Sao Jose do Rio Preto Medical School

São José do Rio Preto, Brazil

Sao Jose do Rio Preto Medical School

São José do Rio Preto, Brazil
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Do Val-da Silva R.A.,University of Sao Paulo | Peixoto-Santos J.E.,University of Sao Paulo | Scandiuzzi R.C.,University of Sao Paulo | Balista P.A.,University of Sao Paulo | And 5 more authors.
Neuroscience | Year: 2016

Preconditioning can induce a cascade of cellular events leading to neuroprotection against subsequent brain insults. In this study, we investigated the chronic effects of hypoxic preconditioning on spontaneous recurrent seizures (SRS), neuronal death, and spatial memory performance in rats subjected to pilocarpine (Pilo)-induced status epilepticus (SE). Rats underwent a short hypoxic episode (7% O2 + 93% N2; 30 min on two consecutive days) preceding a 4-h SE (HSE group). Control groups were rats submitted to SE only (SE), rats subjected to hypoxia only (H) or normoxia-saline (C). Animals were monitored for the occurrence of SRS, and spatial memory performance was evaluated in the radial-arm maze. Hippocampal sections were analyzed for cell death and mossy fiber sprouting at 1 or 60 days after SE. Compared to SE group, HSE had increased SE latency, reduced number of rats with SRS, reduced mossy fiber sprouting at 60 days, and reduced cell death in the hilus and the CA3 region 1 and 60 days after SE. Additionally, HSE rats had better spatial memory performance than SE rats. Our findings indicated that short hypoxic preconditioning preceding SE promotes long-lasting protective effects on neuron survival and spatial memory. © 2016 IBRO

Araujo L.P.,Federal University of São Paulo | Truzzi R.R.,São Paulo State University | Mendes G.E.F.,Sao Jose Do Rio Preto Medical School | Luz M.A.M.,Sao Jose Do Rio Preto Medical School | And 4 more authors.
Inflammation Research | Year: 2012

Background: Cyclosporine (CsA) remains an important immunosuppressant for transplantation and for treatment of autoimmune diseases. The most troublesome side effect of CsA is renal injury. Acute CsA-induced nephrotoxicity is characterized by reduced renal blood flow (RBF) and glomerular filtration rate (GFR) due to afferent arteriole vasoconstriction. Annexin A1 (ANXA1) is a potent anti-inflammatory protein with protective effect in renal ischemia/reperfusion injury. Here we study the effects of ANXA1 treatment in an experimental model of acute CsA nephrotoxicity. Methods: Salt-depleted rats were randomized to treatment with VH (vehicles 1 mL/kg body weight/day), ANXA1 (Ac2-26 peptide 1 mg/kg body weight/day intraperitoneally), CsA (20 mg/kg body weight/day subcutaneously) and CsA + ANXA1 (combination) for seven days. We compared renal function and hemodynamics, renal histopathology, renal tissue macrophage infiltration and renal ANXA1 expression between the four groups. Results: CsA significantly impaired GFR and RBF, caused tubular dilation and macrophage infiltration and increased ANXA1 renal tissue expression. Treatment with ANXA1 attenuated CSA-induced hemodynamic changes, tubular injury and macrophage infiltration. Conclusion: ANXA1 treatment attenuated renal hemodynamic injury and inflammation in an acute CsA nephrotoxicity model. © 2011 Springer Basel AG.

Facio Jr. F.N.,Sao Jose Do Rio Preto Medical School | Sena A.A.,São Paulo State University | Araujo L.P.,São Paulo State University | Mendes G.E.,Sao Jose Do Rio Preto Medical School | And 6 more authors.
Journal of Molecular Medicine | Year: 2011

Inflammation is currently recognized as a key mechanism in the pathogenesis of renal ischemia-reperfusion (I/R) injury. The importance of infiltrating neutrophil, lymphocytes, and macrophage in this kind of injury has been assessed with conflicting results. Annexin 1 is a protein with potent neutrophil anti-migratory activity. In order to evaluate the effects of annexin A1 on renal I/R injury, uninephrectomized rats received annexin A1 mimetic peptide Ac2-26 (100 μg) or vehicle before 30 min of renal artery clamping and were compared to sham surgery animals. Annexin A1 mimetic peptide granted a remarkable protection against I/R injury, preventing glomerular filtration rate and urinary osmolality decreases and acute tubular necrosis development. Annexin A1 infusion aborted neutrophil extravasation and attenuated macrophage infiltration but did not prevent tissue lymphocyte traffic. I/R increased annexin A1 expression (assessed by transmission electron microscopy) in renal epithelial cells, which was attenuated by exogenous annexin A1 infusion. Additionally, annexin A1 reduced I/R injury in isolated proximal tubules suspension. Annexin A1 protein afforded striking functional and structural protection against renal I/R. These results point to an important role of annexin A1 in the epithelial cells defense against I/R injury and indicate that neutrophils are key mediators for the development of tissue injury after renal I/R. If these results were confirmed in clinical studies, annexin A1 might emerge as an important tool to protect against I/R injury in renal transplantation and in vascular surgery. © 2010 Springer-Verlag.

