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Journal articles on the topic "SERV.SOCIALE E SC.FORM"

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Casieri, Arturo, Bernardo De Gennaro, Umberto Medicamento, and Luigi Roselli. "Capitale sociale e performance economica: un'applicazione al sistema di produzione dell'olio extra-vergine di oliva biologico della provincia di Bari." ECONOMIA AGRO-ALIMENTARE, no. 1 (June 2009): 7–23. http://dx.doi.org/10.3280/ecag2009-001002.

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- Social capital and economic firm performances: an application to the organic extravirgin olive oil net-chain in the province of Bari The supply chains of niche market goods like organic products are rapidly evolving. Compared to the conventional supply chains, these are more risky andmarket oriented. Therefore, to build stable networks along and among the chains is becoming an increasingly valuable as a competitive factor. The firms use these networks to exchange tangible and intangible assets. Structural social capital embedded in business networks could influence the firms' competitiveness. In this perspective it can be worthwhile for the possible normative suggestion for policy makers to consider the control over strategic resources spread in the environment out of the firm, as a competitive advantage source, together with the firm's internal resources. The external environment is characterized by a net of inter-firms relationships, which pertain to trade exchange, information exchange, shared norms and resources' association. The strategic resources inside the network, especially information, constitute an asset that companies need to improve their competitive advantage. The structure of relationships enabling the access to those resources, constitute the social capital (sc) which is revealed in the modalities with which firms place themselves in the net: higher the sc, the higher the economic performance. This study aims to show the significance of structural sc in influencing the firms' economic performances in agribusiness. We will try to test this hypothesis by analyzing the organic olive oil production system in the Province of Bari. In this study we refer to the form of sc linked to the firm's position inside the net-chain and to the idea of structural holes. Specifically, we decided to measure sc in terms of network constraints - a more constrained entrepreneurial activity implies less structural holes and therefore less sc. As for the firm performance measures, there are several indexes that could be appropriate: from the well known roi (Return on Investment) and ros (Return on Sale), to revenue. Actually, we selected the last one (revenue). It in fact the results are easier to find, and the productive structure of the firms involved in the organic olive oil processing can be considered quite homogeneous. To measure the structure of the relational web we adopt the Social Network Analysis (sna), a method based on the analysis of the actors (individuals, firms, and institutions) involved in a particular context and on the relationships between them. The subject of the analysis is the extra-virgin organic olive oil net-chain in the province of Bari. A set of economic institutions and organizations both located in this province and out of this territory but involved in processing and in trading the extravirgin organic olive oil. The results obtained, show that also in agribusiness netchains, as the organic olive oil, firms gain a higher competitive advantage if the are able to be central in the network of relationships, both horizontal and vertical, assuming an intermediary role in the transactional and informational flows. Further studies are still necessary, since the analysis completely disregards some key factors of competitiveness (although recognizing their relevance), which are not directly connected to the structure of relationships of the netchain as the relational social capital (e.g. trust, norms and expectations) and cognitive social capital (e.g. shared view, common language).JEL Code: L14Key words: social capital, network analysis, netchain, economic performance, organic olive oil
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Da Silva Sobrinho, Adriano Referino, Israel Luís Diniz Carvalho, Luiz Gutenberg de Miranda Toledo Coelho Júnior, Pedro Henrique Sette-de-Souza, and Herika de Arruda Maurício. "Perfil dos Coordenadores de Saúde Bucal no Brasil: revisão de literatura." ARCHIVES OF HEALTH INVESTIGATION 9, no. 5 (April 20, 2020): 479–84. http://dx.doi.org/10.21270/archi.v9i5.4727.

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Introdução: O gestor de saúde bucal é peça chave para o funcionamento do Sistema Único de Saúde (SUS). Dentre suas atribuições, está a de consolidar os serviços odontológicos, otimizar o processo de trabalho de sua equipe profissional e garantir o direito à saúde para usuários. Para atender a todas as demandas, o gestor precisa estar preparado para o exercício do cargo designado. Objetivo: Conhecer o perfil dos coordenadores de saúde bucal no Brasil. Material e método: O estudo classifica-se como uma revisão narrativa da literatura. O levantamento da literatura foi realizado no período de Março a Abril de 2019, utilizando-se as bases de dados da Biblioteca Virtual de Saúde, Scielo, PubMed e GoogleAcadêmico com os descritores “Gestão em Saúde”, “Gestor de Saúde”, “Saúde Bucal”, “Assistência Odontológica”, “Sistema Único de Saúde”, “Recursos Humanos em Odontologia”, “Serviços de Saúde Bucal”, “Administração em Saúde Pública” e “Gestão da qualidade”. Foram selecionados trabalhos publicados nos últimos 12 anos em qualquer idioma. Resultados: A partir de sete publicações, identificou-se o perfil sociodemográfico dos gestores predominantemente feminino, na faixa etária de quarenta anos e com formação em Odontologia. Observou-se deficiência na formação profissional e precárias condições de trabalho. Conclusão: Os resultados reforçam a necessidade de fortalecimento da Políticas de Recursos Humanos para o SUS.Descritores: Sistema Único de Saúde; Gestão em Saúde; Saúde Bucal; Recursos Humanos em Odontologia.ReferênciasBatista KT. A gestão em saúde como dilema bioético. Brasília méd. 2009;46(4).Brutscher VJ. Gestão, Direito e Participação no SUS. Rev bras ciênc saúde. 2012;16(3):401-10.Paegle ACRO, Souza EHA, Oliveira PA. Coordenação das Equipes de Saúde Bucal: Avaliação para Melhoria da Qualidade (AMQ). Pesq Bras Odontoped Clin Integr. 2012;12(4):497-503.Leal DL, Martins RC, Carneiro NCR, Abreu MHNG, Werneck MAF, Borges-Oliveira AC. Analysis of the oral health care network development in Minas Gerais state, Brazil. J Public Health Dent. 2019;79(2):154-59.Cunha MLS, Hortale VA. Características dos cursos voltados para a formação em gestão em saúde no Brasil. Saúde Debate. 2017;41:425-40.Lorenzetti J, Lanzoni GMM, Assuiti LFC, Pires DEP, Ramos FRS. Gestão em Saúde no Brasil: diálogos com gestores públicos e privados. Texto Contexto Enferm. 