RESUMO
Correlation diagnosis in multivariate process quality management is an important and challenging issue. In this paper, a new diagnostic method based on quality component grouping is proposed. Firstly, three theorems describing the properties of the covariance matrix of multivariate process quality are established based on the statistical viewpoint of product quality, to prove the correlation decomposition theorem, which decomposes the correlation of all the quality components into a series of correlations of components pairs, and then by using the factor analysis method, all quality components are grouped in order to maximize the correlations in the same groups and minimize the ones between different groups. Finally, on the basis of correlations between different groups are ignored, T2 control charts of component pairs in the same groups are established to form the diagnostic model. Theoretical analysis and practice prove that for the multivariate process quality whose the correlations between different components vary considerably, the grouping technique enables the size of the correlation diagnostic model to be drastically reduced, thus allowing the proposed method can be used as a generalized theoretical model for the correlation diagnosis.
RESUMO
Cardiac remodeling is an important mechanism of heart failure, which frequently results from leukocyte infiltration. Vascular cellular adhesion molecule-1 (VCAM-1) plays a critical role in leukocyte adhesion and transmigration. However, the importance of VCAM-1 in the development of angiotensin II (Ang II)-induced cardiac remodeling remains unclear. Wild-type (WT) mice were infused with Ang II (1,000 ng/kg/min) for 14 days and simultaneously treated with VCAM-1 neutralizing antibody (0.1 or 0.2 mg) or IgG control. Systolic blood pressure (SBP) and cardiac function were detected by a tail-cuff and echocardiography. Cardiac remodeling was evaluated by histological staining. Adhesion and migration of bone marrow macrophages (BMMs) were evaluated in vitro. Our results indicated that VCAM-1 levels were increased in the serum of patients with heart failure (HF) and the hearts of Ang II-infused mice. Furthermore, Ang II-caused hypertension, cardiac dysfunction, hypertrophy, fibrosis, infiltration of VLA-4+ BMMs and oxidative stress were dose-dependently attenuated in mice administered VCAM-1 neutralizing antibody. In addition, blocking VCAM-1 markedly alleviated Ang II-induced BMMs adhesion and migration, therefore inhibited cardiomyocyte hypertrophy and fibroblast activation. In conclusion, the data reveal that blocking VCAM-1 ameliorates hypertensive cardiac remodeling by impeding VLA-4+ macrophage infiltration. Selective blockage of VCAM-1 may be a novel therapeutic strategy for hypertensive cardiac diseases.