Simbolismos, Memórias e Narrativas: Redescobrindo a Rua da Lama da Década de 1980

Esta pesquisa teve por objetivo revelar aspectos simbólicos relacionados ao passado de um espaço na cidade de Vitória/ES, a Rua da Lama, a partir de pessoas que a frequentaram na década de 1980. Esta década foi escolhida por se tratar do início dessa região emblemática na cidade, que até hoje permanece sendo um ponto de encontro de lazer das pessoas. O que torna tal espaço contemporâneo e muito frequentado dentro da cidade. O estudo buscou relacionar os aspectos simbólicos de tal espaço, manifestados nas memórias presentes nas narrativas de seus antigos frequentadores. O objeto de pesquisa, composto por diferentes tipos de organizações, foi definido como espaço organizacional. Devido à complexidade do tema, buscou-se um aporte interdisciplinar dentro dos Estudos Organizacionais, abarcando as Ciências Sociais, História e o referencial de memória na Administração. Para o empreendimento, à luz de uma abordagem interdisciplinar nos Estudos Organizacionais, foi desenvolvida uma pesquisa de cunho qualitativo, utilizando a técnica de entrevistas narrativas para a coleta dos dados, gerando um conteúdo denso, que foram transcritas para posterior análise. Esse tipo de entrevista permitiu a pesquisadora entender de forma mais profunda o universo pesquisado. Após a coleta dos dados, o tratamento foi feito através da análise de conteúdo com as categorizações a posteriori. O período de coleta de dados se deu de maio a outubro de 2015, no qual foram realizadas oito entrevistas narrativas. Como resultado, foram encontradas três categorias seguindo um percurso temático, nomeadas por: O rock da Lama; As diferentes relações simbólicas com o espaço da Lama da década de 1980 e A Rua da Lama como um espaço de transgressão. A reflexão deu conta dos diferentes usos do passado para a reapropriação dos espaços simbólicos

Non-viral Smad7 gene delivery and attenuation of postoperative peritoneal adhesion in an experimental model

Background: Postoperative intra-abdominal adhesion is associated with high morbidity and mortality. Smad7, a protein that occupies a strategic position in fibrogenesis, inhibits the transforming growth factor (TGF) β/Smad signalling pathway. In this study the therapeutic potential of exogenous Smad7 in preventing fibrogenesis in postoperative intra-abdominal adhesion was investigated. Methods: Intra-abdominal adhesion was induced in a rodent model by peritoneal abrasion. Smad7 was delivered into the peritoneal cavity by a non-viral ultrasound-microbubble-mediated naked gene transfection system. The effect of Smad7 transgene on adhesion formation was studied by measuring changes in TGF-β, fibrogenic factors, α-SMA and Smad2/3 activation in the anterior abdominal wall. Results: Four weeks after surgical abrasion, all rats developed significant peritoneal adhesion with enhanced TGF-β expression, increased levels of extracellular matrix components and activated myofibroblasts, accompanied by decreased Smad7 expression and increased Smad2/3 activation. In rats treated with the Smad7 transgene, the incidence and severity of peritoneal adhesion were significantly reduced, with biochemical downregulation of fibrogenic factors and inhibition of Smad2/3 activation. Serial quantitation using magnetic resonance imaging revealed a significant reduction in adhesion areas from day 14 onwards. Conclusion: Ultrasound-microbubble-mediated gene transfection provides timely targeted gene delivery for the treatment of postoperative peritoneal adhesions. Copyright © 2009 British Journal of Surgery Society Ltd. Published by John Wiley & Sons Ltd.postprin

Toll-like receptor 4 mediates tubular inflammation in diabetic nephropathy

published_or_final_versionThe 15th Medical Research Conference, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, 16 January 2010. In Hong Kong Medical Journal, 2010, v. 16 n. 1, suppl. 1, p. 39, abstract no. 6

Tissue kallikrein mediates pro-inflammatory pathways and activation of protease-activated receptor-4 in proximal tubular epithelial cells.

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BMP7 reduces inflammation and oxidative stress in diabetic tubulopathy

