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The crater of Mount St. Helens is a unique place to study landscape evolution impacted by volcano-ice interactions. Crater Glacier, which started forming after the 1980 eruption, is one of the world’s last expanding glaciers and provides a remarkable opportunity to characterize the expansion of a glacier in an area of significant thermal flux. Although the lava dome is gradually cooling, present thermal and physical interactions with the encircling glacier are considerable. Glacier surface structures caused by these interactions provide insight to the heat distribution of the dome and illustrate the dynamics of such environments. By combining photographic documentation, subglacial cave surveys, and remote sensing we provide a comprehensive overview of landscape evolution in the active Mount St. Helens crater since the 2004-2008 lava dome was emplaced. Our results show that the glacier toe advanced by several hundred meters, and constant rockfall from the crater walls transformed the glacier into one that is debris-covered, including the development of supraglacial ponds. The shift of the glacier-dome interface towards higher elevations at the dome has led to extensive subglacial cave system formation, particularly around the 2004-2008 dome. Based on the recent evolution of Crater Glacier and our time series analysis of cave surveys and remote sensing data, we speculate about the future development of this volcanic landscape. Investigating volcano-ice interactions may be an important monitoring tool as these interactions provide insight to the evolution of a volcanic edifice and may be an indicator for renewed volcanic activity., The 28th IUGG General Assembly (IUGG2023) (Berlin 2023)

Given the multiple treatment algorithms for advanced cardiovascular life support (ACLS) and the complexity of the associated drug therapies, pharmacist involvement in resuscitation situations could prove valuable through several potential roles. However, the integration of clinical pharmacists in ACLS teams is not widely observed in Canada [1–3]. A current and comprehensive review of the literature around pharmacist involvement in ACLS is not available to guide this integration. Therefore, a scoping review will synthesize the available literature in order to gain a better understanding of the role and impact of pharmacists as ACLS team members as well as identify any literature gaps. The objective of this scoping review is to provide a broad overview of the available literature around pharmacist involvement in ACLS teams, including the following: the roles of pharmacists on ACLS teams, the received and recommended training for pharmacists on ACLS teams, the impact(s)/outcome(s) of pharmacist participation in ACLS teams, the reported barriers and facilitators of having pharmacist involvement in ACLS, and the perceptions around pharmacist involvement from the perspective of the pharmacist(s) or other health care professional(s). The scoping review will also identify any gaps in the literature around pharmacist participation in ACLS teams.

Thrombin is a potent platelet activator, acting through proteinase-activated receptors -1 and -4 (PAR1 and PAR4). Of these, PAR-1 is activated more rapidly and by lower thrombin concentrations. Consequently, PAR-1 has been extensively investigated as a target for anti-platelet drugs to prevent myocardial infarction. Q94 has been reported to act as an allosteric modulator of PAR1, potently and selectively inhibiting PAR1-Gαq coupling in multiple cell lines, but its effects on human platelet activation have not been previously studied. Platelet Ca2+ signaling, integrin αIIbβ3 activation and α-granule secretion were monitored following stimulation by a PAR1-activating peptide (PAR1-AP). Although Q94 inhibited these responses, its potency was low compared to other PAR1 antagonists. In addition, αIIbβ3 activation and α-granule secretion in response to other platelet activators were also inhibited with similar potency. Finally, in endothelial cells, Q94 did not inhibit PAR1-dependent Ca2+ signaling. Our data suggest that Q94 may have PAR1-independent off-target effects in platelets, precluding its use as a selective PAR1 allosteric modulator.

BACKGROUND: During thrombosis, procoagulant platelets expose phosphatidylserine (PS), which enhances local thrombin generation. Reducing platelet PS exposure could be a novel anti-thrombotic approach. PS is confined to the inner leaflet of the plasma membrane in unstimulated platelets by ATP-dependent 'flippase' activity. Ca2+ ionophores trigger all platelets to expose a high level of PS by activating a scramblase protein and inactivating the flippase. Although R5421 was previously shown to reduce Ca2+ ionophore-induced PS exposure, its mechanism of action is unknown. OBJECTIVES: To determine the mechanism by which R5421 reduces platelet PS exposure. METHODS: Washed human platelets were stimulated with the Ca2+ ionophore, A23187, to induce procoagulant platelet formation while bypassing proximal receptor signalling. Platelets PS exposure was detected using annexin V or lactadherin in flow cytometry. NBD-PS was used to assess scramblase and flippase activity. Thrombin generation was monitored using a fluorogenic substrate. RESULTS AND CONCLUSIONS: R5421 reduced the extent of A23187-stimulated platelet PS exposure, as demonstrated with annexin V or lactadherin binding. R5421 also maintained flippase activity in procoagulant platelets. Although R5421 appeared to inhibit scramblase activity in procoagulant platelets, it did not once the flippase had been inhibited, demonstrating that scramblase activity is not directly inhibited. Furthermore, R5421 inhibited the contribution of A23187-stimulated platelets to thrombin generation. Together these data demonstrate that R5421 reduces the extent of PS exposure in procoagulant platelets by maintaining flippase activity. Maintaining flippase activity in procoagulant platelets is a novel and effective approach to reducing thrombin generation.

The objective of the environmental scan is to identify tools, policies, and programs that are currently being used in practice to reduce SHD use or improve sleep in hospitalized patients. The results can be a resource for other acute care institutions to implement their own programs to support evidence-based practice and improve adherence to guidelines. While an environmental scan to change health services delivery or patient outcomes has not been formally defined,(13) the purpose will be to collect and synthesize existing information available electronically in order to make recommendations to shape future policies and improve healthcare practices.