A 10-year retrospective review of Salmonella infections at the Children\u27s Hospital in London, Ontario

OBJECTIVES: To describe Salmonella infections in children presenting to the Children\u27s Hospital (London Health Sciences Centre, London, Ontario), to assess risk factors for infection and to examine whether younger children, particularly infants younger than 12 weeks of age, experience higher morbidity than older children. METHODS: A 10-year retrospective review of children with Salmonella infections at the Children\u27s Hospital was conducted. Patient demographics, risk factors for infection, clinical characteristics, bacteriology and outcome were collected from the hospital charts and laboratory records. Data were separated into groups based on age and recent use of antibiotics to analyze differences in outcomes. RESULTS: Sixty-six children with Salmonella infections presented to the Children\u27s Hospital over a 10-year period. Common risk factors for Salmonella infection included having sick contacts, living in a rural area, recent travel, contact with pets (especially reptiles) and exposure to local water. Younger age was associated with an increased likelihood of admission to hospital, treatment with antibiotics and a longer course of antibiotic therapy. This was true when comparing older infants with those younger than 12 weeks of age. Patients recently treated with antibiotics and those with significant underlying medical conditions were more likely to be admitted. CONCLUSIONS: A wider knowledge of the epidemiological risk factors for Salmonella infection may improve diagnosis. Higher admission rates were expected in children younger than 12 weeks of age, those recently treated with antibiotics and those who had a significant underlying medical condition. A prospective, multicentre study is needed to further address questions regarding increased illness severity and appropriate management of Salmonella infections in children younger than 12 weeks of age. ©2010 Pulsus Group Inc. All rights reserved

The absence of retinal input disrupts the development of cholinergic brainstem projections in the mouse dorsal lateral geniculate nucleus

Abstract Background The dorsal lateral geniculate nucleus (dLGN) of the mouse has become a model system for understanding thalamic circuit assembly. While the development of retinal projections to dLGN has been a topic of extensive inquiry, how and when nonretinal projections innervate this nucleus remains largely unexplored. In this study, we examined the development of a major nonretinal projection to dLGN, the ascending input arising from cholinergic neurons of the brainstem. To visualize these projections, we used a transgenic mouse line that expresses red fluorescent protein exclusively in cholinergic neurons. To assess whether retinal input regulates the timing and pattern of cholinergic innervation of dLGN, we utilized the math5-null (math5 −/−) mouse, which lacks retinofugal projections due to a failure of retinal ganglion cell differentiation. Results Cholinergic brainstem innervation of dLGN began at the end of the first postnatal week, increased steadily with age, and reached an adult-like pattern by the end of the first postnatal month. The absence of retinal input led to a disruption in the trajectory, rate, and pattern of cholinergic innervation of dLGN. Anatomical tracing experiments reveal these disruptions were linked to cholinergic projections from parabigeminal nucleus, which normally traverse and reach dLGN through the optic tract. Conclusions The late postnatal arrival of cholinergic projections to dLGN and their regulation by retinal signaling provides additional support for the existence of a conserved developmental plan whereby retinal input regulates the timing and sequencing of nonretinal projections to dLGN

A 10-year retrospective review of Salmonella infections at the Children’s Hospital in London, Ontario

OBJECTIVES: To describe Salmonella infections in children presenting to the Children’s Hospital (London Health Sciences Centre, London, Ontario), to assess risk factors for infection and to examine whether younger children, particularly infants younger than 12 weeks of age, experience higher morbidity than older children

Research Article Modulation of CREB in the Dorsal Lateral Geniculate Nucleus of Dark-Reared Mice

Copyright © 2012 Thomas E. Krahe et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The cAMP-response element-binding protein (CREB) plays an important role in visual cortical plasticity that follows the disruption of sensory activity, as induced by dark rearing (DR). Recent findings indicate that the dorsal lateral geniculate nucleus (dLGN) of thalamus is also sensitive to altered sensory activity. DR disrupts retinogeniculate synaptic strength and pruning in mice, but only when DR starts one week after eye opening (delayed DR, DDR) and not after chronic DR (CDR) from birth. While DR upregulates CREB in visual cortex, whether it also modulates this pathway in dLGN remains unknown. Here we investigate the role of CREB in the dLGN of mice that were CDR or DDR using western blot and immunofluorescence. Similar to findings in visual cortex, CREB is upregulated in dLGN after CDR and DDR. These findings are consistent with the proposal that DR up-regulates the CREB pathway in response to decreased visual drive. 1

A Molecular Mechanism Regulating the Timing of Corticogeniculate Innervation

Neural circuit formation demands precise timing of innervation by different classes of axons. However, the mechanisms underlying such activity remain largely unknown. In the dorsal lateral geniculate nucleus (dLGN), axons from the retina and visual cortex innervate thalamic relay neurons in a highly coordinated manner, with those from the cortex arriving well after those from retina. The differential timing of retino- and corticogeniculate innervation is not a coincidence but is orchestrated by retinal inputs. Here, we identified a chondroitin sulfate proteoglycan (CSPG) that regulates the timing of corticogeniculate innervation. Aggrecan, a repulsive CSPG, is enriched in neonatal dLGN and inhibits cortical axons from prematurely entering the dLGN. Postnatal loss of aggrecan from dLGN coincides with upregulation of aggrecanase expression in the dLGN and corticogeniculate innervation and, it is important to note, is regulated by retinal inputs. Taken together, these studies reveal a molecular mechanism through which one class of axons coordinates the temporal targeting of another class of axons

Strict Independence of Parallel and Poly-synaptic Axon-Target Matching during Visual Reflex Circuit Assembly

The use of sensory information to drive specific behaviors relies on circuits spanning long distances that wire up through a range of axon-target recognition events. Mechanisms assembling poly-synaptic circuits and the extent to which parallel pathways can “cross-wire” to compensate for loss of one another remain unclear and are crucial to our understanding of brain development and models of regeneration. In the visual system, specific retinal ganglion cells (RGCs) project to designated midbrain targets connected to downstream circuits driving visuomotor reflexes. Here, we deleted RGCs connecting to pupillary light reflex (PLR) midbrain targets and discovered that axon-target matching is tightly regulated. RGC axons of the eye-reflex pathway avoided vacated PLR targets. Moreover, downstream PLR circuitry is maintained; hindbrain and peripheral components retained their proper connectivity and function. These findings point to a model in which poly-synaptic circuit development reflects independent, highly stringent wiring of each parallel pathway and downstream station