Reply to comment on “Mantle plume: the invisible serial killer — Application to the Permian–Triassic boundary mass extinction” by E. Heydari, N. Arzani and J. Hassanzadeh [Palaeogeography, Palaeoclimatology, Palaeoecology 264 (2008) 147–162]

In a recent article, Heydari et al. (2008) suggested that the perturbation at the Permian–Triassic boundary (PTB) was initiated by processes associated with an end-Permian mantle plume including igneous intrusions and uplift. These events resulted in the massive release of CH₄ primarily from the dissociation of marine gas hydrates, and secondarily from maturation of organic-rich sediments and fracturing of petroleum reservoirs. Injection of CH₄ into the ocean changed seawater composition (the acid-bath ocean) leading to marine mass extinction. Transfer of CO₂ and CH₄ from the ocean to the atmosphere created a hot climate (the end-Permian inferno) which caused the terrestrial mass extinction. We suggested that the Siberian trap volcanism and marine anoxia played little role in this catastrophe.Wignall and Racki (2009-this issue) have raised three criticisms to our article. The first is that our interpretation has been previously advocated by others. Our re-evaluation indicates that our interpretation was in fact opposite of those considered by Wignall and Racki (2009-this issue) to have presented scenarios similar to ours.The second, Wignall and Racki (2009-this issue) also suggest that our proposed change in carbonate mineralogy across the PTB did not occur because such a change “should produce a large positive excursion rather than the observed negative excursion”. Wignall and Racki (2009-this issue) have made a basic mathematical error in evaluating the effect of carbonate mineralogy on δ¹³C values. Therefore, they have reached two wrong conclusions: one about the validity of a change in carbonate mineralogy and the other regarding its effect on the shift in δ¹³C values at the PTB. A change in carbonate mineralogy produced a larger negative excursion rather than a positive shift.The third, Wignall and Racki (2009-this issue) indicate that the PTB ocean was anoxic to the rim. This criticism is not supported by the rock record because highly bioturbated strata were deposited in environments ranging from shallow shelves to deep waters under oxygenated water column at the time of the PTB mass extinction. If the ocean were totally stratified for 20 Ma, and if anoxia extended all the way to the shoreline, and if the ocean were anoxic to the rim and H₂S were oozing out of it, then we should see at least 100 m of organic-rich, varved-laminated strata in areas ranging from the abyssal plain to the shoreline environments. Such strata have not yet been found.     

More attention on glial cells to have better recovery after spinal cord injury

Functional improvement after spinal cord injury remains an unsolved difficulty. Glial scars, a major component of SCI lesions, are very effective in improving the rate of this recovery. Such scars are a result of complex interaction mechanisms involving three major cells, namely, astrocytes, oligodendrocytes, and microglia. In recent years, scientists have identified two subtypes of reactive astrocytes, namely, A1 astrocytes that induce the rapid death of neurons and oligodendrocytes, and A2 astrocytes that promote neuronal survival. Moreover, recent studies have suggested that the macrophage polarization state is more of a continuum between M1 and M2 macrophages. M1 macrophages that encourage the inflammation process kill their surrounding cells and inhibit cellular proliferation. In contrast, M2 macrophages promote cell proliferation, tissue growth, and regeneration. Furthermore, the ability of oligodendrocyte precursor cells to differentiate into adult oligodendrocytes or even neurons has been reviewed. Here, we first scrutinize recent findings on glial cell subtypes and their beneficial or detrimental effects after spinal cord injury. Second, we discuss how we may be able to help the functional recovery process after injury.