Effect of diabetes mellitus on markers of left ventricular dysfunction in chronic kidney disease.

Objectives: To identify markers of left ventricular dysfunction in chronic kidney disease (CKD) and the effects of diabetes mellitus on them.

Methods: This was a cross sectional study of 200 consecutive chronic kidney disease patients (stage III-V). Echocardiographic assessment of left ventricular function including left ventricular ejection fraction (LVEF), left ventricular mass index (LVMI), left atrial volume, grade of diastolic dysfunction, E/E', left and right ventricular myocardial performance indices (LVMPI, RVMPI) were compared between diabetic and non-diabetic CKD.

Cathepsin B inhibition attenuates cardiovascular pathology in mucopolysaccharidosis I mice.

Mucopolysaccharidosis type I (MPS I) is a lysosomal storage disorder with multisystemic features, including heart enlargement, heart valve dysfunction, and aortic stiffness and dilatation. Previous studies have shown that MPS I mice overexpress cathepsin B (CtsB) in multiple tissues, including those from the cardiovascular system. Here, we hypothesized that inhibition of CtsB could ameliorate cardiac function parameters, as well as aorta and valve abnormalities found in MPS I.

Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis.

Erythrophagocytosis, the phagocytic removal of damaged red blood cells (RBC), and subsequent phagolysosome biogenesis are important processes in iron/heme metabolism and homeostasis. Phagolysosome biogenesis implies the interaction of nascent phagosomes with endocytic compartments and also autophagy effectors. Here, we report that besides recruitment of microtubule-associated protein-1-light chain 3 (LC3), additional autophagy machinery such as sequestosome 1 (p62) is also acquired by single-membrane phagosomes at very early stages of the phagocytic process and that its acquisition is very important to the outcome of the process.

Modulation of Autophagy by Calcium Signalosome in Human Disease.

Autophagy is a catabolic process that is largely regulated by extracellular and intracellular signaling pathways that are central to cellular metabolism and growth. Mounting evidence has shown that ion channels and transporters are important for basal autophagy functioning and influence autophagy to handle stressful situations. Besides its role in cell proliferation and apoptosis, intracellular Ca(2+) is widely recognized as a key regulator of autophagy, acting through the modulation of pathways such as the mechanistic target of rapamycin complex 1, calcium/calmodulin-dependent protein kinase kinase 2, and protein kinase C.

A Therapeutic Dilemma - Coronary Artery Stenting in the Setting of Thrombocytopaenia.

Coronary artery interventions in the setting of Immune Thrombocytopaenic Purpura (ITP) carry the twin risks of bleeding and thrombosis related to the mandatory dual anti-platelet therapy. This condition therefore may require a splenectomy prior to the coronary intervention. Surgical splenectomy in the presence of high-grade coronary stenosis carries greater morbidity and mortality.

Comparison of the kinetics of maturation of phagosomes containing apoptotic cells and IgG-opsonized particles.

Defective clearance of apoptotic cells has emerged as an important contributing factor to the pathogenesis of many diseases. Although many efforts have been made to understand the machinery involved in the recognition between phagocytes and potential targets, little is known about the intracellular transport of phagosomes containing apoptotic cells within mammalian cells. We have, therefore, performed a detailed study on the maturation of phagosomes containing apoptotic cells in a non-professional phagocytic cell line.

Neuropeptide Y inhibits interleukin-1β-induced phagocytosis by microglial cells.

Background: Neuropeptide Y (NPY) is emerging as a modulator of communication between the brain and the immune system. However, in spite of increasing evidence that supports a role for NPY in the modulation of microglial cell responses to inflammatory conditions, there is no consistent information regarding the action of NPY on microglial phagocytic activity, a vital component of the inflammatory response in brain injury. Taking this into consideration, we sought to assess a potential new role for NPY as a modulator of phagocytosis by microglial cells.