43 research outputs found

    Eating Pathology Symptoms Inventory – Clinician Rated Version (EPSI-CRV)

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    The files in this record contain supplemental information about the EPSI-CRV including: a copy of the EPSI-CRV, suggested training plan, training videos with an example of completed ratings, and a list of items that were removed during the final development process.The Eating Pathology Symptoms Inventory – Clinician Rated Version (EPSI-CRV) is a semi-structured interview that was designed to assess dimensional constructs of eating-disorder psychopathology and generate current Diagnostic and Statistical Manual- Fifth Edition (DSM-5) eating-disorder diagnoses. The EPSI-CRV is based on the self-report version of the EPSI (Forbush et al., 2013). There are 13 modules (or sections) within the EPSI-CRV. Eight modules measure content that is assessed in the self-report version of the EPSI, including: Body Dissatisfaction, Binge Eating, Cognitive Restraint, Excessive Exercise, Restricting, Purging, Muscle Building, and Negative Attitudes Towards Obesity. Five additional modules are included to derive DSM-5 diagnoses. The five DSM-5 modules include: Subjective Binge Episodes, Binge Eating Disorder, Low Weight, Overvaluation of Weight and Shape, and Fear of Weight Gain. The average administration time is approximately 38 minutes. The EPSI-CRV is designed to be used by clinicians and researchers working with adults with eating disorders across a range of settings. The interview may be useful for making admissions decisions, treatment planning, and discharge planning, as well as for research studies

    Subjective experience of sensation in anorexia nervosa

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    The nature of disturbance in body experience in anorexia nervosa (AN) remains poorly operationalized despite its prognostic significance. We examined the relationship of subjective reports of sensitivity to and behavioral avoidance of sensory experience (e.g., to touch, motion) to body image disturbance and temperament in adult women currently diagnosed with AN (n=20), women with a prior history of AN who were weight restored (n=15), and healthy controls with no eating disorder history (n=24). Levels of sensitivity to sensation and attempts to avoid sensory experience were significantly higher in both clinical groups relative to healthy controls. Sensory sensitivity was associated with body image disturbance (r(56) = .51, p < .0001), indicating that body image disturbance increased with increased global sensitivity to sensation. Sensory sensitivity was also negatively and significantly correlated with lowest BMI (r2 = −.32, p < .001), but not current BMI (r2 = .03, p = .18), and to the temperament feature of harm avoidance in both clinical groups. We discuss how intervention strategies that address sensitization and habituation to somatic experience via conditioning exercises may provide a new manner in which to address body image disturbance in AN

    Concurrent inhibition of oncogenic and wild-type RAS-GTP for cancer therapy

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    RAS oncogenes (collectively NRAS, HRAS and especially KRAS) are among the most frequently mutated genes in cancer, with common driver mutations occurring at codons 12, 13 and 611. Small molecule inhibitors of the KRAS(G12C) oncoprotein have demonstrated clinical efficacy in patients with multiple cancer types and have led to regulatory approvals for the treatment of non-small cell lung cancer2,3. Nevertheless, KRASG12C mutations account for only around 15% of KRAS-mutated cancers4,5, and there are no approved KRAS inhibitors for the majority of patients with tumours containing other common KRAS mutations. Here we describe RMC-7977, a reversible, tri-complex RAS inhibitor with broad-spectrum activity for the active state of both mutant and wild-type KRAS, NRAS and HRAS variants (a RAS(ON) multi-selective inhibitor). Preclinically, RMC-7977 demonstrated potent activity against RAS-addicted tumours carrying various RAS genotypes, particularly against cancer models with KRAS codon 12 mutations (KRASG12X). Treatment with RMC-7977 led to tumour regression and was well tolerated in diverse RAS-addicted preclinical cancer models. Additionally, RMC-7977 inhibited the growth of KRASG12C cancer models that are resistant to KRAS(G12C) inhibitors owing to restoration of RAS pathway signalling. Thus, RAS(ON) multi-selective inhibitors can target multiple oncogenic and wild-type RAS isoforms and have the potential to treat a wide range of RAS-addicted cancers with high unmet clinical need. A related RAS(ON) multi-selective inhibitor, RMC-6236, is currently under clinical evaluation in patients with KRAS-mutant solid tumours (ClinicalTrials.gov identifier: NCT05379985).J.E. Klomp is funded by National Cancer Institute grants T32CA009156, F32CA239328 and K99CA276700, and American Cancer Society grant PF-20-069. P.L. is supported in part by the NIH/NCI (1R01CA23074501, 1R01CA23026701A1 and 1R01CA279264-01), The Pew Charitable Trusts, the Damon Runyon Cancer Research Foundation, and the Pershing Square Sohn Cancer Research Alliance. P.L. is also supported by the Josie Robertson Investigator Program and the Support Grant-Core Grant program (P30 CA008748) at Memorial Sloan Kettering Cancer Center. D.S. is funded by AECC Excellence Program 2022 (EPAEC222641CICS). A.J.A. has research funding from Bristol Myers Squibb, Deerfield, Eli Lilly, Mirati Therapeutics, Novartis, Novo Ventures, Revolution Medicines and Syros Pharmaceuticals. A.M.W. was supported by a grant from the NCI (K22CA276632-01). C.J.D. has received research funding support from Deciphera Pharmaceuticals, Mirati Therapeutics, Reactive Biosciences, Revolution Medicines, and SpringWorks Therapeutics, the National Cancer Institute (P50CA257911 and R35CA232113), Department of Defense (W81XWH2110692), and Pancreatic Cancer Action Network (22-WG-DERB). C.A. is funded by grants from the Giovanni Armenise–Harvard Foundation, the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 101001288) and AIRC under IG 2021–ID. 25737 project.Peer reviewe

