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Background: Physical activity, assessed by accelerometers, has been proposed as a quantitative outcome measure for patients with DMD, but research is limited Objective: To assess the total amount and patterns of physical activity in patients with DMD using accelerometers. Methods: Physical activity was assessed in patients with DMD (n = 49, 13.6 ± 4.0-year-old) and age-and sex-matched healthy controls (n = 15, 14.0 ± 2.3-year-old) using wrist-and ankle-worn accelerometers. To assess the amount of activity, accelerometer recordings were converted into acceleration estimates (counts/min). Patterns of activity were assessed as the time that participants spent in sedentary, low-intensity, and moderate-to-vigorous physical activity categories. The sedentary category was divided into three (sedentary-1,-2, and-3) and the low-intensity into two (low-intensity-1, and-2) subcategories. Results: Physical activity across intensity categories differed between study groups (p < 0.001). Patients with DMD spent on average 98.8% of their daytime in the sedentary and low-intensity categories. Compared to non-ambulatory, ambulatory patients spent more time in sedentary-3 and low-intensity-2 subcategories (p < 0.001). Amount of activity was lower in all patients than controls (p < 0.05) and in non-ambulatory than ambulatory patients and controls (p < 0.001), but similar between ambulatory patients and controls. Activity measures in patients were significantly affected by age and ambulation status (p < 0.05) but not corticosteroid use. Conclusion: Patients with DMD spent most of their daytime in sedentary and low-intensity activities. Dividing these intensities into three and two subcategories, respectively, allows better characterization of activity patterns in DMD. Ambulation status and age but not corticosteroid use affected activity measures in patients with DMD.

Arequipa (Peru) is an area where volcanic activity has been persistent during the Quaternary. Studies carried out in this area have highlighted the emplacement of ignimbrite deposits, large volcanic clusters and stratovolcanoes. Monogenetic volcanism is also present, although poorly explored and studied. Due to its location over an ignimbrite plain and poor state of preservation, the only identified monogenetic cone in the Arequipa basin was the Nicholson volcano, while other monogenetic centers remained unknown. This lack of information about the recent volcanism can lead to inadequate definition of scenarios in a hazard assessment in the region. The present study has investigated monogenetic volcanism in the northwestern edge of the Arequipa basin based on geological survey, geochronology and geochemical data. Here, we report for the first time five small volcanic centers such as Yura Viejo, Ccapua, Uyupampa, El Chiral and Patacocha, which together with the Nicholson volcano form the Yura Monogenetic Field. Stratigraphic considerations and new 40Ar/39Ar ages allow us to place the eruptive activity in the Middle–Upper Pleistocene (c. 195–54 ka). Phreatomagmatic, Strombolian and effusive eruptions characterize the monogenetic activity of the field. As a result of these eruptions, small scoria cones, maars, and lava flows/coulées were generated. The eruptive products show ubiquitous olivine phenocryst-rich (&lt;10 vol%) set in a fine pilotaxitic groundmass, suggesting rapid ascent of basaltic magmas to the surface controlled by the tectonic setting. The analyzed rocks lie in a narrow range of basaltic-andesite composition (50.9–55.6 wt% SiO2) being the most mafic Pleistocene - Recent volcanic products identified in the Arequipa basin, along with the least differentiated magmas from the nearby Chachani volcanic cluster. This work shows how monogenetic volcanism can occur contemporaneous and closely spaced to larger volcanic clusters and active stratovolcanoes. We hope the information provided here will contribute to improve the risk management by highlighting the scenario of monogenetic eruptions that should be considered in the hazard assessment.

Non-small cell lung cancer (NSCLC), the most common type of lung cancer, is the leading cause of cancer related deaths in United States. Only 24% of NSCLC patients survive 5-years post diagnosis, which could be attributed to the lack of efficient treatment strategies at the metastatic stage. Thus, understanding the biological mechanisms that promote NSCLC metastasis is critical for developing effective cancer-specific therapeutic agents. The development of cancer metastasis is greatly driven and influenced by intercellular communication. Key mediators of cell-to-cell communication are small extracellular vesicles (sEVs) of approximately 100-150 nm in diameter, often referred as exosomes. Previous report revealed that increased levels of exosomes in NSCLC patients correlated with lower overall survival. Indeed, secretion of sEVs by cancer cells can induce malignant transformation of non-cancerous cells nearby or at distant locations through influencing pre-metastatic niche formation. Therefore, biogenesis and release of cancer derived sEVs are determinant steps for the development of tumor metastasis. However, the mechanisms through which sEVs are produced and secreted by cancer cells are yet to be determined. Here, we isolated and characterized sEVs from a panel of NSCLC cell lines (H358, Calu6, H460, SKMES-1) and non-tumorigenic cells (BEAS-2B and HBEC) to identify mechanisms involved in the elevated secretion of EVs by cancer cells. Contrary to what has been previously reported in literature, our data demonstrated that not all cancer cell lines release high levels of sEVs. Our data suggests that elevated secretion of sEVs could be driven by specific mutations and oncogenic signaling in cancer cells. Among all the cell lines tested, H358 cells which harbor the infamous G12C mutation in KRAS, had the highest sEV release. Therefore, we hypothesize that the KRASG12C can drive high sEV production and secretion in H358 cells. Our preliminary data suggests that siRNA mediated knockdown of oncogenic KRAS signaling in H358 cells significantly decreases secretion of sEVs. Ongoing studies aim to pinpoint the detailed mechanisms by which cancer cells utilize KRAS oncogenic signaling to promote EV biogenesis pathways and tumorigenesis. The current study will provide the foundation to developed new therapeutic strategies against tumor sEVs-driven metastasis. Citation Format: Zulaida M. Soto Vargas, Ikjot Singh Sohal, Humna Hasan, David Arteaga, Andrea L. Kasinski. Uncovering mechanisms of biogenesis and secretion of small extracellular vesicles in non small cell lung cancer (NSCLC) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1581.