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Background:acceptance and commitment therapy (ACT) and cognitive-behavioral therapy (CBT) are empirically supported treatments for anxiety and panic disorder (PD), though they differ in their putative vulnerability and maintenance processes. The present study examined the incremental validity of several of these models’ proposed core processes, including anxiety sensitivity (AS), dispositional avoidance, experiential avoidance (EA), cognitive fusion (CF), and mindfulness, as well as the interaction of the processes within each model, in the prediction of anxiety and panic symptomology.Methods:a sample of US adults (n= 316) completed self-report measures of AS, dispositional avoidance, EA, CF, mindfulness, anxiety, and PD symptoms. A series of hierarchical multiple regression analyses were conducted.Results:hierarchical regression analyses indicated that AS, dispositional avoidance, and EA predicted anxiety and panic symptoms even after controlling for one another, CF, mindfulness, and demographic variables. Although mindfulness and CF was correlated with anxiety and panic at the univariate level, they did not predict either outcome above and beyond AS, dispositional avoidance, and EA. When interaction terms were added to the models, the interaction between AS and ­dispositional avoidance was a significant predictor of panic and anxiety symptoms, whereas the interaction between EA and CF only predicted panic symptoms. None of the interactions that included mindfulness were significant predictors.Conclusions:these findings provide support the independent and interactive predictive value of traditional CBT (AS, dispositional avoidance, and AS-dispositional avoidance) and ACT (EA) processes for anxiety and panic symptoms, but raise questions about the incremental predictive utility of CF and mindfulness.

The cognitive attentional syndrome (CAS) is a core concept within metacognitive theory. The premise of the CAS is related to metacognition, however its role in psychopathology is distinct. Due to the complex nature of the CAS, a theoretically driven and psychometrically sound self-report measure of the CAS for the Arabic population is yet to be developed. We translated the Multidimensional Cognitive Attentional Syndrome Scale (MCASS) into the Arabic language and tested its structural validity. The MCASS was translated according to the standard guidelines of forward-translation followed by backward-translation. In Study 1, the MCASS was administered to a larger sample (

Both post-traumatic stress disorder (PTSD) and traumatic brain injury (TBI) have been linked to subjective cognitive complaints; however, less is known about the unique relationships of PTSD symptoms and TBI severity with domain-specific subjective cognitive declines in older Veterans. The current study included 215 Vietnam-Era Veterans from the Department of Defense-Alzheimer’s Disease Neuroimaging Initiative (age M=69.62 years, SD=4.30). General linear models, adjusting for age, education, apolipoprotein E ε4 status, self-reported health, MMSE score, and depressive symptoms, examined the unique effects of PTSD symptoms (measured using the Clinician-Administered PTSD Scale) and TBI severity (none, mild, moderate/severe) on subjective cognitive decline measured using the Everyday Cognition (ECog) measure. Greater current PTSD symptoms were associated with greater subjective cognitive declines on the ECog total score (t=.198, p=.009) as well as memory (t=.197, p=.008), language (t=.228, p=.004), and visuospatial (t=.216, p=.007) subscales. Compared with participants with no TBI, mild TBI was associated with greater subjective cognitive decline on the ECog total score (t=.329, p=.026) as well as the language (t=.334, p=.030) and divided attention (t=.411, p=.007) subscales, while moderate-to-severe TBI was associated with greater subjective declines in planning (t=.291, p=.049) and divided attention (t=.320, p=.032). There was no interaction between PTSD and TBI severity on ECog scores. Results suggest that PTSD symptoms and mild versus moderate/severe TBI differentially impact specific domains of subjective cognitive decline. Future work should investigate how repetitive TBI may modify these relationships, and whether PTSD and TBI severity are associated with objective cognition and quality of life in older Veterans.

