Exploring silence in short-term psychoanalytic psychotherapy with adolescents with depression

Psychotherapy process research is important in developing technique and enhancing clinical skills. Silence, as an aspect of child and adolescent psychoanalytic psychotherapy, has been a neglected area of research, despite it being acknowledged as an often challenging yet therapeutically useful aspect of the work. This study aims to explore silence in adolescent psychoanalytic psychotherapy, by studying the emergence of silence in therapy sessions. Three Short-Term Psychoanalytic Psychotherapies of adolescents with depression were used in the study, and silences occurring in six sessions of each therapy were coded, using the Pausing Inventory Categorization System (PICS). Findings showed that, in the three therapies sampled, almost one-third of session time was spent on average in silence, and most of this silence was coded as ‘obstructive’. Moreover, the amount of silence in every stage of therapy was different for each patient-therapist dyad. Follow-up interviews conducted with the adolescents were analysed using thematic analysis, and showed that the adolescents generally expressed negative feelings about silence in their therapy. Analysis suggests that the majority of the silence in these therapies related to conflict, which could be viewed as both an aspect of the developmental stage of adolescence, and a symptom of depression. These findings suggest that silences may not always be therapeutically productive in adolescent therapy, even if they are considered to be so in psychotherapy with adults, and so adaptations in therapeutic technique are required

Theory of optical excitations in dipole-coupled hybrid molecule-semiconductor layers: Coupling of a molecular resonance to semiconductor continuum states

We theoretically investigate the optical absorption of a hybrid system consisting of an organic molecular lm on top of a semiconductor substrate. The electronic states of the isolated spatially separated constituents couple due to the Coulomb interaction of the optically induced charge carriers across the lm-substrate interface. Focussing on the coupling of optical active molecular transitions to semiconductor continuum states, we nd that the non-radiative dipole-dipole energy transfer causes the formation of coupled excitations, eectively reducing the excitation energy of the optical resonance in the molecular lm and inducing a broadening of the associated absorption peak. In the framework of the Heisenberg equation of motion technique we derive the Bloch equations for these hybrid systems. The input parameters for our model system of ladder-type quarterphenyl (L4P) molecules on the ZnO(1010) surface are taken from density functional theory calculations

Brain-borne IL-1 adjusts glucoregulation and provides fuel support to astrocytes and neurons in an autocrine/paracrine manner

It is still controversial which mediators regulate energy provision to activated neural cells, as insulin does in peripheral tissues. Interleukin-1β (IL-1β) may mediate this effect as it can affect glucoregulation, it is overexpressed in the ‘healthy’ brain during increased neuronal activity, and it supports high-energy demanding processes such as long-term potentiation, memory and learning. Furthermore, the absence of sustained neuroendocrine and behavioral counterregulation suggests that brain glucose-sensing neurons do not perceive IL-1β-induced hypoglycemia. Here, we show that IL-1β adjusts glucoregulation by inducing its own production in the brain, and that IL-1β-induced hypoglycemia is myeloid differentiation primary response 88 protein (MyD88)-dependent and only partially counteracted by Kir6.2-mediated sensing signaling. Furthermore, we found that, opposite to insulin, IL-1β stimulates brain metabolism. This effect is absent in MyD88-deficient mice, which have neurobehavioral alterations associated to disorders in glucose homeostasis, as during several psychiatric diseases. IL-1β effects on brain metabolism are most likely maintained by IL-1β auto-induction and may reflect a compensatory increase in fuel supply to neural cells. We explore this possibility by directly blocking IL-1 receptors in neural cells. The results showed that, in an activity-dependent and paracrine/autocrine manner, endogenous IL-1 produced by neurons and astrocytes facilitates glucose uptake by these cells. This effect is exacerbated following glutamatergic stimulation and can be passively transferred between cell types. We conclude that the capacity of IL-1β to provide fuel to neural cells underlies its physiological effects on glucoregulation, synaptic plasticity, learning and memory. However, deregulation of IL-1β production could contribute to the alterations in brain glucose metabolism that are detected in several neurologic and psychiatric diseases.This work was supported by a grant from the Deutsche Forschungsgemeinschaft (DFG RE 1451/3-1) to AdR

Brain-borne IL-1 adjusts glucoregulation and provides fuel support to astrocytes and neurons in an autocrine/paracrine manner.

It is still controversial which mediators regulate energy provision to activated neural cells, as insulin does in peripheral tissues. Interleukin-1β (IL-1β) may mediate this effect as it can affect glucoregulation, it is overexpressed in the 'healthy' brain during increased neuronal activity, and it supports high-energy demanding processes such as long-term potentiation, memory and learning. Furthermore, the absence of sustained neuroendocrine and behavioral counterregulation suggests that brain glucose-sensing neurons do not perceive IL-1β-induced hypoglycemia. Here, we show that IL-1β adjusts glucoregulation by inducing its own production in the brain, and that IL-1β-induced hypoglycemia is myeloid differentiation primary response 88 protein (MyD88)-dependent and only partially counteracted by Kir6.2-mediated sensing signaling. Furthermore, we found that, opposite to insulin, IL-1β stimulates brain metabolism. This effect is absent in MyD88-deficient mice, which have neurobehavioral alterations associated to disorders in glucose homeostasis, as during several psychiatric diseases. IL-1β effects on brain metabolism are most likely maintained by IL-1β auto-induction and may reflect a compensatory increase in fuel supply to neural cells. We explore this possibility by directly blocking IL-1 receptors in neural cells. The results showed that, in an activity-dependent and paracrine/autocrine manner, endogenous IL-1 produced by neurons and astrocytes facilitates glucose uptake by these cells. This effect is exacerbated following glutamatergic stimulation and can be passively transferred between cell types. We conclude that the capacity of IL-1β to provide fuel to neural cells underlies its physiological effects on glucoregulation, synaptic plasticity, learning and memory. However, deregulation of IL-1β production could contribute to the alterations in brain glucose metabolism that are detected in several neurologic and psychiatric diseases.Molecular Psychiatry advance online publication, 8 December 2015; doi:10.1038/mp.2015.174