Erratum: Evaluation of Suspected COVID-19 Patients in a Pediatric Emergency Department.

[This corrects the article DOI: 10.1055/s-0041-1735493.].

Evaluation of Suspected COVID-19 Patients in a Pediatric Emergency Department.

Coronavirus disease 2019 (COVID-19) is now a global pandemic. The aim of this study was to investigate the prevalence of COVID-19 in pediatric patients and to compare the characteristics of positive and negative patients. This study conducted from March to May 2020 in a tertiary children's hospital. Patients were included if they were under 18 years old and a SARS-CoV-2 polymerase chain reaction test had been performed. Of the 1,812 patients included in the study, 365 (20.1%) were positive for COVID-19. The median age was 102 months in the positive group, 70 months in the negative group ( p < 0.001). The sex distribution was almost equal. Nearly all positive patients had been in close contact with a COVID-19 infected family household member ( p < 0.001). The most common symptoms were fever (54.4%) and cough (38.6%). The asymptomatic patient rate was higher in the positive group ( p < 0.001). Lymphopenia (<1500/mm 3 ) was found in 29.9% of the positive children ( p = 0.005). When the groups were compared, white blood cell, neutrophil, lymphocyte, and platelet counts; neutrophil-to-lymphocyte ratio; and C-reactive protein level were lower in the positive group. Chest radiography was performed in 95.3% of the positive patients, and the results of 29.7% of them were interpreted as pathological ( p < 0.001). Most of the pediatric patients had a history of contact with COVID-19 positive individuals, and therefore, the diagnosis is generally suspected from a history of household exposure to COVID-19. Lymphopenia can help predict positivity. Awareness, reinforcing infection control measures, and performing health management within families are important steps to manage these patients.

Age-related changes in rat prostate tissue; perspective of protein oxidation.

BACKGROUND: Increased systemic oxidative stress is considered as an important risk factor for prostate cancer occurrence; however, the relationship between impaired redox homeostasis of prostate tissue and aging remains unclear. OBJECTIVE: In our study, we hypothesized that age-related deterioration of redox homeostasis in prostate tissue may be considered as a predisposing factor for prostate cancer occurrence. METHODS: Sprague-Dawley rats were divided into two groups as young control (5 months) and naturally aged (24 months). We investigated the levels of oxidant and antioxidant parameters in prostate tissue. RESULTS: Advanced oxidation protein products, protein carbonyl, non-protein thiol and lipid hydroperoxides levels of aged rats were significantly higher than in the young control rats (p < 0.01, p < 0.05, p < 0.001, p < 0.05, respectively). Additionally, antioxidant activity of Cu-Zn-superoxide dismutase in elderly group was significantly lower than young controls (p < 0.05). CONCLUSIONS: We suggest that increased non-protein thiol levels found in aged rats may prevent further dissemination of oxidative protein damage. We also propose that the increased levels of oxidative protein damage markers and decreased Cu-Zn superoxide dismutase activity in aged prostate may be considered as a predisposing factor for prostate cancer. Further studies are warranted to clarify all these oxidative changes as initiation factors for prostate cancer in the association of aging with prostate cancer.

A comprehensive study of myocardial redox homeostasis in naturally and mimetically aged rats.

Age-related myocardial dysfunction has important implications with impaired redox homeostasis. Current study focused on investigation of redox homeostasis and histopathological changes in the myocardium of mimetically (MA), naturally aged (NA), and young control (YC) rats. Chronic D-galactose administration to young male Wistar rats (5 months old) was used to set up experimental aging models. We investigated 16 different oxidative damage biomarkers which have evaluated redox homeostasis of cellular macromolecules such as protein, lipid, and DNA. As a protein oxidation biomarker, advanced oxidation end products, protein carbonyl groups, protein-bound advanced glycation end products, dityrosine, kynurenine, and N-formylkynurenine concentrations in MA and NA rats were found to be significantly higher compared to those in YC rats. On the other hand, the levels of protein thiol groups were not significantly different between groups, whereas lipid peroxidation biomarkers such as conjugated diens, lipid hydroperoxides, and malondialdehyde in MA and NA rats were found to be significantly higher in comparison to those in YCs. For the assessment of oxidative DNA damage, we analyzed eight hydroxy-5'-deoxyguanosine concentrations of MA and NA groups which were higher than YCs. As an antioxidant status in the MA and NA groups, Cu-Zn superoxide dismutase, ferric reducing antioxidant power, and total thiol levels were lower than those in the YCs. Only nonprotein thiol levels were not significantly different. We also observed similar histopathological changes in MA and NA rats. We concluded that the mimetic aging model could be considered as a reliable experimental model for myocardial senescence.

Oxidation scrutiny in persuaded aging and chronological aging at systemic redox homeostasis level.

BACKGROUND: The effect of the natural aging process on systemic redox homeostasis is previously documented. However, none of the studies specify the effect of experimental aging on systemic redox homeostasis. The purpose of this study is to clarify the ambiguity raised in preliminary reports as to mimetic aging dependency of the type and magnitude of oxidative damage on constituents of plasma. METHODS: In the current study, we investigated the interrelationship among various groups of the systemic oxidative damage markers such as protein oxidation products (protein carbonyl groups, protein hydroperoxides, advanced oxidation protein products, protein thiol groups), lipid peroxidation products (malondialdehyde, lipid hydroperoxides, conjugated dienes), glycoxidation adducts (advanced glycation end products), and antioxidant capacity (ferric reducing/antioxidant power, Cu,Zn-superoxide dismutase, total thiol, non-protein thiol). All these markers were measured in plasma of mimetically aged (MA) rats (5-month-old rats subjected to d-galactose-induced experimental aging), naturally aged (NA) rats (24-month-old), and their corresponding young controls (YC) (5months old). RESULTS AND CONCLUSIONS: Our current results show that systemic oxidation markers of the MA group share significant similarities in terms of impaired redox homeostasis with the NA rats and may be considered as a reliable experimental aging model for intravascular aging. Additional methodological studies including d-galactose dosage and application time are warranted to clarify the potential involvement of all these systemic redox variations as mechanistic factors in the development of mimetic aging related intravascular deterioration. Reversing or preventing systemic oxidative damage in experimental and natural aging should therefore be considered the primary target for the development of effective therapeutic strategies to prevent or treat age-related vascular disorders.