7 research outputs found
Considering the Case for Biodiversity Cycles: Reexamining the Evidence for Periodicity in the Fossil Record
Medvedev and Melott (2007) have suggested that periodicity in fossil
biodiversity may be induced by cosmic rays which vary as the Solar System
oscillates normal to the galactic disk. We re-examine the evidence for a 62
million year (Myr) periodicity in biodiversity throughout the Phanerozoic
history of animal life reported by Rohde & Mueller (2005), as well as related
questions of periodicity in origination and extinction. We find that the signal
is robust against variations in methods of analysis, and is based on
fluctuations in the Paleozoic and a substantial part of the Mesozoic.
Examination of origination and extinction is somewhat ambiguous, with results
depending upon procedure. Origination and extinction intensity as defined by RM
may be affected by an artifact at 27 Myr in the duration of stratigraphic
intervals. Nevertheless, when a procedure free of this artifact is implemented,
the 27 Myr periodicity appears in origination, suggesting that the artifact may
ultimately be based on a signal in the data. A 62 Myr feature appears in
extinction, when this same procedure is used. We conclude that evidence for a
periodicity at 62 Myr is robust, and evidence for periodicity at approximately
27 Myr is also present, albeit more ambiguous.Comment: Minor modifications to reflect final published versio
Concentração de propriedade e desempenho: um estudo nas empresas brasileiras de capital aberto do setor de energia elétrica
Trophic macrophages in development and disease
Specialized phagocytes are found in the most primitive multicellular organisms. Their roles in homeostasis and in distinguishing self from non-self have evolved with the complexity of organisms and their immune systems. Equally important, but often overlooked, are the roles of macrophages in tissue development. As discussed in this Review, these include functions in branching morphogenesis, neuronal patterning, angiogenesis, bone morphogenesis and the generation of adipose tissue. In each case, macrophage depletion impairs the formation of the tissue and compromises its function. I argue that in several diseases, the unrestrained acquisition of these developmental macrophage functions exacerbates pathology. For example, macrophages enhance tumour progression and metastasis by affecting tumour-cell migration and invasion, as well as angiogenesis