Investigating the spatial risk distribution of West Nile virus disease in birds and humans in southern Ontario from 2002 to 2005

<p>Abstract</p> <p>Background</p> <p>The West Nile virus (WNv) became a veterinary public health concern in southern Ontario in 2001 and has continued to threaten public health. Wild bird mortality has been shown to be an indicator for tracking the geographic distribution of the WNv. The purpose of this study was to investigate the latent risk distribution of WNv disease among dead birds and humans in southern Ontario and to compare the spatial risk patterns for the period 2002–2005. The relationship between the mortality fraction in birds and incidence rate in humans was also investigated.</p> <p>Methods</p> <p>Choropleth maps were created to investigate the spatial variation in bird and human WNv risk for the public health units of southern Ontario. The data were smoothed by empirical Bayesian estimation before being mapped. Isopleth risk maps for both the bird and human data were created to identify high risk areas and to investigate the potential relationship between the WNv mortality fraction in birds and incidence rates in humans. This was carried out by the geostatistical prediction method of kriging. A Poisson regression analysis was used to model regional human WNv case counts as a function of the spatial coordinates in the east and north direction and the regional bird mortality fractions. The presence of disease clustering and the location of disease clusters were investigated by the spatial scan test.</p> <p>Results</p> <p>The isopleth risk maps exhibited high risk areas that were relatively constant from year to year. There was an overlap in the bird and human high risk areas, which occurred in the central-west and south-west areas of southern Ontario. The annual WNv cause-specific mortality fractions in birds for 2002 to 2005 were 31.9, 22.0, 19.2 and 25.2 positive birds per 100 birds tested, respectively. The annual human WNv incidence rates for 2002 to 2005 were 2.21, 0.76, 0.13 and 2.10 human cases per 100,000 population, respectively. The relative risk of human WNv disease was 0.72 times lower for a public health unit that was 100 km north of another public health unit. The relative risk of human WNv disease increased by the factor 1.44 with every 10 positive birds per 100 tested. The scan statistic detected disease cluster in the bird and human data. The human clusters were not significant, when the analysis was conditioned on the bird data.</p> <p>Conclusion</p> <p>The study indicates a significant relationship between the spatial pattern of WNv risk in humans and birds.</p

A multi-site study on walkability, data sharing and privacy perception using mobile sensing data gathered from the mk-sense platform

Walking is a fundamental part of a physically active lifestyle, it is one of everyday activities that positively impacts health and wellbeing. In this paper we describe the challenges and experiences of conducting a sensing campaign in the wild. We make use of mk-sense; a software platform to facilitate the deployment of collaborative sensing campaigns. We elaborate on two cross-cultural studies conducted in four different countries (Mexico, Turkey, Spain, and Switzerland) with a total of 77 participants. We present a detailed description of the data collected from one of the studies aimed at measuring walkability around three different university campuses. The analysis of the data shows that walkability can be assessed using information from the sensors in the smartphones and results from surveys answered by participants. In addition, we analyze issues about data sharing and privacy awareness

Methamphetamine induces endoplasmic reticulum stress related gene CHOP/Gadd153/ddit3 in dopaminergic cells

We examined the toxicity of methamphetamine and dopamine in CATH.a cells, which were derived from mouse dopamine-producing neural cells in the central nervous system. Use of the quantitative real-time polymerase chain reaction revealed that transcripts of the endoplasmic reticulum stress related gene (CHOP/Gadd153/ddit3) were considerably induced at 24–48 h after methamphetamine administration (but only under apoptotic conditions), whereas dopamine slightly induced CHOP/Gadd153/ddit3 transcripts at an early stage. We also found that dopamine and methamphetamine weakly induced transcripts for the glucose-regulated protein 78 gene (Grp78/Bip) at the early stage. Analysis by immunofluorescence microscopy demonstrated an increase of　CHOP/Gadd153/ddit3 and Grp78/Bip proteins at 24 h after methamphetamine administration. Treatment of CATH.a cells with methamphetamine caused a re-distribution of dopamine inside the cells, which mimicked the presynaptic activity of neurons with cell bodies located in the ventral tegmental area or the substantia nigra. Thus, we have demonstrated the existence of endoplasmic reticulum stress in a model of presynaptic dopaminergic neurons for the first time. Together with the recent evidence suggesting the importance of presynaptic toxicity, our findings provide new insights into the mechanisms of dopamine toxicity, which might represent one of the most important mechanisms of methamphetamine toxicity and addiction

Striatal Proteomic Analysis Suggests that First L-Dopa Dose Equates to Chronic Exposure

