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Copyright of Revista Eletrônica de Enfermagem is the property of Revista Eletronica de Enfermagem and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Eletrônica de Enfermagem is the property of Revista Eletronica de Enfermagem and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This study aimed to evaluate the effects of radiofrequency (RF) on patellar ligament repair through the analysis of type I and III collagens and immunostaining for TGF-β3. To evaluate the effect of RF on patellar ligament repair of Wistar rats, cross-sectional incision (60% of the width - grade I) was performed in patellar ligaments of the groups: lesion (L, n = 7), treated with RF on the 5-day (5RF, n = 7) and 7-day (7RF, n = 7) post injury were compared to control group (C, n = 7). Histological evaluation, immunohistochemistry, morphometry and statistical analysis were performed. At 10 days post injury, ligament rupture were observed only in L. Active fibroblasts, type 3 collagen and TGF-β3 in L, 5RF and 7RF was significantly (p < 0.05) higher than control (C). Type 1 collagen was significantly (p < 0.05) higher in C than L, 5RF and 7RF. A positive correlation (p < 0.05) was observed: TGF-β3 vs active fibroblasts and TGF-β3 vs type 3 collagen; otherwise, negative correlation (p < 0.05): type I collagen vs TGF-β3. These results suggest that RF seemed to accelerate the wound healing process of the patellar ligament and may be used as a non-invasive treatment of partial ligament injuries., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Aim: To evaluate the serum concentrations of inflammatory mediators in patients with type 2 diabetes mellitus (T2DM) with or without renal alteration (RA) function., Methods: Serum samples from 76 patients with T2DM and 24 healthy individuals were selected. Patients with T2DM were divided into two groups according to eGFR (> or < 60mL/min/1.73m2). Cytokines, chemokines and adipokines levels were evaluated using the Multiplex immunoassay and ELISA., Results: TNFR1 and leptin were higher in the T2DM group with RA than in the T2DM group without RA and control group. All patients with T2DM showed increased resistin, IL-8, and MIP-1α compared to the control group. Adiponectin were higher and IL-4 decreased in the T2DM group with RA compared to the control group. eGFR positively correlated with IL-4 and negatively with TNFR1, TNFR2, and leptin in patients with T2DM. In the T2DM group with RA, eGFR was negatively correlated with TNFR1 and resistin. TNFR1 was positively correlated with resistin and leptin, as well as resistin with IL-8 and leptin., Conclusion: Increased levels of TNFR1, adipokines, chemokines and decrease of IL-4 play important role in the inflammatory process developed in T2DM and decreased renal function. We also suggest that TNFR1 is a strong predictor of renal dysfunction in patients with T2DM., Competing Interests: The authors have declared that no competing interests exist.

Introduction: Mast cells may be involved in inflammation and contribute to the onset of fibrosis in lupus nephritis (LN)., Objective: This study aimed to correlate the presence of mast cells in kidney biopsy specimens of pediatric patients with LN with activity (AI) and chronicity (CI) indices and assess how effectively mast cells may be used as a prognostic factor., Method: The study included 40 patients aged 6-18 years diagnosed with LN at the Renal Disease Service of the Federal University of Triângulo Mineiro between 1996 and 2015. Workup and epidemiological data were evaluated vis-à-vis AI, CI, and mast cell counts (MCC)., Results: Significant positive correlations were found between mast cell counts (MCC) and AI (p = 0.003; r: 0.66) and MCC and CI (p = 0.048; r: 0.48). The ROC curve showed that mast cells were highly sensitive and specific in the differentiation of patients with an AI > 12 from individuals with an AI ≤ 12. Serum creatinine levels were higher in individuals with class IV LN than in patients with class V disease [1.50 (0.40-20.90) vs. 0.70 (0.62-0.90), p = 0.04]. Blood urea nitrogen had a positive significant correlation with MCC (p = 0.002; r: 0.75). A trend toward a negative correlation was observed between MCC and serum albumin (p = 0.06; r: -0.5459). Kidney biopsies of patients with nephrotic syndrome had higher MCC [2.12 (0.41-5.140) vs. 0.53 (0.0-3.94), p = 0.07]., Conclusion: Inflammatory cell infiltration and morphological differences between cell types in the inflammatory infiltrate are relevant factors in the assessment of the LN. Mast cell analysis and AI/CI assessment may be relevant prognostic indicators for pediatric patients with LN.