Bone morphogenetic protein 7 (BMP7) has been reported to confer renoprotective effects in acute and chronic kidney disease models, but its potential role in Type 2 diabetic nephropathy remains unknown. In cultured human proximal tubular epithelial cells (PTECs), exposure to advanced glycation end-products (AGEs) induced overexpression of intercellular adhesion molecule 1 (ICAM1), monocyte chemoattractant protein 1 (MCP1), interleukin 8 (IL-8) and interleukin 6 (IL-6), involving activation of p44/42 and p38 mitogen-activated protein kinase (MAPK) signalling. BMP7 dose-dependently attenuated AGE-induced up-regulation of ICAM1, MCP1, IL-8 and IL-6 at both mRNA and protein levels. Moreover, BMP7 suppressed AGE-induced p38 and p44/42 MAPK phosphorylation and reactive oxygen species production in PTECs. Compared with vehicle control, uninephrectomized db/db mice treated with BMP7 for 8 weeks had significantly lower urinary albumin-to-creatinine ratio (3549±816.2 μg/mg compared with 8612±2037 μg/mg, P=0.036), blood urea nitrogen (33.26±1.09 mg/dl compared with 37.49±0.89 mg/dl, P=0.006), and renal cortical expression of ICAM1 and MCP1 at both gene and protein levels. In addition, BMP7-treated animals had significantly less severe tubular damage, interstitial inflammatory cell infiltration, renal cortical p38 and p44/42 phosphorylation and lipid peroxidation. Our results demonstrate that BMP7 attenuates tubular pro-inflammatory responses in diabetic kidney disease by suppressing oxidative stress and multiple inflammatory signalling pathways including p38 and p44/42 MAPK. Its potential application as a therapeutic molecule in diabetic nephropathy warrants further investigation.postprin

Mesenchymal stem cells modulate albumin-induced renal tubular inflammation and fibrosis.

Bone marrow-derived mesenchymal stem cells (BM-MSCs) have recently shown promise as a therapeutic tool in various types of chronic kidney disease (CKD) models. However, the mechanism of action is incompletely understood. As renal prognosis in CKD is largely determined by the degree of renal tubular injury that correlates with residual proteinuria, we hypothesized that BM-MSCs may exert modulatory effects on renal tubular inflammation and epithelial-to-mesenchymal transition (EMT) under a protein-overloaded milieu. Using a co-culture model of human proximal tubular epithelial cells (PTECs) and BM-MSCs, we showed that concomitant stimulation of BM-MSCs by albumin excess was a prerequisite for them to attenuate albumin-induced IL-6, IL-8, TNF-alpha, CCL-2, CCL-5 overexpression in PTECs, which was partly mediated via deactivation of tubular NF-kappaB signaling. In addition, albumin induced tubular EMT, as shown by E-cadherin loss and alpha-SMA, FN and collagen IV overexpression, was also prevented by BM-MSC co-culture. Albumin-overloaded BM-MSCs per se retained their tri-lineage differentiation capacity and overexpressed hepatocyte growth factor (HGF) and TNFalpha-stimulating gene (TSG)-6 via P38 and NF-kappaB signaling. Albumin-induced tubular CCL-2, CCL-5 and TNF-alpha overexpression were suppressed by recombinant HGF treatment, while the upregulation of alpha-SMA, FN and collagen IV was attenuated by recombinant TSG-6. Neutralizing HGF and TSG-6 abolished the anti-inflammatory and anti-EMT effects of BM-MSC co-culture in albumin-induced PTECs, respectively. In vivo, albumin-overloaded mice treated with mouse BM-MSCs had markedly reduced BUN, tubular CCL-2 and CCL-5 expression, alpha-SMA and collagen IV accumulation independent of changes in proteinuria. These data suggest anti-inflammatory and anti-fibrotic roles of BM-MSCs on renal tubular cells under a protein overloaded condition, probably mediated via the paracrine action of HGF and TSG-6.published_or_final_versio

Semi-individualised Chinese medicine treatment as an adjuvant management for diabetic nephropathy: a pilot add-on, randomised, controlled, multicentre, open-label pragmatic clinical trial

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Human Induced Pluripotent Stem Cell-Derived Mesenchymal Stem Cells Prevent Adriamycin Nephropathy in Mice

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Association of ICAM3 genetic variant with severe acute respiratory syndrome

Genetic polymorphisms have been demonstrated to be associated with vulnerability to human infection. ICAM3, an intercellular adhesion molecule important for T cell activation, and FCER2 (CD23), an immune response gene, both located on chromosome 19p13.3, were investigated for host genetic susceptibility and association with clinical outcome. A case-control study based on 817 patients with confirmed severe acute respiratory syndrome (SARS), 307 health care worker control subjects, 290 outpatient control subjects, and 309 household control subjects unaffected by SARS from Hong Kong was conducted to test for genetic association. No significant association to susceptibility to SARS infection caused by the novel coronavirus (SARS-CoV) was found for the FCER2 and the ICAM3 single nucleotide polymorphisms. However, patients with SARS homozygous for ICAM3 Gly143 showed significant association with higher lactate dehydrogenase levels (P = .0067; odds ratio [OR], 4.31 [95% confidence interval {CI}, 1.37-13.56]) and lower total white blood cell counts (P = .022; OR, 0.30 [95% CI, 0.10-0.89]) on admission. These findings support the role of ICAM3 in the immunopathogenesis of SARS. © 2007 by the Infectious Diseases Society of America. All rights reserved.published_or_final_versio