Usability and Teachability of Continuous Glucose Monitoring Devices in Older Adults and Diabetes Educators: Task Analysis and Ease-of-Use Survey.

BACKGROUND: Continuous glucose monitoring (CGM) devices continuously sense and relay glucose concentration data from the interstitial fluid to a mobile phone or receiver. Older adults benefit from this continuous monitoring of glucose levels. Proper deployment of the sensing wire is facilitated by a specialized applicator. OBJECTIVE: Our aim was to assess a new seventh-generation (G7) CGM device (Dexcom, Inc) for use by adults 65 years of age or older and certified diabetes care and education specialists (CDCESs). Ease of use related to intradermal insertion and mobile app setup will be assessed and compared to the fifth- and sixth-generation systems. METHODS: Formal task analysis was conducted to enumerate the number and complexity of tasks associated with CGM deployment. We recruited 10 older adults with no prior CGM experience and 10 CDCESs to assess ease of use through hands-on insertion and initiation of a G7 system followed by a survey and, for older adults, a system usability scale survey. RESULTS: About half as many tasks are needed to deploy G7 compared to G6. Older adults and CDCESs reported overall high usability of the G7 CGM device. CDCESs noted G7's easier setup compared to previous generations. The system usability scale score for the CGM system was 92.8, which reflects excellent usability. CONCLUSIONS: For CDCESs and for older adults using the G7 CGM system, cognitive burden is relatively low and reduced compared to previous CGM systems. Easing of this burden and simplification of the glucose monitoring aspect of proper diabetes management will likely contribute to improved outcomes in this population.

Support of supervised injection facilities by emergency physicians in Canada.

BACKGROUND: Despite evidence supporting the implementation of supervised injection facilities (SIFs) by multiple stakeholders, no evaluation of emergency physicians' attitudes has ever been documented towards such facilities in Canada or internationally. The primary goal of our study was to determine the opinions and perceptions of emergency physicians regarding the implementation of SIFs in Canada. METHODS: We conducted a national electronic survey of staff and resident emergency physicians in Canada using an iteratively designed survey tool in consultation with content experts. Invitations to complete the survey were sent via email by the Canadian Association of Emergency Physicians. Inclusion criteria required respondents to have treated an adult patient in a Canadian emergency department within the preceding 6 months. The primary measure was the proportion of respondents who would support, not support or were unsure of supporting SIFs in their community with the secondary measure being the likelihood of respondents to refer patients to a SIF if available. RESULTS: We received 280 responses out of 1353 eligible physicians (20.7%), with the analysis conducted on 250 responses that met inclusion criteria (18.5%). The majority of respondents stated they would support the implementation of SIFs in their community (N=172; 74.5%) while 10.8% (N=25) would not and 14.7% (N=34) did not know. The majority of respondents said they would refer their patients to SIFs (N=198; 84.6%), with 4.3% (N=10) who would not and 11.1% (N=26) who were unsure. CONCLUSION: The findings from our study demonstrate that the majority of emergency physician respondents in Canada support the implementation of such sites (74.5%) while 84.6% of respondents would refer patients from the emergency department to such sites if they did exist. Given that many Canadian cities are actively pursuing the creation of SIFs or imminently opening such sites, it appears that our sample population of emergency physicians would both support this approach and would utilize such facilities in an effort to improve patient-centered outcomes for this often marginalized population.

Prolonged Exposure for Treating PTSD Among Female Methadone Patients Who Were Survivors of Sexual Abuse in Israel.

The aims of this pilot study were: (a) to test the feasibility of prolonged exposure (PE) therapy conducted by a social worker staff on female patients in methadone program clinics who were survivors of child sexual abuse or rape and (b) to examine preliminary outcomes of PE on posttraumatic stress disorder (PTSD), depression, and illicit drug use at pre- and posttreatment, and up to 12-month follow-ups. Twelve female methadone patients who were survivors of child sexual abuse or rape diagnosed with PTSD were enrolled in 13-19 weekly individual PE sessions. Assessments were conducted at pre-, mid-, and posttreatment, as well as at 3, 6, and 12-month follow-ups. The treatment outcomes measures included PTSD symptoms, depressive symptoms, and illicit drug use. Ten of the 12 study patients completed treatment. PTSD and depressive symptoms showed significant reduction. No relapse to illicit drug use was detected. These preliminary results suggest that PE may be delivered by methadone social workers with successful outcomes. Further research should test the efficacy of PE among methadone patients in a randomized control trial with standard care as the control condition.

Spatially mapping charge carrier density and defects in organic electronics using modulation-amplified reflectance spectroscopy.

Charge-modulated optical spectroscopy is used to achieve dynamic two-dimensional mapping of the charge-carrier distribution in poly(3-hexylthiophene) thin-film transistors. The resulting in-channel distributions evolve from uniformly symmetric to asymmetrically saturated as the devices are increasingly biased. Furthermore, physical, chemical, and electrical defects are spatially resolved in cases where their presence is not obvious from the device performance.

