Relationships between explanatory style, posttraumatic growth and posttraumatic stress disorder symptoms among Chinese breast cancer patients

Many existing models posit that cognitive processing style is an important factor affecting self-perceived positive changes. In this study, the effects of explanatory style (the manner in which people cognitively process and explain why they experience good and bad events) on both posttraumatic growth (PTG) and posttraumatic stress disorder (PTSD) symptoms were examined among 90 Chinese women with breast cancer. It was found that explanatory style for good events, but not for bad events, was significantly associated with self-reported PTG. Women who attributed the causes of positive events to internal, global and stable factors tended to report more posttraumatic growth. In contrast, explanatory style for bad events, as opposed to good events, was significantly and positively correlated with PTSD symptoms. Among the three dimensions of explanatory style (internal, stable and global), the tendency to globalise the causes of good and bad events were the most important predictors of self-reported PTG and PTSD symptoms, respectively. While enhancing an optimistic explanatory style for bad events might reduce posttraumatic stress symptoms, cultivating an optimistic explanatory style for good events is likely to increase self-perceived positive changes after breast cancer diagnosis and treatment. © 2011 Taylor & Francis.link_to_subscribed_fulltex

Regulation of Ins(3,4,5,6)P-4 signaling by a reversible kinase/phosphatase

Regulation of Cl- channel conductance by Ins(3,4,5,6)P-4 provides receptor-dependent control over salt and fluid secretion [1], cell volume homeostasis [2], and electrical excitability of neurones and smooth muscle [3]. Ignorance of how Ins(3,4,5,6)P4 is synthesized has long hindered our understanding of this signaling pathway. We now show Ins(3,4,5,6)P4 synthesis by Ins(1,3,4,5,6)P,5 1-phosphatase activity by an enzyme previously characterized [4] as an Ins(3,4,5,6)P-4 1-kinase. Rationalization of these phenomena with a ligand binding model unveils Ins(1,3,4)P-3 as not simply an alternative kinase substrate [4, 5], but also an activator of Ins(1,3,4,5,6)P-5 I-phosphatase. Stable overexpression of the enzyme in epithelial monolayers verifies its physiological role in elevating Ins(3,4,5,6)P4 levels and inhibiting secretion. It is exceptional for a single enzyme to catalyze two opposing signaling reactions (1-kinase/1-phosphatase) under physiological conditions. Reciprocal coordination of these opposing reactions offers an alternative to general doctrine that intracellular signals are regulated by integrating multiple, distinct phosphatases and kinases [6].X1139sciescopu

Neuropeptide Y and Epilepsy

It is a central tenet of the epilepsy field that seizures result from the imbalance of excitation over inhibition 1. The bulk of excitation is mediated by the neurotransmitter glutamate, whereas inhibition results mainly from the actions of γ-aminobutyric acid (GABA). In the neocortex and hippocampus, the intrinsic sources of GABA are the interneurons, which lately have come under intense scrutiny. It has become clear that a large number of distinct types of interneurons can be differentiated in part by the array of neuropeptides they coexpress (cf. 2). Evidence is emerging that the neuropeptide complement of interneurons plays important roles in the way that interneurons regulate excitability. Here we discuss what is known about the relation of one well-characterized neuropeptide, neuropeptide Y (NPY), and epilepsy in experimental animals and humans, and suggest possible roles for the receptors as targets for the control of excessive excitation in epilepsy