The Role of Chemerin and Myostatin after Physical Activity

Obesity and overweight is one of the most common metabolic disorders in industrialized countries and in developing countries. One consequence of pathological obesity is cardiovascular disease and metabolic syndrome. Chemerin is an adipocyne that plays a role in the regulation of the adipocyte function and the metabolism of glucose in the liver and musculoskeletal system. Most likely, chemerin is involved in obesity-related disorders such as type 2 diabetes and cardiovascular disease. Aerobic exercises reduce the level of chemerin and cause macrophage penetration into fat cells and inflammatory factors. Several efforts have been made to clarify the cellular and molecular mechanisms of hypertrophy and muscular atrophy. Myostatin, a new member of the TGF-β family, is a transforming growth factor β that its expression negatively regulates the growth of the skeletal muscle; and the increase of this hormone has been observed in conditions of muscular atrophy. While in response to muscle overload, its levels decrease after the atrophy period, TGF-β is the most important cytokine in the development of skeletal muscle. Myostatin plays an important role in muscle control, and animal and human studies show a negative role of myostatin in the growth of skeletal muscle. Separation of myostatin from Golgi begins on the ninth day of the onset period and continues until birth at all times of muscle growth. Higher levels of myostatin are found in obese people. Resistance training for 10 weeks could reduce levels of plasma myostatin.

Hypolipidemic and Antioxidant Effects of Black Tea Extract and Quercetin in Atherosclerotic Rats

Background: Atherosclerosis is the main cause of cardiovascular disease (CVD) with complex and multifactorial process including atherogenic lipoprotein, oxidized low density lipoprotein (LDL), endothelial dysfunction, plaque stability, vascular inflammation, thrombotic and fibrinolytic disorder, exercises and genetic factor Epidemiological studies have shown tea consumption inversely associated with the development and progression of atherosclerosis. The research objectives: to elucidate hypolipidemic, antioxidant effects, as well as ability to improve coronary artery’s histopathologyof black tea extract (BTE) and quercetin in atherosclerotic rats. Methods: The antioxidant activity was determined by using Superoxide Dismutase activity (SOD) of serum and lipid peroxidation product (Malondialdehyde) of plasma and lipid profile including cholesterol total, LDL, triglyceride (TG), High Density Lipoprotein (HDL) of atherosclerotic rats. Inducing atherosclerotic, rats were given cholesterol and cholic acid in feed during ten weeks until rats indicated atherosclerotic symptom with narrowed artery and foamy cells in the artery’s wall. After rats suffered atherosclerotic, the high cholesterol feed and cholic acid were stopped and rats were given BTE 450; 300; 150 mg/kg body weight (BW) daily, quercetin 15; 10; 5 mg/kg BW daily, compared to rats were given vitamin E 60 mg/kg/BW; simvastatin 2.7 mg/kg BW, probucol 30 mg/kg BW daily for 21 days (first treatment) and 42 days (second treatment), negative control (normal feed), positive control (atherosclerotic rats). Results: BTE and quercetin could lower cholesterol total, triglyceride, LDL MDA and increase HDL, SOD were comparable with simvastatin, probucol both for 21 days and 42 days treatment, as well to improve coronary arteries histopathology. Conclusions: BTE andquercetin have hypolipidemic and antioxidant effects, as well as improve coronary arteries histopathology in atherosclerotic rats.

Discovery of Human HMG-Coa Reductase Inhibitors Using Structure-Based Pharmacophore Modeling Combined with Molecular Dynamics Simulation Methodologies

3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) catalyzes the conversion of HMG-CoA to mevalonate using NADPH and the enzyme is involved in rate-controlling step of mevalonate. Inhibition of HMGR is considered as effective way to lower cholesterol levels so it is drug target to treat hypercholesterolemia, major risk factor of cardiovascular disease. To discover novel HMGR inhibitor, we performed structure-based pharmacophore modeling combined with molecular dynamics (MD) simulation. Four HMGR inhibitors were used for MD simulation and representative structure of each simulation were selected by clustering analysis. Four structure-based pharmacophore models were generated using the representative structure. The generated models were validated used in virtual screening to find novel scaffolds for inhibiting HMGR. The screened compounds were filtered by applying drug-like properties and used in molecular docking. Finally, four hit compounds were obtained and these complexes were refined using energy minimization. These compounds might be potential leads to design novel HMGR inhibitor.

Microalbuminuria in Human Immunodeficiency Virus Infection and Acquired Immunodeficiency Syndrome

Human immunodeficiency virus infection and acquired immunodeficiency syndrome is a global pandemic with cases reporting from virtually every country and continues to be a common infection in developing country like India. Microalbuminuria is a manifestation of human immunodeficiency virus associated nephropathy. Therefore, microalbuminuria may be an early marker of human immunodeficiency virus associated nephropathy, and screening for its presence may be beneficial. A strikingly high prevalence of microalbuminuria among human immunodeficiency virus infected patients has been described in various studies. Risk factors for clinically significant proteinuria include African - American race, higher human immunodeficiency virus ribonucleic acid level and lower CD4 lymphocyte count. The cardiovascular risk factors of increased systolic blood pressure and increase fasting blood sugar level are strongly associated with microalbuminuria in human immunodeficiency virus patient. These results suggest that microalbuminuria may be a sign of current endothelial dysfunction and micro-vascular disease and there is substantial risk of future cardiovascular disease events. Positive contributing factors include early kidney disease such as human immunodeficiency virus associated nephropathy, a marker of end organ damage related to co morbidities of diabetes or hypertension, or more diffuse endothelial cells dysfunction. Nevertheless after adjustment for non human immunodeficiency virus factors, human immunodeficiency virus itself is a major risk factor. The presence of human immunodeficiency virus infection is independent risk to develop microalbuminuria in human immunodeficiency virus patient. Cardiovascular risk factors appeared to be stronger predictors of microalbuminuria than markers of human immunodeficiency virus severity person with human immunodeficiency virus infection and microalbuminuria therefore appear to potentially bear the burden of two separate damage related to known vascular end organ damage related to know vascular risk factors, and human immunodeficiency virus specific processes such as the direct viral infection of kidney cells.The higher prevalence of microalbuminuria among the human immunodeficiency virus infected could be harbinger of future increased risks of both kidney and cardiovascular disease. Further study defining the prognostic significance of microalbuminuria among human immunodeficiency virus infected persons will be essential. Microalbuminuria seems to be a predictor of cardiovascular disease in diabetic and non diabetic subjects, hence it can also be used for early detection of micro vascular disease in human immunodeficiency virus positive patients, thus can help to diagnose the disease at the earliest.

Overview of CARDIOSENSOR Project on the Development of a Nanosensor for Assessing the Risk of Cardiovascular Disease

This paper aims at overviewing the topics of a research project (CARDIOSENSOR) on the field of health sciences (biomaterials and biomedical engineering). The project has focused on the development of a nanosensor for the assessment of the risk of cardiovascular diseases by the monitoring of C-reactive protein (CRP), which has been currently considered as the best validated inflammatory biomarker associated to cardiovascular diseases. The project involves tasks such as: 1) the development of sensor devices based on field effect transistors (FET): assembly, optimization and validation; 2) application of sensors to the detection of CRP in standard solutions and comparison with enzyme-linked immunosorbent assay (ELISA); and 3) application of sensors to real samples such as blood and saliva and evaluation of their ability to predict the risk of cardiovascular disease.