The anxiolytic and antidepressant effects of regular physical exercise have been well documented, though the mechanisms through which exercise alleviates symptoms of emotion disorders require further investigation. Mounting research indicates that exercise reduces anxiety sensitivity, a known vulnerability factor for the development and maintenance of psychological disorders, presumably via repeated exposure to feared somatic sensations. The purpose of the present study was to examine whether anxiety sensitivity mediates the relation between exercise frequency and symptoms of anxiety and depression. A large community sample of 955 volunteers completed a demographic questionnaire, the Anxiety Sensitivity Index-3, and the Brief Symptom Inventory-18. Exercise frequency significantly predicted anxiety sensitivity, anxiety, depression, and somatization scores. Mediation analyses indicated that anxiety sensitivity mediated the association between exercise frequency and anxiety, depression, and somatization symptoms. The findings provide further support for the association between exercise and negative affective states and suggest that anxiety sensitivity may be one mechanism through which exercise reduces emotional disorder symptomology. The implications of these findings and recommendations for future research are discussed.

552 Background: It is now well established that AMH can indicate the extent of chemotherapy-induced damage on the ovarian reserve. Very low AMH levels in women after chemotherapy for early breast cancer (eBC) may indicate treatment-induced premature ovarian failure (POI), but the evidence to implement its routine clinical use remains limited. Methods: AMH was measured (Roche cobas autoanalyser) in 197 women aged 40-45 years at diagnosis treated with anthracycline/cyclophosphamide/taxane based chemotherapy for eBC, with no previous endocrine therapy and no subsequent aromatase inhibitor exposure or ovarian suppression. 76% were ER positive and received tamoxifen. The primary objective was to assess the relationships between AMH levels at 6 months after chemotherapy (AMH6) with subsequent ovarian function at 30 months. This included accuracy of prediction of loss of ovarian function at 30 months (E30) after chemotherapy by AMH levels at 6 months (AMH6) and the value of other endocrine/clinical factors pretreatment and at 6 months. Multivariate analysis was performed with data were split into 70% training and 30% testing sets with results reported for model performance on the test set. Results: AMH fell from a median of 0.62 (IQR 0.21-1.31) ng/ml pretreatment to become undetectable ( < 0.01ng/ml) in 137 (70%) of women at 6 months. AMH showed very little recovery, being undetectable in 115 women at 18 months and 119 at 30 months. In those with detectable AMH at 30 months, it remained very low, median 0.07ng/ml, max 0.82ng/ml but nevertheless it reflected ovarian function. Thus median estradiol at 30 months (E30) was 50 pmol/l (IQR 34-68) in women with undetectable AMH at that time, vs 313 pmol/l (IQR 102-1052) in the 80 women with detectable AMH. AMH at 6 months was predictive of ovarian function at 30 months, as E30 was 56 pmol/l (IQR 40-104) in women with undetectable AMH6 vs 258pmol/l (IQR 69-780; p < 0.0001) in women with detectable AMH6, and the positive predictive value (PPV) of AMH being undetectable at 6 months and remaining so at 30 months was 77%. Random forest analysis identified BMI as a non-endocrine predictive factor of E30. Using a stringent cutoff of ≤50pmol/l (13.6 pg/ml) and adding 1:9 weighting to improve PPV gave a test validated PPV of 79.0% while maintaining AUC at 83.7% for prediction of E30. Other classifiers performed less well than random forests. Conclusions: Measurement of AMH at 6 months after chemotherapy has predictive value for later ovarian function, and combining this with other endocrine and baseline data improves discriminative ability. This approach indicates the potential role of multivariate analysis based on AMH measured shortly after chemotherapy to helping optimise subsequent endocrine therapy.