Magnetic bucket for rotating unmagnetized plasma.

A new experiment is described which generates flow in unmagnetized plasma. Confinement is provided by a cage of permanent magnets, arranged to form an axisymmetric, high-order, multipolar magnetic field. This field configuration-sometimes called a "magnetic bucket"-has a vanishingly small field in the core of the experiment. Toroidal rotation is driven by J × B forces applied in the magnetized edge. The cross-field current that is required for this forcing flows from anodes to thermionic cathodes, which are inserted between the magnet rings. The rotation at the edge reaches 3 km/s and is viscously coupled to the unmagnetized core plasma. We describe the conditions necessary for rotation, as well as a 0-dimensional power balance used to understand plasma confinement in the experiment.

Laboratory observation of localized onset of magnetic reconnection.

Magnetic reconnection is a fundamental process in plasmas that results in the often explosive release of stored magnetic energy, but the trigger for its onset is not well understood. We explore this trigger for fast reconnection in toroidal experiments using a magnetic x-type geometry in the strong guide-field regime. We find that the onset occurs asymmetrically: the reconnection begins on one side of the torus and propagates around approximately at the Alfvén speed. The fast reconnection occurs only in the presence of a global plasma mode, which breaks the axisymmetry and enables the current at the x line to decrease sharply. A simple semiempirical model is used to describe the onset's growth rate.

Genetic deletion of fatty acid amide hydrolase alters emotional behavior and serotonergic transmission in the dorsal raphe, prefrontal cortex, and hippocampus.

Pharmacological blockade of the anandamide-degrading enzyme, fatty acid amide hydrolase (FAAH), produces CB(1) receptor (CB(1)R)-mediated analgesic, anxiolytic-like and antidepressant-like effects in murids. Using behavioral and electrophysiological approaches, we have characterized the emotional phenotype and serotonergic (5-HT) activity of mice lacking the FAAH gene in comparison to their wild type counterparts, and their response to a challenge of the CB(1)R antagonist, rimonabant. FAAH null-mutant (FAAH(-/-)) mice exhibited reduced immobility in the forced swim and tail suspension tests, predictive of antidepressant activity, which was attenuated by rimonabant. FAAH(-/-) mice showed an increase in the duration of open arm visits in the elevated plus maze, and a decrease in thigmotaxis and an increase in exploratory rearing displayed in the open field, indicating anxiolytic-like effects that were reversed by rimonabant. Rimonabant also prolonged the initiation of feeding in the novelty-suppressed feeding test. Electrophysiological recordings revealed a marked 34.68% increase in dorsal raphe 5-HT neural firing that was reversed by rimonabant in a subset of neurons exhibiting high firing rates (33.15% mean decrease). The response of the prefrontocortical pyramidal cells to the 5-HT(2A/2C) agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane ((+/-)-DOI) revealed desensitized 5-HT(2A/2C) receptors, likely linked to the observed anxiolytic-like behaviors. The hippocampal pyramidal response to the 5-HT(1A) antagonist, WAY-100635, indicates enhanced tonus on the hippocampal 5-HT(1A) heteroreceptors, a hallmark of antidepressant-like action. Together, these results suggest that FAAH genetic deletion enhances anxiolytic-like and antidepressant-like effects, paralleled by altered 5-HT transmission and postsynaptic 5-HT(1A) and 5-HT(2A/2C) receptor function.

Relevance of norepinephrine-dopamine interactions in the treatment of major depressive disorder.

Central dopaminergic and noradrenergic systems play essential roles in controlling several forebrain functions. Consequently, perturbations of these neurotransmissions may contribute to the pathophysiology of neuropsychiatric disorders. For many years, there was a focus on the serotonin (5-HT) system because of the efficacy of selective serotonin reuptake inhibitors (SSRIs), the most prescribed antidepressants in the treatment of major depressive disorder (MDD). Given the interconnectivity within the monoaminergic network, any action on one system may reverberate in the other systems. Analysis of this network and its dysfunctions suggests that drugs with selective or multiple modes of action on dopamine (DA) and norepinephrine (NE) may have robust therapeutic effects. This review focuses on NE-DA interactions as demonstrated in electrophysiological and neurochemical studies, as well as on the mechanisms of action of agents with either selective or dual actions on DA and NE. Understanding the mode of action of drugs targeting these catecholaminergic neurotransmitters can improve their utilization in monotherapy and in combination with other compounds particularly the SSRIs. The elucidation of such relationships can help design new treatment strategies for MDD, especially treatment-resistant depression.

Chronic exposure to cannabinoids during adolescence but not during adulthood impairs emotional behaviour and monoaminergic neurotransmission.

