40 research outputs found
Protein kinase C and cardiac dysfunction: a review
Heart failure (HF) is a physiological state in which cardiac output is insufficient to meet the needs of the body. It is a clinical syndrome characterized by impaired ability of the left ventricle to either fill or eject blood efficiently. HF is a disease of multiple aetiologies leading to progressive cardiac dysfunction and it is the leading cause of deaths in both developed and developing countries. HF is responsible for about 73,000 deaths in the UK each year. In the USA, HF affects 5.8 million people and 550,000 new cases are diagnosed annually. Cardiac remodelling (CD), which plays an important role in pathogenesis of HF, is viewed as stress response to an index event such as myocardial ischaemia or imposition of mechanical load leading to a series of structural and functional changes in the viable myocardium. Protein kinase C (PKC) isozymes are a family of serine/threonine kinases. PKC is a central enzyme in the regulation of growth, hypertrophy, and mediators of signal transduction pathways. In response to circulating hormones, activation of PKC triggers a multitude of intracellular events influencing multiple physiological processes in the heart, including heart rate, contraction, and relaxation. Recent research implicates PKC activation in the pathophysiology of a number of cardiovascular disease states. Few reports are available that examine PKC in normal and diseased human hearts. This review describes the structure, functions, and distribution of PKCs in the healthy and diseased heart with emphasis on the human heart and, also importantly, their regulation in heart failure
Prevention of acute kidney injury and protection of renal function in the intensive care unit
Acute renal failure on the intensive care unit is associated with significant mortality and morbidity. To determine recommendations for the prevention of acute kidney injury (AKI), focusing on the role of potential preventative maneuvers including volume expansion, diuretics, use of inotropes, vasopressors/vasodilators, hormonal interventions, nutrition, and extracorporeal techniques. A systematic search of the literature was performed for studies using these potential protective agents in adult patients at risk for acute renal failure/kidney injury between 1966 and 2009. The following clinical conditions were considered: major surgery, critical illness, sepsis, shock, and use of potentially nephrotoxic drugs and radiocontrast media. Where possible the following endpoints were extracted: creatinine clearance, glomerular filtration rate, increase in serum creatinine, urine output, and markers of tubular injury. Clinical endpoints included the need for renal replacement therapy, length of stay, and mortality. Studies are graded according to the international Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) group system Several measures are recommended, though none carries grade 1A. We recommend prompt resuscitation of the circulation with special attention to providing adequate hydration whilst avoiding high-molecular-weight hydroxy-ethyl starch (HES) preparations, maintaining adequate blood pressure using vasopressors in vasodilatory shock. We suggest using vasopressors in vasodilatory hypotension, specific vasodilators under strict hemodynamic control, sodium bicarbonate for emergency procedures administering contrast media, and periprocedural hemofiltration in severe chronic renal insufficiency undergoing coronary intervention
How are legal matters related to the access of traditional knowledge being considered in the scope of ethnobotany publications in Brazil?
Atrial fibrillation and risk of dementia in non-demented elderly subjects with and without mild cognitive impairment
REAC technology and hyaluron synthase 2, an interesting network to slow down stem cell senescence
Novel PKCs activate ERK through PKD1 in MCF-7 cells
PKCs can have opposite effects on ERK phosphorylation. Novel (n)PKCs can inhibit ERK by phosphorylation of Raf-1, classical and atypical PKCs can activate ERK by removing an inhibitory protein from Raf-1. The aim of this work was to clarify how PMA-activated PKCs lead to ERK activation in MCF-7 cells expressing mainly nPKCs. Using chemical inhibitors and antibodies against PKCs, delivered into cells by the Chariot transfection system, we found that nPKCs activate ERK through transphosphorylation of PKD1, the blockage of which prevented PMA-stimulated ERK activation. We conclude that the nPKCs/PKD1 cascade is determinant for ERK activation by PMA in MCF-7 cells