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Aims: Anaemia is a frequent comorbidity in patients with chronic heart failure (CHF) and is associated with worse outcomes. It is logical to consider whether correcting anaemia is a novel therapeutic target in such patients. We performed a meta-analysis to explore whether treatment of anaemia with erythropoietin-stimulating agents (ESA) can improve symptoms and progression in patients with CHF. [ABSTRACT FROM PUBLISHER]

Aims: Chronic heart failure with normal left ventricular ejection fraction (HFNEF) is not only common, but also carries a high risk of substantial morbidity and mortality. However, few studies have been conducted in this population and no proven treatment is available. Although β-blockers are evidence-based first-line therapy in systolic heart failure, they have not been well studied in HFNEF. [ABSTRACT FROM PUBLISHER]

Seven new phenolic glucosides, xylocosides A–G 1–7, together with 18 known compounds were isolated from the stems of Xylosma controversumClos. In compounds 3–6, the glucose residue is esterified at C6 by 2hydroxycyclopentanecarboxylic acid. These new structures were established by spectroscopicdata interpretation and chemical methods. [ABSTRACT FROM AUTHOR]

Background: Corneal xenotransplantation is an alternative approach for overcoming shortage of allograft in clinics. However, the mechanism of acute corneal xenograft rejection and the method of prolonging xenograft survival have not been well defined. Methods: In this study, we used an orthotopic corneal guinea pig-to-rat xenotransplantation model to study the effects of CD4 and CD8 T cells, T-cell vaccination (TCV) and TCV-induced T-regulatory (Treg) cells on xenograft survival. Results: The acute rejection of xenografts occurred in untreated rats as early as 6 days post-transplantation, while TCV significantly prolonged xenograft survival from 6–12 to 21–27 days. The lymph node cells of the TCV-treated rats exhibited significant response to the anti-guinea pig T cells and the responding cell populations contained two Treg cell subsets, CD4+ CD25− and CD8+ CD28− T cells, both of which lack expression of Foxp3. Adoptive transfer of CD8+ CD28− T cells resulted in profound inhibition of corneal xenograft rejection, while transfer of CD4+ CD25− T cells alone exhibited no significant inhibition. However, transfer of the CD4+ CD25− and CD8+ CD28− T-cell mixture remarkably enhanced the in vivo protective activity against xenograft rejection. Conclusions: These data suggest that TCV induces the activation of specific Treg cell subsets, CD4+ CD25− and CD8+ CD28− T cells, which may act cooperatively to mediate prolongation of corneal xenograft survival. Therefore, TCV can be used as immunotherapy for suppression of acute xenograft rejection. [ABSTRACT FROM AUTHOR]