The Value of Reflective: Functioning within an Academic Therapeutic Nursery.

The self begins as a social self and is dependent on the other and the self-other relationship. Furthermore, shortly after birth, the intersubjective self is nurtured and sustained by the reciprocal interactions with the significant other. Recent research suggests that the significant other's reciprocity depends on his or her capacity for mentalization, and this reflective functioning capacity influences not only the child's developing sense of I, other, and we, but also his or her developing attachment pattern. Several studies have demonstrated that parental reflective functioning can be improved with intervention, and enhancing parental reflective functioning can lead to a more secure attachment pattern and better outcomes for the child and parent. Therefore, intervention with toddlers and their families requires us to consider this dynamic two-person psychology. In this paper, we describe an academic parent-child nursery program aimed at enhancing parental reflective functioning. A clinical example from the collaborative treatment of a mother and her two-year-old will demonstrate how reflective functioning can be enhanced in the parent-child dyad and lead to a more secure parent-child relationship. We will also discuss the value of reflective functioning to the interdisciplinary team and how we dealt with countertransference issues that arose during the treatment.

Regulation of phototransduction responsiveness and retinal degeneration by a phospholipase D-generated signaling lipid.

Drosophila melanogaster phototransduction proceeds via a phospholipase C (PLC)-triggered cascade of phosphatidylinositol (PI) lipid modifications, many steps of which remain undefined. We describe the involvement of the lipid phosphatidic acid and the enzyme that generates it, phospholipase D (Pld), in this process. Pld(null) flies exhibit decreased light sensitivity as well as a heightened susceptibility to retinal degeneration. Pld overexpression rescues flies lacking PLC from light-induced, metarhodopsin-mediated degeneration and restores visual signaling in flies lacking the PI transfer protein, which is a key player in the replenishment of the PI 4,5-bisphosphate (PIP2) substrate used by PLC to transduce light stimuli into neurological signals. Altogether, these findings suggest that Pld facilitates phototransduction by maintaining adequate levels of PIP2 and by protecting the visual system from metarhodopsin-induced, low light degeneration.