The authors reviewed the psychological research on envy. The authors examined definitional challenges associated with studying envy, such as the important distinction between envy proper (which contains hostile feelings) and benign envy (which is free of hostile feelings). The authors concluded that envy is reasonably defined as an unpleasant, often painful emotion characterized by feelings of inferiority, hostility, and resentment caused by an awareness of a desired attribute enjoyed by another person or group of persons. The authors examined questions such as why people envy, why envy contains hostile feelings, and why it has a tendency to transmute itself. Finally, the authors considered the role of envy in helping understand other research domains and discussed ways in which people cope with the emotion.

Although many scholars have argued that individual differences in proneness to envy can have wide-ranging implications for social interactions, the empirical testing of these claims is largely undeveloped. We created a single-factor Dispositional Envy Scale (DES) to measure individual differences in tendencies to envy, and examined some of the implications of such differences. Study 1 indicated that the DES is a reliable, stable measure, containing items suiting theoretical criteria for the makeup of dispositional envy. Study 2 supported the construct validity of the DES by showing that it is correlated with other individual difference measures in theoretically compatible ways. Studies 3 and 4 supplied diverse ways of establishing the criterion-related validity of the DES by showing that it moderated envious responses to another person’s superiority and that it predicted envy beyond other correlated individual measures of neuroticism, self-esteem, cynical hostility, and socially desirable responding.

Autophagy plays important roles in both cell death and cell survival. Beclin-1, a key regulator of autophagy formation, has been considered as a haploinsufficient tumor suppressor. Loss of expression or point mutation could serve as a mechanism of loss of beclin-1 tumor suppressor function in cancers. However, our recent study revealed that point mutation of the beclin-1 gene is a rare event in common human cancers. In this study we investigated beclin-1 protein expression in 103 colorectal and 60 gastric carcinoma tissues by immunohistochemistry using a tissue microarray approach. In the cancers, expression of beclin-1 was detected in 95% of the colorectal carcinomas and 83% of the gastric carcinomas. In contrast, normal mucosal cells of both stomach and colon showed no or very weak expression of beclin-1. There was no significant association of beclin-1 expression with clinocopathologic characteristics, including invasion, metastasis and stage. The beclin-1 expression of colorectal and gastric cancers in the present study is quite in contrast to that of the breast cancers in the previous study, which showed a decreased beclin-1 expression in breast cancer cells compared to normal breast cells. Our data indicate that beclin-1 inactivation by loss of expression may not occur in colorectal and gastric cancers. Rather, increased expression of beclin-1 in the malignant colorectal and gastric epithelial cells compared to their normal mucosal epithelial cells suggests that neo-expression of beclin-1 may play a role in both colorectal and gastric tumorigenesis.

The combination of TACE and RFA is safe and provides better local tumor control than RFA alone for the treatment of patients with medium-sized HCC. Our multivariate analysis showed that RFA-alone treatment and Child-Pugh class B were poor independent factors for determining the patient survival period.