The psychometric properties of the Varieties of Inner Speech Questionnaire-Revised in Hebrew

IntroductionThe Varieties of Inner Speech Questionnaire-Revised (VISQ-R) is a self-report questionnaire designed to measure characteristics of inner speech. In the current study, we adapted and validated a Hebrew version of VISQ-R. Our first hypothesis was that Confirmatory Factor Analysis (CFA) of the Hebrew VISQ-R would confirm the five subscales replicating the factor structure of the original questionnaire. In addition, building on previous findings that inner speech is involved in tasks that require the executive functions we examined the relationship between VISQ-R and self-reported executive functions questionnaire (BRIEF-A). We hypothesized that correlations between subscales of the Hebrew VISQ-R would reveal covariance between BRIEF-A and some but not all inner speech subscales.Methods406 participants completed the Hebrew VISQ-R and 280 of them also completed the BRIEF-A.ResultsAs hypothesized, CFA confirmed the factor structure revealing the same 5 subscales reported in the original English version, with acceptable internal reliability. Partial support was found for the hypothesized correlations between VISQ-R and BRIEF-A, with covariance of executive functions with some subscales of inner speech (Evaluative, Other-People and Dialogic), and distinct variance with others (Condensed and Positive).DiscussionThese results indicate that the Hebrew version of the VISQ-R has good psychometric properties and that it can be used in future research. The implications concerning the contribution of inner speech for people with difficulties in executive functions are discussed

Can Recovery From an Eating Disorder Be Measured? Toward a Standardized Questionnaire

Background: There is a clear need for a standardized definition of recovery from eating disorders (EDs) and for self-report instruments to assess where individuals with an ED are situated at a given point of time along their process of illness and recovery. It has been acknowledged that psychological and cognitive symptoms are important to recovery in addition to physical and behavioral indices. This study proposes a 28-item multidimensional questionnaire encompassing the main features of recovery from ED, derived from the endorsement of different criteria by people with a lifetime ED diagnosis, family members and ED clinicians.Methods: Participants were 213 volunteers over the age of 18 (118 people with a lifetime ED diagnosis, 58 healthy family members of people with EDs and 37 ED clinicians), who completed the ED-15 and indicated online how important they thought each of 56 criteria were for recovery from an ED.Results: Four factors were identified in an exploratory factor analysis: Lack of Symptomatic Behavior (LSB), Acceptance of Self and Body (ASB), Social and Emotional Connection (SEC), and Physical Health (PH). Confirmatory factor analysis using the seven highest loading items from each subscale confirmed the structure validity of a shortened version of this questionnaire, the Eating Disorders Recovery Endorsement Questionnaire (EDREQ), which had excellent goodness-of-fit indices. Despite a few between-group differences, there was general agreement that LSB was most salient to recovery, followed by ASB, SEC, and PH in that order.Conclusion: Despite the absence of a standardized definition of recovery from ED, there is a general consensus about its components. The EDREQ is a psychometrically sound questionnaire containing items that people with an ED history, their family members and therapists all define as important components of recovery. The inclusion of emotional and psychosocial aspects of recovery in addition to symptomatic and medical aspects is important to expand treatment goals and the concept of recovery from EDs beyond symptom relief and the absence of disease markers. As a clinical tool, the EDREQ stands to assist in setting and refining therapeutic goals throughout therapy, and in establishing standardized, comparable norms for recovery levels in research

RNA Binding Protein CUGBP2/CELF2 Mediates Curcumin-Induced Mitotic Catastrophe of Pancreatic Cancer Cells

Curcumin inhibits the growth of pancreatic cancer tumor xenografts in nude mice; however, the mechanism of action is not well understood. It is becoming increasingly clear that RNA binding proteins regulate posttranscriptional gene expression and play a critical role in RNA stability and translation. Here, we have determined that curcumin modulates the expression of RNA binding protein CUGBP2 to inhibit pancreatic cancer growth.In this study, we show that curcumin treated tumor xenografts have a significant reduction in tumor volume and angiogenesis. Curcumin inhibited the proliferation, while inducing G2-M arrest and apoptosis resulting in mitotic catastrophe of various pancreatic cancer cells. This was further confirmed by increased phosphorylation of checkpoint kinase 2 (Chk2) protein coupled with higher levels of nuclear cyclin B1 and Cdc-2. Curcumin increased the expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) mRNA, but protein levels were lower. Furthermore, curcumin increased the expression of RNA binding proteins CUGBP2/CELF2 and TIA-1. CUGBP2 binding to COX-2 and VEGF mRNA was also enhanced, thereby increasing mRNA stability, the half-life changing from 30 min to 8 h. On the other hand, silencer-mediated knockdown of CUGBP2 partially restored the expression of COX-2 and VEGF even with curcumin treatment. COX-2 and VEGF mRNA levels were reduced to control levels, while proteins levels were higher.Curcumin inhibits pancreatic tumor growth through mitotic catastrophe by increasing the expression of RNA binding protein CUGBP2, thereby inhibiting the translation of COX-2 and VEGF mRNA. These data suggest that translation inhibition is a novel mechanism of action for curcumin during the therapeutic intervention of pancreatic cancers