    Childhood adversity and anxiety versus

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    Eating Disorders and Illness Burden in Patients with Bipolar Spectrum Disorders

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    3sireservedObjectives: The objectives of the study were to evaluate the clinical significance of lifetime eating disorder comorbidity in a well-defined sample of patients with bipolar spectrum disorders and to describe cognitive correlates of disordered eating in this group. Method: Twenty-six bipolar patients with a lifetime history of a Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV)-defined eating disorder (n = 17) or a clinically significant subthreshold eating disorder (n = 9) (ED group) were compared with 46 bipolar patients with no history of an eating disorder (no-ED group) on demographic and clinical characteristics at study presentation, history of bipolar illness, and other psychiatric comorbidity. Measures included the Structured Clinical Interview for the DSM-IV Axis I Disorders, the Clinical Global Impression-Severity Scale-Bipolar Version (CGI-S-BP), and the Eating Disorder Examination. Height and weight were recorded to calculate body mass index. Results: Patients in the ED group were heavier and were rated as more symptomatic on the CGI-S-BP than were patients in the no-ED group. The ED group also had a higher number of lifetime depressive episodes and greater psychiatric comorbidity, excluding eating and mood disorders. Finally, after controlling for body mass index and CGI-S-BP rating, patients in the ED group had significantly higher Eating Disorder Examination Restraint, Eating Concern, Shape Concern, Weight Concern, and Global scores than did patients in the no-ED group. Conclusions: These findings highlight the need for a renewed emphasis on the evaluation and management of weight and eating in the mood disorders. In particular, this research suggests that eating disorder comorbidity may be a marker for increased symptom load and illness burden in bipolar disorder. © 2007 Elsevier Inc. All rights reserved.mixedWILDES, J.E.; MARCUS, M.; FAGIOLINI, A.Wildes, J. E.; Marcus, M.; Fagiolini, A

    Intermittent explosive disorder and eating disorders: Analysis of national comorbidity and research samples

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    Objective Clinical studies suggest comorbidity between eating disorders and aggressive behaviors. This study examined the pattern of comorbidity between intermittent explosive disorder (IED) and eating disorders (ED). Methods Data were analyzed from both the adult and adolescent samples of the National Comorbidity Survey-Replication (n = 19,430) and a clinical research sample (n = 1,642). Results Lifetime prevalence of Any ED was elevated in IED vs. non-IED for both the community and clinical research samples. Though anorexia nervosa displayed no relationship with IED in either sample, bulimia nervosa was associated with IED in the community sample and binge eating disorder was associated with IED in both the community and clinical research samples. Onset of IED preceded onset of Any ED in at least 70% of comorbid IED/ED cases in both community and clinical research samples. Associations of IED with Any ED and bulimia nervosa in the community sample, and associations of IED with binge eating disorder in the clinical research sample, remained significant after controlling for other psychiatric disorders. Conclusions Individuals with IED are more likely to report lifetime prevalence of ED, particularly bulimic spectrum disorders. This finding, and the observation that the onset of IED occurs prior to the onset of ED in the majority of individuals, suggests that longitudinal studies are needed to clarify this relationship and determine whether IED is a risk factor for the development of ED. Early identification of individuals with IED or impulsive aggression may provide clinically useful information to determine most effective treatment interventions
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