Post-breakup tectonics in southeast Brazil from thermochronological data and combined inverse-forward thermal history modeling

The continental margin of southeast Brazil is elevated. Onshore Tertiary basins and Late Cretaceous/Paleogene intrusions are good evidence for post breakup tectono-magmatic activity. To constrain the impact of post-rift reactivation on the geological history of the area, we carried out a new thermochronological study. Apatite fission track ages range from 60.7 +/- 1.9 Ma to 129.3 +/- 4.3 Ma, mean track lengths from 11.41 +/- 0.23 mu m to 14.31 +/- 0.24 mu m and a subset of the (U-Th)/He ages range from 45.1 +/- 1.5 to 122.4 +/- 2.5 Ma. Results of inverse thermal history modeling generally support the conclusions from an earlier study for a Late Cretaceous phase of cooling. Around the onshore Taubate Basin, for a limited number of samples, the first detectable period of cooling occurred during the Early Tertiary. The inferred thermal histories for many samples also imply subsequent reheating followed by Neogene cooling. Given the uncertainty of the inversion results, we did deterministic forward modeling to assess the range of possibilities of this Tertiary part of the thermal history. The evidence for reheating seems to be robust around the Taubate Basin, but elsewhere the data cannot discriminate between this and a less complex thermal history. However, forward modeling results and geological information support the conclusion that the whole area underwent cooling during the Neogene. The synchronicity of the cooling phases with Andean tectonics and those in NE Brazil leads us to assume a plate-wide compressional stress that reactivated inherited structures. The present-day topographic relief of the margin reflects a contribution from post-breakup reactivation and uplift.

Acute inhibition of excessive mitochondrial fission after myocardial infarction prevents long-term cardiac dysfunction

BACKGROUND: Ischemia and reperfusion (IR) injury remains a major cause of morbidity and mortality and multiple molecular and cellular pathways have been implicated in this injury. We determined whether acute inhibition of excessive mitochondrial fission at the onset of reperfusion improves mitochondrial dysfunction and cardiac contractility postmyocardial infarction in rats. METHODS AND RESULTS: We used a selective inhibitor of the fission machinery, P110, which we have recently designed. P110 treatment inhibited the interaction of fission proteins Fis1/Drp1, decreased mitochondrial fission, and improved bioenergetics in three different rat models of IR, including primary cardiomyocytes, ex vivo heart model, and an in vivo myocardial infarction model. Drp1 transiently bound to the mitochondria following IR injury and P110 treatment blocked this Drp1 mitochondrial association. Compared with control treatment, P110 (1 μmol/L) decreased infarct size by 28 ± 2% and increased adenosine triphosphate levels by 70+1% after IR relative to control IR in the ex vivo model. Intraperitoneal injection of P110 (0.5 mg/kg) at the onset of reperfusion in an in vivo model resulted in improved mitochondrial oxygen consumption by 68% when measured 3 weeks after ischemic injury, improved cardiac fractional shortening by 35%, reduced mitochondrial H2O2 uncoupling state by 70%, and improved overall mitochondrial functions. CONCLUSIONS: Together, we show that excessive mitochondrial fission at reperfusion contributes to long-term cardiac dysfunction in rats and that acute inhibition of excessive mitochondrial fission at the onset of reperfusion is sufficient to result in long-term benefits as evidenced by inhibiting cardiac dysfunction 3 weeks after acute myocardial infarction.