Emotion recognition based on physiological signals has been a hot topic and applied in many areas such as safe driving, health care and social security. In this paper, we present a comprehensive review on physiological signal-based emotion recognition, including emotion models, emotion elicitation methods, the published emotional physiological datasets, features, classifiers, and the whole framework for emotion recognition based on the physiological signals. A summary and comparation among the recent studies has been conducted, which reveals the current existing problems and the future work has been discussed.

Abstract-We previously reported that hyperhomocysteinemia (HHcy), an independent risk factor of coronary artery disease (CAD), is associated with increased atherosclerosis and decreased plasma high-density lipoprotein cholesterol (HDL-C) in cystathionine ␤-synthase-/apolipoprotein E-deficient (CBS Ϫ/Ϫ /apoE Ϫ/Ϫ ) mice. We observed that plasma homocysteine (Hcy) concentrations are negatively correlated with HDL-C and apolipoprotein A1 (apoA-I) in patients with CAD. We found the loss of large HDL particles, increased HDL-free cholesterol, and decreased HDL protein in CBS Ϫ/Ϫ /apoE Ϫ/Ϫ mice, and attenuated cholesterol efflux from cholesterol-loaded macrophages to plasma in CBS Ϫ/Ϫ / apoE Ϫ/Ϫ mice. ApoA-I protein was reduced in the plasma and liver, but hepatic apoA-I mRNA was unchanged in CBS Ϫ/Ϫ /apoE Ϫ/Ϫ mice. Moreover, Hcy (0.5 to 2 mmol/L) reduced the levels of apoA-I protein but not mRNA and inhibited apoA-1 protein synthesis in mouse primary hepatocytes. Further, plasma lecithin:cholesterol acyltransferase (LCAT) substrate reactivity was decreased, LCAT specific activity increased, and plasma LCAT protein levels unchanged in apoE

Objective-A risk factor for cardiovascular disease, hyperhomocystinemia (HHcy), is associated with endothelial dysfunction. In this study, we examined the mechanistic role of HHcy in endothelial dysfunction. Methods and Results-Through the use of 2 functional models, aortic rings and intravital video microscopy of the cremaster, we found that arterial relaxation in response to the endothelium-dependent vessel relaxant, acetylcholine or the nitric oxide synthase (NOS) activator (A23187), was significantly impaired in cystathionine ␤-synthase null (CBS Ϫ/Ϫ ) mice. However, the vascular smooth muscle cell (VSMC) response to the nitric oxide (NO) donor (SNAP) was preserved in CBS Ϫ/Ϫ mice. In addition, superoxide dismutase and catalase failed to restore endothelium-dependent vasodilatation. Endothelial nitric oxide synthase (eNOS) activity was significantly reduced in mouse aortic endothelial cells (MAECs) of CBS Ϫ/Ϫ mice, as well as in Hcy-treated mouse and human aortic endothelial cells (HAECs). Hcy-mediated eNOS inhibition-which was not rescued by adenoviral transduction of superoxide dismutase and glutathione peroxidase, or by tetrahydrobiopterin, sepiapterin, and arginine supplementations in MAEC-was associated with decreased protein expression and increased threonine 495 phosphorylation of eNOS in HAECs. Ultimately, a protein kinase C (PKC) inhibitor, GF109203X (GFX), reversed Hcy-mediated eNOS inactivation and threonine 495 phosphorylation in HAECs. Conclusions-These