L-3,4-dihydroxypheylalanine (L-dopa)-induced dyskinesia represent a debilitating complication of therapy for Parkinson's disease (PD) that result from a progressive sensitization through repeated L-dopa exposures. The MPTP macaque model was used to study the proteome in dopamine-depleted striatum with and without subsequent acute and chronic L-dopa treatment using two-dimensional difference in-gel electrophoresis (2D-DIGE) and mass spectrometry. The present data suggest that the dopamine-depleted striatum is so sensitive to de novo L-dopa treatment that the first ever administration alone would be able (i) to induce rapid post-translational modification-based proteomic changes that are specific to this first exposure and (ii), possibly, lead to irreversible protein level changes that would be not further modified by chronic L-dopa treatment. The apparent equivalence between first and chronic L-dopa administration suggests that priming would be the direct consequence of dopamine loss, the first L-dopa administrations only exacerbating the sensitization process but not inducing it

Delta-9-tetrahydrocannabinol, neural oscillations above 20 Hz and induced acute psychosis

Rationale: An acute challenge with delta-9-tetrahydrocannabinol (THC) can induce psychotic symptoms including delusions. High electroencephalography (EEG) frequencies, above 20 Hz, have previously been implicated in psychosis and schizophrenia. Objectives: The objective of this study is to determine the effect of intravenous THC compared to placebo on high-frequency EEG. Methods: A double-blind cross-over study design was used. In the resting state, the high-beta to low-gamma magnitude (21–45 Hz) was investigated (n=13 pairs+4 THC only). Also, the event-related synchronisation (ERS) of motor-associated high gamma was studied using a self-paced button press task (n=15). Results: In the resting state, there was a significant condition × frequency interaction (p=0.00017), consisting of a shift towards higher frequencies under THC conditions (reduced high beta [21–27 Hz] and increased low gamma [27–45 Hz]). There was also a condition × frequency × location interaction (p=0.006), such that the reduction in 21–27-Hz magnitude tended to be more prominent in anterior regions, whilst posterior areas tended to show greater 27–45-Hz increases. This effect was correlated with positive symptoms, as assessed on the Positive and Negative Syndrome Scale (PANSS) (r=0.429, p=0.042). In the motor task, there was a main effect of THC to increase 65–130-Hz ERS (p=0.035) over contra-lateral sensorimotor areas, which was driven by increased magnitude in the higher, 85–130-Hz band (p=0.02) and not the 65–85-Hz band. Conclusions: The THC-induced shift to faster gamma oscillations may represent an over-activation of the cortex, possibly related to saliency misattribution in the delusional state

Food-associated cues alter forebrain functional connectivity as assessed with immediate early gene and proenkephalin expression

<p>Abstract</p> <p>Background</p> <p>Cues predictive of food availability are powerful modulators of appetite as well as food-seeking and ingestive behaviors. The neurobiological underpinnings of these conditioned responses are not well understood. Monitoring regional immediate early gene expression is a method used to assess alterations in neuronal metabolism resulting from upstream intracellular and extracellular signaling. Furthermore, assessing the expression of multiple immediate early genes offers a window onto the possible sequelae of exposure to food cues, since the function of each gene differs. We used immediate early gene and proenkephalin expression as a means of assessing food cue-elicited regional activation and alterations in functional connectivity within the forebrain.</p> <p>Results</p> <p>Contextual cues associated with palatable food elicited conditioned motor activation and corticosterone release in rats. This motivational state was associated with increased transcription of the activity-regulated genes <it>homer1a</it>, <it>arc</it>, <it>zif268</it>, <it>ngfi-b </it>and c-<it>fos </it>in corticolimbic, thalamic and hypothalamic areas and of proenkephalin within striatal regions. Furthermore, the functional connectivity elicited by food cues, as assessed by an inter-regional multigene-expression correlation method, differed substantially from that elicited by neutral cues. Specifically, food cues increased cortical engagement of the striatum, and within the nucleus accumbens, shifted correlations away from the shell towards the core. Exposure to the food-associated context also induced correlated gene expression between corticostriatal networks and the basolateral amygdala, an area critical for learning and responding to the incentive value of sensory stimuli. This increased corticostriatal-amygdalar functional connectivity was absent in the control group exposed to innocuous cues.</p> <p>Conclusion</p> <p>The results implicate correlated activity between the cortex and the striatum, especially the nucleus accumbens core and the basolateral amygdala, in the generation of a conditioned motivated state that may promote excessive food intake. The upregulation of a number of genes in unique patterns within corticostriatal, thalamic, and hypothalamic networks suggests that food cues are capable of powerfully altering neuronal processing in areas mediating the integration of emotion, cognition, arousal, and the regulation of energy balance. As many of these genes play a role in plasticity, their upregulation within these circuits may also indicate the neuroanatomic and transcriptional correlates of extinction learning.</p