tbuckley/cabot-search huggingface dataset:
A rare coding allele in<i>IFIH1</i>is protective for psoriatic arthritis
Authors: Ashley Budu-Aggrey, John Bowes, Philip E Stuart, Matthew Zawistowski, Lam C Tsoi, Rajan Nair, Deepak Rohit Jadon, Neil McHugh, Eleanor Korendowych, James T Elder, Anne Barton, Soumya Raychaudhuri
Journal: Annals of the Rheumatic Diseases (2017)

Psoriatic arthritis (PsA) is an inflammatory arthritis associated with psoriasis. While many common risk alleles have been reported for association with PsA as well as psoriasis, few rare coding alleles have yet been identified.To identify rare coding variation associated with PsA risk or protection, we genotyped 41 267 variants with the exome chip and investigated association within an initial cohort of 1980 PsA cases and 5913 controls. Genotype data for an independent cohort of 2234 PsA cases and 5708 controls was also made available, allowing for a meta-analysis to be performed with the discovery dataset.We identified an association with the rare variant rs35667974 (p=2.39x10-6, OR=0.47), encoding an Ile923Val amino acid change in the IFIH1 gene protein product. The association was reproduced in our independent cohort, which reached a high level of significance on meta-analysis with the discovery and replication datasets (p=4.67x10-10). We identified a strong association with IFIH1 when performing multiple-variant analysis (p=6.77x10-6), and found evidence of independent effects between the rare allele and the common PsA variant at the same locus.For the first time, we report a rare coding allele in IFIH1 to be protective for PsA. This rare allele has also been identified to have the same direction of effect on type I diabetes and psoriasis. While this association further supports existing evidence for IFIH1 as a causal gene for PsA, mechanistic studies will need to be pursued to confirm that IFIH1 is indeed causal.
Challenges and emerging directions in single-cell analysis
Authors: Guo-Cheng Yuan, Long Cai, Michael Elowitz, Tariq Enver, Guoping Fan, Guoji Guo, Rafael Irizarry, Peter Kharchenko, Junhyong Kim, Stuart Orkin, John Quackenbush, Assieh Saadatpour, Timm Schroeder, Ramesh Shivdasani, Itay Tirosh
Journal: Genome biology (2017)

Single-cell analysis is a rapidly evolving approach to characterize genome-scale molecular information at the individual cell level. Development of single-cell technologies and computational methods has enabled systematic investigation of cellular heterogeneity in a wide range of tissues and cell populations, yielding fresh insights into the composition, dynamics, and regulatory mechanisms of cell states in development and disease. Despite substantial advances, significant challenges remain in the analysis, integration, and interpretation of single-cell omics data. Here, we discuss the state of the field and recent advances and look to future opportunities.
Effectiveness of ribavirin use associated with direct-acting antivirals in the treatment of non-cirrhotic patients with genotype 1a or 4 HCV infection in real-world practice
Authors: B. Ruiz-Antorán, D. Rincón, M.H. Conde, I. Fernández, J. García-Samaniego, F. Gea, J. Cabezas, B. Sacristán, F. Jorquera, J. Turnes, M. Prieto, J. Llaneras, J.M. Pascasio, F.S. Royuela, S. Lens, M.A. Serra, R.M. Morillas, X. Torras, R.J. Andrade, M.F. Bermejo, J. Ampuero, E. Molina, L. Bonet, M. Diago, J.R. Salcines, J.M. Moreno, J. Crespo, J.L.C. Panero
Journal: Journal of Hepatology (2017)
Durvalumab in ≥ 3rd-line EGFR mutant/ALK+, locally advanced or metastatic NSCLC: Results from the phase 2 ATLANTIC study
Authors: M.C. Garassino, B.-C. Cho, J.E. Gray, J. Mazières, K. Park, R.A. Soo, P. Dennis, Y. Huang, C. Wadsworth, N. Rizvi
Journal: Annals of Oncology (2017)
Treg-recruiting microspheres prevent inflammation in a murine model of dry eye disease
Authors: Michelle L. Ratay, Andrew J. Glowacki, Stephen C. Balmert, Abhinav P. Acharya, Julia Polat, Lawrence P. Andrews, Morgan V. Fedorchak, Joel S. Schuman, Dario A.A. Vignali, Steven R. Little
Journal: Journal of Controlled Release (2017)
