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Background:Obesity levels in Scotland are amongst the highest in the developing world and psychological co-morbidities are common amongst the obese population. and evidence suggests that psychological approaches, can result in sustained weight loss, improved wellbeing and reduced binge eating. However, there is limited evidence of effective intervention supporting weight outcomes in a general setting.Aim:The aim of this pilot intervention was to determine if the addition of a psychology clinic within a Tier 2 community adult weight management service (CAWMS) supported positive weight management outcomes.Methods:Service evaluation data was gathered at an urban and rural GP practice within Grampian. Patients were referred to the pilot psychology clinic if mild to moderate mental health concerns were highlighted. Eight patients (average age 46 years; mean BMI 46.2) attended between four and eight appointments within the psychology clinic. Progress, goal setting, barriers and relapse prevention were discussed using a motivational interviewing approach. Psycho-education, self-management advice and brief psychological interventions, were offered where appropriate.Results:Mean weight loss for patients who attended the psychology clinic was 7.4kg. Mean HADS anxiety scores did not change, whereas HADS depression scores reduced by 3.5, although not statistically significant (p > 0.001). Qualitative feedback suggests that the majority of patients found the addition of psychological support helpful.Conclusion:The pilot has highlighted the value and importance of a psychology clinic within Tier 2 CAWMS. Feedback from dietitians suggests that the addition of psychological support better informed their understanding of patients concerns. It highlights the need for ‘joined-up’ working within the community weight management service.

This article explores the acceptance and commitment therapy hexaflex in the context of an assistant psychologist aspiring to pursue a career in clinical psychology. The piece aims to highlight the resilience required and challenges that may be faced during this journey. I explore each corner of the hexaflex, often describing my experience becoming ‘stuck’. However, I am able to reflect on the skills I have developed throughout my career and doctorate of clinical psychology application journey, which have allowed me to move towards gaining psychological flexibility and acceptance of my current situation.

Objective To assess the ability of the Australian Modified Lawton's Instrumental Activities of Daily Living (IADL) Scale (Modified Lawton's Scale) to screen for cognitive impairment in patients without physical or sensory deficits. Methods Prospective single-blind study of diagnostic accuracy. Results Data were available for 249 patients. At ≤25 points on the Modified Lawton's Scale, the area under the receiver operating characteristic curve (AUC) for patients with dementia was 0.90 (95% CI 0.83, 0.96), with sensitivity of 95% and specificity of 84%. The scale had decreased ability to identify patients with mild cognitive impairment (MCI) with the AUC highest at 0.76 (95% CI 0.67, 0.84), with a sensitivity of 77% and specificity of 74% at ≤26 points. The Modified Lawton's Scale had a significant strong correlation with the Mini-Mental State Examination (0.73) (P ≤ 0.001). Conclusion A score of ≤25 on the Modified Lawton's Scale may indicate cognitive impairment impacting on IADL.

ObjectivesCardiovascular disease is the leading cause of premature death in patients with mental illness. Metabolic syndrome is a cluster of co-occurring cardiovascular risk factors, seen in high frequency in severe mental illness. Despite ease of diagnosis, monitoring is often poor across psychiatric populations. This report details a quality improvement initiative undertaken on an inpatient psychiatric ward to improve rates of metabolic monitoring.MethodsFour key interventions were developed: (1) A nurse-led intervention, where nurses were upskilled in performing metabolic monitoring, (2) Education was provided to all staff, (3) Introduction of a suite of interventions to improve metabolic risk and (4) Ongoing consumer involvement. A pre–post intervention study design was used to measure effectiveness, with an audit of metabolic monitoring rates performed 12 months after the intervention began.ResultsRates of weight and height monitoring both increased from 46.0% to 69.5% (p=0.0185) and body mass index (BMI) recordings increased from 33% to 63% (p=0.0031). Rates of waist circumference monitoring increased from 44.2% to 65.2% (p=0.0498). Blood pressure (BP) measurements increased from 88.5% to 100% (p=0.0188). Lipid monitoring rates improved from 23% to 69.5% (p=0.001). Rates of glucose monitoring increased from 74% to 82.5% (p=0.8256), although this was not statistically significant.ConclusionsWe found that metabolic monitoring improved following these simple interventions, with a statistically significant increase in measurement rates of weight, BP, height, lipids, BMI and waist circumference (p

p53 acts as a tumor suppressor by inducing both growth arrest and apoptosis. p53-induced apoptosis can occur without new RNA synthesis through an unknown mechanism. In human vascular smooth muscle cells, p53 activation transiently increased surface Fas (CD95) expression by transport from the Golgi complex. Golgi disruption blocked both p53-induced surface Fas expression and apoptosis. p53 also induced Fas-FADD binding and transiently sensitized cells to Fas-induced apoptosis. In contrast, lpr and gld fibroblasts were resistant to p53-induced apoptosis. Thus, p53 can mediate apoptosis through Fas transport from cytoplasmic stores.

