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Background and Purpose: Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity in young adults. The role of iron in potentiating neurodegeneration following TBI has gained recent interest as iron deposition has been detected in the injured brain in the weeks to months post‐TBI, in both the preclinical and clinical setting. A failure in iron homeostasis can lead to oxidative stress, inflammation and excitotoxicity; and whether this is a cause or consequence of the long‐term effects of TBI remains unknown. Experimental Approach: We investigated the role of iron and the effect of therapeutic intervention using a brain‐permeable iron chelator, deferiprone, in a controlled cortical impact mouse model of TBI. An extensive assessment of cognitive, motor and anxiety/depressive outcome measures were examined, and neuropathological and biochemical changes, over a 3‐month period post‐TBI. Key Results: Lesion volume was significantly reduced at 3 months, which was preceded by a reduction in astrogliosis, microglia/macrophages and preservation of neurons in the injured brain at 2 weeks and/or 1 month post‐TBI in mice receiving oral deferiprone. Deferiprone treatment showed significant improvements in neurological severity scores, locomotor/gait performance and cognitive function, and attenuated anxiety‐like symptoms post‐TBI. Deferiprone reduced iron levels, lipid peroxidation/oxidative stress and altered expression of neurotrophins in the injured brain over this period. Conclusion and Implications: Our findings support a detrimental role of iron in the injured brain and suggest that deferiprone (or similar iron chelators) may be promising therapeutic approaches to improve survival, functional outcomes and quality of life following TBI. [ABSTRACT FROM AUTHOR]

Background: The nutritional value and superiority of breast milk against the commercial infant formula has been confirmed by studies results, particularly for premature neonates. Aims: The aims of this study was to: a) explore the factors that are significantly associated and affect the breastfeeding of preterm newborns after their exit from the Neonatal Intensive Care Unit (NICU) and during their stay at home and b) to explore the prevalence and duration of breastfeeding (exclusive or not) in the population of premature neonates in Greece. Methodology: A cross-sectional study was conducted in 2014. A hundred mothers participated via telephone interviews in the study. The newborns of the above mothers were born prematurely and were hospitalized from 2009 to 2010 in a large public hospital pediatric NICU of Athens (Greece). Results: The majority of the women were nulliparous, they had given birth by caesarean section (70%) and most of them had no previous experience of breastfeeding (65%). Just before leaving the NICU and during their stay at home, only 17% of the newborns were fed with exclusive breastfeeding and 24% received exclusively breast milk in any way. The main way of feeding was formula (54%). According to the multivariate logistic regression, breastfeeding at home after NICU discharge is strongly related to: a) mother's support for maintaining lactation (p=0.026), b) past experience of breastfeeding (p=0.049) and c) increased duration of pregnancy (p=0.026). Conclusions: This research highlights factors that seem to have a significant impact on the decision of mothers of premature neonates to breastfeed, a crucial decision for this vulnerable category of newborns. In order to eliminate all obstacles that hinder the positive attitude of mothers towards breastfeeding, further exploration of relevant factors is necessary, in particular after the discharge of premature neonates from the NICU. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) leaves many survivors with long-term disabilities. A prolonged immune response in the brain may cause neurodegeneration, resulting in chronic neurological disturbances. In this study, using a TBI mouse model, we correlate changes in the local immune response with neurodegeneration/neurological dysfunction over an 8-month period. Flow cytometric analysis reveals a protracted increase in effector/memory CD8 + T cells (expressing granzyme B) in the injured brain. This precedes interleukin-17 + CD4 + T cell infiltration and is associated with progressive neurological/motor impairment, increased circulating brain-specific autoantibodies, and myelin-related pathology. Genetic deficiency or pharmacological depletion of CD8 + T cells, but not depletion of CD4 + T cells, improves neurological outcomes and produces a neuroprotective Th2/Th17 immunological shift, indicating a persistent detrimental role for cytotoxic T cells post-TBI. B cell deficiency results in severe neurological dysfunction and a heightened immune reaction. Targeting these adaptive immune cells offers a promising approach to improve recovery following TBI., (Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.)