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A Just-in-Time Adaptive Intervention (Shift) to Manage Problem Anger After Trauma: Co-Design and Development Study

JMIR human factors 2025年 12卷 e62960页

作者： Olivia Metcalf David Forbes Lauren M Henry Tianchen Qian Tracey Varker Melissa A Brotman Sean Cowlishaw Karen E Lamb Meaghan L O'Donnell Centre for Digital Transformation of Health University of Melbourne 700 Swanston St Carlton 3053 Australia 61 404040817. Phoenix Australia - Centre for Posttraumatic Mental Health University of Melbourne Carlton Australia. Neuroscience and Novel Therapeutics Unit Emotion and Development Branch National Institute of Mental Health Intramural Research Program Bethesda MD United States. Department of Statistics University of California Irvine Irvine CA United States. Monash School of Psychological Sciences Turner Institute for Brain and Mental Health Monash University Clayton Australia. MISCH (Methods and Implementation Support for Clinical Health) Research Hub Faculty of Medicine Dentistry and Health Sciences University of Melbourne Carlton Australia.

Background:Problem anger is common after experiencing trauma and is under-recognized relative to other posttraumatic mental health issues. Previous research has shown that digital mental health tools have significant potential to support individuals with problem anger after trauma. Objective:The objective of this study was to describe the co-design and development of a just-in-time adaptive intervention (JITAI) targeting problem anger in individuals who have experienced trauma. Methods:We used a participatory design process following the double-diamond framework. Phase 1 involved one-on-one qualitative interviews with trauma-exposed individuals with problem anger (n=10). Using an inductive approach (interpretative phenomenological analysis), we thematically coded interview data to create design principles for this population and generate potential content for the intervention. Phase 2 involved academic and clinical experts in trauma and experts in digital health reviewing the Phase 1 results and an evidence-based cognitive behavioral approach to treating anger. We then created intervention content and prototypes, which we then took to workshops with all participants for feedback, using group discussions and ratings of desirability and feasibility. Results:From Phase 1, core considerations for a JITAI included look and feel preferences, self-led and personalized support and content, and different support needed for each anger stage. A JITAI was developed with the following components: (1) personalized schedules and content onboarding; (2) psychoeducation about problem anger; (3) crisis support; (4) mood monitoring via anger check-ins; (5) self-led and personalized circuit breakers; (6) cognitive-behavioral based skills; (7) and a digital Coach embedded in the app. Some suggested features, such as social networking and sharing data with loved ones, were not pursued due to feasibility reasons relating to participant safety or technical costs. Conclusions:The resulting

关键词： anger co-design design development digital tool feedback just-in-time adaptive intervention manage mental health monitoring mood participatory design post-traumatic support tool trauma user

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Inclusion of adolescent girls in clinical trials – issues of assent related to pregnancy and contraception

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Fertility and Sterility 2009年第3期92卷 S18-S18页

作者： Stratton, P. Gonzalez, A.C. Khachikyan, I. Wolff, E.F. Idriss, A. Karp, B. Program in Reproductive and Adult Endocrinology Division of Intramural Research NICHD NIH Bethesda MD Unit on Computer Support Services Division of Intramural Research NICHD NIH Bethesda MD Combined Neuroscience IRB Division of Intramural Research NINDS Bethesda MD

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Genome-wide SNP typing reveals signatures of population history

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Genomics 2008年第1期92卷 1-8页

作者： Hughes, Austin L. Welch, Robert Puri, Vinita Matthews, Casey Haque, Kashif Chanock, Stephen J. Yeager, Meredith Department of Biological Sciences University of South Carolina Columbia SC 29208 United States Intramural Research Support Program SAIC-Frederick National Cancer Institute-FCRDC Frederick MD 21702 United States Core Genotyping Facility Division of Cancer Epidemiology and Genetics National Cancer Institute Bethesda MD 20892-4605 United States Section on Genomic Variation Pediatric Oncology Branch National Cancer Institute Gaithersburg MD 20892-4605 United States