2014;23(2):417-25.Costa MBS, Salazar PEL. Análisis de la Gestión Municipal de los Servicios de Salud. Rev enferm UERJ. 2008;16(4):465-71.Mendes JDV, Bittar OJNV. Perspectivas e desafios da gestão pública no SUS. Rev Fac Ciênc Méd. 2014;16(1):35-9.Ferreira J. Celuppi IC, Baseggio L, Geremia DS, Madureira VSF, Souza JB. Planejamento regional dos serviços de saúde: o que dizem os gestores? Saúde Soc. 2018;27(1):69-79.Pimentel FC, Martelli PJL, Araújo Junior JLAC, Acioli RML, Macedo CLSV. Análise da atenção à saúde bucal na Estratégia de Saúde da Família do Distrito Sanitário VI, Recife (PE). Ciênc saúde coletiva. 2010;15(4):2189-96.Cordeiro AM, Oliveira GM, Rentería JM, Guimarães CA. Revisão Sistemática: uma revisão narrativa. Rev Col Bras Cir. 2007;34(6):428-31.Ferenhof HÁ, Fernandes RF. Desmitificando a revisão de literatura como base para redação científica: Método SSF. Revista ACB. 2016;21(3):550-563.Silva HM. O perfil dos municípios e dos coordenadores de saúde bucal pertencentes à região de Bauru (DIR-X) em relação à atenção básica à saúde (SUS)[dissertação]. Bauru: Faculdade de Odontologia de Bauru – USP; 2007.Martelli PJL, Cabral APS, Pimentel FC, Macedo CLSV, Monteiro IS, Silva SF. Análise do modelo de atenção à saúde bucal em municípios do estado de Pernambuco. Ciênc saúde coletiva. 2008;13(5):1669-1674.Lessa CFM, Vettore MV. Gestão da Atenção Básica em Saúde Bucal no Município de Fortaleza, Ceará, entre 1999 e 2006. Saúde Soc. 2010;19(3):547-56.Yokoyama RT, Sousa MLR, Amaral RC, Wada RS. Conhecimento dos Coordenadores de Saúde Bucal no Estado de São Paulo sobre a Lei 6.050 que regulamenta a fluoretação das águas em sistema de abastecimento público. Odontol Clín-Cient. 2011;10(1):37-41.Cascaes AM, Kamimura LCB, Peres KG, Peres MA. Conhecimento sobre uso de fluoretos em saúde bucal coletiva entre coordenadores municipais de saúde bucal do Estado de Santa Catarina, Brasil. Epidemiol Serv Saúde. 2012;21(1):89-98.Morita MC, Haddad AE, Araújo ME. Perfil Atual e Tendências do Cirurgião-Dentista Brasileiro. Maringá: Dental Press; 2010.Santos ALR, Faler CS. A Rede de Atenção Básica na perspectiva dos usuários do SUS de um município do Médio Alto Uruguai Gaúcho. Unoesc & Ciência – ACBS. 2018;9(1):15-22.Martins RJ, Moimaz SAS, Garbin CAS, Garbin AJI, Lima DC. Percepção dos Coordenadores de Saúde Bucal e Cirurgiões-Dentistas do Serviço Público sobre o Sistema Único de Saúde (SUS). Saúde soc. 2009;18(1):75-82.Gondinho BVC, Guerra LM, Bulgarelli JV, Probst LF, Cortellazzi KL, Possobon RF et al. Percepção de coordenadores de saúde bucal sobre a rede de atenção à saúde bucal. Rev Bras Promoç Saúde. 2018;31(Supl):1-8.Vermelho SC, Figueiredo G. A percepção de secretários municipais de saúde sobre a gestão do trabalho e da educação na rede pública do Sistema Único de Saúde (SUS). Saúde Soc. 2017; 26(2):382-96.Limeira FIR, Rebouças PRM, Rocha EALSS, Catão MHCV. O ensino de gestão nos cursos de graduação em Odontologia no Brasil. Rev ABENO. 2018;18(1):161-69.Stein C, Warmling CM, Tôrres LHN, Rech RS, Martins AB, Pires FS et al. Laboratório no estágio de gestão do SUS: integração ensino, pesquisa e gestão. Rev ABENO. 2018;18(2):166-73.Souza LEPF. O SUS necessário e o SUS possível: estratégias de gestão. Uma reflexão a partir de uma experiência concreta. Ciênc saúde coletiva. 2009;14(3):911-18.Pinafo E, Carvalho BG, Nunes EFPA, Domingos CM, Bonfim MCB. Gestor do SUS em município de pequeno porte no estado do Paraná: perfil, funções e conhecimento sobre os instrumentos de gestão. Rev Saúde Pública Paraná. 2016;17(1):130-37.Knevel R, Gussy MG, Farmer J. Exploratory scoping of the literature on factors that influence oral health workforce planning and management in developing countries. Int J Hyg. 2017;15(2):95-105.Chaves SCL, Cruz DN. Desafios contemporâneos à organização da atenção em saúde bucal na Bahia. Rev baiana saúde pública. 2012;36(3):621-39.Soares FF, Chaves SCL, Cangussu MCT. Governo local e serviços odontológicos: análise da desigualdade na utilização. Cad Saúde Pública. 2015;3193):586-96.Melo LMLL. Análise da organização das ações municipais de saúde bucal na atenção básica [dissertação]. Araçatuba: Faculdade de Odontologia – UNESP; 2016.Cunha EN, Souza MKB. A regionalização da saúde enquanto princípio organizativo para a gestão do SUS. Rev enferm UFPE. 2017; 11(suppl 5):2145-56.Maia Júnior AF. Secretários Municipais de Saúde: o SUS visto pela ponta da corda [tese]. Bauru: Faculdade de Odontologia de Bauru – USP; 2014.Scherer CI, Scherer MDA. Advances and challenges in oral health after a decade of the “Smiling Brazil” Program. Rev Saúde Pública. 2015;49:98.Pessoa TRRF, Castro RD, Freitas CHSM, Reichert APS, Forte FDS. Formação em Odontologia e os estágios supervisionados em serviços públicos de saúde: percepções e vivências de estudantes. Rev ABENO. 2018;18(2):144-55.Silva BFS, Benito GAV. A voz de gestores municipais sobre o acesso à saúde nas práticas de gestão. Ciênc saúde coletiva. 2013;18(8):2189-200.Galavote HS, Franco TB, Freitas PSS, Lima EFA, Garcia ACP, Andrade MAC et al. A gestão do trabalho na estratégia saúde da família: (des)potencialidades no cotidiano do trabalho em saúde. Saúde Soc. 2016;25(4):988-1002.Almeida AB, Alves MS, Leite ICG. Reflexões sobre os desafios da odontologia no sistema único de saúde. Rev APS. 2010;13(1):126-32.França MASA, Freire MCM, Pereira EM, Marcelo VC. Oral health indicators in the Interfederative Pacts of the Unified Health System: development in the 1998-2016 period. Rev Odontol UNESP. 2018;47(1):18-24.Hirooka LB, Catanante GV, Porto HS, Caccia-Bava MCGG. Structural factores for public dental health services in Regional Health Care Network 13: an analysis of the Brazilian National Program for Improving Access and Quality of Primaty Care. Rev Odontol UNESP. 2018;47(1):31-9.Patrício WAC. A visão dos gestores acerca da contribuição do programa de capacitação gerencial realizado no hospital do servidor público municipal [dissertação]. São Paulo: Pontifícia Universidade Católica de Saúde Paulo - PUC; 2011.Xavier EA. A inserção profissional dos trabalhadores de apoio à gestão/administrativos no Sistema Único de Saúde no município de Curitiba, PR [dissertação]. Rio de Janeiro: Escola Nacional de Saúde Pública Sergio Arouca; 2012.Molina-Marím G, Oquendo-Lozano T, Rodríguez-Garzón S, Montoya-Gómez N, Vesga-Gómez C, Lagos-Campos N et al. Gestión del talento humano em salud pública. Un análisis en cinco ciudades colombianas, 2014. Rev Gerenc Polít Salud. 2016;15(30):108-25.Felsky CN, Lima RCD, Garcia ACP, França T, Andrade MAC. Gestão do trabalho na saúde: com a palavra, atores da Estratégia Saúde da Família. Rev Bras Pesq Saúde. 2016;18(1):102-10.Moura DCN, Pinto JR, Aragão AEA. Perfil dos profissionais atuantes na Gestão em Saúde frente ao novo modelo de reorganização do SUS: A regionalização. Tempus, actas de saúde colet. 2016;10(1):75-93.Cunha SGS. A tomada de decisão de gestores da atenção secundária à saúde [dissertação] . Belo Horizonte: Escola de Enfermagem – UFMG; 2016.Andraus SHC, Ferreira RC, Amaral JHL, Werneck MAF. Organization of oral health actions in primary care from the perspective of dental managers and dentists: process of work, planning and social control. RGO Rev Gaúch Odontol. 2017;65(4):335-43.Silva BFS, Wandekoken KD, Dalbello-Araujo M, Benito GAV. A importância do planejamento de gestão na microrregião de saúde de Saúde Mateus (ES). Saúde Debate. 2015;39(104):183-96.
