Systemic oxidative stress in children with cystic fibrosis with bacterial infection including Pseudomonas Aeruginosa

IntroductionOxidative stress (OS) occurs in cystic fibrosis (CF).ObjectiveThe objective of this work is to evaluate the influence of bacterial infection on biomarkers of OS (catalase [CAT], glutathione peroxidade [GPx], reduced glutathione [GSH]), markers of oxidative damage (protein carbonyls [PC], thiobarbituric acid reactive substances [TBARS]), together with the nutritional status and lung function in children with CF.MethodsCross‐sectional study including CF group (CFG, n = 55) and control group (CG, n = 31), median age: 3.89 and 4.62 years, respectively. CFG was distributed into CFG negative bacteriology (CFGB−, n = 27) or CFG positive bacteriology (CFGB+, n = 28), and CFG negative Pseudomonas aeruginosa (CFGPa−, n = 36) or CFG positive Pseudomonas aeruginosa (CFGPa+, n = 19).ResultsCompared with CG, CFG (P = .034) and CFGB+ (P = .042) had lower body mass index‐for‐age z‐score; forced expiratory volume in the first second was lower in CFGB+ and CFGPa+ (both P < .001). After adjusting for confounders and compared with CG: CFG showed higher TBARS (P ≤ .001) and PC (P = .048), and lower CAT (P = .004) and GPx (P = .003); the increase in PC levels was observed in CFGB+ (P = .011) and CFGPa+ (P = .001) but not in CFGB− (P = .510) and CFGPa− (P = .460).ConclusionsThese results indicate a systemic OS in children with CF. The presence of bacterial infection particularly Pseudomonas aeruginosa seems to be determinant to exacerbate the oxidative damage to proteins, in which PC may be a useful biomarker of OS in CF.     

Melanotic Neuroectodermal Tumor of Infancy: the Use of Immunohistochemical Analysis

The Melanotic Neuroectodermal Tumor of Infancy (MNTI) is an asymptomatic, pigmented neoplasm characterized by a fast and locally aggressive growth along with a rare tissue formation. In the diagnostic process, the use of imaging exams can suggest a local destruction suggestive of malignancy, a sign of bone remodeling and expansion. Therefore, as any early diagnosis minimizes risks and improves the prognosis of treatment for the patient, the aim of this study was, based on a clinical case report, to corroborate the use of histopathological analysis associated with immunohistochemistry. Thus, we conclude that the immunohistochemical exam is of great importance for a better complementation of the MNTI diagnosis process. In addition, it can reveal signs of possible aggressive growth.     

Checklists for Assessing Skills of Children With Type 1 Diabetes on Insulin Injection Technique

Background:School-aged children often participate in type 1 diabetes (T1D) self-care tasks. Despite widespread discussion about the importance of developing self-care skills in childhood, few explain how the health care team should assess the skills of children with T1D when performing insulin injections.Objective:We sought to assess content validity evidence in two checklists regarding injection technique performed by children.Methods:Two checklists were designed based on a systematic review of the insulin injection technique. Experts in pediatric diabetes, health literacy, and diabetes education assessed the checklists regarding their clarity, objectivity, and relevance. Content validity was assessed using the content validity ratio (CVR).Results:Eleven providers (72% nurses or physicians, professional experience 19.4 ± 10.1 years, 45% of specialists in endocrinology, and 18% in pediatrics) participated in the assessment. Experts considered items containing the word homogeneity inappropriate. Items related to the needle insertion angle and the skin fold did not reach the CVR critical value. The final version of the checklist for syringe injection comprised 22 items with CVR = 0.91, and the checklist for pen injection comprised 18 items with CVR = 0.87.Conclusions:The checklists presented clear, objective, and relevant content that assesses the skills of children with T1D for insulin injection. The checklists formally present the order of the technique and all the steps for insulin injection and allow a quantitative assessment of the operational skills of children. The developed instruments offer providers the possibility of continuous assessment of the progress of the pediatric clientele until they reach independence in diabetes self-care.     