Single-nucleotide polymorphism (SNP) arrays have become a popular technology for disease-association studies, but they also have potential for studying the genetic differentiation of human populations. Application of the Affymetrix GeneChip Human Mapping 500K Array Set to a population of 102 individuals representing the major ethnic groups in the United States (African, Asian, European, and Hispanic) revealed patterns of gene diversity and genetic distance that reflected population history. We analyzed allelic frequencies at 388,654 autosomal SNP sites that showed some variation in our study population and 10% or fewer missing values. Despite the small size (23-31 individuals) of each subpopulation, there were no fixed differences at any site between any two subpopulations. As expected from the African origin of modern humans, greater gene diversity was seen in Africans than in either Asians or Europeans, and the genetic distance between the Asian and the European populations was significantly lower than that between either of these two populations and Africans. Principal components analysis applied to a correlation matrix among individuals was able to separate completely the major continental groups of humans (Africans, Asians, and Europeans), while Hispanics overlapped all three of these groups. Genes containing two or more markers with extraordinarily high genetic distance between subpopulations were identified as candidate genes for health differences between subpopulations. The results show that, even with modest sample sizes, genome-wide SNP genotyping technologies have great promise for capturing signatures of gene frequency difference between human subpopulations, with applications in areas as diverse as forensics and the study of ethnic health disparities. © 2008 Elsevier Inc. All rights reserved.

关键词： Complex disease Human populations Single-nucleotide polymorphism

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PKC is required for EGF-induced chemotaxis of human breast cancer cells

PKC is required for EGF-induced chemotaxis of human breast c...

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第四届全国化学生物学学术会议暨国际化学与生物/医学交叉研讨会

作者： Joost J．Oppenheim Laboratory of Molecular Immunoregulation Center for Cancer Research NCI Intramural Research Support Program Building 560 Room21-89A Frederick MD21702-1201 USA．

Chemotaxis plays an important role in cancer cell metastasis. In this study, we showed that epidermal growth factor (EGF) was a more potent chemoattractant than chemokine SDF-1/CXCL12, for human breast cancer cell MDA... 详细信息

关键词： PKC is required for EGF-induced chemotaxis of human breast cancer cells EGF

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Evaluating the cytotoxicity of innate immune effector cells using the GrB ELISPOT assay

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Journal of Translational Medicine 2004年第1期2卷 1-11页

作者： Shafer-Weaver, Kimberly A. Sayers, Thomas Kuhns, Douglas B. Strobl, Susan L. Burkett, Mark W. Baseler, Michael Malyguine, Anatoli Laboratory of Cell-Mediated Immunity SAIC-Frederick Inc. Natl. Cancer Institute at Frederick Frederick MD United States Clinical Services Program SAIC-Frederick Inc. Natl. Cancer Institute at Frederick Frederick MD United States Lab. of Experimental Immunology Intramural Research Support Program SAIC-Frederick Inc. Frederick MD United States Neutrophil Monitoring Laboratory SAIC-Frederick Inc. Natl. Cancer Institute at Frederick Frederick MD United States

Background: This study assessed the Granzyme B (GrB) ELISPOT as a viable alternative to the 51Cr-release assay for measuring cytotoxic activity of innate immune effector cells. We strategically selected the GrB ELISPO... 详细信息

Background: This study assessed the Granzyme B (GrB) ELISPOT as a viable alternative to the ⁵¹Cr-release assay for measuring cytotoxic activity of innate immune effector cells. We strategically selected the GrB ELISPOT assay because GrB is a hallmark effector molecule of cell-mediated destruction of target cells. Methods: We optimized the GrB ELISPOT assay using the human-derived TALL-104 cytotoxic cell line as effectors against K562 target cells. Titration studies were performed to assess whether the ELISPOT assay could accurately enumerate the number of GrB-secreting effector cells. TALL-104 were treated with various secretion inhibitors and utilized in the GrB ELISPOT to determine if GrB measured in the ELISPOT was due to degranulation of effector cells. Additionally, CD107a expression on effector cells after effector-target interaction was utilized to further confirm the mechanism of GrB release by TALL-104 and lymphokine-activated killer (LAK) cells. Direct comparisons between the GrB ELISPOT, the IFN-γ ELISPOT and the standard ⁵¹Cr-release assays were made using human LAK cells. Results: Titration studies demonstrated a strong correlation between the number of TALL-104 and LAK effector cells and the number of GrB spots per well. GrB secretion was detectable within 10 min of effector-target contact with optimal secretion observed at 3-4 h;in contrast, optimal IFN-γ secretion was not observed until 24 h. The protein secretion inhibitor, brefeldin A, did not inhibit the release of GrB but did abrogate IFN-γ production by TALL-104 cells. GrB secretion was abrogated by BAPTA-AM (1,2-bis-(2-aminophenoxy)ethane-N,N,N′, N′-tetraacetic acid tetra(acetoxymethyl) ester), which sequesters intracellular Ca²⁺, thereby preventing degranulation. The number of effector cells expressing the degranulation associated glycoprotein CD107a increased after interaction with target cells and correlated with the stimulated release of GrB measured in the