High Levels of Circulating Epinephrine Trigger Apical Cardiodepression in a β <sub>2</sub> -Adrenergic Receptor/G <sub>i</sub> –Dependent Manner
Authors: Helen Paur, Peter T. Wright, Markus B. Sikkel, Matthew H. Tranter, Catherine Mansfield, Peter O'Gara, Daniel J. Stuckey, Viacheslav O. Nikolaev, Ivan Diakonov, Laura Pannell, Haibin Gong, Hong Sun, Nicholas S. Peters, Mario Petrou, Zhaolun Zheng, Julia Gorelik, Alexander R. Lyon, Sian E. Harding
Journal: Circulation (2012)

Background— Takotsubo cardiomyopathy is an acute heart failure syndrome characterized by myocardial hypocontractility from the mid left ventricle to the apex. It is precipitated by extreme stress and can be triggered by intravenous catecholamine administration, particularly epinephrine. Despite its grave presentation, Takotsubo cardiomyopathy is rapidly reversible, with generally good prognosis. We hypothesized that this represents switching of epinephrine signaling through the pleiotropic β 2 -adrenergic receptor (β 2 AR) from canonical stimulatory G-protein–activated cardiostimulant to inhibitory G-protein–activated cardiodepressant pathways. Methods and Results— We describe an in vivo rat model in which a high intravenous epinephrine, but not norepinephrine, bolus produces the characteristic reversible apical depression of myocardial contraction coupled with basal hypercontractility. The effect is prevented via G i inactivation by pertussis toxin pretreatment. β 2 AR number and functional responses were greater in isolated apical cardiomyocytes than in basal cardiomyocytes, which confirmed the higher apical sensitivity and response to circulating epinephrine. In vitro studies demonstrated high-dose epinephrine can induce direct cardiomyocyte cardiodepression and cardioprotection in a β 2 AR-Gi–dependent manner. Preventing epinephrine-G i effects increased mortality in the Takotsubo model, whereas β-blockers that activate β 2 AR-G i exacerbated the epinephrine-dependent negative inotropic effects without further deaths. In contrast, levosimendan rescued the acute cardiac dysfunction without increased mortality. Conclusions— We suggest that biased agonism of epinephrine for β 2 AR-G s at low concentrations and for G i at high concentrations underpins the acute apical cardiodepression observed in Takotsubo cardiomyopathy, with an apical-basal gradient in β 2 ARs explaining the differential regional responses. We suggest this epinephrine-specific β 2 AR-G i signaling may have evolved as a cardioprotective strategy to limit catecholamine-induced myocardial toxicity during acute stress.
Donation mode impacts on invariant natural killer T cell population leading to scarce iNKT cells in donation after cardiac death liver grafts despite a significant increase in B cells and CD1d expression
Authors: Y.G. Ghnewa, M. Yuksel, S. Khorsandi, X. Huang, J. Graham, L. Ramsay, L. Fiorou, Z. Milan, Y. Ma, W. Jassem, N. Heaton
Journal: Journal of Hepatology (2017)
Comprehensive Biologic Characterization of 99 Multiple Myeloma Patients Using Cytomorphology, FISH, Gene Expression Profiling and Mutation Screening Leads to Important Clinical and Therapeutic Insights
Authors: Simone Weber, Marietta Truger, Wolfgang Kern, Martin H van Vliet, Erik H van Beers, Niroshan Nadarajah, Manja Meggendorfer, Dennis Haupt, Claudia Haferlach, Torsten Haferlach
Journal: Blood (2016)
Role of Donor Source on Clinical Outcomes and Inpatient Resource Utilization for Hematopoietic Cell Transplantation in Children with Acute Leukemia
Authors: Staci D Arnold, Ruta Brazauskas, Naya He, Yimei Li, Prakash Satwani, Michael A Pulsipher, Matt Hall, Yoshiko Atsuta, Jignesh D Dalal, Theresa Hahn, Carmem Bonfim, Nandita Khera, Richard Aplenc, Wael Saber
Journal: Blood (2016)
Authors’ reply to Spitzer and Chalmers
Authors: Beatrice Clare Cockbain, Tehmina Bharucha, Dianne Irish, Michael Jacobs
Journal: BMJ (2017)

