Sudden death and suicide: a comparison of brain weight.
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BACKGROUND: Recent evidence suggests that the brain weight of individuals over the age of 60 who commit suicide is significantly higher than in those who die of natural causes. AIMS: To ascertain whether brain weight is different in people of a younger age who commit suicide than in those who die accidentally. METHOD: A retrospective review of post-mortem reports collecting height, weight and brain weight in 100 suicide victims (87 males, mean age 38.5 years) and 100 age/gender-matched controls who died accidentally or of natural causes (87 males, mean age 38.7 years). Comparison by t-test was made of brain weight in isolation as well as brain weight corrected for height, weight and body mass index. RESULTS: These results reveal no significant difference in brain weight in suicide cases compared to the general population (P > 0.05). The brain weight of those who died by hanging was significantly higher than of those who died by overdose. CONCLUSIONS: Whatever the significant neuropsychiatric elements are that influence suicidal behaviour, they do not consistently affect brain weight in the population studied. (+info)
Induction of mild hypothermia improves neurologic outcome after global cerebral ischemia. This study measured levels of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in hippocampal tissue of rats after resuscitation from 8 minutes of normothermic, asphyxial cardiac arrest. After resuscitation, rats were maintained either at normal temperature (37 degrees C) or cooled to mild hypothermia (33 degrees C, beginning 60 minutes after resuscitation). After 12 or 24 hours, neurotrophin levels in hippocampus were measured by immunoblotting. Ischemia and reperfusion increased hippocampal levels of BDNF. Induction of hypothermia during reperfusion potentiated the increase in BDNF after 24 hours, but not after 12 hours. Levels of NGF were not increased by postresuscitation hypothermia. Hypothermia also increased tissue levels and tyrosine phosphorylation of TrkB, the receptor for BDNF. Increased BDNF levels were correlated with activation of the extracellularly regulated kinase (ERK), a downstream element in the signal transduction cascade induced by BDNF. In contrast to the many deleterious processes during ischemia and reperfusion that are inhibited by induced hypothermia, increasing BDNF levels is a potentially restorative process that is augmented. Increased activation of BDNF signaling is a possible mechanism by which mild hypothermia is able to reduce the neuronal damage typically occurring after cardiac arrest. (+info)
A confidential enquiry into cases of neonatal encephalopathy.
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OBJECTIVES: To assess the quality of care and timing of possible asphyxial events for infants with neonatal encephalopathy; to compare the quality of care findings with those relating to the deaths from the Confidential Enquiry into Stillbirths and Deaths in Infancy (CESDI); and to assess whether the confidential enquiry method is a useful clinical governance tool for investigating morbidity. DESIGN: Independent, anonymised, multidisciplinary case reviews. SETTING: Trent Health Region, UK. PATIENTS: All cases of grade II and III neonatal encephalopathy born in 1997, excluding those due to congenital malformation, inborn error of metabolism, or infection. All CESDI deaths thought to have resulted from intrapartum asphyxia in 1996 and 1997. MAIN MEASURES: Quality of care provided, timing of possible asphyxial episodes, and the source and timing of episodes of suboptimal care. RESULTS: Significant or major episodes of suboptimal care were identified for 64% of the encephalopathy cases and 75% of the deaths. An average of 2.8 and 2.5 episodes of suboptimal care were identified for the deaths and encephalopathy cases respectively. Over 90% of episodes involved the care provided by health professionals. Results were fed directly back to the units concerned on request and changes in practice have been reported. CONCLUSIONS: The findings were very similar for the encephalopathy cases and the deaths. We have demonstrated that with minor adaptations the CESDI process can be applied to serious cases of morbidity. However, explicit quality standards, control data, and a more formal mechanism for the implementation of findings would strengthen the confidential enquiry process as part of clinical governance. (+info)
Upper airway muscle paralysis reduces reflex upper airway motor response to negative transmural pressure in rat.
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The reflex upper airway (UA) motor response to UA negative pressure (UANP) is attenuated by neuromuscular blockade. We hypothesized that this is due to a reduction in the sensitivity of laryngeal mechanoreceptors to changes in UA pressure. We examined the effect of neuromuscular blockade on hypoglossal motor responses to UANP and to asphyxia in 15 anesthetized, thoracotomized, artificially ventilated rats. The activity of laryngeal mechanoreceptors is influenced by contractions of laryngeal and tongue muscles, so we studied the effect of selective denervation of these muscle groups on the UA motor response to UANP and to asphyxia, recording from the pharyngeal branch of the glossopharyngeal nerve (n = 11). We also examined the effect of tongue and laryngeal muscle denervation on superior laryngeal nerve (SLN) afferent activity at different airway transmural pressures (n = 6). Neuromuscular blockade and denervation of laryngeal and tongue muscles significantly reduced baseline UA motor nerve activity (P < 0.05), caused a small but significant attenuation of the motor response to asphyxia, and markedly attenuated the response to UANP. Motor denervation of tongue and laryngeal muscles significantly decreased SLN afferent activity and altered the response to UANP. We conclude that skeletal muscle relaxation reduces the reflex UA motor response to UANP, and this may be due to a reduction in the excitability of UA motor systems as well as a decrease of the response of SLN afferents to UANP. (+info)
Hepatic inflammatory mediators contribute to intestinal damage in necrotizing enterocolitis.
