A produção em economia da saúde no Brasil: estudo bibliométrico de 1988-2013

A Economia da Saúde (ES) é uma área de conhecimento que tem apresentado nas últimas décadas importantes avanços para a melhoria organizacional e estrutural da gestão pública do Sistema Único de Saúde (SUS). Este estudo bibliométrico teve como objetivo analisar as características da produção de artigos científicos relacionados à ES publicados no período de 1988 a 2013 nas bases de dados SCIELO, LILACS e MEDLINE, Brasil. Foram utilizados os operadores boleanos and e or no cruzamento de palavras-chave, escolhidas a partir dos cinco eixos centrais de pesquisa: a) Saúde e Desenvolvimento Econômico; b) Regulação Econômica em Saúde; c) Alocação de Recursos; d) Eficiência das ações e Serviços de Saúde; e, e) Financiamento das Ações e Serviços de Saúde, estas também foram utilizadas para categorização e análise. A amostra analisada contou com um total de 82 artigos. Os resultados apontam as fragilidades na produção científica, principalmente no eixo B e D e apresentaram predominância nos eixos C e E, os periódicos de maior publicação foram aqueles com maior qualificação na Saúde Coletiva.  Há predomínio nas publicações provenientes da região Sudeste. A ES representa uma área interdisciplinar que carece de políticas de incentivo em pesquisas que desenvolvam novos conhecimentos e práticas de gestão pública do SUS e estimulem o processo de consolidação desta área de conhecimento.

A produção em economia da saúde no Brasil: estudo bibliométrico de 1988-2013

A Economia da Saúde (ES) é uma área de conhecimento que tem apresentado nas últimas décadas importantes avanços para a melhoria organizacional e estrutural da gestão pública do Sistema Único de Saúde (SUS). Este estudo bibliométrico teve como objetivo analisar as características da produção de artigos científicos relacionados à ES publicados no período de 1988 a 2013 nas bases de dados SCIELO, LILACS e MEDLINE, Brasil. Foram utilizados os operadores boleanos and e or no cruzamento de palavras-chave, escolhidas a partir dos cinco eixos centrais de pesquisa: a) Saúde e Desenvolvimento Econômico; b) Regulação Econômica em Saúde; c) Alocação de Recursos; d) Eficiência das ações e Serviços de Saúde; e, e) Financiamento das Ações e Serviços de Saúde, estas também foram utilizadas para categorização e análise. A amostra analisada contou com um total de 82 artigos. Os resultados apontam as fragilidades na produção científica, principalmente no eixo B e D e apresentaram predominância nos eixos C e E, os periódicos de maior publicação foram aqueles com maior qualificação na Saúde Coletiva.  Há predomínio nas publicações provenientes da região Sudeste. A ES representa uma área interdisciplinar que carece de políticas de incentivo em pesquisas que desenvolvam novos conhecimentos e práticas de gestão pública do SUS e estimulem o processo de consolidação desta área de conhecimento.

IL-23–responsive innate lymphoid cells are increased in inflammatory bowel disease

Increased numbers of innate lymphoid cells in patients with inflammatory bowel disease

NOX1 loss-of-function genetic variants in patients with inflammatory bowel disease.

Genetic defects that affect intestinal epithelial barrier function can present with very early-onset inflammatory bowel disease (VEOIBD). Using whole-genome sequencing, a novel hemizygous defect in NOX1 encoding NAPDH oxidase 1 was identified in a patient with ulcerative colitis-like VEOIBD. Exome screening of 1,878 pediatric patients identified further seven male inflammatory bowel disease (IBD) patients with rare NOX1 mutations. Loss-of-function was validated in p.N122H and p.T497A, and to a lesser degree in p.Y470H, p.R287Q, p.I67M, p.Q293R as well as the previously described p.P330S, and the common NOX1 SNP p.D360N (rs34688635) variant. The missense mutation p.N122H abrogated reactive oxygen species (ROS) production in cell lines, ex vivo colonic explants, and patient-derived colonic organoid cultures. Within colonic crypts, NOX1 constitutively generates a high level of ROS in the crypt lumen. Analysis of 9,513 controls and 11,140 IBD patients of non-Jewish European ancestry did not reveal an association between p.D360N and IBD. Our data suggest that loss-of-function variants in NOX1 do not cause a Mendelian disorder of high penetrance but are a context-specific modifier. Our results implicate that variants in NOX1 change brush border ROS within colonic crypts at the interface between the epithelium and luminal microbes

The role of the IL23/IL17 pathway in inflammatory bowel disease

The aetiology of IBD is unknown, but available evidence suggests that an aberrant immune response towards the commensal microbial flora is responsible for intestinal inflammation in genetically susceptible individuals. Studies from animal models of intestinal inflammation have greatly advanced our understanding of the immunological basis of IBD. However, translation of results from animal research into human studies is essential in order to improve treatment options and patient quality of life. In this thesis we present the successful introduction of translational studies on human tissue in our laboratory. In particular, we evaluated the role of the IL23/IL17 pathway in the human immune response and its role in IBD. IL23-driven inflammation has been primarily linked to its activity on Th-17 cells; however, work from our laboratory has identified a novel population of IL23-responsive ILC, which are responsible for innate colitis in mice. Here we have analyzed the role of IL23-responsive innate cells in IBD. Our results show increased expression of Th-17 signature genes amongst intestinal CD3- cells in patients with IBD. Furthermore, we observed a marked and selective increase in IL17 producing CD56- ILC in the inflamed intestine of patients with CD. ILC may contribute to intestinal inflammation through secretion of cytokines, such as IL17A and IL17F, and recruitment of other inflammatory cells, representing a novel tissue-specific target for the treatment of IBD. In addition, we present here our preliminary data on the characterization of human intestinal and systemic DC populations. In particular, we aimed to evaluate if in the context of the intestinal microenvironment DC develop specific regulatory features, as observed in murine CD103+ DC. We show that human intestinal DC populations exhibit specific regulatory properties, such as expression of genes associated with TGF-β and RA activity. Furthermore, CD103+ DC are present in the human gut and are characterized by tolerogenic markers. Remarkably, patients with IBD have reduced frequencies of intestinal CD103+ DC, which display a more pro-inflammatory phenotype. Alteration in DC subset composition and functional activity may result in a distort balance between immune effector and regulatory responses, promoting the development of intestinal inflammation.</p

