Current theories of borderline personality disorder (BPD) suggest that extreme levels of affective instability/emotional dysregulation, impulsivity, or a combination of these traits account for the symptoms of BPD. The present study tested the extent to which personality measures of affective instability and impulsivity could account for BPD features in a nonclinical sample. One hundred forty-one undergraduates completed the Affective Lability Scale, the UPPS Impulsive Behavior Scale, and the Personality Assessment Inventory for Borderlines. Both affective instability and impulsivity were uniquely associated with BPD features. Shifts between euthymia and anger, and between anxiety and depression, were associated with BPD features, as were the urgency and (lack of) premeditation scales. Results indicated that specific BPD features may be differentially accounted for by affective instability vs. impulsivity, consistent with perspectives on BPD emphasizing combinations of affective instability and impulsivity as underlying dimensions of the disorder.
Understanding how human organs respond to ionizing radiation (IR) at a systems biology level and identifying biomarkers for IR exposure at low doses can help provide a scientific basis for establishing radiation protection standards. Little is known regarding the physiological responses to low dose IR at the metabolite level, which represents the end-point of biochemical processes inside cells. Using a full thickness human skin tissue model and GC-MS-based metabolomic analysis, we examined the metabolic perturbations at three time points (3, 24 and 48 h) after exposure to 3, 10 and 200 cGy of X-rays. PLS-DA score plots revealed dose- and time-dependent clustering between sham and irradiated groups. Importantly, delayed metabolic responses were observed at low dose IR. When compared with the high dose at 200 cGy, a comparable number of significantly changed metabolites were detected 48 h after exposure to low doses (3 and 10 cGy) of irradiation. Biochemical pathway analysis showed perturbations to DNA/RNA damage and repair, lipid and energy metabolisms, even at low doses of IR.
There is considerable evidence that understanding reasons for using substances is important for understanding patterns of use and related consequences as well as for developing assessment and intervention strategies. Despite increases in prescription opioid use and related problems (e.g., overdose deaths), a comprehensive measure of prescription opioid motives has yet to be developed. As such, the current study sought to develop and provide validation evidence for a measure of prescription opioid motives. One hundred eleven male and 226 female undergraduate students completed an initial pool of motive items based on the current literature and measures of prescription opioid use and related problems. Confirmatory factor analysis results demonstrated that the predicted 4-factor model provided a good fit to the data. The 4 motives-pain, social, enhancement, and coping-each showed differential patterns of associations with prescription opioid-related contextual and use variables. Enhancement motives were associated with quantity of use (past 3 months and maximum use in 1 day), frequency of use, in multiple contexts, misuse, and related problems. Coping motives demonstrated relations with maximum pills (in 1 day), frequency of use, and prescription opioid misuse, consequences, and dependence features. For social motives, significant associations were found with frequency of use (in past 3 months), typical number of pills (in 1 day), dependence features, and use both on weekdays and on weekends; this motive had a negative association with maximum number of pills taken in 1 day. Pain motives were largely related to frequency of use (in past 3 months), consequencess, and dependence features. The present study is the first to present an empirical measure of prescription opioid motives and demonstrates how these motives have important implications for understanding patterns of prescription opioid use and related problems.
The concern over possible health risks from exposures to low doses of ionizing radiation has been driven largely by the increase in medical exposures, the routine implementation of X-ray backscatter devices for airport security screening, and, most recently, the nuclear incident in Japan. Because of a paucity of direct epidemiological data at very low doses, cancer risk must be estimated from high dose exposure scenarios. However, there is increasing evidence that low and high dose exposures result in different signaling events and may have different response mechanisms than higher doses. We have examined the radiation-induced temporal response after exposure to 10 cGy of an in vitro three dimensional (3D) human skin tissue model using microarray-based transcriptional profiling. Cell type-specific analysis showed significant changes in gene expression with the levels of >1,400 genes altered in the dermis and >400 genes regulated in the epidermis. The two cell layers rarely exhibited overlapping responses at the mRNA level. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) measurements validated the microarray data in both regulation direction and value. Key pathways identified relate to cell cycle regulation, immune responses, hypoxia, reactive oxygen signaling, and DNA damage repair. The proliferation status as well as the expression of PCNA was examined in histological samples. We discuss in particular the role of proliferation, emphasizing how the disregulation of cellular signaling in normal tissue may impact progression toward radiation-induced secondary diseases.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.