Carlos C.P.,Sao Jose Do Rio Preto Medical School | Mendes G.E.F.,Sao Jose Do Rio Preto Medical School | Miquelin A.R.,Sao Jose Do Rio Preto Medical School | Luz M.A.M.,Sao Jose Do Rio Preto Medical School | And 4 more authors.
Transplantation | Year: 2010

BACKGROUND.: Cyclosporine A (CsA)-induced chronic nephrotoxicity is characterized by renal dysfunction and interstitial fibrosis. Early and progressive renal macrophage influx, correlating with latter interstitial fibrotic areas, has been associated with CsA treatment. This study investigated the role of macrophages, the nitric oxide (NO) pathway, and the oxidative stress on chronic CsA nephrotoxicity. METHODS.: The macrophages were depleted by clodronate liposomes. Animals were distributed into four groups: vehicle (olive oil for 21 days), CsA 7.5 mg/kg per day (21 days), CsA plus clodronate (5 mg/mL intraperitoneally on days-4, 1, 4, 11, and 18 of CsA treatment), or vehicle plus clodronate. On day 22, glomerular filtration rate, renal blood flow, renal tubulointerstitial fibrosis, CsA blood levels, serum malondialdehyde and renal tissue immunohistochemistry for macrophages, inducible NO synthase, transforming growth factor-β, nuclear factor-kβ, α-smooth muscle actin, vimentin, and nitrotyrosine were assessed. RESULTS.: CsA-induced increase in the macrophage was prevented by clodronate. Macrophage depletion attenuated the reductions in the glomerular filtration rate and renal blood flow, the development of tubulointerstitial fibrosis, malondialdehyde increase and increases in nuclear factor-kβ, transforming growth factor-β, vimentin, inducible NO synthase, and nitrotyrosine expression provoked by CsA. Clodronate did not affect α-smooth muscle actin expression and CsA blood levels. CONCLUSIONS.: Renal macrophage influx plays an important role in CsA-induced chronic nephrotoxicity. The NO pathway and oxidative stress are likely mechanisms involved in the genesis of this form of renal injury. Copyright © 2010 by Lippincott Williams & Wilkins.

Joaquim A.I.,Hospital Of Base | Mendes G.E.F.,Sao Jose Do Rio Preto Medical School | Ribeiro P.F.F.,Hospital Of Base | Baptista M.A.F.,Sao Jose Do Rio Preto Medical School | Burdmann E.A.,Sao Jose Do Rio Preto Medical School
Nephrology Dialysis Transplantation | Year: 2010

Background. The differentiation between acute interstitial nephritis (AIN) and acute tubular necrosis (ATN) is crucial in patients with acute kidney injury. Gallium-67 citrate (Ga-67) has been used clinically in the differential diagnosis between these entities, but its efficacy is disputed. The aim of this study was to evaluate Ga-67 scintigraphy efficacy in the differentiation between experimental models of drug-induced AIN and ATN.Methods. Animals were divided into three groups: AIN (n = 8), ATN (n = 8) and control (NL, n = 10). The AIN group received intraperitoneal puromycin aminonucleoside (single dose, 150 mg/kg). The ATN group received a single intraperitoneal injection of cisplatin (6 mg/kg). The NL group did not receive active drugs. All of the animals were submitted to Ga-67 scintigraphy, serum creatinine (Cr) and urinary osmolality assessment, and blinded renal histology evaluation. Results. Renal Ga-67 uptake was strikingly more intense in the AIN group when compared to the ATN (P < 0.0001) and NL (P < 0.001) groups. The ATN group had increased Cr when compared to the NL group (P < 0.001) and lower urinary osmolality vs the NL (P < 0.001) and AIN (P < 0.01) groups. Renal histology showed severe acute tubular injury in the ATN group and intense interstitial inflammation in the AIN group, and was normal in control animals.Conclusion. Ga-67 scintigraphy was extremely effective in the differentiation between experimental drug-induced ATN and AIN. © The Author 2010. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

Kozak M.F.,Hospital Of Base | Kozak A.C.L.F.B.M.,Hospital Of Base | Souza A.S.,Sao Jose Do Rio Preto Medical School | Souza Jr. A.S.,Sao Jose Do Rio Preto Medical School
Pediatric Cardiology | Year: 2011

Unilateral pulmonary vein atresia is a rare congenital heart disease. Its symptoms begin to manifest in childhood and may be similar to those of other left-side heart obstructions. The diagnosis of this disorder is difficult and usually requires several imaging methods. This report presents the case of a 7-year-old girl whose diagnosis was aided through the use of multislice computed tomography. © 2010 Springer Science+Business Media, LLC.

