HERALDO POSSOLO DE SOUZA
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina - Docente
Instituto Central, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/02 - Laboratório de Anatomia Médico-Cirúrgica, Hospital das Clínicas, Faculdade de Medicina
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
Instituto Central, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/02 - Laboratório de Anatomia Médico-Cirúrgica, Hospital das Clínicas, Faculdade de Medicina
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
24 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 24
- Effects of diazoxide in experimental acute necrotizing pancreatitis(2017) ANDRADE, Roberta de Oliveira; KUNITAKE, Tiago; KOIKE, Marcia Kiyomi; MACHADO, Marcel C. C.; SOUZA, Heraldo PossoloOBJECTIVE: We aimed to assess the effects of diazoxide on the mortality, pancreatic injury, and inflammatory response in an experimental model of acute pancreatitis. METHODS: Male Wistar rats (200-400 g) were divided randomly into two groups. Fifteen minutes before surgery, animals received physiological (0.9%) saline (3 mL/kg) (control group) or 45 mg/kg diazoxide (treatment group) via the intravenous route. Acute pancreatitis was induced by injection of 2.5% sodium taurocholate via the biliopancreatic duct. Mortality (n= 38) was observed for 72 h and analyzed by the Mantel-Cox Log-rank test. To study pancreatic lesions and systemic inflammation, rats (10 from each group) were killed 3 h after acute pancreatitis induction; ascites volume was measured and blood as well as pancreases were collected. Pancreatic injury was assessed according to Schmidt's scale. Cytokine expression in plasma was evaluated by the multiplex method. RESULTS: Mortality at 72 h was 33% in the control group and 60% in the treatment group (p = 0.07). Ascites volumes and plasma levels of cytokines between groups were similar. No difference was observed in edema or infiltration of inflammatory cells in pancreatic tissues from either group. However, necrosis of acinar cells was lower in the treatment group compared to the control group (3.5 vs. 3.75, p = 0.015). CONCLUSIONS: Treatment with diazoxide can reduce necrosis of acinar cells in an experimental model of acute pancreatitis, but does not affect the inflammatory response or mortality after 72 h.
conferenceObject Intestinal Barrier Dysfunction in Ageing Animals With Acute Pancreatitis: Increased Intestinal Inflammation?(2015) MACHADO, Marcel C.; SILVA, Fabiano Pinheiro da; CUNHA, Debora G.; BARBEIRO, Denise F.; COELHO, Ana Maria M.; SOUZA, Heraldo P.- Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice(2021) SERRA, Mariana B.; KOIKE, Marcia K.; BARBEIRO, Denise F.; MACHADO, Marcel C. C.; SOUZA, Heraldo P. deBiliary acute pancreatitis induction by sodium taurocholate infusion has been widely used by the scientific community due to the representation of the human clinical condition and reproduction of inflammatory events corresponding to the onset of clinical biliary pancreatitis. The severity of pancreatic damage can be assessed by measuring the concentration, speed, and volume of the infused bile acid. This study provides an updated checklist of the materials and methods used in the protocol reproduction and shows the main results from this acute pancreatitis (AP) model. Most of the previous publications have limited themselves to reproducing this model in rats. We have applied this method in mice, which provides additional advantages (i.e., the availability of an arsenal of reagents and antibodies for these animals along with the possibility of working with genetically modified strains of mice) that may be relevant to the study. For acute pancreatitis induction in mice, we present a systematic protocol, with a defined dose of 2.5% sodium taurocholate at an infusion speed 10 mu L/min for 3 min in C57BL/6 mice that reaches its maximal level of severity within 12 h of induction and highlight results with outcomes that validate the method. With practice and technique, the total estimated time, from the induction of anesthesia to the completion of the infusion, is 25 min per animal.
- Reduction of venous pressure during the resection of liver metastases compromises enteric blood flow: IGFBP-1 as a novel biomarker of intestinal barrier injury(2017) BARBEIRO, Hermes Vieira; MACHADO, Marcel Autran Cesar; SOUZA, Heraldo Possolo de; SILVA, Fabiano Pinheiro da; MACHADO, Marcel Cerqueira CesarOBJECTIVES: Disruption of the intestinal barrier and bacterial translocation commonly occur when intestinal blood flow is compromised. The aim of this study was to determine whether liver resection induces intestinal damage. METHODS: We investigated intestinal fatty-acid binding protein and insulin-like growth factor binding protein levels in the plasma of patients who underwent liver resection. RESULTS: We show that liver resection is associated with significant intestinal barrier injury, even if the Pringle maneuver is not performed. CONCLUSION: We propose the use of insulin-like growth factor binding protein-1 as a novel biomarker of intestinal damage in such situations.
- Septic shock in older people: a prospective cohort study(2013) SILVA, Fabiano Pinheiro da; ZAMPIERI, Fernando Godinho; BARBEIRO, Denise Frediani; BARBEIRO, Hermes Vieira; GOULART, Alessandra Carvalho; TORGGLER FILHO, Francisco; VELASCO, Irineu Tadeu; CRUZ NETO, Luiz Monteiro da; SOUZA, Heraldo Possolo de; MACHADO, Marcel Cerqueira CesarBackground: Septic shock is the first cause of death in Intensive Care Units. Despite experimental data showing increased inflammatory response of aged animals following infection, the current accepted hypothesis claims that aged patients are immunocompromised, when compared to young individuals. Results: Here, we describe a prospective cohort study designed to analyze the immune profile of this population. Conclusion: Older people are as immunocompetent as the young individual, regarding the cytokines, chemokines and growth factors response to devastating infection.