Compressive Inverse Scattering I. High Frequency SIMO Measurements

Inverse scattering from discrete targets with the single-input-multiple-output (SIMO), multiple-input-single-output (MISO) or multiple-input-multiple-output (MIMO) measurements is analyzed by compressed sensing theory with and without the Born approximation. High frequency analysis of (probabilistic) recoverability by the $L^1$-based minimization/regularization principles is presented. In the absence of noise, it is shown that the $L^1$-based solution can recover exactly the target of sparsity up to the dimension of the data either with the MIMO measurement for the Born scattering or with the SIMO/MISO measurement for the exact scattering. The stability with respect to noisy data is proved for weak or widely separated scatterers. Reciprocity between the SIMO and MISO measurements is analyzed. Finally a coherence bound (and the resulting recoverability) is proved for diffraction tomography with high-frequency, few-view and limited-angle SIMO/MISO measurements.Comment: A new section on diffraction tomography added; typos fixed; new figures adde

Cyclooxygenase-2 overexpression is common in serrated and non-serrated colorectal adenoma, but uncommon in hyperplastic polyp and sessile serrated polyp/adenoma

<p>Abstract</p> <p>Background</p> <p>Cyclooxygenase-2 (COX-2, <it>PTGS2</it>) plays an important role in colorectal carcinogenesis. COX-2 overexpression in colorectal cancer is inversely associated with microsatellite instability (MSI) and the CpG island methylator phenotype (CIMP). Evidence suggests that MSI/CIMP+ colorectal cancer may arise through the serrated tumorigenic pathway through various forms of serrated neoplasias. Therefore, we hypothesized that COX-2 may play a less important role in the serrated pathway.</p> <p>Methods</p> <p>By immunohistochemistry, we assessed COX-2 expression in 24 hyperplastic polyps, 7 sessile serrated polyp/adenomas (SSA), 5 mixed polyps with SSA and adenoma, 27 traditional serrated adenomas, 515 non-serrated adenomas (tubular adenoma, tubulovillous adenoma and villous adenoma), 33 adenomas with intramucosal carcinomas, 96 adenocarcinomas with serration (corkscrew gland) and 111 adenocarcinomas without serration.</p> <p>Results</p> <p>Strong (2+) COX-2 overexpression was more common in non-serrated adenomas (28% = 143/515) than in hyperplastic polyps (4.2% = 1/24, p = 0.008) and serrated polyps (7 SSAs and 5 mixed polyps) (0% = 0/12, p = 0.04). Furthermore, any (1+/2+) COX-2 overexpression was more frequent in non-serrated adenomas (60% = 307/515) than in hyperplastic polyps (13% = 3/24, p < 0.0001) and serrated polyps (SSAs and mixed polyps) (25% = 3/12, p = 0.03). Traditional serrated adenomas and non-serrated adenomas showed similar frequencies of COX-2 overexpression. Regardless of serration, COX-2 overexpression was frequent (~85%) in colorectal adenocarcinomas. Tumor location was not significantly correlated with COX-2 overexpression, although there was a trend towards higher frequencies of COX-2 overexpression in distal tumors (than proximal tumors) among hyperplastic polyps, SSAs, mixed polyps, traditional serrated adenomas and adenocarcinomas.</p> <p>Conclusion</p> <p>COX-2 overexpression is infrequent in hyperplastic polyp, SSA and mixed polyp with SSA and adenoma, compared to non-serrated and serrated adenoma. COX-2 overexpression becomes more frequent as tumors progress to higher grade neoplasias. Our observations suggest that COX-2 may play a less significant role in the serrated pathway of tumorigenesis; however, COX-2 may still play a role in later stage of the serrated pathway.</p

Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells

Genomic instability is a common feature of cancer etiology. This provides an avenue for therapeutic intervention, since cancer cells are more susceptible than normal cells to DNA damaging agents. However, there is growing evidence that the epigenetic mechanisms that impact DNA methylation and histone status also contribute to genomic instability. The DNA damage response, for example, is modulated by the acetylation status of histone and non-histone proteins, and by the opposing activities of histone acetyltransferase and histone deacetylase (HDAC) enzymes. Many HDACs overexpressed in cancer cells have been implicated in protecting such cells from genotoxic insults. Thus, HDAC inhibitors, in addition to unsilencing tumor suppressor genes, also can silence DNA repair pathways, inactivate non-histone proteins that are required for DNA stability, and induce reactive oxygen species and DNA double-strand breaks. This review summarizes how dietary phytochemicals that affect the epigenome also can trigger DNA damage and repair mechanisms. Where such data is available, examples are cited from studies in vitro and in vivo of polyphenols, organosulfur/organoselenium compounds, indoles, sesquiterpene lactones, and miscellaneous agents such as anacardic acid. Finally, by virtue of their genetic and epigenetic mechanisms, cancer chemopreventive agents are being redefined as chemo- or radio-sensitizers. A sustained DNA damage response coupled with insufficient repair may be a pivotal mechanism for apoptosis induction in cancer cells exposed to dietary phytochemicals. Future research, including appropriate clinical investigation, should clarify these emerging concepts in the context of both genetic and epigenetic mechanisms dysregulated in cancer, and the pros and cons of specific dietary intervention strategies