Picollo Oliveira J.F.,Sao Jose Do Rio Preto Medical School | Burdmann E.A.,University of Sao Paulo
Clinical Kidney Journal | Year: 2015

Dengue is presently the most relevant viral infection transmitted by a mosquito bite that represents a major threat to public health worldwide. Acute kidney injury (AKI) is a serious and potentially lethal complication of this disease, and the actual incidence is unknown. In this review, we will assess the most relevant epidemiological and clinical data regarding dengue and the available evidence on the frequency, etiopathogenesis, outcomes and treatment of dengue-associated AKI. © 2015 The Author.

Galbiatti A.L.S.,Research Unit on Genetics and Molecular Biology | Ruiz M.T.,Federal University of Triângulo Mineiro | Maniglia J.V.,Sao Jose do Rio Preto Medical School | Raposo L.S.,Sao Jose do Rio Preto Medical School | And 2 more authors.
Brazilian Journal of Otorhinolaryngology | Year: 2012

Epidemiological evidence suggests that genetic variants encoding enzymes involved in folate metabolism may modulate HNSCC risk by altering DNA methylation synthesis and genomic estability. Aim: A review of the literature on genetic polymorphisms involved in folate metabolism and risk of head and neck cancer was carried out. Methodology: An electronic search was made on the Medline database to select papers on head and neck cancer and polymorphisms involved in folate metabolism. Results: The association between MTHFR C677T polymorphism and the risk of this tumor type was evaluated in nine studies; there was an association with this disease in three papers. The MTR A2756G and MTRR A66G and RFC1 A80G polymorphisms were also associated with increased risk for HNSCC. MTHFD1 G1958A polymorphism was not associated with increased risk of this disease; the evaluation results of the MTHFR A1298C polymorphism in this neoplasm were contradictory. Other polymorphisms involved in folate metabolism were not studied for this neoplasm. Conclusion: We conclude that polymorphisms involved in folate metabolism may modulate the risk of head and neck cancer, however, these results need to be demonstrated in different populations.

Araujo L.P.,Federal University of São Paulo | Truzzi R.R.,São Paulo State University | Mendes G.E.,Sao Jose Do Rio Preto Medical School | Luz M.A.M.,Sao Jose Do Rio Preto Medical School | And 3 more authors.
American Journal of Nephrology | Year: 2010

Background: Tacrolimus (FK) is currently widely used in transplant immunosuppression and the treatment of autoimmune diseases. However, FK induces nephrotoxicity which is characterized by functional and structural renal injury. The ubiquitous protein annexin A1 (ANXA1) has potent anti-inflammatory effects and protects against ischemia/reperfusion injury. We investigated the effects of exogenous ANXA1 treatment in an experimental model of acute FK nephrotoxicity. Methods: Munich-Wistar rats received a low-salt diet for 1 week and were randomized to treatment with ANXA1 (Ac2-26 peptide 0.5 mg/kg/day s.c.), FK (6 mg/kg/day p.o.), association (FK+ANXA1) and vehicles (1 ml/kg/day) for 7 days. Results: FK induced a significant decrease in glomerular filtration rate and renal blood flow, and a significant increase in renal vascular resistance. In addition, FK caused extensive acute tubule-interstitial damage and an increase in anti-inflammatory ANXA1 expression in renal tissue. Exogenous ANXA1 treatment reduced FK-induced tubular dilatation and macrophage infiltration. For the first time, we observed that FK augmented ANXA1 expression in renal tissue. Conclusion: Exogenous ANXA1 treatment partially protected against FK-induced tubular injury and macrophage infiltration, and may be targeted in renal intervention strategies. Copyright © 2010 S. Karger AG, Basel.

Dos Santos Torres U.,Sao Jose Do Rio Preto Medical School | De Almeida T.E.P.,Sao Jose Do Rio Preto Medical School | Netinho J.G.,Sao Jose Do Rio Preto Medical School
Revista Panamericana de Salud Publica/Pan American Journal of Public Health | Year: 2010

Objective. To determine the trends in hospital admission rates for colorectal cancer (CRC) in the Brazilian Public Health System from 1996 to 2008 and to assess the economic costs. Methods. Data from the Hospital Information Systems database of the Brazilian Unified Health System were used for analysis of all admissions with a primary diagnosis of CRC between 1996 and 2008. Results. There were 297 108 CRC admissions over the study period, with an annual increase from 12 821 in 1996 to 35 040 in 2008. Age-standardized admission rates increased from 8.7 to 23.56 per 100 000 for a percentage increase of 171%. The average length of stay decreased from 11.6 days in 1996 to 7.5 days in 2008. The average hospital mortality declined from 10.4% to 8.5%. Overall costs in United States dollars (US$) of CRC hospitalizations rose from US$ 16.5 million in 1996 to US$ 33.5 million in 2008; the average cost of each admission, however, decreased from US$ 1 283 to US$ 954. Conclusions. Hospitalization rates for CRC in Brazil significantly increased during a 13- year period, incurring a considerable rise in the inflation-adjusted economic burden; national in-hospital mortality rates have remained relatively high.

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