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Necrotizing enterocolitis (NEC) is a common and devastating gastrointestinal disease of premature infants. Along with pathological effects in the ileum, severe NEC is often accompanied by multisystem organ failure, including liver failure. The aim of this study was to determine the changes in hepatic cytokines and inflammatory mediators in experimental NEC. The well-established neonatal rat model of NEC was used in this study, and changes in liver morphology, numbers of Kupffer cells (KC), gene expression, and histological localization of IL-18, TNF-alpha, and inducible nitric oxide synthase were evaluated. Intestinal luminal TNF-alpha levels were also measured. Production of hepatic IL-18 and TNF-alpha and numbers of KC were increased in rats with NEC and correlated with the progression of intestinal damage during NEC development. Furthermore, increased levels of TNF-alpha in the intestinal lumen of rats with NEC was significantly decreased when KC were inhibited with gadolinium chloride. These results suggest an important role of the liver and the gut-liver axis in NEC pathogenesis. (+info)
Respiratory motor recovery after unilateral spinal cord injury: eliminating crossed phrenic activity decreases tidal volume and increases contralateral respiratory motor output.
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By 2 months after unilateral cervical spinal cord injury (SCI), respiratory motor output resumes in the previously quiescent phrenic nerve. This activity is derived from bulbospinal pathways that cross the spinal midline caudal to the lesion (crossed phrenic pathways). To determine whether crossed phrenic pathways contribute to tidal volume in spinally injured rats, spontaneous breathing was measured in anesthetized C2 hemisected rats at 2 months after injury with an intact ipsilateral phrenic nerve, or with ipsilateral phrenicotomy performed at the time of the SCI (i.e., crossed phrenic pathways rendered ineffective) (dual injury). Ipsilateral phrenicotomy did not alter the rapid shallow eupneic breathing pattern in C2 injured rats. However, the ability to generate large inspiratory volumes after either vagotomy or during augmented breaths was impaired if crossed phrenic activity was abolished. We also investigated whether compensatory plasticity in contralateral motoneurons would be affected by eliminating crossed phrenic activity. Thus, contralateral phrenic motor output was recorded in anesthetized, vagotomized, and mechanically ventilated rats with dual injury during chemoreceptor stimulation. Hypercapnia, hypoxia, and asphyxia increased contralateral phrenic burst amplitude in the dual injury group more than in rats with SCI alone. Dual injury rats also had elevated baseline burst frequency. Together, these results demonstrate a functional role of crossed phrenic activity after SCI. Moreover, by preventing ipsilateral phrenic motor recovery in rats with unilateral SCI, segmental and supraspinal changes could be induced in contralateral respiratory motor output beyond that seen with SCI alone. (+info)
A locus for asphyxiating thoracic dystrophy, ATD, maps to chromosome 15q13.
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Asphyxiating thoracic dystrophy (ATD), or Jeune syndrome, is a multisystem autosomal recessive disorder associated with a characteristic skeletal dysplasia and variable renal, hepatic, pancreatic, and retinal abnormalities. We have performed a genome wide linkage search using autozygosity mapping in a cohort of four consanguineous families with ATD, three of which originate from Pakistan, and one from southern Italy. In these families, as well as in a fifth consanguineous family from France, we localised a novel ATD locus (ATD) to chromosome 15q13, with a maximum cumulative two point lod score at D15S1031 (Zmax=3.77 at theta=0.00). Five consanguineous families shared a 1.2 cM region of homozygosity between D15S165 and D15S1010. Investigation of a further four European kindreds, with no known parental consanguinity, showed evidence of marker homozygosity across a similar interval. Families with both mild and severe forms of ATD mapped to 15q13, but mutation analysis of two candidate genes, GREMLIN and FORMIN, did not show pathogenic mutations. (+info)
Differential ranking of causes of fatal versus non-fatal injuries among US children.
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OBJECTIVE: Leading causes of fatal and non-fatal injury among US children aged <15 years were compared. METHOD: A descriptive study was conducted using nationally representative data on injury related deaths (National Vital Statistics System) and on non-fatal injury related emergency department visits (IEDV; National Electronic Injury Surveillance System-All Injury Program). Data were accessed using a publicly available web based system. RESULTS: Annually, an estimated 7100000 pediatric IEDV and 7400 injury deaths occurred. The overall non-fatal to fatal ratio (NF:F) was 966 IEDV:1 death. Among deaths, the leading causes were motor vehicle traffic occupants (n = 1700; NF:F = 150:1), suffocations (n = 1037; NF:F = 14:1), and drownings (n = 971, NF:F = 6:1). Among non-fatal injuries, falls (estimated 2400000) and struck by/against (estimated 1800000) were the most common causes, but substantially less lethal (NF:F = 19000:1 and 15000:1, respectively). CONCLUSIONS: The leading causes of pediatric fatal and non-fatal injuries differed substantially. This study indicates the need for consideration of common causes of non-fatal injury, especially falls. (+info)