关键词： Natural Killer Cell Effector Cell ELISPOT Assay CD107a Expression K562 Target Cell

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A proinflammatory chemokine, CCL3, sensitizes the heat-gated and capsaicin-gated ion channel, TRPV1

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Arthritis research & Therapy 2004年第3期6卷 1-41页

作者： N Zhang R Sun J Wang JJ Oppenheim S Inan A Cowan TJ Rogers AD Guler M Caterina Laboratory of Molecular Immunoregulation Intramural Research Support Program Frederick Maryland USA Department of Pharmacology Fels Institute for Cancer Research and Molecular Biology Center for Substance Abuse Research Temple University School of Medicine Philadelphia Pennsylvania USA Department of Biological Chemistry and Department of Neuroscience The Johns Hopkins University School of Medicine Baltimore Maryland USA

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Identifying and characterizing a five-gene cluster of ATP-binding cassette transporters mapping to human chromosome 17q24: a new subgroup within the ABCA subfamily

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GeneScreen 2002年第3期1卷 157-164页

作者： Isabelle Arnould Lynn M. Schriml Catherine Prades Marcia Lachtermacher-Triunfol Thomas Schneider Christelle Maintoux Cendrine Lemoine Delphine Debono Catherine Devaud Laurent Naudin Stéphanie Bauché Mélanie Annat Tarmo Annilo Rando Allikmets Bert Gold Patrice Denèfle Marie Rosier Michael Dean Evry Genomics Center Aventis Pharma Evry France These authors contributed equally to the study. Human Genetics Section Laboratory of Genomic Diversity Present address: National Center for Biotechnology Information NLM NIH Bethesda MD U.S.A. Intramural Research and Support Program SAIC-Frederick Frederick MD 21702 U.S.A. Laboratory of Experimental and Computational Biology National Cancer Institute-Frederick Cancer Research and Development Center Departments of Ophthalmology and Pathology Columbia University New York NY

Abstract Introduction The ATP-binding cassette (ABC) gene superfamily encodes a series of transporter proteins that move a wide variety of substances across extra- and intracellular membranes. Forty-eight known human ABC genes can be divided into seven phylogenetically distinct subfamilies. The ABCA gene subfamily is found exclusively in multicellular eukaryotes. Results We report here on a unique tandem array of five ABCA genes on chromosome 17q24 defining a phylogenetically distinct group. This is the largest cluster of mammalian ABC genes described to date. They are arranged head-to-tail and have similar intron/exon organization in both mouse and human. Northern analysis reveals a heterogeneous pattern of expression in human tissues, with ABCA5 and ABCA10 expressed in skeletal muscle, ABCA6 in the liver, ABCA9 in the heart, and ABCA8 in ovaries. This suggests that these proteins have distinct functions.

关键词： ABC gene cluster chromosome 17 ATP-binding cassette transporter ABCA subfamily

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Plasma pharmacokinetics of a liver-selective nitric oxide-donating diazeniumdiolate in the male C57BL/6 mouse

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Xenobiotica 2002年第4期32卷 339-347页

作者： Stinson, S.F. House, T. Bramhall, C. Saavedra, J.E. Keefer, L.K. Nims, R.W. Developmental Therapeutics Program Laboratory of Comparative Carcinogenesis National Cancer Institute at Frederick Frederick MD 20702-1201 United States Intramural Research Support Programme Laboratory of Comparative Carcinogenesis National Cancer Institute at Frederick Frederick MD 20702-1201 United States Chemistry Section Laboratory of Comparative Carcinogenesis National Cancer Institute at Frederick Frederick MD 20702-1201 United States

1. The single-dose plasma pharmacokinetics of O2-vinyl 1-(pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO) following intravenous (i.v.) and intraperitoneal (i.p.) bolus administration to the male C57BL/6 mouse wa...

