Search

Background: Rheumatic heart disease (RHD) results from group A beta-hemolytic streptococcal pharyngeal infection is an autoimmune sequela of acute or recurrent episodes of acute rheumatic fever (ARF). This study is focused on identifying heart tissue-specific proteins implicated in the secondary immunopathogenesis of RHD. Methods: Sera from 49 RHD patients and 32 controls were probed in 2DE to study the differential expression of proteins. After 2DE, the spots were analyzed and identified using ESI-MS. A total of 1082 protein spots were detected in RHD patients and controls. Results: Two protein spots were significantly down-regulated (p≤0.01) and 34 protein spots were significantly up-regulated (p≤0.01) compared to controls. The differentially expressed protein spots were trypsin-digested and identified as hyaluronan-mediated motility receptor (RHAMM), troponin 1, janus kinase and microtubule interacting protein 1 (Jakmip 1), nuclear ubiquitous casein and cyclin-dependent kinase substrate 1, basal body-orientation factor 1 and muscle-related coiled-coil protein. A positive correlation was established with the up-regulated and down-regulated expression of these proteins suggests them as potential biomarker for RHD. Conclusion: This study highlights rheumatic mitral stenosis and regurgitation, an active inflammatory process and provides novel information about the proteins thereby elaborates the knowledge of physiology and etiology of this disease.

Background: Type-2 diabetes mellitus (T2DM) is a major risk factor for coronary artery disease (CAD) resulting in high morbidity and mortality. Glutathione S-transferases (GSTM1, GSTT1 and GSTP1) are known for their broad range of detoxification and in the metabolism of xenobiotics. Recent studies revealed the relationship of GSTs variants with T2DM and CAD. In this case-control study we ascertained the association of GSTs variants in association with the development of CAD in patients with T2DM. Methods: From the Southern part of India, we enrolled 222 T2DM patients, 290 T2DM patients with CAD and 270 healthy controls matched for age, sex and origin. Serum lipid profiles were measured and DNA was extracted from the blood samples. Multiplex PCR for GSTM1/T1 (null polymorphism) and PCR-RFLP for GSTP1 (105 A > G), were performed for genotyping of study participants. Gene frequency and lipid profiles were statistically analyzed for disease association. Results: Regression analysis showed that. GSTM1-null genotype is associated with a 2-fold increase (OR = 2.925; 95% CI = 2.078-4.119; P < 0.0001) and CSTT1-null genotype is associated with a 3-fold increase (OR = 3.114; 95% CI = 2.176-4.456; P < 0.0001) to T2DM development. Ile/Val and Val/Val genotypes of GSTP1 also showed a significant risk for T2DM (OR = 1.423, CI = 1.041-1.946; P=0.027 and OR = 1.829, CI = 1.064-3.142; P = 0.029). Increased odds ratio showed that GSTT1-null genotype had a moderately higher occurrence in T2DM-CAD patients (OR = 1.918, 95% CI = 1.144-3.214; P = 0.014) than T2DM patients without CAD. The level of HDL has significantly decreased in GSTT1-present than in GSTT1-null genotype (43.50 +/- 4.10 vs. 45.20 +/- 3.90; P = 0.004) when compared with control and T2DM patients. However, LDL level showed a significant increase in GSTT1-null than GSTT1-present genotype (108.70 +/- 16.90 vs. 102.20 +/- 12.60; P = 0.005). Although the GSTM1-null polymorphism showed no correlation with lipid profiles among T2DM and T2DM with CAD patients, GSTT1-null polymorphism attained a statistical significance for the level of LDL (127 +/- 28.20 vs. 134 +/- 29.10; P = 0.039) and triglycerides in T2DM with CAD patients (182.10 +/- 21.10 vs. 191.20 +/- 24.10; P = 0.018). Conclusion: Our work concludes that GSTM1, GSTT1 and GSTP1 variants might contribute to the development of T2DM and GSTT1 variant alone is involved in the development of T2DM associated CAD complications in the South Indian population. (C) 2011 Elsevier Inc. All rights reserved.

Endothelium forms an innermost lining of blood vessel and it regulates the vascular tone and permeability. A healthy vascular endothelium is antiatherogenic in nature because of its properties such as inhibition of platelet aggregation, adhesion cascades, smooth muscle cell proliferation and leukocyte adhesion. Vascular endothelial dysfunction (VED) is associated with reduced synthesis and release of nitric oxide, proinflammatory and prothrombotic properties followed by diminished vasodilation. VED has been implicated in the pathogenesis of artherosclerosis, hypertension, myocardial infarction, heart failure, renal failure and stroke. Various pharmacological interventions such as angiotensin converting enzyme (ACE) inhibitors, statins, insulin sensitizers, L-arginine as well as agents that target endothelial nitric oxide synthase (eNOS) ``coupling'' such as folates or tetrahydrobiopterin (BH4) have been noted to improve the function of vascular endothelium. In this review, we discussed various recently developed pharmacological interventions to improve the function of endothelium. Moreover, the novel targets sites involved in the pathogenesis of vascular endothelial dysfunction have been delineated.

