis sur la collaboration extĂ©rieure rejoint la «troisiĂšme mission» des universitĂ©s, qui existe depuis longtemps, mais les innovateurs sociaux ont des objectifs, des mĂ©thodes et des processus distincts pour mener Ă bien cette mission. Nous concluons avec les orientations pour les recherches futures.
Keywords / Mots clĂ©s: Universities; Higher education; Social innovation; Community engagement; Service mission; Social change; Canada / UniversitĂ©s; Ătablissements dâenseignement supĂ©rieur; Innovation sociale; Engagement communautaire; Mission de service; Changement social; Canad
Wireless Environmental Weather Monitor
The goal of this senior design/honors project is to create a device that monitors environmental conditions in order to detect a wildfire. This device should notify a user of the status of the environment. The device should also last for 6 months without any human interaction. My role on the team is to design the power supply system that maximizes efficiency and uses renewable energy
Liquefaction of hydrothermally pretreated wheat straw at high-solids content by purified Trichoderma enzymes
Peer reviewe
Vasodilator effect of glucagon: receptorial crosstalk among glucagon, GLP-1, and receptor for glucagon and GLP-1
Glucagon is known for its insulin-antagonist effect in the blood glucose homeostasis, while it also reduces vascular resistance. The mechanism of the vasoactive effect of glucagon has not been studied before; thereby we aimed to investigate the mediators involved in the vasodilatation induced by glucagon. The vasoactive effect of glucagon, insulin, and glucagon-like peptide-1 was studied on isolated rat thoracic aortic rings using a wire myograph. To investigate the mechanism of the vasodilatation caused by glucagon, we determined the role of the receptor for glucagon and the receptor for GLP-1, and studied also the effect of various inhibitors of gasotransmitters, inhibitors of reactive oxygen species formation, NADPH oxidase, prostaglandin synthesis, protein kinases, potassium channels, and an inhibitor of the Na(+)/Ca(2+)-exchanger. Glucagon causes dose-dependent relaxation in the rat thoracic aorta, which is as potent as that of insulin but greater than that of GLP-1 (7-36) amide. Vasodilatation by GLP-1 is partially mediated by the glucagon receptor. The vasodilatation due to glucagon evokes via the glucagon-receptor, but also via the receptor for GLP-1, and it is endothelium-independent. Contribution of gasotransmitters, prostaglandins, the NADPH oxidase enzyme, free radicals, potassium channels, and the Na(+)/Ca(2+)-exchanger is also significant. Glucagon causes dose-dependent relaxation of rat thoracic aorta in vitro, via the receptor for glucagon and the receptor for GLP-1, while the vasodilatation evoked by GLP-1 also evolves partially via the receptor for glucagon, thereby, a possible crosstalk between the 2 hormones and receptors could occur
Role of Cystathionine Gamma-Lyase in Immediate Renal Impairment and Inflammatory Response in Acute Ischemic Kidney Injury
Hydrogen sulfide (H2S) is known to act protectively during renal
ischemia/reperfusion injury (IRI). However, the role of the endogenous H2S in
acute kidney injury (AKI) is largely unclear. Here, we analyzed the role of
cystathionine gamma-lyase (CTH) in acute renal IRI using CTH-deficient
(Cthâ/â) mice whose renal H2S levels were approximately 50% of control (wild-
type) mice. Although levels of serum creatinine and renal expression of AKI
marker proteins were equivalent between Cthâ/â and control mice, histological
analysis revealed that IRI caused less renal tubular damage in Cthâ/â mice.
Flow cytometric analysis revealed that renal population of infiltrated
granulocytes/macrophages was equivalent in these mice. However, renal
expression levels of certain inflammatory cytokines/adhesion molecules
believed to play a role in IRI were found to be lower after IRI only in Cthâ/â
mice. Our results indicate that the systemic CTH loss does not deteriorate but
rather ameliorates the immediate AKI outcome probably due to reduced
inflammatory responses in the kidney. The renal expression of CTH and other
H2S-producing enzymes was markedly suppressed after IRI, which could be an
integrated adaptive response for renal cell protection
Levosimendan: a cardiovascular drug to prevent liver ischemia-reperfusion injury?
