Stages of development and injury: an epidemiological survey of young children presenting to an emergency department

<p><b>Background:</b> The aim of our study was to use a local (Glasgow, west of Scotland) version of a Canadian injury surveillance programme (CHIRPP) to investigate the relationship between the developmental stage of young (pre-school) children, using age as a proxy, and the occurrence (incidence, nature, mechanism and location) of injuries presenting to a Scottish hospital emergency department, in an attempt to replicate the findings of a recent study in Kingston, Canada.</p> <p><b>Methods:</b> We used the Glasgow CHIRPP data to perform two types of analyses. First, we calculated injury rates for that part of the hospital catchment area for which reasonably accurate population denominators were available. Second, we examined detailed injury patterns, in terms of the circumstances, mechanisms, location and types of injury. We compared our findings with those of the Kingston researchers.</p> <p><b>Results:</b> A total of 17,793 injury records for children aged up to 7 years were identified over the period 1997–99. For 1997–2001, 6,188 were used to calculate rates in the west of the city only. Average annual age specific rates per 1000 children were highest in both males and females aged 12–35 months. Apart from the higher rates in Glasgow, the pattern of injuries, in terms of breakdown factors, mechanism, location, context, and nature of injury, were similar in Glasgow and Kingston.</p> <p><b>Conclusion:</b> We replicated in Glasgow, UK, the findings of a Canadian study demonstrating a correlation between the pattern of childhood injuries and developmental stage. Future research should take account of the need to enhance statistical power and explore the interaction between age and potential confounding variables such as socio-economic deprivation. Our findings highlight the importance of designing injury prevention interventions that are appropriate for specific stages of development in children.</p&gt

Pattern of injury mortality by age-group in children aged 0–14 years in Scotland, 2002–2006, and its implications for prevention

<p>Abstract</p> <p>Background</p> <p>Knowledge of the epidemiology of injuries in children is essential for the planning, implementation and evaluation of preventive measures but recent epidemiological information on injuries in children both in general and by age-group in Scotland is scarce. This study examines the recent pattern of childhood mortality from injury by age-group in Scotland and considers its implications for prevention.</p> <p>Methods</p> <p>Routine mortality data for the period 2002–2006 were obtained from the General Register Office for Scotland and were analysed in terms of number of deaths, mean annual mortality rates per 100,000 population, leading causes of death, and causes of injury death. Mid-year population estimates were used as the denominator. Chi-square tests were used to determine statistical significance.</p> <p>Results</p> <p>186 children aged 0–14 died from an injury in Scotland during 2002–06 (MR 4.3 per 100,000). Injuries were the leading cause of death in 1–14, 5–9 and 10–14 year-olds (causing 25%, 29% and 32% of all deaths respectively). The leading individual causes of injury death (0–14 years) were pedestrian and non-pedestrian road-traffic injuries and assault/homicide but there was variation by age-group. Assault/homicide, fire and suffocation caused most injury deaths in young children; road-traffic injuries in older ones. Collectively, intentional injuries were a bigger threat to the lives of under-15s than any single cause of unintentional injury. The mortality rate from assault/homicide was highest in infants (<1 year) and decreased with increasing age. Children aged 5–9 were significantly less likely to die from an injury than 0–4 or 10–14 year-olds (p < 0.05). Suicide was an important cause of injury mortality in 10–14 year-olds.</p> <p>Conclusion</p> <p>Injuries continue to be a leading cause of death in childhood in Scotland. Variation in causes of injury death by age-group is important when targeting preventive efforts. In particular, the threats of assault/homicide in infants, fire in 1–4 year-olds, pedestrian injury in 5–14 year-olds, and suicide in 10–14 year-olds need urgent consideration for preventive action.</p

Independent Risk Factors for Injury in Pre-School Children: Three Population-Based Nested Case-Control Studies Using Routine Primary Care Data