Correctly identifying Koplik’s spots is not an easy feat, as noted in Spitzer’s excellent letter.12 Koplik’s spots are still thought to be pathognomonic for measles, but oral lesions, similar in appearance to Koplik’s spots, can be found in other illnesses, such as parvovirus B12 infection.3 Zenner and Nacul’s study included reporting of “Koplik’s spots” by clinicians with variable levels of experience and did not include independent assessment …
Recurrence of primary sclerosing cholangitis is associated with lower survival after liver transplantation: an analysis of the European liver transplant registry data base
Authors: T. Visseren, W.G. Polak, R. Adam, J. Klempnauer, B.-G. Ericzon, R.J. Porte, F. Van der Heide, A. Paul, P. Nemec, M. Salizzoni, J. Pirenne, B.E. Hansen, H.J. Metselaar, J.N. IJzermans, S.D. Murad
Journal: Journal of Hepatology (2017)
Quantification of serum hepatitis B core-related antigen to understanding the hepatitis B virus and hepatitis D virus chronic infection
Authors: A. Ruiz-Ripa, M. Riveiro-Barciela, D. Tabernero, C. Godoy, S. Sopena, R.M. López-Martínez, M. Buti, F. Rodríguez-Frías
Journal: Journal of Hepatology (2017)
Gut microbiota are associated with impaired brain recovery after liver transplant
Authors: J.S. Bajaj, A. Fagan, J. Wade, A. Fagan, E.A. Gavis, M. White, D. Ganapathy, D. Heuman, M. Sikaroodi, M. Fuchs, B. John, H.C. Gilles, P. Gillevet
Journal: Journal of Hepatology (2017)
Can modest alcohol intake be dismissed as a co-factor in diabetic patients with non-alcoholic fatty liver disease?
Authors: P.J. Patel, D.D. Smith, K.A. Stuart, L.U. Horsfall, K.L. Hayward, F. Hossain, S. Williams, T. Johnson, N.N. Brown, N. Saad, A.D. Clouston, K.M. Irvine, A.W. Russell, P.C. Valery, E.E. Powell
Journal: Journal of Hepatology (2017)
Real life retreatment of patients failing DAAs in Spain: data from the HCVREsp cohort
Authors: A.B. Pérez, N. Chueca, J.Á. Fernández-Caballero, M.G.-D. Toro, A. Martínez-Sapiña, D. Navarro, D. Merino, M. Jiménez, J.M. Pascasio, A. Rivero-Juárez, J.C. Alados, F. Téllez, F.J. Vera, V. Hontañón, A. Collado, F.J. Salmerón, M. Delgado, M. Diago, M. Casado, T. Aldamiz-Echevarría, J. Santos, J.A. Pineda, A. Poyato, P. Viciana, S. Reus, C. Hidalgo, I. García-Arata, M. Masià, M.M. Lara, M. Omar-Balghata, E. Bernal, C. Delgado, J. Antón, C. Mínguez, J.M. Fernández-Martín, J. Primo, R. Hernández, J. Guilarte, A. Fernández, C. Galera, V. Navarro, M. Chicano, R. Alonso, C. Guerrero, F. García
Journal: Journal of Hepatology (2017)
Controlled attenuation parameter as an additional tool for the non-invasive prediction of first clinical decompensation in compensated advanced chronic liver disease
Authors: C. Margini, G. Murgia, G. Stirnimann, A. De Gottardi, N. Semmo, S. Casu, J. Bosch, J.-F. Dufour, A. Berzigotti
Journal: Journal of Hepatology (2017)
The role of the microbiome in cancer development and therapy
Authors: Aadra P. Bhatt, Matthew R. Redinbo, Scott J. Bultman
Journal: CA A Cancer Journal for Clinicians (2017)

Answer questions and earn CME/CNE The human body harbors enormous numbers of microbiota that influence cancer susceptibility, in part through their prodigious metabolic capacity and their profound influence on immune cell function. Microbial pathogens drive tumorigenesis in 15% to 20% of cancer cases. Even larger numbers of malignancies are associated with an altered composition of commensal microbiota (dysbiosis) based on microbiome studies using metagenomic sequencing. Although association studies cannot distinguish whether changes in microbiota are causes or effects of cancer, a causative role is supported by rigorously controlled preclinical studies using gnotobiotic mouse models colonized with one or more specific bacteria. These studies demonstrate that microbiota can alter cancer susceptibility and progression by diverse mechanisms, such as modulating inflammation, inducing DNA damage, and producing metabolites involved in oncogenesis or tumor suppression. Evidence is emerging that microbiota can be manipulated for improving cancer treatment. By incorporating probiotics as adjuvants for checkpoint immunotherapy or by designing small molecules that target microbial enzymes, microbiota can be harnessed to improve cancer care. CA Cancer J Clin 2017;67:326-344. © 2017 American Cancer Society.