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Admin, Admin, and Dr Mustafa Arslan. "Effect of dexmedetomidine on ischemia-reperfusion injury of liver and kidney tissues in experimental diabetes and hepatic ischemia-reperfusion injury induced rats." Anaesthesia, Pain & Intensive Care, May 9, 2019, 143–49. http://dx.doi.org/10.35975/apic.v0i0.641.

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Background: Reperfusion following ischemia can lead to more injuries than ischemia itself especially in diabetic patients. The aim of this study was to evaluate the effect of dexmedetomidine on ischemia-reperfusion injury (IRI) in rats with have hepatic IRI and diabetes mellitus. Methodology: Twenty-eight Wistar Albino rats were randomised into four groups as control (C), diabetic (DC), diabetic with hepatic ischemia-reperfusion injury (DIR), and diabetic but administered dexmedetomidine followed by hepatic IRI (DIRD) groups. Hepatic tissue samples were evaluated histopathologically by semiquantitative methods. Malondialdehyde (MDA), superoxide dismutase (SOD), glutathion s-transpherase (GST), and catalase (CAT) enzyme levels were investigated in liver and kidney tissues as oxidative state parameters. Results: In Group DIR; hepatocyte degeneration, sinusoidal dilatation, pycnotic nucleus, and necrotic cells were found to be more in rat hepatic tissue; while mononuclear cell infiltration was higher in the parenchyme. MDA levels were significantly lower; but SOD levels were significantly higher in Group DIRD with regard to Group DIR. In the IRI induced diabetic rats’ hepatic and nephrotic tissues MDA levels, showing oxidative injury, were found to be lower. SOD levels, showing early antioxidant activity, were higher. Conclusion: The enzymatic findings of our study together with the hepatic histopathology indicate that dexmedetomidine has a potential role to decrease IRI. Key words: Hepatic ischemia reperfusion injury; Diabetes mellitus; Dexmedetomidine; Rat; MDA; SOD Citation: Sezen SC, Işık B, Bilge M, Arslan M, Çomu FM, Öztürk L, Kesimci E, Kavutçu M. Effect of dexmedetomidine on ischemia-reperfusion injury of liver and kidney tissues in experimental diabetes and hepatic ischemia-reperfusion injury induced rats. Anaesth Pain & Intensive Care 2016;20(2):143-149 Received: 21 November 2015; Reviewed: 10, 24 December 2015, 9, 10 June 2016; Corrected: 12 December 2015; Accepted: 10 June 2016 INTRODUCTİON Perioperative acute tissue injury induced by ischemia-reperfusion is a comman clinical event caused by reduced blood supply to the tissue being compromised during major surgery. Ischemia leads to cellular injury by depleting cellular energy deposits and resulting in accumulation of toxic metabolites. The reperfusion of tissues that have remained in ischemic conditions causes even more damage.1 Furthermore hepatic ischemia-reperfusion injury (IRI) demonstrates a strong relationship with peri-operative acute kidney injury.2 The etiology of diabetic complications is strongly associated with increased oxidative stress (OS). Diabetic patients are known to have a high risk of developing OS or IRI which results with tissue failure.3 The most important role in ischemia and reperfusion is played by free oxygen radicals.1 In diabetes, characterized by hyperglycemia, even more free oxygen radicals are produced due to oxidation of glucose and glycosylation of proteins.3 The structures which are most sensitive to free oxygen radicals in the cells are membrane lipids, proteins, nucleic acids and deoxyribonucleic acids.1 It has been reported that endogenous antioxidant enzymes [superoxide dismutase (SOD), glutathion s-transpherase (GST), catalase (CAT)] play an important role to alleviate IRI.4-8 Also some pharmacological agents have certain effects on IRI.1 The anesthetic agents influence endogenous antioxidant systems and free oxygen radical formation.9-12 Dexmedetomidine is a selective α-2 adrenoceptor agonist agent. It has been described as a useful and safe adjunct in many clinical applications. It has been found that it may increase urine output by considerably redistributing cardiac output, inhibiting vasopressin secretion and maintaining renal blood flow and glomerular filtration. Previous studies demonstrated that dexmedetomidine provides protection against renal, focal cerebral, cardiac, testicular, and tourniquet-induced IRI.13-18 Arslan et al observed that dexmedetomidine protected against lipid peroxidation and cellular membrane alterations in hepatic IRI, when given before induction of ischemia.17 Si et al18 demonstrated that dexmedetomidine treatment results in a partial but significant attenuation of renal demage induced by IRI through the inactivation of JAK/STAT signaling pathway in an in vivo model. The efficacy of the dexmedetomidine for IRI in diabetic patient is not resarched yet. The purpose of this experimental study was to evaluate the biochemical and histological effects of dexmedetomidine on hepatic IRI in diabetic rat’s hepatic and renal tissue. METHODOLOGY Animals and Experimental Protocol: This study was conducted in the Physiology Laboratory of Kirikkale University upon the consent of the Experimental Animals Ethics Committee of Kirikkale University. All of the procedures were performed according to the accepted standards of the Guide for the Care and Use of Laboratory Animals. In the study, 28 male Wistar Albino rats, weighing between 250 and 300 g, raised under the same environmental conditions, were used. The rats were kept under 20-21 oC at cycles of 12-hour daylight and 12-hour darkness and had free access to food until 2 hours before the anesthesia procedure. The animals were randomly separated into four groups, each containing 7 rats. Diabetes was induced by a single intraperitoneal injection of streptozotocin (Sigma Chemical, St. Louis, MO, USA) at a dose of 65 mg/kg body weight. The blood glucose levels were measured at 72 hrs following this injection. Rats were classified as diabetic if their fasting blood glucose (FBG) levels exceeded 250 mg/dl, and only animals with FBGs of > 250 mg/dl were included in the diabetic groups (dia­betes only, diabetes plus ischemia-reperfusion and diabetes plus dexmedetomidine-ischemia-reperfusion). The rats were kept alive 4 weeks after streptozotocin injection to allow development of chronic dia­betes before they were exposed to ischemia-reperfusion.(19) The rats were weighed before the study. Rats were anesthetized with intraperitoneal ketamine 100 mg/kg. The chest and abdomen were shaved and each animal was fixed in a supine position on the operating table. The abdomen was cleaned with 1% polyvinyl iodine and when dry, the operating field was covered with a sterile drape and median laparotomy was performed. There were four experimental groups (Group C (sham-control; n = 7), (Group DC (diabetes-sham-control; n = 7), Group DIR (diabetes-ischemia-reperfusion; n = 7), and Group DIRD (diabetes-ischemia-reperfusion-dexmedetomidine; n = 7). Sham operation was performed on the rats in Group C and Group DC. The sham operation consisted of mobilization of the hepatic pedicle only. The rats in this group were sacrificed 90 min after the procedure. Hepatic I/R injury was induced in Groups DIR and DIRD respectively with hepatic pedicle clamping using a vascular clamp as in the previous study of Arslan et al.