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Antenatal steroid administration to pregnant women at risk of prematurity provides pulmonarymaturation in infants, while it has limited effects on incidence of bronchopulmonary dysplasia (BPD), the clinical expression of hyperoxia-induced lung injury (HILI). Cytidine-5'-diphosphate choline (CDP-choline) was shown to alleviate HILI when administered to newborn rats. Therefore, we investigated effects of maternal administration of CDP-choline, alone or in combination with betamethasone, on lung maturation in neonatal rats subjected to HILI immediately after birth. Pregnant rats were randomly assigned to one of the four treatments: saline (1mL/kg), CDP-choline (300 mg/kg), betamethasone (0.4mg/kg), or CDP-choline plus betamethasone (combination therapy). From postnatal day 1 to 11, pups born to mothers in the same treatment group were pooled and randomly assigned to either normoxia or hyperoxia group. Biochemical an d histopathological effects of CDP-choline on neonatal lung tissue were evaluated. Antenatal CDP-choline treatment increased levels of phosphatidylcholine and total lung phospholipids, decreased apoptosis, and improved alveolarization. The outcomes were further improved with combination therapy compared to the administration of CDP-choline or betamethasone alone. These results demonstrate that antenatal CDP-choline treatment provides benefit in experimental HILI either alone or more intensively when administered along with a steroid, suggesting a possible utility for CDP-choline against BPD. Key words: betamethasone, bronchopulmonary dysplasia, citicoline, newborn rat, 1. Introduction Bronchopulmonary dysplasia (BPD) is the most common long-term respiratory complication of premature birth. Despite improvements such as antenatal corticosteroid therapy, non-invasive ventilation practices, surfactant replacement therapy, and advanced [...]

Background: The study was carried out to determine the knowledge level of nursing students about oxygen therapy in neonatal intensive care units. Material and Methods: This study was carried out with 89 students who agreed to participate in the study between January-March 2019. The data were collected by using the questionnaire which were prepared by the researchers to determine the knowledge level of the participants about oxygen application in neonatal intensive care units. The statistical analyses were performed by using Shapiro Wilk test, Mann Whitney U test and descriptive statistical methods. Result: The mean total knowledge level of the students about oxygen application in neonatal intensive care units was determined as 25.75 ± 3.56. The mean score of female students was 26.47 ± 3.10 while the mean score of male students was 23.42 ± 4.03. In terms of groups there was a statistically significant difference between the knowledge level about oxygen application in newborn intensive care units. Conclusion: In the study, the level of knowledge of the nursing students about oxygen administration in neonatal intensive care units was found as high. [ABSTRACT FROM AUTHOR]

Aim: Apoptosis after cerebral ischemia/reperfusion (I/R) injury leads to the process of cell death. The deal therapeutic approach would target the apoptosis after I/R. Ischemic postconditioning is a recently discovered neuroprotective strategy that involves the application of brief mechanical reperfusion with a specific algorithm at the onset of reperfusion following an ischemic period., Material and Methods: Transient MCAo was performed on male SD (275+/-25 g) rats with intraluminal thread insertion for 2 hrs. Rats (n:36) were treated with postconditioning after 60 minutes of occlusion. The postconditioning algorithm was 30 secs of brief reperfusion followed by 30 secs of MCAo and this cycle was repeated 3 times at the onset of reperfusion., Results: After I/R injury, % change of the malonyldialdehyde (MDA) levels in the cortex, which is an index of lipid peroxidation, was found significantly higher in the I/R group. On the other hand postconditioning upregulated Bcl-2 and Bax translocation to the mitochondria, and caspase-3 activity and also reduced oxidative stress levels., Conclusion: These findings indicated this neuroprotective effect is most likely achieved by antiapoptotic mechanisms through caspase pathways.

Elucidation of the endogenous cell survival pathways involved in ischemic tolerance (preconditioning) and postconditioning has significant clinical implications for preventing neuronal damage in susceptible patients. Ischemic tolerance is a phenomenon in which the brain protects itself against future injury by adapting to low doses of noxious insults. Ischemic postconditioning is defined as brief periods of reperfusion alternating with re-occlusion applied during the very early minutes of reperfusion that mechanically alters the hydrodynamics of reperfusion. Similar pathways and molecules play a role in pre-and postconditioning but their roles and timing are different in each conditioning. Understanding the neuroprotective effects of mechanisms underlying conditioning has been elusive, but NMDA receptor activation, nitric oxide, inflammatory cytokines, and suppression of the innate immune system appear to have a role. Reactive oxygen species and classical ligand stimuli play a role in postconditioning with KATP channels and protein kinase C pathways acting as mediators.