Climate change is an important predictor of extinction risk on macroevolutionary timescales

Anthropogenic climate change is increasing rapidly and already impacting biodiversity. Despite its importance in future projections, understanding of the underlying mechanisms by which climate mediates extinction remains limited. We present an integrated approach examining the role of intrinsic traits versus extrinsic climate change in mediating extinction risk for marine invertebrates over the past 485 million years. We found that a combination of physiological traits and the magnitude of climate change is necessary to explain marine invertebrate extinction patterns. Our results suggest that taxa previously identified as extinction resistant may still succumb to extinction if the magnitude of climate change is great enough.</p

Phanerozoic trends in the ecological tolerance of Lingula and extinction selectivity of marine invertebrates.

Environmental affinity analyses of Lingula throughout the Phanerozoic for depth, lithology, grainsize, and latitude using three different affinity metrics reveal that lingulids have high ecological tolerance relative to other brachiopods and marine invertebrates. Lingulids were generalist with regards to depth, grainsize, and latitude, and were siliciclastic specialists throughout much of the Phanerozoic. Generalist behavior was observed for all four metrics following certain mass extinction events such as the end-Permian mass extinction. Logistic regression analyses reveal that generalists and specialists are selected for during many extinction and background times throughout the Phanerozoic. Depth and Lithology ecological tolerance were the most significant determinants of extinction risk. Taxa with a high depth or lithology tolerance were more likely to survive many extinction events, whereas specialist selectivity is more common during background intervals. Overall, ecological tolerance plays a role in determining extinction risk over geologic time and the high ecological tolerance of Lingula could provide a mechanism for its longevity and success following mass extinction events

Subgroup analyses of maraviroc in previously treated R5 HIV-1 infection.

BACKGROUND: We conducted subanalyses of the combined results of the Maraviroc versus Optimized Therapy in Viremic Antiretroviral Treatment-Experienced Patients (MOTIVATE) 1 and MOTIVATE 2 studies to better characterize the efficacy and safety of maraviroc in key subgroups of patients. METHODS: We analyzed pooled data from week 48 from the two studies according to sex, race or ethnic group, clade, CC chemokine receptor 5 (CCR5) delta32 genotype, viral load at the time of screening, the use or nonuse of enfuvirtide in optimized background therapy (OBT), the baseline CD4 cell count, the number of active antiretroviral drugs coadministered, the first use of selected background agents, and tropism at baseline. Changes in viral tropism and the CD4 count at treatment failure were evaluated. Data on aminotransferase levels in patients coinfected with hepatitis B virus (HBV) or hepatitis C virus (HCV) were also analyzed. RESULTS: A treatment benefit of maraviroc plus OBT over placebo plus OBT was shown in all subgroups, including patients with a low CD4 cell count at baseline, those with a high viral load at screening, and those who had not received active agents in OBT. Analyses of the virologic response according to the first use of selected background drugs showed the additional benefit of adding a potent new drug to maraviroc at the initiation of maraviroc therapy. More patients in whom maraviroc failed had a virus binding to the CXC chemokine receptor 4 (CXCR4) at failure, but there was no evidence of a decrease in the CD4 cell count at failure in such patients as compared with those in whom placebo failed. Subanalyses involving patients coinfected with HBV or HCV revealed no evidence of excess hepatotoxic effects as compared with baseline. CONCLUSIONS: Subanalyses of pooled data from week 48 indicate that maraviroc provides a valuable treatment option for a wide spectrum of patients with R5 HIV-1 infection who have been treated previously. (ClinicalTrials.gov numbers, NCT00098306 and NCT00098722.