‘What is the self anyway?’ : towards a more parsimonious conceptualisation of the self : a review

The ‘self’ is of interest across multiple psychological, cognitive, and social sciences. Unhelpfully, a plethora of terms are used across different theoretical and empirical areas. This leads to inconsistency, confusion and lack of clarity and impedes cross-disciplinary communication and progress. To improve clarity, increase parsimony and support theoretical and empirical advances, it is important to establish clear terms that can be applied consistently across psychology. The aim of this paper is to present a comprehensive initial inventory of synthesised self-terms that can be used by, and across psychology. We review self-terms used across different areas in psychology and identify a set of terms that are most frequently and consistently used across these domains. We then present a synthesis of commonly used ‘self-terms’ that are specifically related to six psychological sub-disciplines; Cognitive, Social, Developmental, Neuroscience, Clinical and Personality psychology. A glossary of self-terms, together with frequently used synonymous self-terms are presented

Do non-steroidal anti-inflammatory drugs or smoking predispose to Helicobacter pylori infection?

Susceptibility to Helicobacter pylori infection is a poorly understood phenomenon. This study was undertaken to establish whether either smoking or chronic non-steroidal anti-inflammatory drug (NSAID) consumption might in some way predispose to H. pylori infection and hence lead to peptic ulceration. Serological evidence of H. pylori infection was assessed in 100 consecutive subjects receiving NSAIDs without any evidence of gastrointestinal upset and 100 matched controls. All subjects had a full assessment of their smoking habits. Sixty-three per cent of patients taking NSAIDs compared to 51% of controls had evidence of H. pylori infection (NS). Smoking habit also had no effect on H. pylori colonization. The ulcerogenic potential of NSAIDs and smoking does not appear to be mediated via a prediposition to H. pylori infection

The mechanisms of coronary restenosis: insights from experimental models

Since its introduction into clinical practice, more than 20 years ago, percutaneous transluminal coronary angioplasty (PTCA) has proven to be an effective, minimally invasive alternative to coronary artery bypass grafting (CABG). During this time there have been great improvements in the design of balloon catheters, operative procedures and adjuvant drug therapy, and this has resulted in low rates of primary failure and short-term complications. However, the potential benefits of angioplasty are diminished by the high rate of recurrent disease. Up to 40% of patients undergoing angioplasty develop clinically significant restenosis within a year of the procedure. Although the deployment of endovascular stents at the time of angioplasty improves the short-term outcome, ‘in-stent’ stenosis remains an enduring problem. In order to gain an insight into the mechanisms of restenosis, several experimental models of angioplasty have been developed. These have been used together with the tools provided by recent advances in molecular biology and catheter design to investigate restenosis in detail. It is now possible to deliver highly specific molecular antagonists, such as antisense gene sequences, to the site of injury. The knowledge provided by these studies may ultimately lead to novel forms of intervention. The present review is a synopsis of our current understanding of the pathological mechanisms of restenosis