Circulating microparticles in cardiovascular disease: going on stage!

Cardiovascular diseases (CVDs) are the leading cause of death worldwide. In spite of the fact that treatments are based on risk calculators which in turn are based on population characteristics, it is well known that these methods have definite levels of uncertainty. Recently, more precise diagnostic or predictive methods have been developed based on indicators of vascular and/or cardiac damage in order to supplement this risk evaluation.

A REDCap application that links researchers, animal facility staff and members of the IACUC in animal health monitoring.

Research studies involving animal experimentation are regulated by the Institutional Animal Care and Use Committee (IACUC). To this end, the IACUC must integrate the information provided by the investigators of each preclinical study and the veterinarians from the animal facility in order to monitor and approve the process. Using a paper-based system to collect animal health and welfare data is a common, albeit time-consuming practice, prone to transcription and reading errors, not to mention inconvenient for veterinarians and investigators wishing to make timely and collaborative decisions when animal welfare is at risk.

Circulating miR-19b and miR-181b are potential biomarkers for diabetic cardiomyopathy.

Diabetic cardiomyopathy is characterized by metabolic changes in the myocardium that promote a slow and silent dysfunction of muscle fibers, leading to myocardium remodelling and heart failure, independently of the presence of coronary artery diseases or hypertension. At present, no imaging methods allow an early diagnosis of this disease. Circulating miRNAs in plasma have been proposed as biomarkers in the prognosis of several cardiac diseases.

Visualization and Analysis of MiRNA-Targets Interactions Networks.

MicroRNAs are a class of small, noncoding RNA molecules of 21-25 nucleotides in length that regulate the gene expression by base-pairing with the target mRNAs, mainly leading to down-regulation or repression of the target genes. MicroRNAs are involved in diverse regulatory pathways in normal and pathological conditions. In this context, it is highly important to identify the targets of specific microRNA in order to understand the mechanism of its regulation and consequently its involvement in disease.

Rab24 interacts with the Rab7/Rab interacting lysosomal protein complex to regulate endosomal degradation.

Endocytosis is a multistep process engaged in extracellular molecules internalization. Several proteins including the Rab GTPases family coordinate the endocytic pathway. The small GTPase Rab7 is present in late endosome (LE) compartments being a marker of endosome maturation.

Two complementary strategies to improve cell engraftment in mesenchymal stem cell-based therapy: Increasing transplanted cell resistance and increasing tissue receptivity.

Over the past 2 decades, therapies based on mesenchymal stem cells (MSC) have been tested to treat several types of diseases in clinical studies, due to their potential for tissue repair and regeneration. Currently, MSC-based therapy is considered a biologically safe procedure, with the therapeutic results being very promising. However, the benefits of these therapies are not stable in the long term, and the final outcomes manifest with high inter-patient variability.

Subclinical Detection of Diabetic Cardiomyopathy with MicroRNAs: Challenges and Perspectives.

The prevalence of cardiac diabetic diseases has been increased around the world, being the most common cause of death and disability among diabetic patients. In particular, diabetic cardiomyopathy is characterized with a diastolic dysfunction and cardiac remodelling without signs of hypertension and coronary artery diseases. In an early stage, it is an asymptomatic disease; however, clinical studies demonstrate that diabetic myocardia are more vulnerable to injury derived by acute myocardial infarct and are the worst prognosis for rehabilitation.

Mesenchymal stem cell therapy for doxorubicin cardiomyopathy: hopes and fears.

Chemotherapy has made an essential contribution to cancer treatment in recent decades despite its adverse effects. As cancer survivors have increased, concern about ex-patient lifespan has become more important too. Doxorubicin is an effective anti-neoplastic drug that produces a cardiotoxic effect.

Intravenous administration of bone marrow-derived multipotent mesenchymal stromal cells has a neutral effect on obesity-induced diabetic cardiomyopathy.

Obesity is a major global health issue. Obese patients develop metabolic syndrome, which is a cluster of clinical features characterized by insulin resistance and dyslipidemia. Its cardiac manifestation, diabetic cardiomyopathy, leads to heart failure.

Mice long-term high-fat diet feeding recapitulates human cardiovascular alterations: an animal model to study the early phases of diabetic cardiomyopathy.

Background/aim: Hypercaloric diet ingestion and sedentary lifestyle result in obesity. Metabolic syndrome is a cluster of clinical features secondary to obesity, considered as a pre-diabetic condition and recognized as an independent risk factor for cardiovascular diseases. To better understand the relationship between obesity, metabolic syndrome and cardiovascular disease as well as for the development of novel therapeutic strategies, animal models that reproduce the etiology, course and outcomes of these pathologies are required.

Cardiac stress test induced by dobutamine and monitored by cardiac catheterization in mice.

Dobutamine is a β-adrenergic agonist with an affinity higher for receptor expressed in the heart (β1) than for receptors expressed in the arteries (β2). When systemically administered, it increases cardiac demand. Thus, dobutamine unmasks abnormal rhythm or ischemic areas potentially at risk of infarction.

Autophagy: for better or for worse, in good times or in bad times.

Autophagy is a bulk cytosolic degradative process which in the last few years has become a key pathway for the advancement of molecular medicine. Autophagy (cellular self-eating) has several implications in human disorders involving accumulation of cytosolic protein aggregates such as Alzheimer, Parkinson, Huntington diseases, as well as in myopathies caused by deficient lysosomal functions and in cancer. Moreover, autophagy affects intracellular microorganism lifespan, acting either as a cellular defense mechanism or, on the contrary, promoting pathogen replication.

Cytotoxicity is predicted by unbound and not total bilirubin concentration.

Although it has been suggested that the unbound, free, (B(f)) rather than total (B(T)) bilirubin level correlates with cell toxicity, direct experimental evidence supporting this conclusion is limited. In addition, previous studies never included a direct measurement of B(f), using newer, accurate methods. To test "the free bilirubin hypothesis", in vitro cytotoxicity was assessed in four cell lines exposed to different B(f) concentrations obtained by varying B(T)/Albumin ratio, using serum albumins with different binding affinities, and/or displacing unconjugated bilirubin (UCB) from albumin with a sulphonamide.

Bilirubin-induced cell toxicity involves PTEN activation through an APE1/Ref-1-dependent pathway.

Unconjugated bilirubin (UCB) is the major degradation product of the heme catabolism. A growing body of evidences suggests that UCB plays major biological effects by inhibiting cell proliferation in cancer cell lines and eliciting cell toxicity particularly in neurons and glial cells. Early molecular events responsible for bilirubin-induced cytotoxicity remain poorly understood.

Ammonium detoxifying activity is maintained after 72 hours of cold preservation of rat hepatocytes in University of Wisconsin (UW) solution.

The ammonium removal efficiency (ARE) and cell viability was investigated in freshly isolated rat hepatocytes exposed to increasing ammonium loads (0.1-2.0 mM).