The study was carried to determine the association of angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism with the risk of hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), and restrictive cardiomyopathy (RCM).A total of 174 patients diagnosed with cardiomyopathy (118 with HCM, 51 with DCM, and 5 with RCM) and 164 ethnically, age- and gender-matched controls were included in the study. ACE I/D genotyping was performed by PCR. In total, 25.86% of the patients were in New York Heart Association (NYHA) class III and IV at presentation. A total of 67.24% patients had dyspnea, 56.89% had angina pectoris, and 25.28% of the patients had at least one event of syncope. Frequency of occurrence of the disease was more in male patients compared to female patients (P0.05). After adjustment for age, sex, body mass index (BMI), and smoking habit, the prevalence of ACE DD genotype, and ACE 'D' allele was significantly higher in patients as compared to controls and was associated with increased risk (DD: OR 2.11, 95% CI 1.27-3.52, P0.05; 'D': OR 1.91, 95% CI 1.08-3.35, P0.05). The mean septal thickness was higher for DD and ID genotypes (20.40 +/- 3.73 mm and 21.82 +/- 5.35 mm, respectively) when compared with II genotype (18.63 +/- 6.69 mm) in HCM patients, however, the differences were not significant statistically (P0.05). The DCM patients with ID genotype showed significantly decreased left ventricular ejection fraction (LVEF) at enrolment (26.50 +/- 8.04%) (P = 0.04).Our results suggest that D allele of ACE I/D polymorphism significantly influences the HCM and DCM phenotypes.

Cardiac isoform of alpha-2 macroglobulin [cardiac alpha2M] has been shown to be an early marker in cardiac hypertrophy and left ventricular mass in humans. We, here, for the first time report its presence in myocardial infarcted humans and tried to explore the possibility of using this protein as a novel diagnostic marker for myocardial infarcted diabetic patients. A total of 260 samples were analyzed in this study for the presence of cardiac alpha2M. These include 55 patients of diabetic with post myocardial infarction [PMI], 45 diabetic patients without PMI, 60 patients of PMI alone and 100 controls without any ailments. Levels of cardiac alpha2M present in the sera of diabetic patients with PMI are significantly higher than that of normal human sera and diabetic patients without PMI but not with PMI alone group, suggesting this protein as a marker for PMI itself. However, our results reveal that cardiac alpha2M could be a valuable marker for the diagnosis of myocardial infarcted diabetic patients and differentiating them from diabetic patients without myocardial infarction by sandwich ELISA.

Background Cardiac isoform of alpha 2 macroglobulin (CA2M), a serum protein (182000Mr) has been used as a diagnostic molecular marker for cardiac manifestations in HIV and diabetic patients. This study investigates the reliability of CA2M as an early diagnostic marker for cardiac manifestations in HIV patients and factors that could possibly influence their levels. Methods A total of 206 serum samples were analysed from HIV patients with cardiac diseases (68), with non-cardiac ailments (48), opportunistic infections (34) and without other co-morbidities (56). The immuno-cross-reactivity between human serum CA2M and anti-rat CA2M antibody was tested and quantified by sandwich enzyme linked immunosorbent assay (ELISA). Results The CA2M levels were high in HIV patients with cardiac diseases irrespective of the manifestations. The CA2M levels were not influenced by opportunistic infections, non-cardiac ailments and patient parameters like age, sex, duration of illness, past history of other co-morbidities. Conclusion CA2M can be used as a reliable early diagnostic marker in HIV patients with cardiac manifestations. CA2M levels were not influenced by other patient parameters.

This study investigated the possible role of the cardiac isoform of alpha 2-macroglobulin (CA2M) as an early diagnostic marker for HIV-associated cardiovascular manifestations. A total of 349 samples were analysed by Western blot and quantified by sandwich enzyme-linked immunosorbent assay. The levels of CA2M present in sera of HIV-associated cardiac diseases were significantly higher than those of HIV without cardiac involvement and healthy sera. CA2M may act as a novel diagnostic marker to identify cardiac manifestations in HIV/AIDS patients.

BACKGROUND Earlier we showed cardiac isoform of alpha-2 macroglobulin (CA2M) to be an early marker of cardiac hypertrophy. DESIGN In this study, we tried to explore the possibility of using this protein as a marker for diagnosis of cardiac diseases. METHODS A total of 593 samples were analyzed for the presence of CA2M using sandwich enzyme-linked immunosorbent assay. RESULTS Samples include various cardiac diseases (230), non-cardiac ailments (263) and controls (100). CONCLUSION Levels of CA2M in cardiac diseases were significantly higher than other sample groups but moderately elevated in leprosy. This protein could be considered for diagnosis of cardiac diseases as a serum marker.

Cardiovascular diseases (CVDs) have a complex aetiology determined by risk factors, which include genetic and environmental factors. Chronic infection and inflammation is reported to be a pathogenic determinant for the development of CVDs. Here, we report the prevalence of bacterial pathogens in the circulation of CVD patients in Madurai, India. Blood culturing was performed using BD BACTEC automated culture system and organisms were identified by16S rRNA gene sequence analysis. From a total of 133 samples screened, 47 samples showed culture positive which indicates a high level of bacteraemia in CVD patients. From the 47 samples that showed growth, we have identified 57 bacterial isolates comprising 35 different species. Coagulase negative Staphylococci (CoNS) was the most predominant group of bacteria and other notable bacterial species isolated in this study are discussed.