Background: Injuries in childhood are largely preventable yet an estimated 2,400 children die every day because of injury and violence. Despite this, the factors that contribute to injury occurrence have not been quantified at the population scale using primary care data. We used The Health Improvement Network (THIN) database to identify risk factors for thermal injury, fractures and poisoning in pre-school children in order to inform the optimal delivery of preventative strategies. Methods: We used a matched, nested case-control study design. Cases were children under 5 with a first medically recorded injury, comprising 3,649 thermal injury cases, 4,050 fracture cases and 2,193 poisoning cases, matched on general practice to 94,620 control children. Results: Younger maternal age and higher birth order increased the odds of all injuries. Children’s age of highest injury risk varied by injury type; compared with children under 1 year, thermal injuries were highest in those age 1-2 (OR = 2.43, 95%CI 2.23–2.65), poisonings in those age 2-3 (OR = 7.32, 95%CI 6.26–8.58) and fractures in those age 3-5 (OR = 3.80, 95%CI 3.42–4.23). Increasing deprivation was an important modifiable risk factor for poisonings and thermal injuries (tests for trend p#0.001) as were hazardous/harmful alcohol consumption by a household adult (OR = 1.73, 95%CI 1.26–2.38 and OR = 1.39, 95%CI 1.07–1.81 respectively) and maternal diagnosis of depression (OR = 1.45, 95%CI 1.24–1.70 and OR = 1.16, 95%CI 1.02–1.32 respectively). Fracture was not associated with these factors, however, not living in single-adult household reduced the odds of fracture (OR = 0.88, 95%CI 0.82–0.95). Conclusions: Maternal depression, hazardous/harmful adult alcohol consumption and socioeconomic deprivation represent important modifiable risk factors for thermal injury and poisoning but not fractures in preschool children. Since these risk factors can be ascertained from routine primary care records, pre-school children’s frequent visits to primary care present an opportunity to reduce injury risk by implementing effective preventative interventions from existing national guidelines

Influence of Caloric Restriction on Constitutive Expression of NF-κB in an Experimental Mouse Astrocytoma

Many of the current standard therapies employed for the management of primary malignant brain cancers are largely viewed as palliative, ultimately because these conventional strategies have been shown, in many instances, to decrease patient quality of life while only offering a modest increase in the length of survival. We propose that caloric restriction (CR) is an alternative metabolic therapy for brain cancer management that will not only improve survival but also reduce the morbidity associated with disease. Although we have shown that CR manages tumor growth and improves survival through multiple molecular and biochemical mechanisms, little information is known about the role that CR plays in modulating inflammation in brain tumor tissue.Phosphorylation and activation of nuclear factor κB (NF-κB) results in the transactivation of many genes including those encoding cycloxygenase-2 (COX-2) and allograft inflammatory factor-1 (AIF-1), both of which are proteins that are primarily expressed by inflammatory and malignant cancer cells. COX-2 has been shown to enhance inflammation and promote tumor cell survival in both in vitro and in vivo studies. In the current report, we demonstrate that the p65 subunit of NF-κB was expressed constitutively in the CT-2A tumor compared with contra-lateral normal brain tissue, and we also show that CR reduces (i) the phosphorylation and degree of transcriptional activation of the NF-κB-dependent genes COX-2 and AIF-1 in tumor tissue, as well as (ii) the expression of proinflammatory markers lying downstream of NF-κB in the CT-2A malignant mouse astrocytoma, [e.g. macrophage inflammatory protein-2 (MIP-2)]. On the whole, our date indicate that the NF-κB inflammatory pathway is constitutively activated in the CT-2A astrocytoma and that CR targets this pathway and inflammation.CR could be effective in reducing malignant brain tumor growth in part by inhibiting inflammation in the primary brain tumor

Neuroprotection by adenosine in the brain: From A1 receptor activation to A2A receptor blockade

Adenosine is a neuromodulator that operates via the most abundant inhibitory adenosine A1 receptors (A1Rs) and the less abundant, but widespread, facilitatory A2ARs. It is commonly assumed that A1Rs play a key role in neuroprotection since they decrease glutamate release and hyperpolarize neurons. In fact, A1R activation at the onset of neuronal injury attenuates brain damage, whereas its blockade exacerbates damage in adult animals. However, there is a down-regulation of central A1Rs in chronic noxious situations. In contrast, A2ARs are up-regulated in noxious brain conditions and their blockade confers robust brain neuroprotection in adult animals. The brain neuroprotective effect of A2AR antagonists is maintained in chronic noxious brain conditions without observable peripheral effects, thus justifying the interest of A2AR antagonists as novel protective agents in neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease, ischemic brain damage and epilepsy. The greater interest of A2AR blockade compared to A1R activation does not mean that A1R activation is irrelevant for a neuroprotective strategy. In fact, it is proposed that coupling A2AR antagonists with strategies aimed at bursting the levels of extracellular adenosine (by inhibiting adenosine kinase) to activate A1Rs might constitute the more robust brain neuroprotective strategy based on the adenosine neuromodulatory system. This strategy should be useful in adult animals and especially in the elderly (where brain pathologies are prevalent) but is not valid for fetus or newborns where the impact of adenosine receptors on brain damage is different