(17) After an ischemic period of 45 min, the vascular clamp was removed. A reperfusion period was maintained for 45 min. In Group DIRD, dexmedetomidine hydrochloride 100 μg/kg, (Precedex 100 μg/2 ml, Abbott®, Abbott Laboratory, North Chicago, Illinois, USA) was administrated via intraperitoneal route 30 minutes before surgery. All the rats were given ketamine 100 mg/kg intraperitoneally and intracardiac blood samples were obtained. Preserving the tissue integrity by avoiding trauma, liver and renal biopsy samples were obtained. Biochemical Analysis: The liver and renal tissues were first washed with cold deionized water to discard blood contamination and then homogenized in a homogenizer. Measurements on cell contest require an initial preparation of the tissues. The preparation procedure may involve grinding of the tissue in a ground glass tissue blender using a rotor driven by a simple electric motor. The homogenizer as a tissue blender similar to the typical kitchen blender is used to emulsify and pulverize the tissue (Heidolph Instruments GMBH & CO KGDiax 900 Germany®) at 1000 U for about 3 min. After centrifugation at 10,000 g for about 60 min, the upper clear layer was taken. MDA levels were determined using the method of Van Ye et al,(20) based on the reaction of MDA with thiobarbituric acid (TBA). In the TBA test reaction, MDA and TBA react in acid pH to form a pink pigment with an absorption maximum at 532 nm. Arbitrary values obtained were compared with a series of standard solutions (1,1,3,3-tetraethoxypropane). Results were expressed as nmol/mg.protein. Part of the homogenate was extracted in ethanol/chloroform mixture (5/3 v/v) to discard the lipid fraction, which caused interferences in the activity measurements of T-SOD, CAT and GST activities. After centrifugation at 10.000 x g for 60 min, the upper clear layer was removed and used for the T-SOD, CAT, GST enzyme activity measurement by methods as described by Durak et al21, Aebi22 and Habig et al23 respectively. One unit of SOD activity was defined as the enzyme protein amount causing 50% inhibition in NBTH2 reduction rate and result were expressed in U/mg protein. The CAT activity method is based on the measurement of absorbance decrease due to H2O2 consumption at 240 nm. The GST activity method is based on the measurement of absorbance changes at 340 nm due to formation of GSH-CDNB complex. Histological determinations: Semiquantitative evaluation technique used by Abdel-Wahhab et al(24) was applied for interpreting the structural changes investigated in hepatic tissues of control and research groups. According to this, (-) (negative point) represents no structural change, while (+) (one positive point) represents mild, (++) (two positive points) medium and (+++) (three positive points) represents severe structural changes. Statistical analysis: The Statistical Package for the Social Sciences (SPSS, Chicago, IL, USA) 20.0 softwre was used for the statistical analysis. Variations in oxidative state parameters, and histopathological examination between study groups were assessed using the Kruskal-Wallis test. The Bonferroni-adjusted Mann-Whitney U-test was used after significant Kruskal-Wallis to determine which groups differed from the others. Results were expressed as mean ± standard deviation (Mean ± SD). Statistical significance was set at a p value < 0.05 for all analyses. RESULTS There was statistically significant difference observed between the groups with respect to findings from the histological changes in the rat liver tissue (hepatocyte degeneration, sinüsoidal dilatation, pycnotic nucleus, prenecrotic cell) determined by light microscopy according to semiquantitative evaluation techniques (p < 0.0001). In Group DIR, hepatocyte degeneration was significantly high compared to Group C, Group DC and Group DIRD (p < 0.0001, p < 0.0001, p = 0.002, respectively), (Table 1, Figure 1-4). Similarly, sinüsoidal dilatation was significantly higher in Group DIR (p < 0.0001, p = 0.004, p = 0.015, respectively). Although, pcynotic nucleus was decreased in Group DIRD, it did not make a significant difference in comparison to Group DIR (p = 0.053), (Table 1, Figure 1-4). The prenecrotic cells were significantly increased in Group DIR, with respect to Group C, Group DC and Group DIRD (p < 0.0001, p = 0.004, p < 0.0001, respectively), (Table 1, Figure 1-4). Table 1. The comparison of histological changes in rat hepatic tissue [Mean ± SD)] p**: Statistical significance was set at a p value < 0.05 for Kruskal-Wallis test *p < 0.05: When compared with Group DIR Figure 1: Light microscopic view of hepatic tissue of Group C (control). VC: vena centralis, *: sinusoids. ®: hepatocytes, k: Kupffer cells, G: glycogen granules, mc: minimal cellular changes, Hematoxilen & Eosin x 40 Figure 2: Light-microscopic view of hepatic tissue of Group DC (diabetes mellitus control) (G: Glycogen granules increased in number, (VC: vena centralis, *:sinusoids. ®:hepatocytes, k:Kupffer cells, G: glycogen granules, mc: minimal cellular changes; Hematoxylin & Eosin x 40) Figure 3: Light-microscopic view of hepatic tissue of Group DIR (Diabetes Mellitus and ischemia-reperfusion) (VC: vena centralis, (H) degenerative and hydrophic hepatocytes, (dej) vena centralis degeneration (centrolobar injury) (*): sinusoid dilatation. (←) pycnotic and hyperchromatic nuclei, MNL: mononuclear cell infiltration, (¯) congestion, K: Kupffer cell hyperplasia, (­) vacuolar degeneration (Hematoxylin & Eosin x 40) Figure 4: Light-microscopic view of hepatic tissue of Group DIRD (Diabetes Mellitus and ischemia-reperfusion together with dexmedetomidine applied group) (VC: vena centralis, (MNL) mononuclear cell infiltration, (dej) hydrophilic degeneration in hepatocytes around vena centralis, (conj) congestion, G: glycogen granules, (←) pycnotic and hyperchromatic nuclei, sinusoid dilatation (*) (Hematoxylin & Eosin x 40) Besides, in liver tissue parenchyma, MN cellular infiltration was a light microscopic finding; and showed significant changes among the groups (p < 0.0001). This was significantly higher in Group DIR, compared to Group C, DC, and DIRD (p < 0.0001, p=0.007, p = 0.007, respectively), (Table 1, Figure 1-4). The enzymatic activity of MDA, SOD and GST in hepatic tissues showed significant differences among the groups [(p = 0.019), (p = 0.034). (p = 0.008) respectively]. MDA enzyme activity was significantly incresed in Group DIR, according to Group C and Group DIRD (p = 0.011, p = 0.016, respectively), (Table 2). In Group DIR SOD enzyme activity was lower with respect to Group C and Group DIRD (p = 0.010, p = 0.038, respectively), (Table 2). The GST enzyme activity was significantly higher in Group DIR, when compared to Group C, DC and DIRD (p = 0.007, p = 0.038, p = 0.039, respectively), (Table 2). Table 2. Oxidative state parameters in rat hepatic tissue [Mean ± SD] p**: Statistical significance was set at a p value < 0.05 for Kruskal-Wallis test *p < 0.05: When compared with Group DIR The enzymatic activity of MDA, SOD in renal tissues, showed significant differences among the groups [(p < 0.0001), (p = 0.008) respectively ]. MDA enzyme activity was significantly