The extended evolutionary synthesis and human origins: Archaeological perspectives.

Recent developments in evolutionary biology have led to a call for an extension of standard evolutionary theory, with its emphasis on processes such as selection and drift, into a much larger theoretical framework that includes processes such as niche construction, developmental plasticity, inclusive inheritance, and developmental bias. Skeptics argue that these processes are already subsumed within the standard theory and thus an extension is not required. Here, we outline what this evolutionary "rethink" might mean for the study of human origins.

Practice gaps in the care of mitral valve regurgitation: Insights from the American College of Cardiology mitral regurgitation gap analysis and advisory panel.

Background: The revised 2014 American College of Cardiology (ACC)/American Heart Association valvular heart disease guidelines provide evidenced-based recommendations for the management of mitral regurgitation (MR). However, knowledge gaps related to our evolving understanding of critical MR concepts may impede their implementation.

Methods: The ACC conducted a multifaceted needs assessment to characterize gaps, practice patterns, and perceptions related to the diagnosis and treatment of MR.

Persistent Friend virus replication and disease in Apobec3-deficient mice expressing functional B-cell-activating factor receptor.

Rfv3 is an autosomal dominant gene that influences the recovery of resistant mice from Friend retrovirus (FV) infection by limiting viremia and promoting a more potent neutralizing antibody response. We previously reported that Rfv3 is encoded by Apobec3, an innate retrovirus restriction factor. However, it was recently suggested that the Rfv3 susceptible phenotype of high viremia at 28 days postinfection (dpi) was more dominantly controlled by the B-cell-activating factor receptor (BAFF-R), a gene that is linked to but located outside the genetically mapped region containing Rfv3.

Innate retroviral restriction by Apobec3 promotes antibody affinity maturation in vivo.

Apobec3/Rfv3 is an innate immune factor that promotes the neutralizing Ab response against Friend retrovirus (FV) in infected mice. Based on its evolutionary relationship to activation-induced deaminase, Apobec3 might directly influence Ab class switching and affinity maturation independently of viral infection. Alternatively, the antiviral activity of Apobec3 may indirectly influence neutralizing Ab responses by reducing early FV-induced pathology in critical immune compartments.

Apobec3 encodes Rfv3, a gene influencing neutralizing antibody control of retrovirus infection.

Recovery from Friend virus 3 (Rfv3) is a single autosomal gene encoding a resistance trait that influences retroviral neutralizing antibody responses and viremia. Despite extensive research for 30 years, the molecular identity of Rfv3 has remained elusive. Here, we demonstrate that Rfv3 is encoded by Apobec3.