Variability of Suspended-Sediment Concentration in the Connecticut River Estuary

Thesis advisor: Gail KinekeTurbidity maxima are areas of elevated suspended-sediment concentration commonly found at the head of the salt intrusion in partially-mixed estuaries. The suspended-sediment distribution in the Connecticut River estuary was examined to determine where turbidity maxima exist and how they form. Areas of enhanced suspended-sediment concentration were found to exist at all phases of the tide near the head of the salt intrusion as well as downstream of this point in deeper parts of the estuarine channel. These areas are locations where peaks in the longitudinal salinity gradient exist, suggesting the presence of a front, or zone of flow convergence. During flood conditions there is a layer of landward-flowing water in the middle of the water column that decelerates upon entering deep parts of the estuary; thus enhancing particle settling. During ebb conditions, stratification and therefore settling from surface waters is enhanced. The combination of processes acting throughout the tidal cycle focuses and, potentially, traps sediment in the deeper parts of the Connecticut River estuary.Thesis (BS) — Boston College, 2012.Submitted to: Boston College. College of Arts and Sciences.Discipline: College Honors Program.Discipline: Geology & Geophysics Honors Program.Discipline: Earth and Environmental Sciences

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice