Why people enter treatment for alcohol problems: Findings from UK Alcohol Treatment Trial pre‐treatment interviews

Aim: To develop a model of why people seek professional treatment for drinking problems, grounded in what clients say about the process at treatment entry.

Participants: Three sets of consecutive entrants to the UK Alcohol Treatment Trial, sets commencing at intervals during trial recruitment (total n = 98).

Location: Statutory and non‐statutory alcohol problem treatment agencies in three areas of England and Wales.

Data: Open‐ended interviews according to a brief interview guide, leading to 400–800‐word post‐interview reports used for analysis (tape recordings used for auditing the interview and analysis process).

Analysis: Reports analysed by a team according to grounded theory principles, involving an iterative process with successive refinement of interviewing and analysis with each successive set of data.

Findings: A model of professional treatment entry was developed, refined and “tested” with the last set of data. The process of seeking professional treatment was depicted in the model as involving a realization of worsening, accumulating and multiple problems related to drinking, especially in health and family domains; in conjunction with, in most cases (but not all), a trigger event and/or family or professional influence; combined with rejection of the possibility of unaided change or non‐professional help; leading to the seeking or accepting of professional help.

Conclusions: The findings support conclusions already in the literature about the process of seeking professional help for a drinking problem, but provide further refinement of existing ideas: for example regarding the accumulation of drinking‐related problems, the ways in which a realization of those problems combines with triggers or pressure, and the complex role of the family and primary care professionals in assisting motivation to seek treatment.     

Mechanism of vascular smooth muscle cells activation by hydrogen peroxide: role of phospholipase C gamma.

BACKGROUND: Hydrogen peroxide (H2O2) formation is a critical factor in processes involving ischaemia/ reperfusion. However, the precise mechanism by which reactive oxygen species (ROS) induce vascular damage are insufficiently known. Specifically, activation of phospholipase C gamma (PLCgamma) is a probable candidate pathway involved in vascular smooth muscle cells (VSMC) activation by H2O2. METHODS: The activation of human venous VSMC was measured as cytosolic free calcium mobilization, shape change and protein phosphorylation, focusing on the role of tyrosine phosphorylation-activated PLCgamma. RESULTS: The exposure of VSMC to exogenous H2O2 caused a rapid increase in cytosolic free calcium concentration ([Ca2+]i), and induced a significant VSMC shape change. Both effects were dependent on a tyrosine kinase-mediated mechanism, as determined by the blockade of short-term treatment of VSMC with the protein tyrosine kinase inhibitor, genistein. Giving further support to the putative role of phospholipase C (PLC)-dependent pathways, the [Ca2+]i and VSMC shape change response were equally inhibited by the specific PLC blocker, 1-(6-((17-beta-methoxyestra-1,3,5(10)trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). In addition, U73122 had a protective effect against the deleterious action (24 h) of H2O2 on non-confluent VSMC. As a further clarification of the specific pathway involved, the exposure to H2O2 significantly stimulated the tyrosine phosphorylation of PLCgamma with a concentration- and time-profile similar to that of [Ca(2+)](i) mobilization. CONCLUSIONS: The present study reveals that H(2)O(2) activates PLCgamma on VSMC through tyrosine phosphorylation and that this activation has a major role in rapid [Ca(2+)](i) mobilization, shape-changing actions and damage by H(2)O(2) in this type of cells. These findings have direct implications for understanding the mechanisms of the vascular actions of H(2)O(2) and may help to design pharmacologically protective strategies.     

Growth impairment shows an age-dependent pattern in boys with chronic kidney disease

The impact of chronological age on longitudinal body growth from early childhood through adolescence using detailed anthropometric methods has not yet been studied in children with chronic kidney disease (CKD). We have evaluated growth failure by measuring four components of linear growth: body height (HT), sitting height (SHT), arm length (AL) and leg length (LL). Data were prospectively collected for up to 7 years on 190 boys (3–21 years old) with congenital or hereditary CKD (all had developed at least stage 2 CKD by the age of 10 years). Patients showed the most severe growth failure in early childhood, followed by an acceleration in growth in pre-puberty, a slowing-down of growth at puberty, as expected, and thereafter a late speeding-up of growth until early adulthood. This pattern was observed irrespective of the degree of CKD and different treatment modalities, such as conservative treatment, recombinant human growth hormone (rhGH) therapy or transplantation. LL showed the most dynamic growth changes of all the parameters evaluated and emerged as the best indicator of statural growth in children with CKD. A specific age-dependent pattern of physical growth was identified in pediatric male CKD patients. This growth pattern should be considered in the evaluation of individual growth and the assessment of treatment efficacy such as rhGH therapy.