Geochemical Evaluation of the Permian Ecca Shale in Eastern Cape Province, South Africa:Implications for Shale Gas Potential

Shale gas has been the exploration focus for future energy supply in South Africa in recent time. Specifically, the Permian black shales of the Prince Albert, Whitehill, Collingham, Ripon and Fort Brown Formations are considered to be most prospective rocks for shale gas exploration. In this study,outcrop and core samples from the Ecca Group were analyzed to assess their total organic carbon(TOC), organic matter type, thermal maturity and hydrocarbon generation potential. These rocks have TOC ranging from 0.11 to 7.35 wt%. The genetic potential values vary from 0.09 to 0.53 mg HC/g,suggesting poor hydrocarbon generative potential. Most of the samples have Hydrogen Index(HI) values of less than 50 mg HC/g TOC, thus suggesting Type-Ⅳ kerogen. Tmax values range from 318℃ to601℃, perhaps indicating immature to over-maturity of the samples. The vitrinite reflectance values range from 2.22% to 3.93%, indicating over-maturity of samples. Binary plots of HI against Oxygen Index(OI), and HI versus Tmax show that the shales are of Type II and mixed Type Ⅱ-Ⅲ kerogen.Based on the geochemical data, the potential source rocks are inferred as immature to over-matured and having present-day potential to produce gas.

Classification and Diagenetic Characteristics of the Cretaceous Sandstones in the Southern Bredasdorp Basin,Offshore South Africa

A systematic petrographic and geochemical studies of 92 representative sandstone samples from exploration wells E-AH1,E-AJ1,E-BA1,E-BB1 and E-D3 in the southern part of the Bredasdorp Basin was undertaken to classify the sandstones as well as unravel the main diagenetic processes and their time relations.Petrographic study shows that the sandstones are largely subarkosic arenite and arkosic litharenite,which have underwent series of diagenetic processes as a result burial,rifting and subsequent uplift.The main diagenetic processes that have affected the reservoir properties of the sandstones are cementation by authigenic clay,carbonate and silica,growth of authigenic glauconite,dissolution of minerals and load compaction.The major diagenetic processes reducing the porosity are calcite cementation in the subarkosic arenite,and compaction and quartz cementation in arkosic litharenite.On the other hand,the formation of secondary porosity due to the partial to complete dissolution of early calcite cement,feldspars and minor grain fracturing has improved the reservoir property of the sandstone to some extent.The clay minerals in the sandstones commonly acts as pore choking cement,which reduces porosity.In general,there is no particular diagenetic process that exclusively controls the type or form of porosity evolution in the sandstones.

Exosomes secreted from cardiomyocytes suppress the sensitivity of tumor ferroptosis in ischemic heart failure

Heart failure(HF)patients in general have a higher risk of developing cancer.Several animal studies have indicated that cardiac remodeling and HF remarkably accelerate tumor progression,highlighting a cause-and-effect relationship between these two disease entities.Targeting ferroptosis,a prevailing form of non-apoptotic cell death,has been considered a promising therapeutic strategy for human cancers.Exosomes critically contribute to proximal and distant organ-organ communications and play crucial roles in regulating diseases in a paracrine manner.However,whether exosomes control the sensitivity of cancer to ferroptosis via regulating the cardiomyocyte-tumor cell crosstalk in ischemic HF has not yet been explored.Here,we demonstrate that myocardial infarction(MI)decreased the sensitivity of cancer cells to the canonical ferroptosis activator erastin or imidazole ketone erastin in a mouse model of xenograft tumor.Post-MI plasma exosomes potently blunted the sensitivity of tumor cells to ferroptosis inducers both in vitro in mouse Lewis lung carcinoma cell line LLC and osteosarcoma cell line K7M2 and in vivo with xenograft tumorigenesis model.The expression of miR-22-3p in cardiomyocytes and plasma-exosomes was significantly upregulated in the failing hearts of mice with chronic MI and of HF patients as well.Incubation of tumor cells with the exosomes isolated from post-MI mouse plasma or overexpression of miR-22-3p alone abrogated erastin-induced ferroptotic cell death in vitro.Cardiomyocyte-enriched miR-22-3p was packaged in exosomes and transferred into tumor cells.Inhibition of cardiomyocyte-specific miR-22-3p by AAV9 sponge increased the sensitivity of cancer cells to ferroptosis.ACSL4,a pro-ferroptotic gene,was experimentally established as a target of miR-22-3p in tumor cells.Taken together,our findings uncovered for the first time that MI suppresses erastin-induced ferroptosis through releasing miR-22-3p-enriched exosomes derived from cardiomyocytes.Therefore,targeting exosome-mediated cardiomyocyte/tumor pathological communication may offer a novel approach for the ferroptosis-based antitumor therapy.

Mettl13 protects against cardiac contractile dysfunction by negatively regulating C-Cbl-mediated ubiquitination of SERCA2a in ischemic heart failure

Ischemic heart failure(HF)remains a leading cause of morbidity and mortality.Maintaining homeostasis of cardiac function and preventing cardiac remodeling deterioration are critical to halting HF progression.Methyltransferase-like protein 13(Mettl13)has been shown to regulate protein translation efficiency by acting as a protein lysine methyltransferase,but its role in cardiac pathology remains unexplored.This study aims to characterize the roles and mechanisms of Mettl13 in cardiac contractile function and HF.We found that Mettl13 was downregulated in the failing hearts of mice post-myocardial infarction(MI)and in a cellular model of oxidative stress.Cardiomyocyte-specific overexpression of Mettl13 mediated by AAV9-Mettl13 attenuated cardiac contractile dysfunction and fibrosis in response to MI,while silencing of Mettl13 impaired cardiac function in normal mice.Moreover,Mettl13 overexpression abrogated the reduction in cell shortening,Ca^(2+)transient amplitude and SERCA2a protein levels in the cardiomyocytes of adult mice with MI.Conversely,knockdown of Mettl13 impaired the contractility of cardiomyocytes,and decreased Ca^(2+)transient amplitude and SERCA2a protein expression in vivo and in vitro.Mechanistically,Mettl13 impaired the stability of c-Cbl by inducing lysine methylation of c-Cbl,which in turn inhibited ubiquitination-dependent degradation of SERCA2a.Furthermore,the inhibitory effects of knocking down Mettl13 on SERCA2a protein expression and Ca^(2+)transients were partially rescued by silencing c-Cbl in H_(2)O_(2)-treated cardiomyocytes.In conclusion,our study uncovers a novel mechanism that involves the Mettl13/c-Cbl/SERCA2a axis in regulating cardiac contractile function and remodeling,and identifies Mettl13 as a novel therapeutic target for ischemic HF.