1. The single-dose plasma pharmacokinetics of O²-vinyl 1-(pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO) following intravenous (i.v.) and intraperitoneal (i.p.) bolus administration to the male C57BL/6 mouse was studied in an effort to characterize the disposition of the agent and to serve as a basis for the design of in vivo efficacy studies. 2. Plasma V-PYRRO/NO concentrations declined rapidly in a bi-exponential manner after i.v. administration of 5 mg kg^-1 body weight to mouse. The terminal half-life was 9.4 min and the mean residence time was 3.4 min. 3. V-PYRRO/NO was absorbed rapidly following i.p. administration, with peak plasma concentrations being observed 3 min after injection. Levels then declined with a terminal half-life of 11.7 min. The bioavailable fraction from the i.p. compartment was 19%, indicating a high first-pass effect. 4. The results provide additional evidence for a liver-selective metabolism of this nitric oxide-donating prodrug.

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AAA proteins: In search of a common molecular basis. International meeting on cellular functions of AAA proteins

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EMBO Reports 2001年第11期2卷 980-985页

作者： Maurizi, Michael R. Li, Chou-Chi H. Laboratory of Cell Biology National Cancer Institute Bethesda MD United States Basic Research Laboratory National Cancer Institute at Frederick Intramural Research Support Program Frederick MD United States

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Enhancement of N-Nitrosodiethylamine-lnitiated Hepatocarcinogenesis by Phenytoin in Male F344/NCr Rats at a Dose Causing Maximal Induction of CYP2B

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International Journal of Toxicology 2001年第2期20卷 81 - 87页

作者： Bhalchandra A. Diwan John R. Henneman Raymond W. Nims Intramural Research Support Program SAIC Frederick NCI–Frederick Cancer Research and Development Center Frederick Maryland USA Laboratory of Comparative Carcinogenesis National Cancer Institute Frederick Cancer Research and Development Center Frederick Maryland USA

The effect of the clinically important anticonvulsant phenytoin (DPH) on hepatocarcinogenesis of male F344/NCr rats initiated with a single i.p. dose of N-nitrosodiethylamine (75 mg/kg b.w.) was studied. Beginning 2 weeks post-initiation, the rats received control diet or diet containing 500 or 1500 ppm DPH or 500 ppm phenobarbital. At 52 weeks age, the incidences (and multiplicities, in units of tumors per tumor-bearing rat) of hepatocellular adenomas were 0%, 17% (1 ± 0), 42% (1.8 ± 0.8), or 67% (2.5 ± 1.9) in rats exposed to N-nitrosodiethylamine alone, or the carcinogen followed by 500 ppm DPH, 1500 ppm DPH, or 500 ppm phenobarbital, respectively. Between 53 and 79 weeks of age, 39% of rats receiving N-nitrosodiethylamine alone developed multiple (1.5 ± 0.8) hepatocellular adenomas. A similar incidence (41%) occurred in the rats administered the carcinogen followed by 500 ppm DPH. The incidence of hepatocellular adenomas (88% and 89%) was significantly greater in rats exposed to N-nitrosodiethylamine followed by 1500 ppm DPH or 500 ppm phenobarbital, respectively. Multiplicities of hepatocellular adenomas were significantly greater than the control value in rats fed 1500 ppm DPH or 500 ppm phenobarbital (5.9 ± 4.8 and 10.1 ± 6.7, respectively), but not in the rats receiving 500 ppm DPH (2.3 ± 1.6). No rats exposed to N-nitrosodiethylamine alone or the carcinogen followed by 500 ppm DPH developed hepatocellular carcinomas, while hepatocellular carcinomas occurred in 29% or 67% of the rats given 1500 ppm DPH or 500 ppm phenobarbital, respectively, following initiation. Increases in hepatic CYP2B-mediated benzyloxyresorufin O-dealkylation activity in rats exposed to 500 and 1500 ppm DPH for 2 or 23 weeks were ∼50% and ∼100%, respectively, of the maximal induction caused by 500 ppm phenobarbital. Thus, in the rat model, DPH enhanced N-nitrosodiethyl-amine-initiated hepatocarcinogenesis when administered at a dose causing maximal CYP2B induction.

关键词： Cytochrome(s) P450 Induction F344 Rats Liver Tumor Promotion Phenytoin

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