Effect of d-amphetamine repeated administration on rat antioxidant defences

The purpose of this study was to evaluate rat tissue antioxidant status after repeated administration of d-amphetamine. Three groups of four rats each were used: control, d-amphetamine sulphate dosed (s.c., 20 mg/kg per day), and pair-fed. After 14 days of d-amphetamine daily administration, superoxide dismutase (CuZnSOD and MnSOD), catalase, glutathione peroxidase (GPx), glutathione reductase (GRed), glutathione-S-transferase (GST), glutathione (GSH), cysteine and thiobarbituric acid reactive substances (TBARS) were measured in liver, kidney, and heart. Various serum and urine parameters were also analysed. d-Amphetamine treatment induced an increase of liver GSH, as well as a decrease of cysteine and MnSOD levels in this organ. A small increase in serum transaminases was also observed in comparison to the pair-fed group. Hepatic levels of TBARS, GPx, GRed and CuZnSOD were found to be similar among the three groups of rats. d-Amphetamine treatment induced an increase of kidney GST, GRed and catalase levels, and an elevation of N-acetyl-β-d-glucosaminidase efflux to the urine, accompanied by a decrease in urinary creatinine, compared to the pair-fed group. In d-amphetamine treated animals, heart cysteine levels were significantly depleted when compared to the pair-fed group, but all three groups of rats were found to have similar heart antioxidant enzyme levels. These results indicate that repeated administration of d-amphetamine caused a certain degree of stress in liver and kidney, which was followed by adaptations of antioxidant defences. The mechanisms involved in d-amphetamine-induced toxicity may explain the different adaptations observed for the studied organs. Received: 19 October 1998 / Accepted: 11 January 1999     

Sex-Dependent Effects of the Intake of NOVA Classified Ultra-Processed Foods on Syndrome Metabolic Components in Brazilian Adults

Longitudinal studies evaluating the relationship between UPF consumption and the incidence of Metabolic Syndrome (MetS) and its components are still scarce. This study aimed to evaluate the effect of UPF consumption on the incidence of MetS and its components in adults. A prospective study was conducted with 896 participants from the 1978/79 Ribeirão Preto cohort, São Paulo, Brazil. UPF consumption was evaluated in %kcal and %g at ages 23–25 years. Incidence of MetS and its components were estimated at ages 37–39 years, according to the Joint Interim Statement criteria. Poisson regression was used to assess associations, and interactions with sex were investigated. UPF consumption had no association with MetS (%kcal Adjusted PR: 1.00; 95% CI: 0.99–1.01; %g Adjusted PR: 1.00; 95% CI: 0.99–1.01). However, women with higher UPF consumption, in %kcal and %g, had a higher risk of abdominal obesity (%kcal: p = 0.030; %g: p = 0.003); and women with higher UPF consumption, in %g, had a higher risk of low HDL-cholesterol (p = 0.041). For the other components of MetS, no significant associations were observed in either sex. These findings suggest evidence of no association between UPF consumption and MetS; however, consumption of UPF was associated with increased WC and low HDL-c, but only in women.     

Molecular analysis of the β-catenin gene in patients with the Mayer-Rokitansky-Küster-Hauser syndrome

Purpose

To study the β-catenin gene in a group of Mayer-Rokitansky-Küster-Hauser patients.

Methods

Twelve patients with the Mayer-Rokitansky-Küster-Hauser syndrome were included in this study. DNA was extracted from peripheral blood and the region codifying β-catenin GSK-3β phosphorylation sites on exon 3 was amplified. PCR products were purified and directly sequenced.

Results

No mutations were found in the GSK-3β phosphorylation sites on exon 3 of β-catenin gene in this group of patients with the MRKH syndrome.

Conclusions

β-catenin gene mutations are an unlikely cause of the MRKH syndrome.