Background: Physiopathological processes in hypertensive heart disease are controlled by complex interactions between cardiomyocytes, extracellular matrix, microvasculature and other cells present in the myocardium., Objective: To analyze morphological changes in hypertensive cardiopathy and to describe and compare findings in order to help clarify determinant factors., Methods: 42 fragments of the left ventricular myocardium and circumflex branch of the left coronary artery were obtained from individuals autopsied at the Clinical Hospital of the Federal University of Triângulo Mineiro (UFTM) in the period ranging from 1984 to 2018. Groups were split into individuals with hypertensive heart disease (HD) and individuals without heart disease (ND). Wall thickness was measured with a digital caliper and Computed Tomography. Quantification of collagen fibers was conducted by computerized morphometry and mast cell density was assessed by immunohistochemical methods., Results: There was a significant increase of heart weight in the HD group compared to the ND group, (p = 0.0002). There was a significant increase of thickness of the middle third of the free wall in the HD group compared to the ND group, (p = 0.04). There was a significant increase of collagen fibers in the left ventricle in the HD group compared to the ND group, (p < 0.0001). Concerning mast cell density, there was a significant increase in the left ventricle of individuals with HD immuno-labeled by the set anti-chymase/anti-tryptase (p < 0.0001). There was a significant increase of mast cell density in the circumflex branch of the left coronary artery of individuals with HD immuno-labeled by the set anti-chymase/anti-tryptase (p = 0.01)., Conclusions: Mast cells are involved in the development of hypertensive heart disease, contributing to the remodeling of collagen fibers in this disease., (Copyright © 2019 Elsevier Inc. All rights reserved.)

There are controversies whether Minimal Change Disease (MCD) and Focal and Segmental Glomerulosclerosis (FSGS) are distinct glomerular lesions or different manifestations within the same spectrum of diseases. The uPAR (urokinase-type plasminogen activator receptor) and some slit diaphragm proteins may be altered in FSGS glomeruli and may function as biomarkers of the disease in renal biopsies. Thus, this study aims to evaluate the diagnostic potential of uPAR and glomerular proteins for differentiation between MCD and FSGS in renal pediatric biopsy. Renal biopsies from 50 children between 2 and 18 years old were selected, with diagnosis of MCD (n = 29) and FSGS (n = 21). Control group consisted of pediatric autopsies (n = 15) from patients younger than 18 years old, with no evidences of renal dysfunction. In situ expressions of WT1, nephrin, podocin and uPAR were evaluated by immunoperoxidase technique. Renal biopsy of patients with MCD and FSGS expressed fewer WT1 (p≤0.0001, F = 19.35) and nephrin (p<0.0001; H = 21.54) than patients in the control group. FSGS patients expressed fewer podocin than control (p<0.0359, H = 6.655). FSGS cases expressed more uPAR than each of control and MCD (p = 0.0019; H = 12.57) and there was a positive and significant correlation between nephrin and podocin (p = 0.0026, rS = 0.6502) in these cases. Podocin had sensitivity of 73.3% and specificity of 86.7% (p = 0.0068) and uPAR had sensitivity of 78.9% and specificity of 73.3% (p = 0.0040) for diagnosis of FSGS patients. The main limitation of the study is the limited number of cases due to the difficulty in performing biopsy in pediatric patients. Podocin and uPAR are good markers for FSGS and differentiate these cases from MCD, reinforcing the theory of distinct glomerular diseases. These findings suggest that podocin and uPAR can be used as biomarkers in the routine analysis of renal biopsies in cases of podocytopathies when the lesion (sclerosis) is not sampled., Competing Interests: The authors have declared that no competing interests exist.

Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are primary glomerulopathies leading to proteinuria, known as podocytopathies, which share syndromic and morphological similarities. Morphological similarity occurs in cases of FSGS in which the sclerotic lesion was not sampled in renal biopsy, due to the focal nature of the disease. Differentiating these entities is very important, especially in cases of suspected FSGS but with sclerotic lesion not sampled, as they are diseases that apparently have different pathogenic mechanisms and prognosis. The difference in uPAR expression in situ among these two entities may be related to a distinct molecular mechanism involved in pathogenesis. Thus, finding biomarkers involved in the pathogenesis and that can also help in differential diagnosis is very relevant. The aim of this work was to evaluate the potential of urokinase-type plasminogen activator receptor (uPAR) as a biomarker in renal biopsies of patients with podocytopathies ( n = 38). Immunohistochemistry showed that FSGS ( n = 22) had increased uPAR expression in podocytes compared with both the MCD group ( n = 16; p = 0.0368) and control group ( n = 21; p = 0.0076). ROC curve ( p = 0.008) showed that this biomarker has 80.95% of specificity in biopsies of patients with FSGS. Therefore, uPAR presented a high specificity in cases of podocytopathies associated with sclerosis and it can be considered a potential biomarker for FSGS.