incresed in Group DIR, according to Group C and Group DIRD (p < 0.0001, p < 0.0001, respectively). Also MDA enzyme activity level was significantly increased in Group DC, in comparison to Group C and Group DIRD (p = 0.003, p = 0.001, respectively), (Table 3). In Group DIR SOD enzyme activity was lower with respect to Group C and Group DIRD (p = 0.032, p = 0.013, respectively), (Table 3). The GST enzyme activity was significantly higher in Group DIR than the other three groups, however; CAT levels were similar among the groups (Table 3). Table 3: Oxidative state parameters in rat nephrotic tissue [Mean ± SD)] p**: Statistical significance was set at a p value < 0.05 for Kruskal-Wallis test *p < 0.05: When compared with Group DIR DISCUSSION In this study, we have reported the protective effect of dexmedetomidine in experimental hepatic and renal IRI model in the rat by investigating the MDA and SOD levels biochemically. Besides, hepatic histopathological findings also supported our report. Ischemic damage may occur with trauma, hemorrhagic shock, and some surgical interventions, mainly hepatic and renal resections. Reperfusion following ischemia results in even more injury than ischemia itself. IRI is an inflammatory response accompanied by free radical formation, leucocyte migration and activation, sinusoidal endothelial cellular damage, deteoriated microcirculation and coagulation and complement system activation.1 We also detected injury in hepatic and renal tissue caused by reperfusion following ischemia in liver. Experimental and clinical evidence indicates that OS is involved in both the pathogenesis and the complications of diabetes mellitus.25,26 Diabetes mellitus is a serious risk factor for the development of renal and cardiovascular disease. It is also related to fatty changes in the liver.27 Diabetes-related organ damage seems to be the result of multiple mechanisms. Diabetes has been associated with increased free radical reactions and oxidant tissue damage in STZ-induced diabetic rats and also in patients.26Oxidative stress has been implicated in the destruction of pancreatic β-cells28 and could largely contribute to the oxidant tissue damage associated with chronic hyperglycemia.29 A number of reports have shown that antioxidants can attenuate the complications of diabetes in patients30 and in experimental models.28,31 This study demonstrated that diabetes causes a tendency to increase the IRI. There is a lot of investigations related to the pharmacological agents or food supplements applied for decreasing OS and IRI. Antioxidant agents paly an important role in IRI by effecting antioxidant system or lessening the formation of ROS. It has been reported that anesthetic agents too, are effective in oxidative stress.1 During surgical interventions, it seems rational to get benefit from anesthetic agents in prevention of OS caused by IRI instead of using other agents. It has been declared that; dexmedetomidine; as an α-2 agonist with sedative, hypnotic properties; is important in prevention of renal, focal, cerebral, cardiac, testicular and tourniquet-induced IRI.13-18 On the other hand Bostankolu et al. concluded that dexmedetomidine did not have an additional protective role for tournique induced IRI during routine general anesthesia.32 In this study; we have shown that dexmedetomidine has a reducing effect in IRI in diabetic rats. Some biochemical tests and histopathological evaluations are applied for bringing up oxidative stress and IRI in the tissues. Reactive oxygen species (ROS) that appear with reperfusion injury damage cellular structures through the process of the lipid peroxidation of cellular membranes and yield toxic metabolites such as MDA.33 As an important intermidiate product in lipid peroxidation, MDA is used as a sensitive marker of IRI.34 ROS-induced tissue injury is triggered by various defense mechanisms.35 The first defence mechanisms include the antioxidant enzymes of SOD, CAT, and GPx. These endogenous antioxidants are the first lines of defence against oxidative stres and act by scavenging potentially damaging free radical moieties.36 There is a balance between ROS and the scavenging capacity of antioxidant enzymes.1-8 In this study, for evaluation of oxidative damage and antioxidant activity, MDS, SOD, GST and CAT levels were determined in liver and kidney tissues. MDA levels in hepatic and renal tissues were higher in Group DIR compared to Group C and Group DIRD. GST levels were higher in Group DIR compared to all the other three groups. When the groups were arranged from highest to lowest order, with respect to CAT levels, the order was; Group DIR, Group DIRD, Group DC and Group C. However, the difference was not significant. The acute phase reactant MDA, as a marker of OS, was found to be high in Group DIR and low in Group DIRD. This could be interpreted as the presence of protective effect of dexmedetomidine in IRI. IRI developing in splanchnic area causes injury also in the other organs.35 Leithead et al showed that clinically significant hepatic IRI demonstrates a strong relationship with peri-operative acute kidney injury.2 In our experimental research that showed correlation to that of research by Leithead et al. After hepatic IRI in diabetic rats renal OS marker MDA levels were significantly more in Group DIR than Group DIRD. In our study, we observed histopathological changes in the ischemic liver tissue and alterations in the level of MDA, SOD, GST and CAT levels which are OS markers. Histopathological changes of the liver tissues are hepatocyt degeneration, sinusoidal dilatation, nuclear picnosis, celluler necrosis, mononuclear cell infiltrationat paranchimal tissue. These histopathological injury scores were significantly lower in the Group DIRD than those in group DIR. LIMITATION Study limitation is there was no negative control group, as this type of surgical intervention is not possible in rats without anesthesia. CONCLUSION The enzymatic findings of our study together with the hepatic histopathology indicate that dexmedetomidine has a potential role to decrease ischemia-reperfusion injury. Conflict of interest and funding: The authors have not received any funding or benefits from industry or elsewhere to conduct this study. Author contribution: ŞCS: Concept, conduction of the study work and manuscript editing; BI: the main author to write the article; MB & MK: biochemical analysis; MA: manuscript writing; FMÇ: helped us with experimental study; LÖ & EK: collection of data REFERENCES Collard CD, Gelman S. Pathophysiology, clinical manifestations, and prevention of ischemia-reperfusion injury. Anesthesiology. 2001;94(6):1133. [PubMed] [Free full text] Leithead JA, Armstrong MJ, Corbett C, Andrew M, Kothari C, Gunson BK, et al. Hepatic ischemia reperfusion injury is associated with acute kidney injury following donation after brain death liver transplantation. Transpl Int. 2013;26(11):1116. doi: 10.1111/tri.12175. [PubMed] [Free full text] Panés J, Kurose I, Rodriguez-Vaca D, Anderson DC, Miyasaka M, Tso P, et al. Diabetes exacerbates inflammatory responses to ischemia-reperfusion. Circulation. 