Unveiling relationships between crime and property in England and Wales via density scale-adjusted metrics and network tools

Scale-adjusted metrics (SAMs) are a significant achievement of the urban scaling hypothesis. SAMs remove the inherent biases of per capita measures computed in the absence of isometric allometries. However, this approach is limited to urban areas, while a large portion of the world’s population still lives outside cities and rural areas dominate land use worldwide. Here, we extend the concept of SAMs to population density scale-adjusted metrics (DSAMs) to reveal relationships among different types of crime and property metrics. Our approach allows all human environments to be considered, avoids problems in the definition of urban areas, and accounts for the heterogeneity of population distributions within urban regions. By combining DSAMs, cross-correlation, and complex network analysis, we find that crime and property types have intricate and hierarchically organized relationships leading to some striking conclusions. Drugs and burglary had uncorrelated DSAMs and, to the extent property transaction values are indicators of affluence, twelve out of fourteen crime metrics showed no evidence of specifically targeting affluence. Burglary and robbery were the most connected in our network analysis and the modular structures suggest an alternative to "zero-tolerance" policies by unveiling the crime and/or property types most likely to affect each other

Pertussis resurgence in Toronto, Canada: a population-based study including test-incidence feedback modeling

<p>Abstract</p> <p>Background</p> <p>Pertussis continues to challenge medical professionals; recently described increases in incidence may be due to age-cohort effects, vaccine effectiveness, or changes in testing patterns. Toronto, Canada has recently experienced increases in pertussis incidence, and provides an ideal jurisdiction for evaluating pertussis epidemiology due to centralized testing. We evaluated pertussis trends in Toronto using all available specimen data, which allowed us to control for changing testing patterns and practices.</p> <p>Methods</p> <p>Data included all pertussis culture and PCR test records for Greater Toronto from 1993 to 2007. We estimated incidence trends using Poisson regression models; complex relationships between disease incidence and test submission were explored with vector autoregressive models.</p> <p>Results</p> <p>From 1993 to 2007, 26988 specimens were submitted for testing; 2545 (9.4%) were positive. Pertussis incidence was 2 per 100,000 from 1993 to 2004 and increased to 10 per 100,000 from 2005-2007, with a concomitant 6-fold surge in test specimen submissions after the introduction of a new, more sensitive PCR assay. The relative change in incidence was less marked after adjustment for testing volumes. Bidirectional feedbacks between test positivity and test submissions were identified.</p> <p>Conclusions</p> <p>Toronto's recent surge in pertussis reflects a true increase in local disease activity; the apparent size of the outbreak has likely been magnified by increasing use of pertussis testing by clinicians, and by improved test sensitivity since 2005. These findings may be applicable to changes in pertussis epidemiology that have been noted elsewhere in North America.</p

2017 Research & Innovation Day Program

A one day showcase of applied research, social innovation, scholarship projects and activities.https://first.fanshawec.ca/cri_cripublications/1004/thumbnail.jp

[Depression and addiction comorbidity: towards a common molecular target?]

La dépression est le trouble mental le plus souvent associé aux addictions. La prévalence de la dépression parmi les patients souffrant d’une addiction est de 30 %. Cette forte comorbidité suggère l’existence de voies moléculaires et anatomiques communes à ces deux pathologies. C’est le cas du noyau accumbens (NAc) dont le dysfonctionnement est impliqué dans la dépression et l’addiction. Nous résumons ici des résultats récents montrant que la protéine p11 (S100A10) dans le NAc permet de réguler des comportements liés à l’addiction et à la dépression chez la souris. Notamment, la manipulation des niveaux de p11 dans les interneurones cholinergiques ou dans les neurones épineux moyens de la voie directe striato-nigrale permet de contrôler des comportements liés à la dépression et à l’addiction respectivement. Des traitements visant à normaliser les niveaux d’expression de p11 dans le NAc pourraient donc avoir un intérêt thérapeutique dans ces pathologies

Neurotrophic-priming of glucocorticoid receptor signaling is essential for neuronal plasticity to stress and antidepressant treatment

International audienc

Gene therapy blockade of dorsal striatal p11 improves motor function and dyskinesia in parkinsonian mice.

Complications of dopamine replacement for Parkinson's disease (PD) can limit therapeutic options, leading to interest in identifying novel pathways that can be exploited to improve treatment. p11 (S100A10) is a cellular scaffold protein that binds to and potentiates the activity of various ion channels and neurotransmitter receptors. We have previously reported that p11 can influence ventral striatal function in models of depression and drug addiction, and thus we hypothesized that dorsal striatal p11 might mediate motor function and drug responses in parkinsonian mice. To focally inhibit p11 expression in the dorsal striatum, we injected an adeno-associated virus (AAV) vector producing a short hairpin RNA (AAV.sh.p11). This intervention reduced the impairment in motor function on forced tasks, such as rotarod and treadmill tests, caused by substantia nigra lesioning in mice. Measures of spontaneous movement and gait in an open-field test declined as expected in control lesioned mice, whereas AAV.sh.p11 mice remained at or near normal baseline. Mice with unilateral lesions were then challenged with l-dopa (levodopa) and various dopamine receptor agonists, and resulting rotational behaviors were significantly reduced after ipsilateral inhibition of dorsal striatal p11 expression. Finally, p11 knockdown in the dorsal striatum dramatically reduced l-dopa-induced abnormal involuntary movements compared with control mice. These data indicate that focal inhibition of p11 action in the dorsal striatum could be a promising PD therapeutic target to improve motor function while reducing l-dopa-induced dyskinesias