Adolescence is a challenging developmental period marked with declines in emotional well-being; however, self-compassion has been suggested as a protective factor. This cross-sectional survey study (N=765, grades 7th to 12th; 53% female; 4% Hispanic ethnicity; 64% White and 21% Black) examined whether adolescents’ self-compassion differed by age and gender, and secondly, whether its associations with emotional well-being (perceived stress, life satisfaction, distress intolerance, depressive symptoms, and anxiety) also differed by age and gender. The findings indicated that older females had the lowest self-compassion levels compared to younger females or all-age males. Self-compassion was associated with all emotional well-being measures, and gender and/or age moderated the associations with anxiety and depressive symptoms. Among older adolescents, self-compassion had a greater protective effect on anxiety for boys than for girls. Additionally, older adolescents with low and average self-compassion had greater levels of depressive symptoms than those with high self-compassion. These results may inform for whom and at what age self-compassion interventions may be implemented to protect adolescents from further declines in emotional well-being.

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A method has been developed for the selective delivery of lipophilic immunomodulators to macrophages, which results in the induction of antitumor activity. This method utilizes exhaustively acetylated low density lipoprotein (acetyl-LDL) effector-to-target ratio using 18 ,sg of the acetyl-LDL:MTPPtdEtn complex containing 3.6 ,ig of MTP-PtdEtn (=80 molecules per particle). These studies describe a method for the induction of antitumor activity by use of a chemically modified serum component, acetyl-LDL, to direct lipophilic immunomodulators to Mo.The development of biological response modifiers to modulate antitumor activity has been an area of great interest (1-6). Muramyl dipeptide (MDP; N-acetylmuramyl-L-alanyl-Disoglutamine), a component of the mycobacterium cell wall, is a powerful inducer of antitumor activity in the macrophage (M*). MDP, however, is quickly excreted from the body and has limited usefulness for regimens in vivo (7). The lipophilic derivative muramyl tripeptide phosphatidylethanolamine (MTP-PtdEtn; amide composed of N-acetylmuramyl-L-alanyl-D-isoglutamyl-L-alanine and dipalmitoyl phosphatidylethonolamine) (8) and $To whom reprint requests should be addressed. 6112The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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Macrophage (M+) phenotype and function can be modulated by various T-cell lymphokines (LK). The alteration of M4 phenotype is a result of LK concentration, duration of exposure, and the level of M4 activation when obtained from in vivo sources through elicitation by either-sterile irritants or cellular immune mechanisms. To dissect M4 activation into discrete signals, we constructed T-cell hybridomas by fusing hypoxanthine-aminopterin-thymidine-sensitive BW5147 cells with nylon wool-purified, concanavalin Astimulated T cells. The resulting T-cell hybrids were screened for their ability to (i) protect M4 from the cytopathic effect of Naegleria lysates, (ii) induce class II major histocompatibility complex gene product (Ia antigen) expression, (iii) increase tumoricidal and cytostatic activity, and (iv) alter ectoenzyme profiles on either resident or thioglycolate-elicited M+. Two hybridomas (T-3 and T-9) were selected for further evaluation because of their activity patterns. Supernatants from T-3 and T-9 were compared with cloned gammainterferon (IFN--y) for alterations of biological activities. Both T-3 and T-9 were able to protect resident-M4 cells from Naegleria lysate but had no protective effect on thioglycolate-induced M+. T-9 supernatant had patterns of activity similar to IFN-y, whereas T-3 patterns were different. The addition of anti-IFN--y removed T-9 cytostatic activity while not affecting T-3-induced activity. The LK inducing protection from the cytopathic effect of Naegleria lysate is not IFN--y but another molecular moiety. We conclude that the activation of M4 for the destruction of tumor cells and amoebae may occur via different mechanisms.

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