Nanocomposites consisting of oblong ultrathin plate shaped calcium phosphate nanoparticles and graphene oxide microflakes were synthesized and have demonstrated markedly synergistic effect in accelerating stem cell differentiation to osteoblasts.

We studied the relationship of apolipoprotein E (apoE) isoforms and coronary artery disease (CAD) in 224 African Americans and 326 Caucasians undergoing diagnostic coronary angiography. The presence of CAD was defined as .50% stenosis in at least one artery. ApoE allele frequencies were 0.12, 0.62, and 0.26 for e2, e3, and e4, respectively, in African Americans and 0.08, 0.78, and 0.14 for e2, e3, and e4, respectively, in Caucasians. Among African Americans, CAD was present in 9 of 34 e2 carriers (26%), significantly smaller (P , 0.05) in proportion compared with 39 of 82 e3 carriers and 43 of 92 e4 carriers (48% and 47%, respectively), suggesting a protective effect of the e2 allele. No such difference was seen in Caucasians. In African Americans but not Caucasians, LDL cholesterol was lower in e2 carriers than in e3 and e4 carriers (106 vs. 127 and 134 mg/dl, respectively; P , 0.005). After adjusting for lipid levels, the association between apoE2 and CAD was no longer significant. Thus, the protective effect of apoE2 seen in African Americans could be explained by a favorable lipid profile in e2 carriers, whereas in Caucasians, the absence of such a protective effect could be attributable to the lack of effect of apoE2 on the lipid

In conclusion, plasma MPO levels were not elevated in patients with stable CAD, suggesting that systemic release of MPO is not a characteristic feature of asymptomatic CAD.

The genetic variability of apolipoprotein E (apoE) influences plasma lipoprotein levels, and allele frequencies differ between African Americans and Caucasians. As African Americans have higher lipoprotein [a] (15,18,19). Furthermore, as described above, we and others have identified several genetic variations that affect allele-specific apo[a] levels (8,16,17,20). Genetic variability of apolipoprotein E (apoE) is a major determinant of plasma lipoprotein levels (21), and furthermore, apoE genotype frequencies differ between African Americans and Caucasians (22,23). As the African AmericanCaucasian differences in allele-specific apo[a] levels for large apo[a] sizes remain unexplained, we focused on apoE as a possible genetic factor potentially contributing to this difference. Earlier studies have investigated the impact of apoE genotypes on Lp[a] levels, but the results have been

The hypothesis was tested that plasma levels of adiponectin would be associated with coronary artery disease (CAD) across African-American and Caucasian ethnicity and gender. Adiponectin levels, cardiovascular risk factors, and extent of CAD were measured in 453 subjects (173 African-American and 280 Caucasian men and women). The distribution of adiponectin levels differed significantly between African-Americans and Caucasians (P<0.0001). Among African-Americans, the adiponectin distribution was skewed toward lower levels. For women, adiponectin levels were higher among Caucasians compared with African-Americans (P<0.001), whereas no interethnic difference was observed for men. Irrespective of ethnic group, subjects with CAD had lower levels of adiponectin than did subjects without CAD. Adiponectin was negatively and significantly associated with waist-hip ratio, body mass index, diastolic blood pressure, insulin level, and homeostasis model assessment-insulin resistance in both ethnic groups. Among lipid parameters, total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels were negatively correlated with adiponectin, whereas the high-density lipoprotein cholesterol level correlated positively for both African-Americans and Caucasians. In a multiple regression model, controlling for gender, ethnicity, and other CAD risk factors, adiponectin levels were negatively associated with CAD (P<0.05). The results indicate that, across gender and ethnicity, low adiponectin levels may be an independent risk factor for CAD.