- Septic Shock in Advanced Age: Transcriptome Analysis Reveals Altered Molecular Signatures in Neutrophil Granulocytes(2015) PELLEGRINA, Diogo Vieira da Silva; SEVERINO, Patricia; BARBEIRO, Hermes Vieira; ANDREGHETTO, Flavia Maziero; VELASCO, Irineu Tadeu; SOUZA, Heraldo Possolo de; MACHADO, Marcel Cerqueira Cesar; REIS, Eduardo Moraes; SILVA, Fabiano Pinheiro daSepsis is one of the highest causes of mortality in hospitalized people and a common complication in both surgical and clinical patients admitted to hospital for non-infectious reasons. Sepsis is especially common in older people and its incidence is likely to increase substantially as a population ages. Despite its increased prevalence and mortality in older people, immune responses in the elderly during septic shock appear similar to that in younger patients. The purpose of this study was to conduct a genome-wide gene expression analysis of circulating neutrophils from old and young septic patients to better understand how aged individuals respond to severe infectious insult. We detected several genes whose expression could be used to differentiate immune responses of the elderly from those of young people, including genes related to oxidative phosphorylation, mitochondrial dysfunction and TGF-a signaling, among others. Our results identify major molecular pathways that are particularly affected in the elderly during sepsis, which might have a pivotal role in worsening clinical outcomes compared with young people with sepsis.
- Molecular Basis of Hyperammonemic Encephalopathy in Fibrolamellar Hepatocellular Carcinoma(2023) SURJAN, Rodrigo Canada T.; LIMA, Thais M. de; SOUZA, Heraldo P. de; MACHADO, Marcel Cerqueira C.; ARDENGH, Jose C.Hyperammonemic encephalopathy is a potentially fatal condition associated with fibrolamellar hepatocellular carcinoma. The mechanism involved in hyperammonemia in patients with fibrolamellar carcinoma was unclear until a possible physiopathological pathway was recently proposed. An ornithine transcarboxylase dysfunction was suggested as a result of increased ornithine decarboxylase activity induced by c-Myc overexpression. This c-Myc overexpression resulted from Aurora kinase A overexpression derived from the activity of a chimeric kinase that is the final transcript of a deletion in chromosome 19, common to all fibrolamellar carcinomas. We performed the analysis of the expression of all enzymes involved and tested for the mutation in chromosome 19 in fresh frozen samples of fibrolamellar hepatocellular carcinoma, non-tumor liver, and hepatic adenomatosis. The specific DNAJB-PRKACA fusion protein that results from the recurrent mutation on chromosome 19 common to all fibrolamellar carcinoma was detected only in the fibrolamellar carcinoma sample. Fibrolamellar carcinoma and adenomyomatosis samples presented increased expression of Aurora kinase A, c-MYC, and ornithine decarboxylase when compared to normal liver, while ornithine transcarbamylase was decreased. The proposed physiopathological pathway is correct and that overexpression of c-Myc may also be responsible for hyperammonemia in patients with other types of rapidly growing hepatomas. This gives further evidence to apply new and adequate treatment to this severe complication.
- Circulating fatty acid binding protein as a marker of intestinal failure in septic patients(2012) MACHADO, Marcel Cerqueira Cesar; BARBEIRO, Hermes Vieira; SILVA, Fabiano Pinheiro da; SOUZA, Heraldo Possolo de
conferenceObject LIVER RESECTION INDUCES ACUTE INTESTINAL BARRIER DYSFUNCTION IGFBP-1 AS A NOVEL BIOMARKER OF INTESTINAL INJURY(2017) MACHADO, Marcel C. C.; BARBEIRO, Hermes; SOUZA, Heraldo P.; PINHEIRO, Fabiano; MACHADO, Marcel Autran- Cathelicidin LL-37 bloodstream surveillance is down regulated during septic shock(2013) BARBEIRO, Denise Frediani; BARBEIRO, Hermes Vieira; ZAMPIERI, Fernando Godinho; MACHADO, Marcel Cerqueira Cesar; TORGGLER FILHO, Francisco; CUNHA, Debora Maria Gomes; GOULART, Alessandra Carvalho; VELASCO, Irineu Tadeu; CRUZ NETO, Luiz Monteiro da; SOUZA, Heraldo Possolo de; SILVA, Fabiano Pinheiro daHost defense peptides are ancient weapons of the innate immunity. The human cathelicidin LL-37 protects the epithelial barrier against infection and is constitutively secreted in the bloodstream by immune cells. Current knowledge claims that LL-37 is up regulated upon infection. LL-37 can protect against bacterial infections and possesses many immunomodulatory properties. Here, we show that the human host defense peptide LL-37 is down regulated during septic shock. Furthermore, we show that these effects are not related to vitamin D serum levels, a potent inducer of LL-37 gene expression, pointing out the complex regulation of cathelicidins during septic shock.
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