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As illustrated by the 2010 eruption of Eyjafjallajökull, even small eruptions can have big impacts. Our 5E lesson begins with several different Engage activities including the exploration of what is Eyjafjallajökull through the use of Google Earth and looking into whether Michigan could be affected by a similar eruption. Explore activities track the rate of movement and trajectory of the Eyjafjallajökull ash and review news articles about the economy, air safety, and social impacts. In Explain, we add details about the Volcanic Explosivity Index, the jet stream, and ash plumes. In Elaborate, participants select a Cascade or Alaskan volcano and use NOAA's HYSPLIT trajectory model to predict if, under today's atmospheric conditions, an ash plume would reach Michigan. We evaluate understanding by using a scenario for the Redoubt volcano in Alaska. The lesson is aligned to NGSS MS-ESS3-2 and HS-ESS3-1. [ABSTRACT FROM AUTHOR]

Hepatic lipase deficiency is a rare genetic condition caused by biallelic loss-of-function variants in the LIPC gene encoding hepatic lipase. These variants reduce or abolish the protein's lipolytic activity, resulting in elevated plasma lipids. The condition is classified as autosomal recessive, since dyslipidemia is inconsistently observed in heterozygous patients with only one LIPC variant. However, this has been concluded from historical studies encompassing a few families and having very small sample sizes. Here, we conduct a retrospective chart review of 46 heterozygous subjects, each harboring one rare pathogenic LIPC variant. We compare plasma levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides, and apolipoprotein B to those of matched controls without LIPC variants. Variant pathogenicity is classified according to the guidelines of the American College of Medical Genetics and Genomics. We observe that levels of total cholesterol, LDL-C, and triglycerides are significantly elevated in the LIPC variant heterozygotes, but HDL-C and apolipoprotein B are not. When filtering solely with respect to pathogenic or likely pathogenic variants, all lipid variables emerge as significantly elevated compared to controls. Thus, hepatic lipase deficiency may not necessarily be a recessive condition, but perhaps semi-dominant since individuals with one variant are phenotypically distinct from the controls. These hypothesis-generating findings regarding LIPC genetic variations observed in a clinical cohort should be evaluated in larger populations and databases. [ABSTRACT FROM AUTHOR]