The role of pain self-efficacy and pain catastrophising in the relationship between chronic pain and depression: A moderated mediation model.

Chronic pain is a substantial health problem with a high prevalence of comorbid depression. To understand the link between chronic pain and depression, cognitive factors including pain catastrophising and pain self-efficacy have been theorised as significant contributing variables. There is relatively strong evidence that pain catastrophising mediates the relationship between pain severity and depression symptoms.

Smartphone use and study behavior: A Korean and Australian comparison.

Smartphone use amongst university students is widespread and a common practice while studying. However, this usage can lead to academic performance costs. This study examined the relationship between smartphone use during study, problematic smartphone use and academic performance in Korean and Australian university students.

Progress in bipolar disorder drug design toward the development of novel therapeutic targets: a clinician's perspective.

Bipolar disorder (BD) is a considerable burden to the affected individual. The need for novel drug targets and improved drug design (DD) in BD is therefore clear. Areas covered: The following article provides a brief, narrative, clinician-oriented overview of the most promising novel pharmacological targets for BD along with a concise overview regarding the general DD process and the unmet needs relevant to BD.

T cell-mediated neuroprotection involves antithrombin activity.

Functional loss after injury to the mammalian central nervous system (CNS) has been attributed not only to the immediate loss of neurons but also to secondary neuronal degeneration caused by the toxicity of physiological compounds present in abnormally high amounts as a result of the injury. One such compound appears to be the protease thrombin. Here we show that the beneficial effect of T cells directed against myelin self-antigens can be attributed, at least in part, to the ability of these 'autoimmune' T cells to produce antithrombin III.