The current study investigated several factors that might increase the risk of mortality in elderly patients with hip fracture. Further studies are needed to evaluate the effectiveness of specific interventions to reduce the risk of mortality.

Pathological cardiac hypertrophy is characterized by deleterious changes developed in cardiovascular diseases, whereas microRNAs (miRNAs) are involved in the mediation of cardiac hypertrophy. To investigate the role of microRNA-26a (miR-26a) in regulating cardiac hypertrophy and its functioning mechanisms, overexpression and suppression of miR‑26a via its mimic and inhibitor in a transverse abdominal aortic constriction (TAAC)-induced rat model and in angiotensin II (Ang II)-induced cardiomyocytes (CMs) was performed. In the rat model, the heart weight (HW) compared with the body weight (BW), the CM area, and expression of the hypertrophy‑associated factors, atrial natriuretic factor (ANF) and β‑myosin heavy chain (β‑MHC), were assessed. In CMs, the protein synthesis rate was determined using a leucine incorporation assay. Mutation of the GATA‑binding protein 4 (GATA4) 3'‑untranslated region (UTR) and overexpression of GATA4 were performed to confirm whether GATA4 is the target of miR‑26a. The results indicated that miR-26a was significantly downregulated in the heart tissue of the rat model, as well as in Ang II‑induced CMs (P<0.05). The TAAC-induced rat model exhibited a higher HW/BW ratio, a larger CM area, and higher expression levels of ANF and β‑MHC. CMs, upon Ang II treatment, also demonstrated a larger CM area, higher levels of ANF and β‑MHC, as well as accelerated protein synthesis. miR‑26a was not able to regulate GATA4 with mutations in the 3'‑UTR, indicating that GATA4 was the direct target of miR‑26a. Overexpression of GATA4 abrogated the inhibitory functions of miR‑26a in cardiac hypertrophy. Taken together, the present study suggested an anti‑hypertrophic role of miR‑26a in cardiac hypertrophy, possibly via inhibition of GATA4. These findings may be useful in terms of facilitating cardiac treatment, with potential therapeutic targets and strategies.

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Background: To improve therapy for slow coronary flow (SCF), the effects of hyperbaric oxygen (HBO) therapy on vascular endothelial function in divided into two groups according to the following treatment: HBO group (n = 48) and the control group (n = 50). Patients in the control group were administrated with conventional treatment, while those in the HBO group were administrated HBO therapy for 4 weeks in addition to conventional treatment. To evaluate the effects of HBO on vascular endothelial functions, plasma levels of nitric oxide (NO), calcitonin gene-related peptide (CGRP), endothelin-1 (ET-1), high sensitivity C-reactive protein (hsCRP) as well as endothelial-dependent flowmediated vasodilation (FMD) of the brachial artery were measured in both groups before and after their respective treatments.Results: There were no significant differences in plasma levels of NO, CGRP, hsCRP (Cardiol J 2018; 25, 1: 106-112)

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Cardiovascular diseases remain the leading causes of death worldwide. Stem cell therapy offers a promising option to regenerate injured myocardium. Among the various types of stem cells, cardiosphere cells represent a mixture of intrinsic heart stem cells and supporting cells. The safety and efficacy of cardiosphere cells have been demonstrated in recent clinical trials. Cell–matrix interaction plays an important role in mediating the engraftment of injected stem cells. Here, we studied the role of integrin β‐3 in cardiosphere‐mediated cell therapy in a mouse model of myocardial infarction. Our results indicated that inhibiting integrin β‐3 reduced attachment, retention and therapeutic benefits of human cardiospheres in mice with acute myocardial infarction. This suggests integrin β‐3 plays an important role in cardiosphere‐mediated heart regeneration.

Background: The study sought to analyze the predictive value of the early measurement of pregnancy associated plasma protein-A (PAPP-A), prealbumin (PAB), C-reactive protein (CRP), brain natriuretic peptide (BNP), and other indicators of heart failure (HF) after acute myocardial infarction (AMI).