Coral Reef Fish Rapidly Learn to Identify Multiple Unknown Predators upon Recruitment to the Reef

Organisms often undergo shifts in habitats as their requirements change with ontogeny

Association of air quality during forest fire season with respiratory emergency department visits in Vancouver, British Columbia

Background: Climate change has been deemed the biggest global health threat of the 21st century. One consequence of climate change is the increasing frequency and severity of forest fires. Smoke from wildfires has the ability to negatively impact air quality over large distances. The aim of this study was to examine the association that air quality had on emergency department visits for cardiac, respiratory and psychiatric/behavioral health chief complaints during forest fire season in Vancouver, British Columbia. Methods: The study period was January 1, 2009 – December 31, 2019. Forest fire season was defined as April 1- September 30. Air quality (measured by PM2.5 in ug/m3) was obtained from the Vancouver International Airport (YVR) Air Quality station. Emergency department visit data (CEDIS triage complaint) was acquired from a regional emergency department database. A generalized linear mixed model with Poisson link function was used to determine the relative risk (as a percentage) for respiratory, cardiac and psychiatric/behavioral health CEDIS triage complaints associated with a 10 unit increase in PM2.5. Results: PM2.5 during forest fire season was significantly associated with emergency department visits for respiratory chief complaints. For every 10 ug/m3 increase in PM2.5, there was a 4.61% (95% CI: 3.07, 6.17) increase in relative risk of respiratory chief complaints presenting to emergency departments. No association was found between PM2.5 and cardiac or psychiatric/behavioral health chief complaints during forest fire season or non-forest fire season. During non-forest fire season, PM2.5 was found to be negatively associated with respiratory (-3.57, 95% CI: -5.44, -1.66) and cardiac chief complaints (-2.77, 95% CI: -4.16, -1.47). Conclusion: Our results indicate a probable association between air quality during forest fire season and emergency department visits for respiratory chief complaints. This provides further illustration of the widespread impact of climate change, and underscores the importance of efforts to address it

Soluble T Cell Immunoglobulin Mucin Domain 3 Is Shed from CD8+ T Cells by the Sheddase ADAM10, Is Increased in Plasma during Untreated HIV Infection, and Correlates with HIV Disease Progression

UnlabelledChronic HIV infection results in a loss of HIV-specific CD8(+) T cell effector function, termed "exhaustion," which is mediated, in part, by the membrane coinhibitory receptor T cell immunoglobulin mucin domain-3 (Tim-3). Like many other receptors, a soluble form of this protein has been described in human blood plasma. However, soluble Tim-3 (sTim-3) is poorly characterized, and its role in HIV disease is unknown. Here, we show that Tim-3 is shed from the surface of responding CD8(+) T cells by the matrix metalloproteinase ADAM10, producing a soluble form of the coinhibitory receptor. Despite previous reports in the mouse model, no alternatively spliced, soluble form of Tim-3 was observed in humans. Shed sTim-3 was found in human plasma and was significantly elevated during early and chronic untreated HIV infection, but it was not found differentially modulated in highly active antiretroviral therapy (HAART)-treated HIV-infected subjects or in elite controllers compared to HIV-uninfected subjects. Plasma sTim-3 levels were positively correlated with HIV load and negatively correlated with CD4 counts. Thus, plasma sTim-3 shedding correlated with HIV disease progression. Despite these correlations, we found that shedding Tim-3 did not improve the function of CD8(+) T cells in terms of gamma interferon production or prevent their apoptosis through galectin-9. Further characterization studies of sTim-3 function are needed to understand the contribution of sTim-3 in HIV disease pathogenesis, with implications for novel therapeutic interventions.ImportanceDespite the overall success of HAART in slowing the progression to AIDS in HIV-infected subjects, chronic immune activation and T cell exhaustion contribute to the eventual deterioration of the immune system. Understanding these processes will aid in the development of interventions and therapeutics to be used in combination with HAART to slow or reverse this deterioration. Here, we show that a soluble form of T cell exhaustion associated coinhibitory molecule 3, sTim-3, is shed from the surface of T cells. Furthermore, sTim-3 is elevated in the plasma of treatment-naive subjects with acute or chronic HIV infection and is associated with markers of disease progression. This is the first study to characterize sTim-3 in human plasma, its source, and mechanism of production. While it is still unclear whether sTim-3 contributes to HIV pathogenesis, sTim-3 may represent a new correlate of HIV disease progression