Preterm birth accounts for nearly one million deaths among children under five years of age, and although its etiopathogenesis is not fully elucidated, ascending intrauterine infection and fetal inflammatory response seem to be the main triggers. The intense inflammatory response mediated by IL-1β, TNF-α, PAF, IFN-γ and IL-6, PGE 2 and MMP-1 and MMP-9 causes fetal membrane damage and rupture, increased uterine contractions and biochemical and structural changes in the cervix. Furthermore, preterm neonates have deficient innate and adaptive immune responses characterized by reduced levels of IgG, opsonization and phagocytosis, as well as increased activation of Th1 cells in relation to Th2 cells. Therefore, this triad is favors the occurrence of neonatal complications, such as respiratory distress syndrome, necrotizing enterocolitis, retinopathy of prematurity and bronchopulmonary dysplasia. Due to serious maternal and child health complications of intrauterine infection, several studies have tried to identify biomarkers for the early diagnosis of this entity. This literature review aims to discuss the main scientific findings regarding the association between ascending intrauterine infection, immune system and preterm birth.

Background: Pre-eclampsia is a multifactorial hypertensive disorder that is triggered by placental insufficiency and that accounts for up to 15% of maternal deaths. In normal pregnancies, this process depends on the balance between the expression of angiogenic factors and antiangiogenic factors, which are responsible for remodeling the spiral arteries, as well as for neoangiogenesis and fetal development., Purpose: The aim of this review is to discuss the main scientific findings regarding the role of angiogenic and antiangiogenic factors in the etiopathogenesis of preeclampsia., Methods: An extensive research was conducted in the Pubmed database in search of scientific manuscripts discussing potential associations between angiogenic and antiangiogenic factors and preeclampsia. Ninety-one papers were included in this review., Results: There is an increased expression of soluble fms-like tyrosine kinase receptor and soluble endoglin in pre-eclampsia, as well as reduced placental expression of vascular endothelial growth factor and placental growth factor. Systemic hypertension, proteinuria and kidney injury - such as enlargement and glomerular fibrin deposit, capillary occlusion due to edema, and hypertrophy of endocapillary cells - are some of these changes. The complex etiopathogenesis of preeclampsia instigates research of different biomarkers that allow for the early diagnosis of this entity, such as vascular endothelial growth factor, placental growth factor, soluble fms-like tyrosine kinase receptor, soluble endoglin, placental glycoprotein pregnancy-associated plasma protein-A and protein 13., Conclusion: Even though it is possible to establish an efficient and effective diagnostic tool, three key principles must be observed in the management of preeclampsia: prevention, early screening and treatment., (Copyright © 2017 Elsevier GmbH. All rights reserved.)

Vascular endothelial growth factor (VEGF) and von Willebrand factor (Factor VIII) are important components involved in the regulation of vascular development and identification of endothelial cells in many tissues. This study aimed to evaluate the presence of these substances in the placenta of pig fetuses located in different uterine regions and at different gestational ages and correlate them with fetal development. One hundred seventy-five pig fetuses from fifteen gilts slaughtered at 50, 80 and 106 days of pregnancy were used. Each uterine horn was divided into three segments, the apex, base and middle region, and also into left and right sides. The fetuses were sexed before determining their weight and anatomical measurements. The weights of the placentas were obtained for the calculation of placental efficiency, and VEGF and factor VIII were determined by immunohistochemistry. There was no significant interaction between gestational age, uterine segment or side and fetal sex in any of the variables studied. Higher VEGF and factor VIII concentrations were found at 80 and 105 days of pregnancy, and there was no significant difference between the right and left sides of the uterus, uterine segments or fetal sex. Positive correlations between VEGF and fetal weights were observed at 80 and 105 days of pregnancy, whereas factor VIII showed positive correlations with the weight and length of fetuses and placental weight and efficiency throughout pregnancy. It was concluded that VEGF and factor VIII are important growth factors associated with fetal development in pigs and are identified in all uterine segments. The concentration of these substances increases until the middle third of pregnancy which suggests that most of the uterine vascular development occurs before this stage., (Copyright © 2017 Elsevier Inc. All rights reserved.)