This brief review on perceived control and aging is organized according to 3 perspectives of research involving description, explanation, and modification. An extensive body of literature has utilized cross-sectional and correlational methods to describe the sociodemographic variations and outcomes associated with perceived control. This work has focused on differences in perceived control as a function of age, sex, education, socioeconomic status, and culture and has identified positive associations with many aging-related outcomes involving health and well-being. With growing evidence regarding the health benefits of perceived control in the context of a declining sense of control with aging, there has been an increased effort to uncover the mechanisms involved, with the hopes of developing methods to maintain and/or promote adaptive control beliefs throughout adulthood. Through longitudinal and experimental work, researchers are beginning to clarify the directionality and elucidate the mechanisms to explain the associations. Recent evidence from longitudinal studies shows that control beliefs have an impact on subsequent changes in health. Yet, the findings suggest that it is not a unidirectional relationship. A conceptual model suggesting an ongoing reciprocal relationship between perceived control and health and well-being is discussed. Research examining the mechanisms that link perceived control to aging-related outcomes can help to inform and to develop effective interventions that are tailored to the individual's specific barriers and goals. We consider new directions for research, including more attention to intraindividual variability and reactivity to daily challenges, such as stress, with the goal of advancing our understanding of how perceived control contributes to aging-related outcomes. More work is needed to develop strategies to enhance control beliefs in later life. Although it will not always be possible to modify control beliefs, researchers can take these beliefs into account when developing interventions. A personalized approach is recommended as a way to tailor interventions that are compatible with individuals' beliefs about control to facilitate adaptive behavior change. Conclusions focus on selected issues and considerations for future research.

The synthesis of protein–protein and protein–peptide conjugates is an important capability for producing vaccines, immunotherapeutics, and targeted delivery agents. Herein we show that the enzyme tyrosinase is capable of oxidizing exposed tyrosine residues into o -quinones that react rapidly with cysteine residues on target proteins. This coupling reaction occurs under mild aerobic conditions and has the rare ability to join full-size proteins in under 2 h. The utility of the approach is demonstrated for the attachment of cationic peptides to enhance the cellular delivery of CRISPR-Cas9 20-fold and for the coupling of reporter proteins to a cancer-targeting antibody fragment without loss of its cell-specific binding ability. The broad applicability of this technique provides a new building block approach for the synthesis of protein chimeras.

The phosphatidylcholine-using phospholipase D (PLD) isoform PLD2 is widely expressed in mammalian cells and is activated in response to a variety of promitogenic agonists. In this study, active and inactive hemagglutinin-tagged human PLD2 (HA-PLD2) constructs were stably expressed in an EL4 cell line lacking detectable endogenous PLD1 or PLD2. The overall goal of the study was to examine the roles of PLD2 in cellular signal transduction and cell phenotype. HA-PLD2 confers PLD activity that is activated by phorbol ester, ionomycin, and okadaic acid. Proliferation and Erk activation are unchanged in cells transfected with active PLD2; proliferation rate is decreased in cells expressing inactive PLD2. Basal tyrosine phosphorylation of focal adhesion kinase (FAK) is increased in cells expressing active PLD2, as is phosphorylation of Akt; inactive PLD2 has no effect. Expression of active PLD2 is associated with increased spreading and elongation of cells on tissue culture plastic, whereas inactive PLD2 inhibits cell spreading. Inactive PLD2 also inhibits cell adhesion, migration, and serum-induced invasion. Cells expressing active PLD2 form metastases in syngeneic mice, as do the parental cells; cells expressing inactive PLD2 form fewer metastases than parental cells. In summary, active PLD2 enhances FAK phosphorylation, Akt activation, and cell invasion in EL4 lymphoma cells, whereas inactive PLD2 exerts inhibitory effects on adhesion, migration, invasion, and tumor formation. Overall, expression of active PLD2 enhances processes favorable to lymphoma cell metastasis, whereas expression of inactive PLD2 inhibits metastasis.

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Only two-thirds of participants started treatment. Although there were significant group x time interactions for bingeing and vomiting, favouring the CD-ROM group at 3 months and the waiting-list group at 7 months, post hoc group comparisons at 3 and 7 months found no significant differences for bingeing or vomiting. CD-ROM-based delivery of this intervention, without support from a clinician, may not be the best way of exploiting its benefits.