1996;93(1):161. [PubMed] [Free full text] Touyz RM. Reactive oxygen species and angiotensin II signaling in vascular cells-implications in cardiovascular disease. Braz J Med Biol Res. 2004;37:1263. [PubMed] [Free full text] Olivares-Corichi IM, Ceballos G, Ortega-Camarillo C, Guzman-Grenfell AM, Hicks JJ. Reactive oxygen species (ROS) induce chemical and structural changes on human insulin in vitro, including alterations in its immunoreactivity. Front Biosci. 2005;10:834. [PubMed] Witko-Sarsat V, Friedlander M, Capeillere-Blandin C, Nguyen-Khoa T, Nguyen AT, Zingraff J, et al. Advanced oxidation protein products as a novel marker of oxidative stress in uremia. Kidney Int. 1996;49:1304. [PubMed] Harman D. Free radical theory of aging: An update: Increasing the functional life span. Ann N Y Acad Sci. 2006;1067:10. [PubMed] Nita DA, Nita V, Spulber S, Moldovan M, Popa DP, Zagrean AM, Zagrean L. Oxidative damage following cerebral ischemia depends on reperfusion – a biochemical study in rat. J Cell Mol Med. 2001;5:163–170. [PubMed] [Free full text] Annecke T, Kubitz JC, Kahr S, Hilberath JM, Langer K, Kemming GI, et al. Effects of sevoflurane and propofol on ischaemia-reperfusion injury after thoracic-aortic occlusion in pigs. Br J Anaesth. 2007;98(5):581. [PubMed] [Free full text] De Hert SG, Van der Linden PJ, Cromheecke S, Meeus R, Nelis A, Van Reeth V, ten Broecke PW, et al. Cardioprotective properties of sevoflurane in patients undergoing coronary surgery with cardiopulmonary bypass are related to the modalities of its administration. Anesthesiology. 2004;101(2):299. [PubMed] [Free full text] Yuzer H, Yuzbasioglu MF, Ciralik H, Kurutas EB, Ozkan OV, Bulbuloglu E, et al. Effects of intravenous anesthetics on renal ischemia/reperfusion injury. Ren Fail. 2009;31(4):290. [PubMed] [Free full text] Lee HT, Ota-Setlik A, Fu Y, Nasr SH, Emala CW. Differential protective effects of volatile anesthetics against renal ischemia-reperfusion injury in vivo. Anesthesiology. 2004;101(6):1313. [PubMed] [Free full text] Lai YC, Tsai PS, Huang CJ. Effects of dexmedetomidine on regulating endotoxin-induced up-regulation of inflammatory molecules in murine macrophages. J Surg Res. 2009;154(2):212. doi: 10.1016/j.jss.2008.07.010. [PubMed] Yoshitomi O, Cho S, Hara T, Shibata I, Maekawa T, Ureshino H, Sumikawa K. Direct protective effects of dexmedetomidine against myocardial ischemia-reperfusion injury in anesthetized pigs. Shock. 2012;38(1):92. doi: 10.1097/SHK.0b013e318254d3fb. [PubMed] Jolkkonen J, Puurunen K, Koistinaho J, Kauppinen R, Haapalinna A, Nieminen L, et al. Neuroprotection by the alpha2-adrenoceptor agonist, dexmedetomidine, in rat focal cerebral ischemia. Eur J Pharmacol. 1999;372(1):31. [PubMed] Kocoglu H, Ozturk H, Ozturk H, Yilmaz F, Gulcu N. Effect of dexmedetomidine on ischemia-reperfusion injury in rat kidney: a histopathologic study. Ren Fail. 2009;31(1):70. doi: 10.1080/08860220802546487. [PubMed] Arslan M, Çomu FM, Küçük A, Öztürk L, Yaylak F. Dexmedetomidine protects against lipid peroxidation and erythrocyte deformability alterations in experimental hepatic ischemia reperfusion injury. Libyan J Med. 2012;7. doi: 10.3402/ljm.v7i0.18185 [PubMed] [Free full text] Si Y, Bao H, Han L, Shi H, Zhang Y, Xu L, et al. Dexmedetomidine protects against renal ischemia and reperfusion injury by inhibiting the JAK/STAT signaling activation. J Transl Med. 2013;11(1):141. doi: 10.1186/1479-5876-11-141. [PubMed][Free full text] Türeci E, İş M, Üzüm G, Akyüz F, Ulu MO, Döşoğlu M, et al. Alterations in blood-brain barrier after traumatic brain injury in streptozotocin-induced diabetic rats. J Nervous Sys Surgery 2009;2(2):79. [Free full text] Van Ye TM, Roza AM, Pieper GM, Henderson J Jr, Johnson JP, Adams MB. Inhibition of intestinal lipid peroxidation does not minimize morphological damage. J Surg Res 1993;55:553. [PubMed] Durak I, Canbolat O, Kavutcu M, Öztürk HS, Yurtarslanı Z. Activities of total, cytoplasmic and mihochondrial superoxide dismutase enzymes in sera and pleural fluids from patient with lung cancer. J Clin Lab Anal 1996;10:17. [PubMed] Aebi H. Catalase. In: H.U.Bergmeyer (Ed): Methods of Enzymatic Analysis, Academic Press , New York and London, 1974;pp.673-677. Habig WH, Pabst MJ, Jakoby WB. Glutathione S-transferases. The first enzymatic step in mercapturic acid formation. J Biol Chem 1974;249:7130. [PubMed] [Free full text] Abdel-Wahhab MA, Nada SA, Arbid MS. Ochratoxicosis: Prevention of developmental toxicity by L-methionine in rats. J Appl Toxicol 1999;19:7. [PubMed] Wolff SP. Diabetes mellitus and free radicals: free radicals, transition metals and oxidative stress in the aetiology of diabetes mellitus and complications. Br Med Bull. 1993;49:642. [PubMed] [Free full text] West IC. Radicals and oxidative stress in diabetes. Diabet Med. 2000;17:171–180. [PubMed] Wanless IR, Lentz JS. Fatty liver hepatitis (steatohepatitis) and obesity: an autopsy study with analysis risk factors. Hepatology. 1990;12:1106. [PubMed] Hotta M, Tashiro F, Ikegami H, Niwa H, Ogihara T, Yodoi J, Miyazaki J. Pancreatic cell-specific expression of thioredoxin, an antioxidative and antiapoptotic protein, prevents autoimmune and streptozotocin-induced diabetes. J Exp Med. 1998;188:1445. [PubMed] [Free full text] Baynes JW. Role of oxidative stress in the development of complications in diabetes. Diabetes. 1991;40:405. [PubMed] Borcea V, Nourooz-Zadeh J, Wolff SP, Klevesath M, Hofmann M, Urich H, et al. α-Lipoic acid decreases oxidative stress even in diabetic patients with poor glycemic control and albuminuria. Free Radic Biol Med. 1999;26:1495. [PubMed] Fitzl G, Martin R, Dettmer D, Hermsdorf V, Drews H, Welt K. Protective effect of ginkgo biloba extract EGb 761 on myocardium of experimentally diabetic rats, I: ultrastructural and biochemical investigation on cardiomyocytes. Exp Toxicol Pathol. 1999;51:189. [PubMed] Bostankolu E, Ayoglu H, Yurtlu S, Okyay RD, Erdogan G, Deniz Y, et al. Dexmedetomidine did not reduce the effects of tourniquet-induced ischemia-reperfusion injury during general anesthesia. Kaohsiung J Med Sci. 2013;29(2):75. doi: 10.1016/j.kjms.2012.08.013. [PubMed] [Free full text] Wakai A, Wang JH, Winter DC, Street JT, O’Sullivan RG, Redmond HP. Tourniquet-induced systemic inflammatory response in extremity surgery. J Trauma 2001;51:922. [PubMed] Concannon MJ, Kester CG, Welsh CF, Puckett CL. Patterns of free-radical production after tourniquet ischemia implications for the hand surgeon. Plast Reconstr Surg 1992;89:846. [PubMed] Grisham MB, Granger DN. Free radicals: reactive metabolites of oxygen as mediators of postischemic reperfusion injury. In: Martson A, Bulkley GB, Fiddian-Green RG, Haglund U, editors. Splanchnic İschemia and Multiple Organ Failure. St Louis, MO: Mosby;1989. pp. 135–144. Mccard JM. The evolution of free radicals and oxidative stress. Am J Med 2000;108:652. [PubMed]
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Book chapters on the topic "SERV.SOCIALE E SC.FORM"

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STINGHEN TONET, NATÁLIA, and IAGO WEBER PITZ. "VAMOS FALAR SOBRE SEXUALIDADE?: O DIÁLOGO EM AMBIENTE ESCOLAR COMO FERRAMENTA PARA A PROTEÇÃO FÍSICA E EMOCIONAL DE CRIANÇAS E ADOLESCENTES." In Itinerários de resistência: pluralidade e laicidade no Ensino de Ciências e Biologia. Editora Realize, 2021. http://dx.doi.org/10.46943/viii.enebio.2021.01.553.

