Smoke Sense Initiative Leverages Citizen Science to Address the Growing Wildfire-Related Public Health Problem.

Smoke Sense is a citizen science project with investigative, educational, and action-oriented objectives at the intersection of wildland fire smoke and public health. Participants engage with a smartphone application to explore current and forecast visualizations of air quality, learn about how to protect health from wildfire smoke, and record their smoke experiences, health symptoms, and behaviors taken to reduce their exposures to smoke. Through participation in the project, individuals engage in observing changes in their environment and recording changes in their health, thus facilitating progression on awareness of health effects of air pollution and adoption of desired health-promoting behaviors. Participants can also view what others are reporting. Data from the pilot season (1 August 2017 to 7 January 2018; 5,598 downloads) suggest that there is a clear demand for personally relevant data during wildfire episodes motivated by recognition of environmental hazard and the personal concern for health. However, while participants shared clear perceptions of the environmental hazard and health risks in general, they did not consistently recognize their own personal health risk. The engagement in health protective behavior was driven in response to symptoms rather than as preventive courses of action. We also observed clear differences in the adoption likelihood of various health protective behaviors attributed to barriers and perceived benefits of these actions. As users experience a greater number and severity of symptoms, the perceived benefits of taking health protective actions exceeded the costs associated with the barriers and thus increased adoption of those actions. Based on pilot season data, we summarize key insights which may improve current health risk communications in nudging individuals toward health protective behavior; there is a need to increase personal awareness of risk and compelling evidence that health protective behaviors are beneficial.

Pharmacodynamics, pharmacokinetics, and safety of AM211: a novel and potent antagonist of the prostaglandin D2 receptor type 2.

The prostaglandin D(2) receptor type 2 (DP2) and its ligand, PGD(2), have been implicated in the development of asthma and other inflammatory diseases. The authors evaluated the pharmacodynamics, pharmacokinetics and safety of [2'-(3-benzyl-1-ethyl-ureidomethyl)-6-methoxy-4'-trifluoromethyl-biphenyl-3-yl]-acetic acid sodium salt (AM211), a novel and potent DP2 antagonist, in healthy participants. Single and multiple doses of AM211 demonstrated dose-dependent inhibition of eosinophil shape change in blood with near-complete inhibition observed at trough after dosing 200 mg once daily for 7 days. Maximum plasma concentrations and exposures of AM211 increased in a greater-than-dose-proportional manner after single and multiple dosing. After multiple dosing, the exposures on day 7 were higher than on day 1 with accumulation ratio values ranging from 1.4 to 1.5. Mean terminal half-life values ranged from 14 to 25 hours across the dose range of 100 to 600 mg. AM211 was well tolerated at all doses in both the single- and multiple-dose cohorts. These data support additional clinical studies to evaluate AM211 in asthma and other inflammatory diseases.

Comparison of the antinociceptive profiles of gabapentin and 3-methylgabapentin in rat models of acute and persistent pain: implications for mechanism of action.

The anticonvulsant gabapentin (GBP) has been shown effective for the treatment of neuropathic pain, although its mechanism of action remains unclear. A recent report has suggested that binding to the alpha(2)delta subunit of voltage-gated calcium channels contributes to its antinociceptive effect, based on the stereoselective efficacy of two analogs: (1S,3R)3-methylgabapentin (3-MeGBP) (IC(50) = 42 nM), which is effective in neuropathic pain models; and (1R,3R)3-MeGBP (IC(50) > 10,000 nM), which is ineffective (Field et al., 2000). The present study was designed to further examine the profiles of GBP and 3-MeGBP in rat models of acute and persistent pain. Systemic administration of GBP or (1S,3R)3-MeGBP inhibited tactile allodynia in the spinal nerve ligation model of neuropathic pain, whereas (1R,3R)3-MeGBP was ineffective. The antiallodynic effect of GBP, but not (1S,3R)3-MeGBP, was blocked by i.t. injection of the GABA(B) receptor antagonist [3-[[(3,4-dichlorophenyl)methyl]amino]propyl](diethoxymethyl)phosphinic acid (CGP52432). Systemic GBP or (1S,3R)3-MeGBP also inhibited the second phase of formalin-evoked nociceptive behaviors, whereas (1R,3R)3-MeGBP was ineffective. However, both (1S,3R)3-MeGBP and (1R,3R)3-MeGBP, but not GBP, inhibited first phase behaviors. In the carrageenan model of inflammatory pain, systemic GBP or (1R,3R)3-MeGBP failed to inhibit thermal hyperalgesia, whereas (1S,3R)3-MeGBP had a significant, albeit transient, effect. Systemic (1S,3R)3-MeGBP, but not GBP or (1R,3R)3-MeGBP, also produced an antinociceptive effect in the warm water tail withdrawal test of acute pain. These data demonstrate that GBP and 3-MeGBP display different antinociceptive profiles, suggesting dissimilar mechanisms of antinociceptive action. Thus, the stereoselective efficacy of 3-MeGBP, presumably related to alpha(2)delta binding, likely does not completely account for the mechanism of action of GBP.

Ultrasonographic description of succenturiate placenta.

Postpartum hemorrhage may occur in cases of a retained succenturiate lobe. More catastrophic is rupture of the fetal vessels connecting the lobe to the placenta. A case is presented demonstrating the sonographic description of a large succenturiate lobe.