CYTOKINE RESISTIN IN METABOLIC AND CARDIOVASCULAR DISEASE.

The rise in metabolic syndromes is known to be the root cause of major cardiovascular diseases mainly Coronary Artery Disease (CAD) in India. A biological marker will thus help to determine the disease before its onset and help cure it at early stages, reducing the chances of development of further complications. There are various pro-inammatory markers (cytokines) which can be used to determine the onset of disease one such marker known is resistin. Resistin is known to be a pro-inammatory adipokine secreted mainly from Peripheral mononuclear cell (PMNC), bone marrow cells and macrophages in humans [1]. Inammatory response is generated due to rise in metabolic syndromes which in turn leads to the secretion of various cytokines. The levels of these cytokines released help in determining the severity of disease.

Cardiac Migration of Endogenous Mesenchymal Stromal Cells in Patients with Inflammatory Cardiomyopathy

Introduction. Mesenchymal stromal cells (MSC) have immunomodulatory features. The aim of this study was to investigate the migration and homing potential of endogenous circulating MSC in virus negative inflammatory cardiomyopathy (CMi).Methods. In 29 patients withn=23or withoutn=6CMi undergoing endomyocardial biopsies (EMB), transcardiac gradients (TCGs) of circulating MSC were measured by flow cytometry from blood simultaneously sampled from aorta and coronary sinus. The presence of MSC in EMB, cardiac inflammation, and SDF-1αmRNA expression were detected via immunohistochemistry and real-time PCR.Results. MSC defined as CD45−CD34−CD11b−CD73+CD90+cells accounted for 0.010 [0.0025–0.048]%/peripheral mononuclear cell (PMNC) and as CD45−CD34−CD11b−CD73+CD105+cells for 0.019 [0.0026–0.067]%/PMNC, both with similar counts in patients with or without cardiac inflammation. There was a 29.9%P<0.01transcardiac reduction of circulating MSC in patients with CMi, correlating with the extent of cardiac inflammation (P<0.05, multivariate analysis). A strong correlation was found between the TCG of circulating MSC and numbers of MSC (CD45−CD34−CD90+CD105+) in EMB (r=-0.73,P<0.005). SDF-1αwas the strongest predictor for increased MSC in EMB (P<0.005, multivariate analysis).Conclusions. Endogenous MSC continuously migrate to the heart in patients with CMi triggered by cardiac inflammation.

Protection against Loss of Innate Defenses in Adulthood by Low Advanced Glycation End Products (AGE) Intake: Role of the Antiinflammatory AGE Receptor-1

Context: Increased oxidant stress and inflammation (OS/infl) are linked to both aging-related diseases and advanced glycation end products (AGEs). Whereas AGE receptor-1 (AGER1) reduces OS/infl in animals, this has not been assessed in normal humans. Objective: The objectives of the study were to determine whether AGER1 correlates with AGEs and OS/infl and a reduction of dietary AGEs (dAGEs) lowers OS/infl in healthy adults and chronic kidney disease (CKD-3) patients. Design: This study was cross-sectional with 2-yr follow-up studies of healthy adults and CKD-3 patients, a subset of which received a reduced AGE or regular diet. Setting: The study was conducted at general community and renal clinics. Participants: Participants included 325 healthy adults (18–45 and &gt;60 yr old) and 66 CKD-3 patients. Intervention: An isocaloric low-AGE (30–50% reduction) or regular diet was given to 40 healthy subjects for 4 months and to nine CKD-3 patients for 4 wk. Main Outcome: Relationships between age, dAGEs, serum AGEs, peripheral mononuclear cell AGE-receptors, and OS/Infl before and after reduction of dAGE intake were measured. Results: AGEs, oxidant stress, receptor for AGE, and TNFα were reduced in normal and CKD-3 patients after the low-AGE diet, independently of age. AGER1 levels in CKD-3 patients on the low-AGE diet resembled 18- to 45-yr-old normal subjects. Dietary, serum, and urine AGEs correlated positively with peripheral mononuclear cell AGER1 levels in healthy participants. AGER1 was suppressed in CKD-3 subjects, whereas receptor for AGE and TNFα were increased. Conclusions: Reduction of AGEs in normal diets may lower oxidant stress/inflammation and restore levels of AGER1, an antioxidant, in healthy and aging subjects and CKD-3 patients. AGE intake has implications for health outcomes and costs and warrants further testing. Reduction of advanced glycation endproducts (AGE) in normal diets lowers oxidant stress/inflammation, and restores levels of AGE receptor-1 in healthy, aging, and chronic kidney disease-3 patients.