The pathophysiological neural mechanism underlying the depressogenic and anxiogenic effects of chronic adolescent cannabinoid use may be linked to perturbations in monoaminergic neurotransmission. We tested this hypothesis by administering the CB(1) receptor agonist WIN55,212-2, once daily for 20 days to adolescent and adult rats, subsequently subjecting them to tests for emotional reactivity paralleled by the in vivo extracellular recordings of serotonergic and noradrenergic neurons. Chronic adolescent exposure but not adult exposure to low (0.2 mg/kg) and high (1.0 mg/kg) doses led to depression-like behaviour in the forced swim and sucrose preference test, while the high dose also induced anxiety-like consequences in the novelty-suppressed feeding test. Electrophysiological recordings revealed both doses to have attenuated serotonergic activity, while the high dose also led to a hyperactivity of noradrenergic neurons only after adolescent exposure. These suggest that long-term exposure to cannabinoids during adolescence induces anxiety-like and depression-like behaviours in adulthood and that this may be instigated by serotonergic hypoactivity and noradrenergic hyperactivity.

Effects of acute and sustained administration of the catecholamine reuptake inhibitor nomifensine on the firing activity of monoaminergic neurons.

Nomifensine potently inhibits the reuptake of norepinephrine and dopamine in vitro. It is one of few antidepressants with marked potency to block dopamine reuptake that has ever been used clinically. Acute and sustained administration of nomifensine was investigated on the firing of monoaminergic neurons to understand its mechanism of action. In vivo extracellular recordings of locus coeruleus, ventral tegmental area and dorsal raphe nucleus neurons were obtained from male Sprague-Dawley rats. The intravenous injection of nomifensine in the locus coeruleus and ventral tegmental area yielded ED(50) values of 40 +/- 1 and 450 +/- 41 microg/kg, respectively, suggesting that nomifensine directly acted upon dopamine and norepinephrine neurons, since these values are proportional to its affinities for norepinephrine and dopamine transporters. There was no effect on 5-HT neurons. Nomifensine (5 mg/kg/day, subcutaneous, using minipumps) potently and significantly inhibited dopamine neuronal firing in the ventral tegmental area after 2 days, with recovery to normal after the 14-day treatment due to D(2) autoreceptor desensitization. Norepinephrine neuronal firing in the locus coeruleus was significantly decreased after 2 and 14 days. A significant increase in dorsal raphe nucleus 5-HT neuronal firing was seen after a two-day regimen, and remained elevated after 14 days. Desensitization of the 5-HT(1A) receptor on 5-HT neurons of the dorsal raphe nucleus occurred after two days of nomifensine administration. Nomifensine likely treated depression by acting on dopamine, norepinephrine and 5-HT neurons, highlighting the importance of the functional connectivity between these three monoaminergic systems.

Experiments on the propagation of plasma filaments.

We investigate experimentally the motion and structure of isolated plasma filaments propagating through neutral gas. Plasma filaments, or "blobs," arise from turbulent fluctuations in a range of plasmas. Our experimental geometry is toroidally symmetric, and the blobs expand to a larger major radius under the influence of a vertical electric field. The electric field, which is caused by nabla B and curvature drifts in a 1/R magnetic field, is limited by collisional damping on the neutral gas. The blob's electrostatic potential structure and the resulting E x B flow field give rise to a vortex pair and a mushroom shape, which are consistent with nonlinear plasma simulations. We observe experimentally this characteristic mushroom shape for the first time. We also find that the blob propagation velocity is inversely proportional to the neutral density and decreases with time as the blob cools.

Cannabinoids elicit antidepressant-like behavior and activate serotonergic neurons through the medial prefrontal cortex.

Preclinical and clinical studies show that cannabis modulates mood and possesses antidepressant-like properties, mediated by the agonistic activity of cannabinoids on central CB1 receptors (CB1Rs). The action of CB1R agonists on the serotonin (5-HT) system, the major transmitter system involved in mood control and implicated in the mechanism of action of antidepressants, remains however poorly understood. In this study, we demonstrated that, at low doses, the CB1R agonist WIN55,212-2 [R(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)]pyrrolo[1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl) methanone mesylate] exerts potent antidepressant-like properties in the rat forced-swim test (FST). This effect is CB1R dependent because it was blocked by the CB1R antagonist rimonabant and is 5-HT mediated because it was abolished by pretreatment with the 5-HT-depleting agent parachlorophenylalanine. Then, using in vivo electrophysiology, we showed that low doses of WIN55,212-2 dose dependently enhanced dorsal raphe nucleus 5-HT neuronal activity through a CB1R-dependent mechanism. Conversely, high doses of WIN55,212-2 were ineffective in the FST and decreased 5-HT neuronal activity through a CB1R-independent mechanism. The CB1R agonist-induced enhancement of 5-HT neuronal activity was abolished by total or medial prefrontocortical, but not by lateral prefrontocortical, transection. Furthermore, 5-HT neuronal activity was enhanced by the local microinjection of WIN55,212-2 into the ventromedial prefrontal cortex (mPFCv) but not by the local microinjection of WIN55,212-2 into the lateral prefrontal cortex. Similarly, the microinjection of WIN55,212-2 into the mPFCv produced a CB1R-dependent antidepressant-like effect in the FST. These results demonstrate that CB1R agonists possess antidepressant-like properties and modulate 5-HT neuronal activity via the mPFCv.