The objective of this study was to explore the relationship between the Perception of Control Scale (PCS) and other measures that incorporate physical disability, optimism, self-efficacy and hopelessness components in a Multiple Sclerosis (MS) sample. One hundred and fifteen participants comprising 44 males and 71 females with a mean age of 45.65 years (standard deviation: 10.43) diagnosed with MS attending the centre for the first time to consult the Rehabilitation Physician, participated in this cohort study. The main outcome measures used were the Expanded Disability Status Scale, the Life Orientation Test (LOT), the Multiple Sclerosis Self-Efficacy Scale (MSSE-control and MSSE-function), the Beck Hopelessness Scale and the PCS. There were at best moderate relationships found between the PCS and the LOT (r = 0.45; P0.01) and the Beck Hopelessness Scale (r = -0.41; P0.01). A weak relationship was found between the PCS and the MSSE-control (r = 0.34; P0.01). There was negligible correlation between the PCS and the MSSE-function (r = 0.15; P0.05) and the Expanded Disability Status Scale (r = -0.15; P0.05). It can be concluded that Negative perception of control showed an association with decreased optimism, decreased self-efficacy and increased hopelessness in a sample of participants diagnosed with MS. No association was found with perception of control and ambulatory/functional abilities.

Abstract —Increasing evidence indicates that the control of cell proliferation and apoptosis are linked. The c- myc proto-oncogene is induced early after cell-cycle entry in vascular smooth muscle cells (VSMCs) in vitro and after arterial injury and regulates both cell proliferation and apoptosis. Although both proliferation and apoptosis are likely to be mediated via transcriptional activation of target genes, few c- myc targets have been identified. Therefore, the recent identification that cdc25A, a cell-cycle phosphatase involved in G 1 progression, is transcriptionally activated by c- myc and regulates c- myc –induced apoptosis has suggested that cdc25A may be the principal mediator of c- myc in VSMCs. We examined cdc25A regulation of c- myc –induced proliferation and apoptosis by expressing cdc25A or antisense cdc25A in primary rat VSMCs or in VSMCs expressing deregulated c- myc or adenovirus E1A. Ectopic c- myc increased cdc25A expression, but cdc25A was still responsive to serum components, which indicated that c- myc alone is not the main determinant of cdc25A expression. Antisense cdc25A inhibited c- myc –induced proliferation and apoptosis; however, drug and metabolic blocks indicated that this effect was limited to G 1 . Ectopic cdc25A augmented the proproliferative and proapoptotic action of c- myc but did not increase cell proliferation or apoptosis in the absence of ectopic c- myc . In contrast, E1A/E2F-induced apoptosis was independent of cdc25A. We conclude that cdc25A expression modulates the ability of c- myc to induce apoptosis in G 1 . However, cdc25A alone does not induce apoptosis and cannot substitute for c- myc in VSMCs. Additional targets of c- myc are therefore involved in apoptosis of both G 1 and post-G 1 VSMCs.

Abstract —Compared with vascular smooth muscle cells (VSMCs) from normal vessels, VSMCs from human atherosclerotic plaques proliferate more slowly, undergo earlier senescence, and demonstrate higher levels of apoptosis in culture. The tumor suppressor genes p105 RB (retinoblastoma, acting through the E2F transcription factor family) and p53 regulate cell proliferation, cell senescence, and apoptosis in many cell types. We have therefore determined whether these stable growth properties of plaque VSMCs reflect altered activity of RB and/or p53. VSMCs were derived from coronary atherectomies or from normal coronary arteries from transplant recipients. Compared with normal VSMCs, plaque VSMCs showed a higher ratio of the active (hypophosphorylated) to the inactive (phosphorylated) form of RB and a lower level of E2F transcriptional activity. Cells were stably transfected with retrovirus constructs that inhibited RB or p53 alone or in combination. Suppression of RB alone increased rates of cell proliferation and apoptosis and inhibited cell senescence in normal VSMCs. Suppression of p53 and RB together had similar effects but, additionally, resulted in immortalization of normal VSMC cultures. In contrast, inhibition of RB binding to E2F or ectopic expression of E2F-1 in plaque VSMCs induced massive apoptosis, which required suppression of p53 to rescue cells. Suppression of RB and p53 together increased cell proliferation and delayed senescence but failed to immortalize plaque VSMCs. Inhibition of p53 alone had minimal effects on plaque VSMCs but increased the lifespan of normal VSMCs. We conclude that human plaque VSMCs have slower rates of cell proliferation and earlier senescence than do cells from normal vessels because of a defect in phosphorylation of RB. Furthermore, both disruption of RB/E2F and inhibition of p53 are required for plaque VSMCs to proliferate without apoptosis. This observation may explain the relatively low level of cell proliferation and high level of apoptosis seen in VSMCs in human atherosclerotic plaques.