Salvador, Brazil
Salvador, Brazil

Time filter

Source Type

Palma Zochio Tozzato G.,Laboratory of Pharmacology | Taipeiro E.F.,Discipline of Biochemistry | Spadella M.A.,Discipline of Human Embryology | Marabini Filho P.,Discipline of Pathology | And 3 more authors.
Clinical and Experimental Immunology | Year: 2016

Rheumatoid arthritis (RA) may promote endothelial dysfunction. This phenomenon requires further investigation, especially in collagen-induced arthritis (CIA), as it is considered the experimental model most similar to RA. The objectives of this study were to identify CIA-induced changes in noradrenaline (NE) and acetylcholine (ACh) responses in mice aortas that may suggest endothelial dysfunction in these animals. Moreover, we characterize CIA-induced modifications in inducible nitric oxide synthase (iNOS) expression in the aortas and cardiac and renal tissues taken from these mice that may be related to possible endothelial dysfunction. Male DBA/1J mice were immunized with 100 μg of emulsified bovine collagen type II (CII) plus complete Freund's adjuvant. Twenty-one days later, these animals received a boost of an additional 100μg plus incomplete Freund's adjuvant. Fifteen days after the onset of the disease, aortic rings from CIA and control mice were challenged with NE and ACh in an organ bath. In these animals, iNOS was detected through immunohistochemical analysis of aorta, heart and kidneys. Plasma nitrite concentration was determined using the Griess reaction. CIA did not change NE or ACh responses in mice aorta but apparently increased the iNOS expression not only in aorta, but also in cardiac and renal microcirculation. In parallel, CIA reduced nitrite plasma concentration. In mice, CIA appears to increase the presence of iNOS in aorta, as well as in heart and in kidney microcirculation. This iNOS increase occurs apparently in parallel to a reduction of the bioavailability of NO. This phenomenon does not appear to change NE or ACh responses in aorta. © 2016 British Society for Immunology.


Bonassa C.E.G.,Universidade São Francisco | Pereira J.A.,Discipline of Pathology | de Campos F.G.C.M.,University of Sao Paulo | Chaim F.D.M.,Universidade São Francisco | Martinez C.A.R.,USF
Acta Cirurgica Brasileira | Year: 2015

Purpose: To measure the content of acidic mucin, sialomucin, and sulfomucins in the colonic mucosa without fecal stream submit to intervention with sucralfate (SCF). Methods: Thirty-six rats were submitted to a right colostomy and a distal mucous fistula and divided into two groups according to sacrifice to be performed two or four weeks. Each group was divided into three subgroups according daily application of enemas containing saline, SCF at 1.0 g/kg/day or 2.0 g/kg/day. Colitis was diagnosed by histological analysis. Acid mucins were determined with the Alcian-Blue and sulfomucin and sialomucin by high iron diamine-alcian blue (HID-AB) techniques. The mucins were quantified by computer-assisted image analysis. Mann-Whitney and ANOVA tests were used to analyze the results establishing the level of significance of 5% for both (p<0.05). Results: SCF enemas decreased the inflammation score and was related to the concentration used and time of the intervention. SCF at both concentrations increased the content of acid mucin, which was related to the concentration used and to the improvement in the inflammatory score. There was an increase in the content of sulfomucins and sialomucins in SCF groups. SCF increased sulfomucins from 2 weeks of intervention, which was not related to the dose or time of application. The increase in sialomucin content was related to the time and dose used in the intervention. Conclusion: Sucralfate increased the content of acidic mucins, primarily at the expense of sialomucin, which was affected by the dose and time of intervention. © 2015, Sociedade Brasileira para o Desenvolvimento de Pesquisa em Cirurgia. All rights reserved.


PubMed | Laboratory of Immunohistochemistry, Discipline of Human Embryology, Laboratory of Pharmacology, Discipline of Rheumatology and 2 more.
Type: Journal Article | Journal: Clinical and experimental immunology | Year: 2016

Rheumatoid arthritis (RA) may promote endothelial dysfunction. This phenomenon requires further investigation, especially in collagen-induced arthritis (CIA), as it is considered the experimental model most similar to RA. The objectives of this study were to identify CIA-induced changes in noradrenaline (NE) and acetylcholine (ACh) responses in mice aortas that may suggest endothelial dysfunction in these animals. Moreover, we characterize CIA-induced modifications in inducible nitric oxide synthase (iNOS) expression in the aortas and cardiac and renal tissues taken from these mice that may be related to possible endothelial dysfunction. Male DBA/1J mice were immunized with 100 g of emulsified bovine collagen type II (CII) plus complete Freunds adjuvant. Twenty-one days later, these animals received a boost of an additional 100g plus incomplete Freunds adjuvant. Fifteen days after the onset of the disease, aortic rings from CIA and control mice were challenged with NE and ACh in an organ bath. In these animals, iNOS was detected through immunohistochemical analysis of aorta, heart and kidneys. Plasma nitrite concentration was determined using the Griess reaction. CIA did not change NE or ACh responses in mice aorta but apparently increased the iNOS expression not only in aorta, but also in cardiac and renal microcirculation. In parallel, CIA reduced nitrite plasma concentration. In mice, CIA appears to increase the presence of iNOS in aorta, as well as in heart and in kidney microcirculation. This iNOS increase occurs apparently in parallel to a reduction of the bioavailability of NO. This phenomenon does not appear to change NE or ACh responses in aorta.