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NESTE DOCUMENTO, APRESENTA-SE A EXPERI?NCIA DO GRUPO PIBID BIOLOGIA UFSC NO DESENVOLVIMENTO DA ATIVIDADE ?VAMOS FALAR SOBRE SEXUALIDADE??, REALIZADA COM AS TURMAS DE 8? ANO, NA DISCIPLINA DE CI?NCIAS, EM UMA ESCOLA RURAL DO MUNIC?PIO DE FLORIAN?POLIS/SC. AQUI, EXP?E-SE A MOTIVA??O E A FORMA DE ORGANIZA??O E DID?TICA ESCOLHIDA PARA CRIA??O DE UM AMBIENTE DE EMPATIA E ACOLHIMENTO, ONDE OS ALUNOS PUDESSEM EXPOR SEUS MEDOS E D?VIDAS, A FIM DE QUE SE INFORMASSEM E SA?SSEM CERTOS DE SEUS DIREITOS, DEVERES E LIBERDADES INDIVIDUAIS, PARA PROMO??O DE RESPEITO PARA CONSIGO E COM OS DEMAIS, NO ?MBITO DA SA?DE E DO BEM-ESTAR F?SICO E EMOCIONAL. OS RESULTADOS POSITIVOS OBTIDOS NA ATIVIDADE REFOR?ARAM A NECESSIDADE DE DI?LOGOS ABERTOS, E O PAPEL SOCIAL DA ESCOLA COMO PROMOTORA DESTES. PARA AL?M DO ?MBITO FISIOL?GICO, A EDUCA??O SEXUAL DEVE SER TRATADA PELA ESCOLA ATRAV?S DA ESFERA DAS RELA??ES SOCIAIS E CULTURAIS DA SOCIEDADE.
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Conference papers on the topic "SERV.SOCIALE E SC.FORM"

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Victoria, Isabel Cristina Moreira, Attilio Bolivar Ourives de Figueiredo, Eliete Auxiliadora Assunção Ourives, Luiz Fernando Gonçalves de Figueiredo, Giovana De Freitas Rabelo Ribeiro, and Francisco Gómez Castro. "A COMPREENSÃO SISTÊMICA E O PENSAMENTO DO DESIGN PARA O DESENVOLVIMENTO DE PRODUTOS PARA A CULTURA SLOW FOOD E DE PRATICAS COLABORATIVAS." In Systems & Design 2017. Valencia: Universitat Politècnica València, 2017. http://dx.doi.org/10.4995/sd2017.2017.6645.

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RESUMO A sociedade atual vive em um contexto tumultuoso, sendo comum as pessoas viverem de forma mais estressadas, se alimentando mal e convivendo cada vez menos com as pessoas, perdendo oportunidades de fazer e manter relacionamentos pessoais. Como este estilo de vida está saturado, gerando problemas de saúde aos indivíduos, existem diversos estudos que comprovam a tendência de que as pessoas buscarão um melhor aproveitamento do seu tempo, com um maior contato com a natureza, dando valor ao seu próprio bem-estar, prestando mais atenção no que consome e em como consome, assim como a valorização do prazer de estar em um meio social. Nesse contexto, o objetivo deste trabalho é contribuir por meio da visão sistêmica e do design, o incentivo e a prática da filosofia Slow Food, e dessa forma, promover a preocupação com uma saudável forma de alimentação e a ação colaborativa entre as pessoas, em que um indivíduo possa cooperar com o outro, resgatando o convívio e socialização. Assim, pretende-se atuar em pequenas unidades urbanas externas, como prédios, condomínios, praças e avenidas com intuito de criação de um artefato que motive a prática dessa filosofia, assim como impulsione também as práticas colaborativas nestes locais, buscando a integração social e desenvolvimento econômico e ambiental, atendendo os princípios da sustentabilidade e o desenvolvimento local. O método de pesquisa usado é descritivo, em que se observou e analisou as situações e relações dos indivíduos, tanto de forma individual quanto as relações em sociedade. Os instrumentos escolhidos para coleta de dados foram o questionário, entrevistas e observações abertas, feitas informalmente ao decorrer das entrevistas. Neste trabalho integrou-se dois métodos de projeto, a ferramenta HCD/IDEO (Human Centered Design - Design Centrado no Ser Humano), usado como base, com técnicas para o entendimento dos desejos e necessidades da comunidade estudada e o Guia de projeto NASDesign/UFSC (Núcleo de Abordagem Sistêmica do Design/Universidade Federal de Santa Catarina), dividido em três fases: Sentir, Agir e Realizar, como complementação. Ao final, conclui-se que o modelo físico do produto proposto atende uma lista de requisitos divididos em três grande grupo: requisitos de produto, referentes à forma, materiais e texturas do objeto; requisitos do usuário, referente a necessidade entendida a partir do tipo de ambiente em que o produto está, e de como ele está sendo usado e aos requisitos do contexto de uso, que consiste nas necessidades do usuário observado durante a pesquisa.Palavras Chaves: design de produto, slow food, sustentabilidade. REFERÊNCIAS ANDRADE, Aurélio L. et al. Pensamento sistêmico: caderno de campo: o desafio das mudanças sustentada nas organizações e na sociedade. Porto Alegre: Bookman, 2006. AROS, Kammiri Corinaldesi. Elicitação do processo projetual do Núcleo de Abordagem Sistêmica do Design da Universidade Federal de Santa Catarina. Orientador: Luiz Fernando Gonçalves de Figueiredo – Florianópolis, SC, 2016. BARBOSA FILHO, Antonio Nunes. Projeto e Desenvolvimento de Produtos - São Paulo: Editora Atlas S.A. - 2009. BERTALANFFY, Ludwig Von. Teoria geral dos sistemas. 3.ed. Petrópolis: Vozes, 2008. BEST, Kathryn. Fundamentos de gestão do design. Porto Alegre: Bookman, 2012. 