Search

Background: Early detection of melanoma is crucial to improving the detection of thin curable melanomas. Noninvasive, computer-assisted methods have been developed to use at the bedside to aid in diagnoses but have not been compared directly in a clinical setting.Objective: We conducted a prospective diagnostic accuracy study comparing a dermatologist's clinical examination at the bedside, teledermatology, and noninvasive imaging techniques (FotoFinder, MelaFind, and Verisante Aura).Methods: A total of 184 patients were recruited prospectively from an outpatient dermatology clinic, with lesions imaged, assessed, and excised. Skin specimens were assessed by 2 blinded pathologists, providing the gold standard comparison.Results: Fifty-nine lesions from 56 patients had a histopathologic diagnosis of melanoma, whereas 150 lesions from 128 patients were diagnosed as benign. Sensitivities and specificities were, respectively, MelaFind (82.5%, 52.4%), Verisante Aura (21.4%, 86.2%), and FotoFinder Moleanalyzer Pro (88.1%, 78.8%). The sensitivity and specificity of the teledermoscopist (84.5% and 82.6%, respectively) and local dermatologist (96.6% and 32.2%, respectively) were also compared.Limitations: There are inherent limitations in using pathology as the gold standard to compare sensitivities and specificities.Conclusion: This study demonstrates that the highest sensitivity and specificity of the instruments were established with the FotoFinder Moleanalyzer Pro, which could be a valuable tool to assist with, but not replace, clinical decision making. [ABSTRACT FROM AUTHOR]

Abstract Inadequate delivery of oxygen to organisms during development can lead to cell dysfunction/death and life-long disabilities. Although the susceptibility of developing cells to low oxygen conditions changes with maturation, the cellular and molecular pathways that govern responses to low oxygen are incompletely understood. Here we show that developing Caenorhabditis elegans are substantially more sensitive to anoxia than adult animals and that this sensitivity is controlled by nervous system generated hormones (e.g., neuropeptides). A screen of neuropeptide genes identified and validated nlp-40 and its receptor aex-2 as a key regulator of anoxic survival in developing worms. The survival-promoting action of impaired neuropeptide signaling does not rely on five known stress resistance pathways and is specific to anoxic insult. Together, these data highlight a novel cell non-autonomous pathway that regulates the susceptibility of developing organisms to anoxia. Graphical abstract fx1 Highlights • Developing C. elegans lacking neuropeptide signaling survive anoxic stress better. • This effect does not rely on canonical stress resistance pathways. • Neurons, not other tissues, are the source of the neuropeptides underlying survival. • We employed a directed screen of worm neuropeptides to identify candidates. • The screen suggests nlp-40 partially accounts for anoxic survival phenotype. [ABSTRACT FROM AUTHOR]

Abstract: Objective: The current study aimed to investigate the difference in the levels of core beliefs between eating disordered women and those who showed milder forms of symptomatology. Methods: Thirty-five eating disordered women, 16 symptomatic dieters, 39 normal dieters and 34 non-clinical comparison women completed questionnaires measuring eating symptomatology (Eating Disorders Inventory [EDI]), core beliefs (Young Schema Questionnaire [YSQ]), depression (The Beck Depression Inventory-II [BDI-II]) and self-esteem (Rosenberg Self-Esteem Inventory [RSE]). Results: With the exception of Entitlement beliefs, there were significant differences in the levels of core beliefs across all four groups. In particular, symptomatic dieters and eating disordered women differed on 8 YSQ subscales despite showing very similar level of eating symptomatology. Discussion: The current findings lend support to the discontinuity model that suggests that there are fundamental differences between women with a clinical eating disorder and those with milder eating psychopathology. The clinical and research implications of the present results were discussed. [Copyright &y& Elsevier]

Many viruses shut off host gene expression to inhibit antiviral responses. Viral proteins and host proteins required for viral replication are typically spared in this process, but the mechanisms of target selectivity during host shutoff remain poorly understood. Using transcriptome-wide and targeted reporter experiments, we demonstrate that the influenza A virus endoribonuclease PA-X usurps RNA splicing to selectively target host RNAs for destruction. Proximity-labeling proteomics reveals that PA-X interacts with cellular RNA processing proteins, some of which are partially required for host shutoff. Thus, PA-X taps into host nuclear pre-mRNA processing mechanisms to destroy nascent mRNAs shortly after their synthesis. This mechanism sets PA-X apart from other viral host shutoff proteins that target actively translating mRNAs in the cytoplasm. Our study reveals a unique mechanism of host shutoff that helps us understand how influenza viruses suppress host gene expression. • Influenza A virus PA-X targets the majority of host mRNAs for destruction • Downregulation by PA-X correlates with the number of splice sites in a transcript • Splicing renders RNAs susceptible to PA-X • The cellular CFIm complex interacts with PA-X and contributes to PA-X activity Gaucherand et al. uncover a unique relationship between RNA degradation by the influenza A virus ribonuclease PA-X and host RNA splicing, which allows PA-X to selectively target host RNAs for destruction. [ABSTRACT FROM AUTHOR]