Background: Necrotizing enterocolitis (NEC) is one of the most important life- threatening diseases in neonates. Recurrent episodes of supraventricular tachycardia (SVT) can lead to gut ischemia, with subsequent reperfusion injury resulting in NEC. Mesenchymal stem cells (MSCs) are multi-potential cells which can differentiate into multiple cell types. Case report: A 22-day old male baby delivered to 34 yr old mother at 37-weeks’ gestation via cesarean section, birth weight 3550 g, developed NEC 14 hours after being treated with cardioversion for SVT. At laparotomy, there was pan-NEC, and 60 cm of necrotic and perforated bowel was resected. 1 × 10⁷ umbilical cord origin allogeneic MSCs were given intravenously, with subsequent improvement of the remaining bowel. Conclusion: MSC may be a promising treatment for adjacent ischemic bowel in NEC helping prevent short bowel syndrome.

Objective: It is suggested that folic acid and/or multivitamins, taken periconceptionally, have a role in the prevention of many congenital anomalies. The aim of this study was to determine the serum micronutrient levels in mother–infant pairs with CHD compared with those with healthy newborns and their mothers.Methods: Serum levels of folic acid, homocysteine, zinc, vitamin A, vitamin D, and vitamin B₁₂were measured from 108 newborns with CHD (study group) and 103 healthy newborns (control group). The mothers’ micronutrient levels were also measured simultaneously.Results: When compared with healthy newborns, for both maternal and neonatal data, homocysteine and zinc levels were higher and vitamin D levels were lower in the study group. In multivariate analysis, only maternal high zinc levels were associated with CHD in the newborns (p=0.02, OR: 0.9, 95% CI 0.8–0.9). The results did not change when analysed for truncal anomalies including truncus arteriosus, tetralogy of Fallot, and d-transposition of great arteries. There were positive correlations between maternal and neonatal levels of micronutrients, except vitamin B₁₂.Conclusion: We thought that high homocysteine and zinc levels and low vitamin D levels in mother–infant pairs might have a role in the aetiopathogenesis of CHD. Large-scale, prospective studies are needed to clarify the role of micronutrients in CHDs.

Objective This study aimed to ascertain the effects of astaxanthin (ASX) in an experimental necrotizing enterocolitis (NEC) model using rat pups. Study Design Forty-two pups born from five Wistar albino rats were randomly divided into three groups as the control group, NEC + placebo (saline), and NEC + ASX. Pups in the NEC + ASX group were given 100 mg/kg/day oral ASX from day 1 to day 4 of the study. Saline of 2 mL/kg was given to the NEC + placebo group. Histopathological, immunohistochemical (caspase-3), and biochemical evaluations including the total antioxidant status (TAS), total oxidant status (TOS), superoxide dismutase (SOD), glutathione (GSH), lipid hydroperoxide (LPO), 8-hydroxydeoxyguanosine (8-OHdG), advanced oxidation protein products (AOPP), myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and nuclear factor erythroid 2–related factor 2 (Nfr-2) activities were all performed. Results A better survival rate and weight gain were demonstrated in the NEC + ASX group (p < 0.05). In the histopathological evaluation, the severity of intestinal damage was significantly reduced in the NEC + ASX group, as well as decreased apoptosis (enzyme-linked immunosorbent assay [ELISA] for caspase-3; p = 0.001). The biochemical analyses of intestinal tissue TOS, oxidative stress index (OSI; TOS/TAS), IL-1β, LPO, 8-OHdG, AOPP, caspase-3 (p < 0.001 for all), and TNF-α and MPO (p = 0.001 for both parameters) levels were lower in the NEC + ASX group than in the NEC + placebo group. Nrf-2, TAS, GSH, and SOD levels were higher in the NEC + ASX group than in the NEC + placebo group (p = 0.001, 0.001, <0.001, and 0.01, respectively). Conclusion ASX treatment has been shown to effectively reduce the severity of intestinal damage in NEC due to its antioxidant, anti-inflammatory, and antiapoptotic properties. Key Points

Background/Aims: This study aimed to ascertain the effects of astaxanthin on the lungs of rat pups with bronchopulmonary dysplasia (BPD) induced by hyperoxia and lipopolysaccharide (LPS). Materials and Methods: Forty-two newborn Wistar rats, born to spontaneous pregnant rats, were divided into three groups: Hyperoxia (95% O2) + lipopolysaccharide (LPS) group, hyperoxia + LPS + astaxhantin group, and control: no treatment group (21% O2). Pups in the hyperoxia + LPS + astaxanthin group were given 100 mg/kg/day oral astaxanthin from the first day to the fifth day. Histopathologic and biochemical evaluations, including glutathione (GSH), total anti-oxidant status (TAS), total oxidant status (TOS), lipid hydroperoxide (LPO), 8-hydroxydeoxyguanosine (8-OHdG), advanced oxidation protein products (AOPP), myeloperoxidase (MPO), total thiol, tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), and caspase-3 activities, were performed. Results: Better survival rates and weight gain were demonstrated in the hyperoxia + LPS + astaxanthin group (p <0.001). In the histopathologic evaluation, the severity of lung damage was significantly reduced in the hyperoxia+LPS+astaxanthin group, as well as decreased apoptosis (ELİSA for caspase-3) (p <0.001). The biochemical analyses of lung tissues showed that TAS, GSH, and Total thiol levels were significantly higher in the astaxanthin treated group compared to the hyperoxia + LPS group (p <0.05) while TOS, AOPP, LPO, 8-OHdG, MPO levels were significantly lower (p <0.001). In addition, unlike the hyperoxia + LPS group, TNF-α and IL-1β levels in lung tissue were significantly lower in the astaxanthin-treated group (p <0.001). Conclusion: Astaxanthin was shown to reduce lung damage caused by inflammation and hyperoxia with its anti-inflammatory, anti-oxidant, anti-apoptotic properties, and to protect the lung from severe destruction.

Background and aim: The thiol-disulphide homeostasis is essential for the body to maintain effective antioxidant defence mechanisms. We aimed to show the relationship between sepsis and thiol-disulphide homeostasis in newborns. Materials and methods: In this prospective study,66 newborns with sepsis (Group 1) and 51 healthy controls (Group 2) were included. In Group 1, 53 newborns were diagnosed as clinical sepsis (Group 1a) and 13 as definite sepsis (Group 1b). The study has to time points; the day of diagnosis (Step 1) and 3 days after the treatment (Step 2). At step 1, Group 1 and Group 2 were compared for thiol-disulphide homeostasis as well as inflammatory markers At step 2, the same laboratory tests were repeated only in Group 1. Results: At step 1, the levels of C-reactive protein (CRP) and interleukin-6 (IL-6) were higher, while native thiol and total thiol levels were lower in Group 1 compared to controls. Serum disulphide / total thiol ratio was also significantly higher in Group 1. When analyzed for subgroups of Group 1, demonstration of microorganism in did not affect the serum thiol levels. Within Group 1, at step 2, although CRP and IL-6 levels were significantly lowered compared to step 1, we did not observe significant changes in thiol-disulphide parameters. Conclusion: The thiol-disulphide homeostasis may have a role in the pathogenesis of sepsis in newborns. The related parameters might be new markers for the diagnosis of sepsis in newborn patients. Further studies are needed to define the role of thiol-disulphide homeostasis in the course of neonatal sepsis.

Lung ultrasonography (LUS) is a noninvasive bed-side test and increasingly used by clinicians in the management and follow-up of respiratory distress syndrome (RDS) in premature infants.To compare ...