INTRODUCTION: Temporary occlusion of the hepatoduodenal ligament leads to an ischemic-reperfusion (IR) injury in the liver. Levosimendan is a new positive inotropic drug, which induces preconditioning-like adaptive mechanisms due to opening of mitochondrial KATP channels. The aim of this study was to examine possible protective effects of levosimendan in a rat model of hepatic IR injury. MATERIAL AND METHODS: Levosimendan was administered to male Wistar rats 1 hour (early pretreatment) or 24 hours (late pretreatment) before induction of 60-minute segmental liver ischemia. Microcirculation of the liver was monitored by laser Doppler flowmeter. After 24 hours of reperfusion, liver and blood samples were taken for histology, immuno- and enzyme-histochemistry (TUNEL; PARP; NADH-TR) as well as for laboratory tests. Furthermore, liver antioxidant status was assessed and HSP72 expression was measured. RESULTS: In both groups pretreated with levosimendan, significantly better hepatic microcirculation was observed compared to respective IR control groups. Similarly, histological damage was also reduced after levosimendan administration. This observation was supported by significantly lower activities of serum ALT (pearly = 0.02; plate = 0.005), AST (pearly = 0.02; plate = 0.004) and less DNA damage by TUNEL test (pearly = 0.05; plate = 0.034) and PAR positivity (pearly = 0.02; plate = 0.04). Levosimendan pretreatment resulted in significant improvement of liver redox homeostasis. Further, significantly better mitochondrial function was detected in animals receiving late pretreatment. Finally, HSP72 expression was increased by IR injury, but it was not affected by levosimendan pretreatment. CONCLUSION: Levosimendan pretreatment can be hepatoprotective and it could be useful before extensive liver resection
Vitamin D depletion aggravates hypertension and target-organ damage
BACKGROUND: We tested the controversial hypothesis that vitamin D depletion aggravates hypertension and target-organ damage by influencing renin. METHODS AND RESULTS: Four-week-old double-transgenic rats (dTGR) with excess angiotensin (Ang) II production due to overexpression of the human renin (hREN) and angiotensinogen (hAGT) genes received vitamin D-depleted (n=18) or standard chow (n=15) for 3 weeks. The depleted group had very low serum 25-hydroxyvitamin D levels (mean+/-SEM; 3.8+/-0.29 versus 40.6+/-1.19 nmol/L) and had higher mean systolic BP at week 5 (158+/-3.5 versus 134.6+/-3.7 mm Hg, P<0.001), week 6 (176.6+/-3.3 versus 162.3+/-3.8 mm Hg, P<0.01), and week 7 (171.6+/-5.1 versus 155.9+/-4.3 mm Hg, P<0.05). Vitamin D depletion led to increased relative heart weights and increased serum creatinine concentrations. Furthermore, the mRNAs of natriuretic peptides, neutrophil gelatinase-associated lipocalin, hREN, and rRen were increased by vitamin D depletion. Regulatory T cells in the spleen and in the circulation were not affected. Ang metabolites, including Ang II and the counter-regulatory breakdown product Ang 1 to 7, were significantly up-regulated in the vitamin D-depleted groups, while ACE-1 and ACE-2 activities were not affected. CONCLUSIONS: Short-term severe vitamin D depletion aggravated hypertension and target-organ damage in dTGR. Our data suggest that even short-term severe vitamin D deficiency may directly promote hypertension and impacts on renin-angiotensin system components that could contribute to target-organ damage. The findings add to the evidence that vitamin D deficiency could also affect human hypertension
Supplementary material for the article: Wedmann, R.; Onderka, C.; Wei, S.; SzijĂĄrtĂł, I. A.; Miljkovic, J. L.; Mitrovic, A.; Lange, M.; Savitsky, S.; Yadav, P. K.; Torregrossa, R.; et al. Improved Tag-Switch Method Reveals That Thioredoxin Acts as Depersulfidase and Controls the Intracellular Levels of Protein Persulfidation. Chemical Science 2016, 7 (5), 3414â3426. https://doi.org/10.1039/c5sc04818d
Supplementary material for: [https://doi.org/10.1039/c5sc04818d]Related to published version: [http://cherry.chem.bg.ac.rs/handle/123456789/1925
Levosimendan Administration in Limb Ischemia: Multicomponent Signaling Serving Kidney Protection
AIMS AND OBJECTIVES: Acute renal failure is a severe complication of lower extremity major arterial reconstructions, which could even be fatal. Levosimendan is a dual-acting positive inotropic and vasodilatory agent, which is suspected to have protective effects against cardiac ischemia. However, there is no data available on lower limb or remote organ ischemic injuries therefore the aim of the study was to investigate the effect of levosimendan on lower limb ischemia-reperfusion injury and the corollary renal dysfunction. METHODS: Male Wistar rats underwent 180 min bilateral lower limb ischemia followed by 4 or 24 hours of reperfusion. Intravenous Levosimendan was administered continuously (0.2mug/bwkg/min) throughout the whole course of ischemia and the first 3h of reperfusion. Results were compared with sham-operated and ischemia-reperfusion groups. Hemodynamic monitoring was performed by invasive arterial blood pressure measurement. Kidney and lower limb muscle microcirculation was registered by a laser Doppler flowmeter. After 4h and 24h of reperfusion, serum, urine and histological samples were collected. RESULTS: Systemic hemodynamic parameters and microcirculation of kidney and the lower limb significantly improved in the Levosimendan treated group. Muscle viability was significantly preserved 4 and 24 hours after reperfusion. At the same time, renal functional laboratory tests and kidney histology demonstrated significantly less expressive kidney injury in Levosimendan groups. TNF-alpha levels were significantly less elevated in the Levosimendan group 4 hours after reperfusion. CONCLUSION: The results claim a protective role for Levosimendan administration during major vascular surgeries to prevent renal complications
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