Felzemburgh V.A.,Discipline of Surgical Technique and Experimental Surgery I | Nunes V.L.C.,Discipline of Pathology | Campos J.H.O.,Discipline of Surgical Technique and Experimental Surgery I
Acta Cirurgica Brasileira | Year: 2012

PURPOSE: To evaluate the donor site of adipocytes as well as histopathological alterations secondary to liposuction. METHODS: All animals underwent liposuction with a syringe on the right side of the back. While the left side of the back was used as control and did not undergo intervention. The 10 rabbits were divided into two groups A and B according the postoperative day which were submitted to euthanasia: 90 and 120 days. All adipose tissue from the donor site was analyzed and compared with the control macroscopic and light microscopy. Tissues were weighed and analyzed searching for histological changes and late inflammatory response to trauma such as fbrosis, fat necrosis and infammation and macrophage infltration. RESULTS: There was wide variation in adipose tissue volume between the experimental and the control on macroscopic analysis. The presence of histopathological changes was found in two samples at 90 days. CONCLUSIONS: There was a relationship between the presence of fbrosis with the weight and number of days after liposuction surgery in rabbits. The study show macroscopic difference between control and experiment sides in all rabbits.


PubMed | Discipline of Pathology, Federal University of São Paulo and University of Sao Paulo
Type: Journal Article | Journal: Arquivos brasileiros de cirurgia digestiva : ABCD = Brazilian archives of digestive surgery | Year: 2017

Gastric cancer is the fifth most frequent cancer and the third most common cause of cancer-related deaths worldwide.It has been reported that Wnt/ betacatenin pathway is activated in 30-50% of these tumors. However,the deregulation of this pathway has not been fully elucidated.To determine the expression of E-cadherin, betacatenin, APC, TCF-4 and survivin proteins in gastric adenocarcinoma tissues and correlate with clinical and pathological parameters.Seventy-one patients with gastric adenocarcinoma undergoing gastrectomy were enrolled. The expression of E-cadherin, betacatenin, APC, TCF-4 and survivin proteins was detected by immunohistochemistryand related to the clinical and pathological parameters.The expression rates of E-cadherin in the membrane was 3%; betacatenin in the cytoplasm and nucleus were 23,4% and 3,1% respectively; APC in the cytoplasm was 94,6%; TCF-4 in the nucleus was 19,4%; and survivin in the nucleus 93,9%. The expression rate of E-cadherin was correlated with older patients (p=0,007), while betacatenin with tumors <5 cm (p=0,041) and APC with proximal tumors (p=0,047). Moreover, the expression of TCF-4 was significantly higher in the diffuse type (p=0,017) and T4 tumors (p=0,002).The Wnt/betacatenin is not involved in gastric carcinogenesis. However, the high frequency of survivin allows to suggest that other signaling pathways must be involved in the transformation of gastric tissue.O cncer gstrico encontra-se entre as principais neoplasias malignas do mundo sendo o quinto mais incidente e o terceiro em relao ao ndice de mortalidade. Acredita-se que a via Wnt/betacatenina esteja ativada em 30-50% desses tumores, porm a desregulao dela ainda no est completamente esclarecida.Avaliar a imunoexpresso das protenas E-caderina, betacatenina, APC, TCF-4 e survivina em tecidos de adenocarcinoma gstrico e correlacion-las com as variveis clnicas dos doentes e anatomopatolgicas do tumor.Foram coletados os dados clnicos e anatomopatolgicos dos pronturios de 71 doentes com adenocarcinoma gstrico submetidos gastrectomia. O material obtido na operao foi submetido anlise imunoistoqumica e a frequncia da expresso de cada protena pde ser analisada de acordo com a sua localizao na clula e relacionada com as variveis clinicopatolgicas.A graduao percentualda expresso e da localizao das protenas foi a seguinte: E-caderina em 3% na membrana; betacatenina em 23,4% no citoplasma e 3,1% no ncleo; APC em 94,6% no citoplasma; TCF-4 em19,4% no ncleo; e survivina em 93,9% no ncleo. Houve relao entre expresso da protena E-caderina com a idade mais avanada (p=0,007); betacatenina com tumores <5 cm de dimetro (p=0,041);APC com tumores proximais (p=0,047); e TCF-4 com tipo difuso da classificao de Lauren (p=0,017) e com o grau de penetrao tumoral (p=0,002).A via Wnt/betacatenina no est envolvida na carcinognese gstrica. Porm, a frequncia elevada de survivina permite sugerir que outras vias sinalizadoras devam estar envolvidas na transformao do tecido gstrico.


