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While there has been an increasing professional and political focus on the prevalence and harmfulness of child neglect, little has been done to explore what child neglect means outside child protection circles. This qualitative study explores lay constructions of child neglect by thematically analyzing focus group discussions between 46 self-defined ‘lay’ people in England. Participants viewed neglect as extremely damaging for children and as arising when children’s physical, emotional, training and supervisory needs were unmet due to abnormal parental behavior. Children with unmet needs were positioned as deprived, unloved, uncontrolled and escaping. They were only positioned as neglected when failure to meet their needs was attributable to a lack of parental knowledge and skill (clueless parents), a lack of appropriate parental disposition (underinvested parents) or both (unsuitable parents). ‘Normal’ parents – those with the appropriate parental disposition, skills and knowledge – who failed to meet their children’s needs were not seen as neglectful but rather as overburdened. As ‘normal parenting’ has fragmented in late modernity, society wide consensus on child neglect was felt by participants to have retreated to child protection definitions, alienating lay understandings. If child neglect really is ‘everybody’s business’, then it is important that lay people are included in forging new definitions of and responses to meeting the needs of children. [ABSTRACT FROM AUTHOR]

Purpose The purpose of this paper is to provide an analysis of the changes in child protection policy and practice in England over the last 30 years, in particular to critically analyse the nature and impact of the “refocusing” initiative of the mid-1990s.Design/methodology/approach Policy analysis.Findings While the period from the mid-1990s until 2008 can be seen to show how policy and practice attempted to build on a number of the central principles of the “refocusing” initiative, the period since 2008 has been very different. Following the huge social reaction to the death of Peter Connelly, policy and practice moved in directions quite contra to the “refocusing” initiative’s aims and aspirations such that we can identify a refocusing of “refocusing”. Such developments were given a major impetus with the election of the Coalition government in 2010 and have been reinforced further following the election of the Conservative government in May 2015.Originality/value The paper places the changes in child protection policy and practice in England in their political and economic contexts and makes explicit how the changes impact on the role and responsibilities of professionals, particularly social workers. [ABSTRACT FROM AUTHOR]

Zika virus (ZIKV) infection during pregnancy has been causally linked to a constellation of neurodevelopmental deformities in the fetus resulting in a disease termed congenital Zika syndrome (CZS). Here we detail how ZIKV infection produces extensive neuropathology in the developing mouse brain and spinal cord of both sexes. Surprisingly, neuropathology differs depending on viral strain with a French Polynesian isolate producing primarily excitotoxicity and a Brazilian isolate being almost exclusively apoptotic but occurring over a prolonged period that is more likely to produce severe hypoplasia. We also show exposure can produce a characteristic pattern of infection that mirrors neuropathology and ultimately results in gross morphological deformities strikingly similar to CZS. This research provides a valuable mouse model mirroring the clinical course of disease that can be used to test potential therapies to improve treatment and gain a better understanding of the disabilities associated with CZS. [ABSTRACT FROM AUTHOR]

Sedatives and anesthetics can injure the developing brain. They cause apoptosis of neurons and oligodendrocytes, impair synaptic plasticity, inhibit neurogenesis and trigger long-term neurocognitive deficits. The projected vulnerable period in humans extends from the third trimester of pregnancy to the third year of life. Despite all concerns, there is no ethically and medically acceptable alternative to the use of sedatives and anesthetics for surgeries and painful interventions. Development of measures that prevent injury while allowing the medications to exert their desired actions has enormous translational value. Here we investigated protective potential of hypothermia against histological toxicity of the anesthetic sevoflurane in the developing nonhuman primate brain. Neonatal rhesus monkeys underwent sevoflurane anesthesia over 5 h. Body temperature was regulated in the normothermic (>36.5 °C), mild hypothermic (35–36.5 °C) and moderately hypothermic (<35 °C) range. Animals were euthanized at 8 h and brains examined immunohistochemically (activated caspase 3) and stereologically to quantify apoptotic neuronal and oligodendroglial death. Sevoflurane anesthesia was well tolerated at all temperatures, with oxygen saturations, end tidal CO 2 and blood gases remaining at optimal levels. Compared to controls, sevoflurane exposed brains displayed significant apoptosis in gray and white matter affecting neurons and oligodendrocytes. Mild hypothermia (35–36.5 °C) conferred significant protection from apoptotic brain injury, whereas moderate hypothermia (<35 °C) did not. Hypothermia ameliorates anesthesia-induced apoptosis in the neonatal primate brain within a narrow temperature window (35–36.5 °C). Protection is lost at temperatures below 35 °C. Given the mild degree of cooling needed to achieve significant brain protection, application of our findings to humans should be explored further. • Sevoflurane triggers apoptosis of neurons and oligodendrocytes in neonatal primates; • Mild hypothermia conferred significant protection from apoptosis; • Moderate hypothermia did not protect from sevoflurane-induced apoptosis; • The protective temperature window in the neonatal primate brain is very narrow; • Application of our findings to humans should be explored further. [ABSTRACT FROM AUTHOR]

Epidemiological studies suggest exposures to anesthetic agents and/or sedative drugs (AASDs) in children under three years old, or pregnant women during the third trimester, may adversely affect brain development. Evidence suggests lengthy or repeated AASD exposures are associated with increased risk of neurobehavioral deficits. Animal models have been valuable in determining the type of acute damage in the developing brain induced by AASD exposures, as well as in elucidating long-term functional consequences. Few studies examining very early exposure to AASDs suggest this may be a critical period for inducing long-term functional consequences, but the impact of repeated exposures at these ages has not yet been assessed. To address this, we exposed mouse pups to a prototypical general anesthetic, isoflurane (ISO, 1.5% for 3 hr), at three early postnatal ages (P3, P5 and P7). We quantified the acute neuroapoptotic response to a single versus repeated exposure, and found age- and brain region-specific effects. We also found that repeated early exposures to ISO induced subtle, sex-specific disruptions to activity levels, motor coordination, anxiety-related behavior and social preference. Our findings provide evidence that repeated ISO exposures may induce behavioral disturbances that are subtle in nature following early repeated exposures to a single AASD. [ABSTRACT FROM AUTHOR]