Renin and renin blockade have no role in complement activity.

Renin, an aspartate protease, regulates the renin-angiotensin system by cleaving its only known substrate angiotensinogen to angiotensin. Recent studies have suggested that renin may also cleave complement component C3 to activate complement or contribute to its dysregulation. Typically, C3 is cleaved by C3 convertase, a serine protease that uses the hydroxyl group of a serine residue as a nucleophile.

Mechanistic modeling of climate effects on redistribution and population growth in a community of fish species.

Understanding community responses to climate is critical for anticipating the future impacts of global change. However, despite increased research efforts in this field, models that explicitly include important biological mechanisms are lacking. Quantifying the potential impacts of climate change on species is complicated by the fact that the effects of climate variation may manifest at several points in the biological process.

Complement Factor I Variants in Complement-Mediated Renal Diseases.

C3 glomerulopathy (C3G) and atypical hemolytic uremic syndrome (aHUS) are two rare diseases caused by dysregulated activity of the alternative pathway of complement secondary to the presence of genetic and/or acquired factors. Complement factor I (FI) is a serine protease that downregulates complement activity in the fluid phase and/or on cell surfaces in conjunction with one of its cofactors, factor H (FH), complement receptor 1 (CR1/CD35), C4 binding protein (C4BP) or membrane cofactor protein (MCP/CD46). Because altered FI activity is causally related to the pathogenesis of C3G and aHUS, we sought to test functional activity of select missense variants in these two patient cohorts.

Jointly modeling marine species to inform the effects of environmental change on an ecological community in the Northwest Atlantic.

Single species distribution models (SSDMs) are typically used to understand and predict the distribution and abundance of marine fish by fitting distribution models for each species independently to a combination of abiotic environmental variables. However, species abundances and distributions are influenced by abiotic environmental preferences as well as biotic dependencies such as interspecific competition and predation. When species interact, a joint species distribution model (JSDM) will allow for valid inference of environmental effects.

Shifting seas, shifting boundaries: Dynamic marine protected area designs for a changing climate.

Marine protected areas (MPAs) are valuable tools for marine conservation that aim to limit human impacts on marine systems and protect valuable species or habitats. However, as species distributions shift due to ocean warming, acidification, and oxygen depletion from climate change, the areas originally designated under MPAs may bear little resemblance to their past state. Different approaches have been suggested for coping with species on the move in conservation.

Substrate-dependent fish have shifted less in distribution under climate change.

Analyses of the impacts of climate change on fish species have primarily considered dynamic oceanographic variables that are the output of predictive models, yet fish species distributions are determined by much more than just variables such as ocean temperature. Functionally diverse species are differentially influenced by oceanographic as well as physiographic variables such as bottom substrate, thereby influencing their ability to shift distributions. Here, we show that fish species distributions that are more associated with bottom substrate than other dynamic environmental variables have shifted significantly less over the last 30 years than species whose distributions are associated with bottom salinity.