Dennis C.V.,Discipline of Pathology | Sheahan P.J.,Discipline of Pathology | Graeber M.B.,Discipline of Medicine | Graeber M.B.,Brain and Mind Research Institute | And 5 more authors.
Metabolic Brain Disease | Year: 2014

Hepatic encephalopathy (HE) is a common complication of chronic alcoholism and patients show neurological symptoms ranging from mild cognitive dysfunction to coma and death. The HE brain is characterized by glial changes, including microglial activation, but the exact pathogenesis of HE is poorly understood. During a study investigating cell proliferation in the subventricular zone of chronic alcoholics, a single case with widespread proliferation throughout their adjacent grey and white matter was noted. This case also had concomitant HE raising the possibility that glial proliferation might be a pathological feature of the disease. In order to explore this possibility fixed postmortem human brain tissue from chronic alcoholics with cirrhosis and HE (n = 9), alcoholics without HE (n = 4) and controls (n = 4) were examined using immunohistochemistry and cytokine assays. In total, 4/9 HE cases had PCNA- and a second proliferative marker, Ki-67-positive cells throughout their brain and these cells co-stained with the microglial marker, Iba1. These cases were termed ‘proliferative HE’ (pHE). The microglia in pHEs displayed an activated morphology with hypertrophied cell bodies and short, thickened processes. In contrast, the microglia in white matter regions of the non-proliferative HE cases were less activated and appeared dystrophic. pHEs were also characterized by higher interleukin-6 levels and a slightly higher neuronal density. These findings suggest that microglial proliferation may form part of an early neuroprotective response in HE that ultimately fails to halt the course of the disease because underlying etiological factors such as high cerebral ammonia and systemic inflammation remain. © 2013, Springer Science+Business Media New York.


Machado F.A.,Federal University of Triângulo Mineiro | Abdalla D.R.,Federal University of Triângulo Mineiro | Montes L.,Federal University of Triângulo Mineiro | Etchebehere R.M.,Discipline of Pathology | And 2 more authors.
European Journal of Gynaecological Oncology | Year: 2014

The aim of this study was to characterize infiltrating immune cells in cervical stroma biopsy samples from patients diagnosed with cervical intraepithelial neoplasias (CINs) who were treated with IFN-α 2b. The authors studied 13 volunteers who were diagnosed with Cervical intraepithelial neoplasiaCIN II or III and who received intra-lesional treatment with IFN-α 2b. They collected pre- and post-treatment biopsies from each patient. They also examined the slides under a common optical microscope with a X400 lens for biopsy sample sections that were labeled with immunohistochemistry for T lymphocyte, B lymphocyte, natural killer cell, macrophage, iNOS, and perforin markers. The presence of immune response cells in the lesion was observed after treatment with intralesional IFN-α 2b in patients with CIN II/III changes, a reduction in CD4+ and CD8+ T lymphocyte infiltration in the women who responded well to treatment. However, there was a significant increase in these markers in samples from women who did not respond to treatment. Nonetheless, immunotherapy with IFN-α 2b administered intralesionally in patients with CIN II/III yields favorable results in patients who do not smoke.


PubMed | Discipline of Pathology
Type: Journal Article | Journal: Metabolic brain disease | Year: 2014

Hepatic encephalopathy (HE) is a common complication of chronic alcoholism and patients show neurological symptoms ranging from mild cognitive dysfunction to coma and death. The HE brain is characterized by glial changes, including microglial activation, but the exact pathogenesis of HE is poorly understood. During a study investigating cell proliferation in the subventricular zone of chronic alcoholics, a single case with widespread proliferation throughout their adjacent grey and white matter was noted. This case also had concomitant HE raising the possibility that glial proliferation might be a pathological feature of the disease. In order to explore this possibility fixed postmortem human brain tissue from chronic alcoholics with cirrhosis and HE (n=9), alcoholics without HE (n=4) and controls (n=4) were examined using immunohistochemistry and cytokine assays. In total, 4/9 HE cases had PCNA- and a second proliferative marker, Ki-67-positive cells throughout their brain and these cells co-stained with the microglial marker, Iba1. These cases were termed proliferative HE (pHE). The microglia in pHEs displayed an activated morphology with hypertrophied cell bodies and short, thickened processes. In contrast, the microglia in white matter regions of the non-proliferative HE cases were less activated and appeared dystrophic. pHEs were also characterized by higher interleukin-6 levels and a slightly higher neuronal density . These findings suggest that microglial proliferation may form part of an early neuroprotective response in HE that ultimately fails to halt the course of the disease because underlying etiological factors such as high cerebral ammonia and systemic inflammation remain.

Loading Discipline of Pathology collaborators
Loading Discipline of Pathology collaborators