Análise do conhecimento dos discentes de ciências contábeis acerca dos red flags no processo investigativo da fraude

Objetivo: A presente pesquisa tem por objetivo analisar as percepções dos discentes de Ciências Contábeis, das universidades públicas da cidade de Mossoró/RN, sobre os red flags no processo investigativo de fraude contábil. Metodologia: A amostra foi composta por 90 discentes de duas universidades públicas. A coleta de dados ocorreu através de questionário, que dispôs de 45 red flags, divididos em seis grupos, avaliados na escala do tipo Likert. Para cada ‘bandeira vermelha’, foi atribuído um nível de conhecimento, sendo: Não possui conhecimento (0), Muito baixo (1), Baixo (2), Médio (3), Alto (4) e Muito alto (5). Posteriormente, para a análise dos resultados, utilizou-se estatística descritiva, com cálculo da média, mediana, moda e desvio padrão. Resultados: A interpretação dos achados, evidenciaram que os acadêmicos compreendem à nível “médio” os sinalizadores de fraudes relacionados aos relatórios contábeis e serviços de auditoria independente. Nesse sentido, comparando as médias, percebe-se que discentes têm maior percepção de conhecimento acerca dos registros inadequados, arquivos incompletos, ajustes excessivos na contabilidade e transações não registradas. Além disso, os estudantes também percebem, em grau “médio”, a influência do caráter e ética dos agentes de recursos (gestores) na elaboração e repassem informacional. Contudo, apresentam déficits quanto ao entendimento dos red flags associados ao segmento de mercado o qual estão inseridas as entidades. Contribuições do Estudo: O avanço que o presente estudo proporciona é acentuar a discussão relativa ao nível de domínio, dos estudantes, sobre as fraudes financeiras que incorrem em prejuízos para as entidades. Desse modo, a relevância desta pesquisa é expor os déficits autoavaliados pelos graduandos de Contabilidade, quanto aos red flags no ambiente organizacional, concedendo resultados que fomentem as coordenações dos Cursos a mitigarem os déficits decorrentes de baixos níveis de conhecimento acerca dos indicadores de fraude

Macrophage Trafficking as Key Mediator of Adenine-Induced Kidney Injury

Macrophages play a special role in the onset of several diseases, including acute and chronic kidney injuries. in this sense, tubule interstitial nephritis (TIN) represents an underestimated insult, which can be triggered by different stimuli and, in the absence of a proper regulation, can lead to fibrosis deposition. Based on this perception, we evaluated the participation of macrophage recruitment in the development of TIN. Initially, we provided adenine-enriched food to WT and searched for macrophage presence and action in the kidney. Also, a group of animals were depleted of macrophages with the clodronate liposome while receiving adenine-enriched diet. We collected blood and renal tissue from these animals and renal function, inflammation, and fibrosis were evaluated. We observed higher expression of chemokines in the kidneys of adenine-fed mice and a substantial protection when macrophages were depleted. Then, we specifically investigated the role of some key chemokines, CCR5 and CCL3, in this TIN experimental model. Interestingly, CCR5 KO and CCL3 KO animals showed less renal dysfunction and a decreased proinflammatory profile. Furthermore, in those animals, there was less profibrotic signaling. in conclusion, we can suggest that macrophage infiltration is important for the onset of renal injury in the adenine-induced TIN.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Instituto Nacional de Ciencia e Tecnologia de Fluidos Complexos (INCT Complex Fluids)Univ São Paulo, Inst Biomed Sci, Dept Immunol, Lab Transplantat Immunobiol, BR-05508900 São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, Lab Clin & Expt Immunol, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biophys, BR-04023062 São Paulo, BrazilUniv São Paulo, Inst Chem, Dept Biochem, BR-05508000 São Paulo, BrazilUniv São Paulo, Sch Med Ribeirao Preto, Dept Biochem & Immunol, BR-14049900 Ribeirao Preto, SP, BrazilUniversidade Federal de São Paulo, Div Nephrol, Lab Clin & Expt Immunol, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biophys, BR-04023062 São Paulo, BrazilFAPESP: 2009/54474-8FAPESP: 2012/02270-2FAPESP: 2013/25010-9Web of Scienc

MyD88 Signaling Pathway Is Involved in Renal Fibrosis by Favoring a T(H)2 Immune Response and Activating Alternative M2 Macrophages

Inflammation contributes to the pathogenesis of chronic kidney disease (CKD). Molecules released by the inflamed injured tissue\ud can activate toll-like receptors (TLRs), thereby modulating macrophage and CD4+ T-cell activity. We propose that in renal fibrogenesis,\ud M2 macrophages are recruited and activated in a T helper subset 2 cell (TH2)-prone inflammatory milieu in a MyD88-\ud dependent manner. Mice submitted to unilateral ureteral ligation (UUO) demonstrated an increase in macrophage infiltration with\ud collagen deposition after 7 d. Conversely, TLR2, TLR4 and MyD88 knockout (KO) mice had an improved renal function together with\ud diminished TH2 cytokine production and decreased fibrosis formation. Moreover, TLR2, TLR4 and MyD88 KO animals exhibited less M2\ud macrophage infiltration, namely interleukin (IL)-10+ and CD206+ CD11bhigh cells, at 7 d after surgery. We evaluated the role of a TH2\ud cytokine in this context, and observed that the absence of IL-4 was associated with better renal function, decreased IL-13 and TGF-\ud β levels, reduced arginase activity and a decrease in fibrosis formation when compared with IL-12 KO and wild-type (WT) animals.\ud Indeed, the better renal outcomes and the decreased fibrosis formation were restricted to the deficiency of IL-4 in the hematopoietic\ud compartment. Finally, macrophage depletion, rather than the absence of T cells, led to reduced lesions of the glomerular filtration\ud barrier and decreased collagen deposition. These results provide evidence that future therapeutic strategies against renal\ud fibrosis should be accompanied by the modulation of the M1:M2 and TH1:TH2 balance, as TH2 and M2 cells are predictive of fibrosis\ud toward mechanisms that are sensed by innate immune response and triggered in a MyD88-dependent pathway.Brazilian Foundation - FAPESP (Fundacao de Apoio a Pesquisa do Estado de Sao Paulo) [07/07139-3, 10/52180-4]Brazilian Foundation FAPESP (Fundacao de Apoio a Pesquisa do Estado de Sao Paulo)International Associated Laboratory (CNPq/Inserm)International Associated Laboratory (CNPq/Inserm)National Institute of Science and Technology (INCT)National Institute of Science and Technology (INCT