These results suggest that TP receptor stimulation by 8-iso-PGF2alpha may involve salt loading-induced stroke through activation of cerebrovascular inflammation and damage.

No abstract

To overcome the challenge of synthesizing new and promising iron fluoride cathode materials, high-pressure synthesis was employed to obtain a new form of LiFe2F6 crystallized in the trigonal P321 α-LiMnFeF6 structure. Starting from solid fluorine sources, the trigonal structure was obtained for the first time for LiFe2F6 at 2.7 GPa, 500 °C, and characterized by synchrotron X-ray diffraction. Rietveld refinements revealed that a new form of LiFe2F6 possesses the Na2SiF6-type structure, which would provide enhanced Li+ diffusions. A Mössbauer spectrometry analysis was done with a paramagnetic structure obtained at 300 K and a magnetic sextet at 77 K with a 53 T hyperfine field for Fe3+ similarly to α-LiMnFeF6. The first electrochemistry tests indicate a good first cycle capacity of ∼150 mAh·g–1 with a charge process corresponding to Li+ disinsertion, a value doubled when compared to α-LiMnFeF6. These first experimental results show a new synthetic idea to discover materials designed for next generation batteries.

Epidemiological and clinical studies have demonstrated that excessive salt intake causes severe hypertension and exacerbates organ derangement, such as in chronic kidney disease (CKD). In this study, we focused on evaluating the histological and gene expression effects in the kidneys of stroke‐prone spontaneously hypertensive rats (SHRSP) with a high salt intake and the thromboxane A2/ prostaglandin H2 receptor (TPR) blocker ONO‐8809. Six‐week‐old SHRSPs were divided into three groups and were fed normal chow containing 0.4% NaCl, 2.0%NaCl or 2.0%NaCl + ONO‐8809 (0.6 mg/kg p.o. daily). Histological analyses with immunohistochemistry and a gene expression assay with a DNA kidney microarray were performed after 8 weeks. The following changes were observed in SHRSPs with the high salt intake. Glomerular sclerotic changes were remarkably observed in the juxtamedullary cortex areas. The ED1, monocyte chemoattractant protein‐1 (MCP‐1), nitrotyrosine and hypoxia inducible factor 1α (HIF‐1α) staining areas were increased in the glomeruli and interstitial portion of the kidneys. The genes Tbxa2r (that encodes TPR), Prcp and Car7 were significantly underexpressed in the kidneys. The plasma 8‐isoprostane level was significantly elevated and was attenuated with the ONO‐8809 treatment. Thromboxane A2 (TXA2) and oxidative stress exaggerated renal dysfunction in the salt‐loaded SHRSPs, and ONO‐8809 as a TPR blocker suppressed these changes. Therefore, ONO‐8809 is a candidate drug to prevent CKD in hypertensive patients when CKD is associated with a high salt intake.

Background. Epidemiological and clinical studies demonstrated that excessive salt intake causes severe hypertension and exacerbated organ derangement such as chronic kidney disease (CKD). In this study, we focused on evaluating histological and gene-expression findings in the kidney using stroke-prone spontaneously hypertensive rats (SHRSP) with high-salt intake and thromboxane A2/ prostaglandin H2 receptor (TPR) blocker ONO-8809. Methods. SHRSP aged 6 weeks were divided into three groups eating normal chow containing 0.4% NaCl, 2.0%NaCl, or 2.0%NaCl +ONO-8809 (0.6mg/kg p.o. daily). Histological analyses with immunohistochemistry and a gene-expression assay with a DNA kidney microarray were performed after 8 weeks. Results. The following changes were observed with high-salt intake. Glomerular sclerotic changes were remarkably observed in the juxtaglomerular cortex areas. ED1, MCP-1, nitrotyrosine, and HIF-1α staining areas were increased in the glomeruli and interstitial portion. Tbxa2r which encodes TPR, Prcp, and Car7 were significantly underexpressed in the kidney. The plasma 8-isoprostane level was significantly elevated, and was attenuated with ONO-8809 treatment. Conclusion. TXA2 and oxidative stresses exaggerated renal dysfunction in salt-loading SHRSP, and ONO-8809 as a TPR blocker suppressed these changes. Therefore, ONO-8809 is a candidate drug to prevent CKD for hypertensive patients associated with high-salt intake.