This work was funded in part by an NHS Fife Research and Development Bursary Award to all authors. In addition, we have received funding from the University of St Andrews’ EPSRC Impact Acceleration Account. In 2013, Schick received a LEADERS award from the Scottish Universities Life Sciences Alliance that started this project. Background: Approximately 11,000 people die in Scotland each year as a result of smoking-related causes. Quitting smoking is relatively easy; maintaining a quit attempt is a very difficult task with success rates for unaided quit attempts stubbornly remaining in the single digits. Pharmaceutical treatment can improve these rates by lowering the overall reward factor of nicotine. However, these and related nicotine replacement therapies do not operate on, or address, the spatial and contextual aspects of smoking behaviour. With the ubiquity of smartphones that can log spatial, quantitative and qualitative data related to smoking behaviour, there exists a person-centred clinical opportunity to support smokers attempting to quit by first understanding their smoking behaviour and subsequently sending them dynamic messages to encourage health behaviour change within a situational context. Methods: We have built a smartphone app—MapMySmoke—that works on Android and iOS platforms. The deployment of this app within a clinical National Health Service (NHS) setting has two distinct phases: (1) a 2-week logging phase where pre-quit patients log all of their smoking and craving events; and (2) a post-quit phase where users receive dynamic support messages and can continue to log craving events, and should they occur, relapse events. Following the initial logging phase, patients consult with their general practitioner (GP) or healthcare provider to review their smoking patterns and to outline a precise, individualised quit attempt plan. Our feasibility study consists of assessment of an initial app version during and after use by eight patients recruited from an NHS Fife GP practice. In addition to evaluation of the app as a potential smoking cessation aid, we have assessed the user experience, technological requirements and security of the data flow. Results: In an initial feasibility study, we have deployed the app for a small number of patients within one GP practice in NHS Fife. We recruited eight patients within one surgery, four of whom actively logged information about their smoking behaviour. Initial feedback was very positive, and users indicated a willingness to log their craving and smoking events. In addition, two out of three patients who completed follow-up interviews noted that the app helped them reduce the number of cigarettes they smoked per day, while the third indicated that it had helped them quit. The study highlighted the use of pushed notifications as a potential technology for maintaining quit attempts, and the security of collection of data was audited. These initial results influenced the design of a planned second larger study, comprised of 100 patients, the primary objectives of which are to use statistical modelling to identify times and places of probable switches into smoking states, and to target these times with dynamic health behaviour messaging. Conclusions: While the health benefits of quitting smoking are unequivocal, such behaviour change is very difficult to achieve. Many factors are likely to contribute to maintaining smoking behaviour, yet the precise role of cues derived from the spatial environment remains unclear. The rise of smartphones, therefore, allows clinicians the opportunity to better understand the spatial aspects of smoking behaviour and affords them the opportunity to push targeted individualised health support messages at vulnerable times and places. Publisher PDF

A recount of the latest work on the collection and the analysis of the medieval paintings of Hexham Abbey is provided. Medieval pigments of the panel paintings such as blue azurite pigment and post-1840 restoration substitute pigments such as French ultramarine were detected with visible light and ultraviolet fluorescence microscopy. A recently found painting in the Abbey's collection, was studied by means of multispectral imaging and was attributed to the 15th century 'Dance of Death' sequence of panels. After a virtual varnish removal on highly pigmented colour spots with the aid of non-negative least squares analysis resulting in quantitative heat-maps of the panel, the pigment concentration on the painting surface and enhanced reflectance image spectra were extracted. With the aid of these spectra the presence of original medieval pigments such as yellow ochre, verdigris, madder and Egyptian blue was indicated.

