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Big data is an emerging technological field that encompasses massive datasets. Its role in the healthcare field is currently being explored and has the potential to greatly improve healthcare and disease surveillance through pattern analysis of health data. Concerns had by the general public focus primarily on potential breaches of privacy and confidentiality of patient medical health records in the context of research. These concerns relate to the innate characteristics of big data, such as large size and fast data acquisition speed, which increases the risk of breaching confidentiality. Therefore, it is important for physicians to be mindful of privacy concerns and maintain trust as big data becomes more prominent. Doing so is a key factor in building public trust in the use. Understanding strategies and limitations of current practice standards will allow physicians to build on existing guidelines to incorporate the rise of big data. This means prioritizing privacy when handling big data through anonymization, creating safe havens and promoting dynamic informed consent practice standards.

Chronic pain is a common condition that impacts quality of life and often precipitates the need for medical attention. Despite evidence that long-term opioid use provides limited relief, prescription opioid therapy remains a cornerstone in the medical management of chronic non-cancer pain. Presently, 13% of Canadians are prescribed opioids for pain management, and physicians play a crucial role in preventing the development of opioid use disorders. However, Canadian physicians lack knowledge of and comfort with evidence-based principles of opioid stewardship. In this article, we aim to highlight ongoing Canadian efforts to address physician discomfort and improve clinical practice. We focus on 2017 Canadian guidelines that provide clinicians with evidence-based recommendations for opioid use in chronic non-cancer pain management. In addition, we call attention to provincial efforts to implement physician accountability measures. In reviewing the existing literature, we uncovered inadequacies in pain management curricula within the Canadian undergraduate and continuing medical education (CME) systems. We consulted the educational practices of the European Pain Federation and the Centers for Disease Control and Prevention to make recommendations for improvement to current Canadian pain curricula. Based on our findings, we recommend that (1) Canadian medical institutions expand upon current core pain curricula, (2) pain management education be made compulsory, (3) academic detailing be emphasized as a means of CME, and (4) multidisciplinary non-medical management of chronic pain be featured more extensively.

Hearing loss is a chronic health condition that affects millions of people worldwide. In addition to age-related hearing impairment, excessive noise exposure is a leading cause of hearing loss. Beyond the devastating effects of hearing impairment itself, epidemiological studies have identified hearing loss as a major risk factor for age-related cognitive decline, including dementia. At present, we currently lack a full understanding of the brain regions and underlying molecular changes that are responsible for mediating the link between hearing loss and cognitive impairment across aging. In the present study, we exposed 6-month-old rats to an occupational-like noise (100 dB SPL, 4 h/day × 30 days) or sham exposure and investigated both hippocampal-dependent (i.e., spatial learning and memory, assessed using the Morris water maze) and striatal-dependent (i.e., visuomotor associative learning, assessed using an operant-conditioning task) cognitive function across aging at 7, 10, and 13 months of age. We also investigated brain region-specific changes in microglial expression following noise/sham exposure in order to assess the potential contribution of this cell type to noise-induced cognitive impairments. Consistent with human studies, the occupational-like noise exposure resulted in high-frequency hearing loss, evidenced by a significant increase in hearing thresholds at 20 kHz. Ultimately, our results suggest that not all higher-level cognitive tasks or their associated brain regions appear to be equally susceptible to noise-induced deficits during aging, as the occupational-like noise exposure caused an age-dependent deficit in spatial but not visuomotor associative learning, as well as altered microglial expression in the hippocampus but not the striatum. Interestingly, we found no significant relationships between spatial learning ability and the level of hearing loss or altered microglial density in the hippocampus following noise exposure, suggesting that other changes in the brain likely contribute to hippocampal-dependent cognitive dysfunction following noise exposure. Lastly, we found that a subset of younger animals also showed noise-induced deficits in spatial learning; findings which suggest that noise exposure may represent an increased risk for cognitive impairment in vulnerable subjects. Overall, our findings highlight that even a mild occupational-like noise exposure earlier in adulthood can have long lasting implications for cognitive function later in life.

Hearing loss is one of the most prevalent chronic health conditions worldwide, with excessive exposure to loud noise as a leading cause of hearing loss. Beyond the devastating effects of hearing impairment itself, epidemiological studies have identified hearing loss as a major risk factor for cognitive decline. Furthermore, preclinical studies on rodents have identified that the hippocampus—a brain region outside of the classical auditory pathway which subserves spatial navigation—appears to be vulnerable to noise exposure. For example, two hours of exposure to very loud noise (e.g., 123 dB sound pressure level, SPL) has been shown to cause long‐term impairment in spatial learning and memory, as well as suppress hippocampal neurogenesis (i.e., the processes by which new neurons are generated from neural stem cells in the adult brain). That said, because these past studies used noise levels that far exceed those frequently experienced by humans who work in noisy environments, it remains uncertain whether a more modest degree of hearing loss, consistent with that caused by daily, occupational noise exposure, is also problematic for normal hippocampal function. In the present study, we are using a rat model to study the effect of daily noise exposure on spatial learning, memory and hippocampal neurogenesis. Following baseline hearing testing using the auditory brainstem response (i.e., an electrophysiologically‐measured evoked potential from the brain in response to sound), 6‐month old Fischer 344 rats were exposed to 100 dB SPL white noise (or silence) for 4 hours/day for 30 days. Separate cohorts of noise‐ and sham‐exposed rats then underwent behavioral testing at 7, 10, or 13 months old using a Morris water maze (MWM) protocol to assess hippocampal‐dependent spatial acquisition learning and reference memory. After completion of the behavioral testing and post‐exposure hearing assessments, the rats were sacrificed, and their brains harvested for tissue processing. As predicted, the noise‐exposed rats had a mild degree of high‐frequency hearing loss, evidenced by a ~25 dB increase in the rats’ hearing threshold to a 20 kHz acoustic stimulus. Overall, both treatment groups demonstrated spatial acquisition learning over the 5 training days on the MWM hidden platform task; however, the noise‐exposed rats performed slightly, albeit significantly worse than the shams at 10 months of age. Moreover, in contrast to past studies that used very loud noise exposures, none of the cohorts of noise‐exposed rats in the present study were impaired during the MWM probe task; findings which identify that deficits in spatial reference memory are not an inevitable consequence of repeated exposure to sounds that cause a mild degree of hearing loss. Histological analysis of hippocampal neurogenesis is ongoing. Ultimately, given that not all individuals exposed to occupational noise suffer the same degree of hearing loss, it will be important that we correlate each rat's hearing sensitivity with its’ cognitive‐behavioral performance and ...