The role of the IL23/IL17 pathway in inflammatory bowel disease

The aetiology of IBD is unknown, but available evidence suggests that an aberrant immune response towards the commensal microbial flora is responsible for intestinal inflammation in genetically susceptible individuals. Studies from animal models of intestinal inflammation have greatly advanced our understanding of the immunological basis of IBD. However, translation of results from animal research into human studies is essential in order to improve treatment options and patient quality of life. In this thesis we present the successful introduction of translational studies on human tissue in our laboratory. In particular, we evaluated the role of the IL23/IL17 pathway in the human immune response and its role in IBD. IL23-driven inflammation has been primarily linked to its activity on Th-17 cells; however, work from our laboratory has identified a novel population of IL23-responsive ILC, which are responsible for innate colitis in mice. Here we have analyzed the role of IL23-responsive innate cells in IBD. Our results show increased expression of Th-17 signature genes amongst intestinal CD3- cells in patients with IBD. Furthermore, we observed a marked and selective increase in IL17 producing CD56- ILC in the inflamed intestine of patients with CD. ILC may contribute to intestinal inflammation through secretion of cytokines, such as IL17A and IL17F, and recruitment of other inflammatory cells, representing a novel tissue-specific target for the treatment of IBD. In addition, we present here our preliminary data on the characterization of human intestinal and systemic DC populations. In particular, we aimed to evaluate if in the context of the intestinal microenvironment DC develop specific regulatory features, as observed in murine CD103+ DC. We show that human intestinal DC populations exhibit specific regulatory properties, such as expression of genes associated with TGF-β and RA activity. Furthermore, CD103+ DC are present in the human gut and are characterized by tolerogenic markers. Remarkably, patients with IBD have reduced frequencies of intestinal CD103+ DC, which display a more pro-inflammatory phenotype. Alteration in DC subset composition and functional activity may result in a distort balance between immune effector and regulatory responses, promoting the development of intestinal inflammation.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Innate Lymphoid Cells in Intestinal Inflammation

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the intestine that encompasses Crohn’s disease (CD) and ulcerative colitis. The cause of IBD is unknown, but the evidence suggests that an aberrant immune response toward the commensal bacterial flora is responsible for disease in genetically susceptible individuals. Results from animal models of colitis and human studies indicate a role for innate lymphoid cells (ILC) in the pathogenesis of chronic intestinal inflammation in IBD. ILC are a population of lymphocytes that are enriched at mucosal sites, where they play a protective role against pathogens including extracellular bacteria, helminthes, and viruses. ILC lack an antigen-specific receptor, but can respond to environmental stress signals contributing to the rapid orchestration of an early immune response. Several subsets of ILC reflecting functional characteristics of T helper subsets have been described. ILC1 express the transcription factor T-bet and are characterized by secretion of IFNγ, ILC2 are GATA3+ and secrete IL5 and IL13 and ILC3 depend on expression of RORγt and secrete IL17 and IL22. However, ILC retain a degree of plasticity depending on exposure to cytokines and environmental factors. IL23 responsive ILC have been implicated in the pathogenesis of colitis in several innate murine models through the production of IL17, IFNγ, and GM-CSF. We have previously identified IL23 responsive ILC in the human intestine and found that they accumulate in the inflamed colon and small bowel of patients with CD. Other studies have confirmed accumulation of ILC in CD with increased frequencies of IFNγ-secreting ILC1 in both the intestinal lamina propria and the epithelium. Moreover, IL23 driven IL22 producing ILC have been shown to drive bacteria-induced colitis-associated cancer in mice. Interestingly, our data show increased ILC accumulation in patients with IBD and primary sclerosing cholangitis, who carry an increased risk of developing colorectal cancer. ILC may play an important amplifying role in IBD and IBD-associated cancer, through secretion of inflammatory cytokines and interaction with other immune and non-immune cells. Here, we will review the evidence indicating a role for ILC in the pathogenesis of chronic intestinal inflammation

Information management and ante-mortem inspection procedures for the emerging diseases control: Experiences acquired in the epidemiological surveillance of bluetongue and lumpy skin disease

The spread of exotic, emerging and reemerging diseases, has become, in the last years, one of the most important threats to the animal productions and public health, representing a new challenge for the European Community. In a global-market framework, where trade and contacts between countries are simplified, effective and well-developed surveillance systems are necessary. Multiple factors are, in fact, associated with the emergence of new, known or exotic diseases in this new economic panorama and for these reasons controls on animal imports, traceability and timeliness detection of infected animals should be considered the basis of a sound surveillance. In this work, we focused our attention on the management of Bluetongue and on the risk of introduction of the Lumpy Skin Disease in Italy, in order to describe the national and European surveillance systems for these diseases. In particular, we underlined the crucial role of information that reach the Official Veterinarian at the slaughterhouse concerning the epidemiological situation of the sending countries. Information that are important for the management of the ante-mortem inspection and for increasing the awareness of the Veterinary Inspectors of their role in the surveillance