This study was funded by NHS Lothian Cancer and Leukaemia Endowments Fund. Part of this work was undertaken in the MRC Centre for Reproductive Health which is funded by the MRC Centre grant MR/N022556/1 . STUDY QUESTION What is the impact of cancer in females aged ≤39 years on subsequent chance of pregnancy? SUMMARY ANSWER Cancer survivors achieved fewer pregnancies across all cancer types, and the chance of achieving a first pregnancy was also lower. WHAT IS KNOWN ALREADY The diagnosis and treatment of cancer in young females may be associated with reduced fertility but the true pregnancy deficit in a population is unknown. STUDY DESIGN, SIZE, DURATION We performed a retrospective cohort study relating first incident cancer diagnosed between 1981 and 2012 to subsequent pregnancy in all female patients in Scotland aged 39 years or less at cancer diagnosis (n = 23 201). Pregnancies were included up to end of 2014. Females from the exposed group not pregnant before cancer diagnosis (n = 10 271) were compared with general population controls matched for age, deprivation quintile and year of diagnosis. PARTICIPANTS/MATERIALS, SETTING, METHODS Scottish Cancer Registry records were linked to hospital discharge records to calculate standardized incidence ratios (SIR) for pregnancy, standardized for age and year of diagnosis. Linkage to death records was also performed. We also selected women from the exposed group who had not been pregnant prior to their cancer diagnosis who were compared with a matched control group from the general population. Additional analyses were performed for breast cancer, Hodgkin lymphoma, leukaemia, cervical cancer and brain/CNS cancers. MAIN RESULTS AND THE ROLE OF CHANCE Cancer survivors achieved fewer pregnancies: SIR 0.62 (95% CI: 0.60, 0.63). Reduced SIR was observed for all cancer types. The chance of achieving a first pregnancy was also lower, adjusted hazard ratio = 0.57 (95% CI: 0.53, 0.61) for women >5 years after diagnosis, with marked reductions in women with breast, cervical and brain/CNS tumours, and leukaemia. The effect was reduced with more recent treatment period overall and in cervical cancer, breast cancer and Hodgkin lymphoma, but was unchanged for leukaemia or brain/CNS cancers. The proportion of pregnancies that ended in termination was lower after a cancer diagnosis, and the proportion ending in live birth was higher (78.7 vs 75.6%, CI of difference: 1.1, 5.0). LIMITATIONS, REASONS FOR CAUTION Details of treatments received were not available, so the impact of specific treatment regimens on fertility could not be assessed. Limited duration of follow-up was available for women diagnosed in the most recent time period. WIDER IMPLICATIONS OF THE FINDINGS This analysis provides population-based quantification by cancer type of the effect of cancer and its treatment on subsequent pregnancy across the reproductive age range, and how this has changed in recent decades. The demonstration of a reduced chance of pregnancy across all cancer types and the changing impact in some but not other common cancers highlights the need for appropriate fertility counselling of all females of reproductive age at diagnosis. STUDY FUNDING/COMPETING INTEREST(S) This study was funded by NHS Lothian Cancer and Leukaemia Endowments Fund. Part of this work was undertaken in the MRC Centre for Reproductive Health which is funded by the MRC Centre grant MR/N022556/1. RAA has participated in Advisory Boards and/or received speaker’s fees from Beckman Coulter, IBSA, Merck and Roche Diagnostics. He has received research support from Roche Diagnostics, Ansh labs and Ferring. The other authors have no conflicts to declare. Publisher PDF

HIF-1α is a hypoxia-inducible protein that regulates many cell and molecular processes, including those involved in angiogenesis and stem cell maintenance. Prior studies demonstrated constitutive HIF-1α stabilization in neural stem cells (NSCs) of the adult mouse SVZ, but its role there has not been elucidated. Here, we tested the hypothesis that HIF-1α plays an essential role in the maintenance of adult NSCs and stabilization of the SVZ vascular niche using conditional, tamoxifen-inducibleHif1aknock-out mice. We generated nestin-CreERT2/R26R-YFP/Hif1afl/fltriple transgenic mice, to enable tamoxifen-inducibleHif1agene inactivation in nestin-expressing NSCs within the adult SVZ.Hif1agene deletion resulted in a significant loss of YFP+NSCs within the SVZ by 45 d post recombination, which was preceded by significant regression of the SVZ vasculature at 14 d, and concomitant decrease of VEGF expression by NSCs. Loss of YFP+NSCs followingHif1agene inactivationin vivowas likely an indirect consequence of vascular regression, since YFP+neurosphere formation over serial passage was unaffected. These results identify NSC-encoded HIF-1α as an essential factor in the maintenance of the adult SVZ, and demonstrate that NSCs within the SVZ maintain the integrity of their vascular niche through HIF-1α-mediated signaling mechanisms.

RTM is supported by a Wellcome Trust Intermediate Clinical Fellowship (Grant No: 098522). Inhibin B has been identified as a potential marker of Sertoli cell function in males. The aim of this study is to produce a normative model of serum inhibin B in males from birth to seventeen years. We used a well-defined search strategy to identify studies containing data that can contribute to a larger approximation of the healthy population. We combined data from four published studies (n = 709) and derived an internally validated model with high goodness-of-fit and normally distributed residuals. Our results show that inhibin B increases following birth to a post-natal peak of 270 pg/mL (IQR 210–335 pg/mL) and then decreases during childhood followed by a rise at around 8 years, peaking at a mean 305 pg/mL (IQR 240–445 pg/mL) at around age 17. Following this peak there is a slow decline to the standard mature adult normal range of 170 pg/mL (IQR 125–215 pg/mL). This normative model suggests that 35% of the variation in Inhibin B levels in young males is due to age alone, provides an age-specific reference range for inhibin B in the young healthy male population, and will be a powerful tool in evaluating the potential of inhibin B as a marker of Sertoli cell function in pre-pubertal boys. Publisher PDF