208 p. BISTAGNINO, Luigi. Design sistêmico: uma abordagem interdisciplinar para a inovação. p.13-30. In: BOAS, Eduardo Villas. Perfils de consumo: VALS2 aponta oito tipos de consumidores. Disponível em: &lt; http://www.audaces.com/br/educacao/falando-de-educacao/2013/10/16/perfis-de-consumo-vals2-aponta-oito-tipos-de-consumidores-2&gt;. Acesso em: 7 out. 2016. BRUNDTLAND, Gro Harlem. Nosso futuro comum: Comissão Mundial sobre Meio Ambiente e Desenvolvimento. 2a. ed. Rio de Janeiro: FGV, 1991. BRUNEL, Felipe Kanarek; O design estratégico em nível metaprojetual como suporte para a inovação social: o caso slow food, p. 202-210 . In: Anais do 5º Simpósio Brasileiro de Design Sustentável [=Blucher Design Proceedings, v.2, n.5]. São Paulo: Blucher, 2016. ISSN 2318-6968, DOI 10.5151/despro-sbds15-2st701b CAPELLO, Giuliana. Slow Life: vida mais calma, lenta e confortável. Planeta Sustentável: 16 set 2008. Disponível em: &lt;http://planetasustentavel.abril.com.br/blog/gaiatos-e-gaianos/109647/&gt;. Acesso em: 4 out. 2016. CAPRA, Fritjof. Teia da vida: uma nova compreensão científica dos sistemas vivos. São Paulo: Cultrix, 1998 CARDOSO, Rafael. Uma Introdução à História do Design. São Paulo: Edgard Blucher, 2008. 56. COGO, Rodrigo. Tendências Globais de Consumo. Disponível em: &lt; http://www.aberje.com.br/blogs/post/tendencias-globais-de-consumo-para-2016/&gt;. Acesso em: 1 nov. 2016. DEHEINZELIN, Lala. Desejável Mundo novo: vida sustentável, diversa e criativa em 2042. 1ª edição. São Paulo, SP | 2012 ERLHOFF, Michael; MARSHALL, Timothy (Ed.) Design Dictionary: Perspectives on Design Terminology. Basel, Switzerland: Birkhauser Verlang Ag, 2008. (Board of International Research in Design). GIL, A. C. Como elaborar projetos de pesquisa. 4. ed. São Paulo: Atlas, 2010. ICSID. Definition of Design. About ICSID: 2013. Disponível em: &lt;http://www.icsid.org/about/about/articles31.htm&gt;. Acesso em: 04 out. 2016. IDEO. HCD: Human Centered Design - kit de ferramentas. 2. ed. 2010. KRUCKEN, L. Design e Território: valorização de identi- dades e produtos locais. São Paulo: Studio Nobel, 2009. KRUCKEN, L.; TRUSEN, C. A comunicação da sustentabilidade em produtos e serviços. In: DE MORAES, D., KRUCKEN, L. Design e Sustentabilidade. Coleção Cadernos de Estudos Avançados em Design, Belo Horizonte: EdUEMG, 2009. KUEHR, R. Environmental technologies: from a misleading interpretations to an operational categorization and definition. Journal of Cleaner Production, 2007. MANZINI, Ezio. Design para a inovação social e sustentabilidade: Comunidades criativas, organizações colaborativas e novas redes projetuais. Rio de Janeiro: E-papers, 2008. 104 p. (Caderno do Grupo de Altos Estudos do PEP/UFRJ; v.1). MANZINI, Ezio. Design, when everbody designs: an introduction to design for social innovattion. Cambridge: MIT Press Book, 2015. 241p. MANZINI, Ezio. Making Things Happen: Social Innovation and Design. Design Issues: v.30 n.1, 2014. MANZINI, Ezio; VEZZOLI, Carlo. O desenvolvimento de produtos sustentáveis: os requisitos ambientais dos produtos industriais. São Paulo: Edusp – Editora da Universidade de São Paulo, 2008. MARCONI, M. A.; Lakatos, E. M. Fundamentos de metodologia científica. São Paulo: Atlas, 2007. MELO FILHO, Álvaro de. Designing marketing. Fragmentos de Cultura, Goiânia, 2009. Disponível em: seer.ucg.br/index.php/fragmentos/article/viewFile/994/696. Acesso em: 14/04/2011. MORARES, Dijon de. Metaprojeto: o design do design. São Paulo: Blucher, 2010. MORARES, Dijon de; KRUCKEN, Lia. Cadernos de estudos avançados em design: Sustentabilidade II. Barbacena: EdUEMG, 2009. 79p. MOZOTA, B. B. Gestão do design: usando o design para construir valor de marca e inovação corporativa. Porto Alegre: Bookman, 2011. POTTER, N. Qué es un diseñador: objetos, lugares,mensajes. Buenos Aires: Paidós, 1999. REID, Mariana. A contribuição do design na motivação da prática do Slow Food; Florianopolis,SC, 2014. 149 p. RICHARDSON, R. J. Pesquisa social: métodos e técnicas. 3 ed. São Paulo: Atlas, 2008. Slow Food Brasil, 2013. Disponível em: &lt;http://www.slowfoodbrasil.com/&gt;. Acesso em: 4 out. 2016. Slow Moviment Portugal, 2014. Disponível em: &lt;http://www.slowmovementportugal.com/&gt; Acesso em: 4 de out. 2016. Slow Moviment, 2016. Disponível em &lt;http://www.slowmovement.com/slow_living.php&gt; Acesso em: 4 de out. 2016. STICKDORN,Marc. Isto é design thinking de serviços/ Marc Stickdorn, Jakob Schneider e coautores ; tradução: Mariana Bandarra ; revisão técnica : Clarissa Biolchini. Porto Alegre : Bookman, 2014. SUDJIC, Deyan. A Linguagem das Coisas. Rio de Janeiro: Intrínseca, 2010. THACKARA, John. Plano B: o design e as alternativas viáveis em um mundo complexo - tradução Cristina Yamagami - São Paulo : Saraiva : Versar, 2008. 299 p. VALENTE, Edison. Slow Design. Revista Planeta: Ambiente: out.2013. Disponível em: &lt;http://revistaplaneta.terra.com.br/secao/ambiente/slow-design&gt;. Acesso em: 30 out. 2016. 58 VEZZOLI, Carlo. Design de sistemas para a sustentabilidade: teoria, métodos e ferramentas para o design sustentável de sistemas de satisfação. Salvador: EDUFUBRA, 2010. 343p.
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