Mental Health Outcomes After Having or Being Denied an Abortion
Authors: Michael A. Erdek
Journal: JAMA Psychiatry (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Psychiatry HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Psychiatry journal
Treatment and prognosis of acute severe autoimmune hepatitis
Authors: E. De Martin, A. Coilly, P. Houssel-Debry, I. Ollivier-Hourmand, A. Heurgue-Berlot, F. Artru, S. Barge, O. Chazouilleres, C. Silvain, C. Duvoux, G.-P. Pageaux, C. Besch, M. Bourlière, H. Fontaine, V. de Ledinghen, J. Dumortier, F. Conti, S. Radenne, M. Debette-Gratien, O. Goria, J. Boursier, J.-M. Peron, F. Durand, P. Borrentain, P. Potier, A. Minello, A. Abergel, J.-M. Perarnau, J.-B. Nousbaum, M. Rudler, L. Alric, R. Anty, N. Sturm, M. Sebagh, H. Agostini, D. Samuel, J.-C. Duclos-Vallée
Journal: Journal of Hepatology (2017)
CHK1 Inhibition in Small-Cell Lung Cancer Produces Single-Agent Activity in Biomarker-Defined Disease Subsets and Combination Activity with Cisplatin or Olaparib
Authors: Triparna Sen, Pan Tong, C Allison Stewart, Sandra Cristea, Aly Valliani, David S Shames, Abena B Redwood, You Hong Fan, Lerong Li, Bonnie S Glisson, John D Minna, Julien Sage, Don L Gibbons, Helen Piwnica-Worms, John V Heymach, Jing Wang, Lauren Averett Byers
Journal: Cancer Research (2017)

Effective targeted therapies for small-cell lung cancer (SCLC), the most aggressive form of lung cancer, remain urgently needed. Here we report evidence of preclinical efficacy evoked by targeting the overexpressed cell-cycle checkpoint kinase CHK1 in SCLC. Our studies employed RNAi-mediated attenuation or pharmacologic blockade with the novel second-generation CHK1 inhibitor prexasertib (LY2606368), currently in clinical trials. In SCLC models in vitro and in vivo, LY2606368 exhibited strong single-agent efficacy, augmented the effects of cisplatin or the PARP inhibitor olaparib, and improved the response of platinum-resistant models. Proteomic analysis identified CHK1 and MYC as top predictive biomarkers of LY2606368 sensitivity, suggesting that CHK1 inhibition may be especially effective in SCLC with MYC amplification or MYC protein overexpression. Our findings provide a preclinical proof of concept supporting the initiation of a clinical efficacy trial in patients with platinum-sensitive or platinum-resistant relapsed SCLC. Cancer Res; 77(14); 3870-84. ©2017 AACR.
An interpenetrating network-strengthened and toughened hydrogel that supports cell-based nucleus pulposus regeneration
Authors: Yibo Gan, Pei Li, Liyuan Wang, Xiumei Mo, Lei Song, Yuan Xu, Chen Zhao, Bin Ouyang, Bing Tu, Lei Luo, Linyong Zhu, Shiwu Dong, Fuyou Li, Qiang Zhou
Journal: Biomaterials (2017)
Molecular effects of the soluble guanylyl cyclase stimulator riociguat on biliary cirrhosis and effects on transaminases in patients
Authors: P. Schwabl, K. Brusilovskaya, P. Königshofer, P. Supper, D. Bauer, F. Riedl, N. Rohr-Udilova, H. Hayden, S. Aschauer, D. Bonderman, G. Oberhuber, B. Podesser, M. Peck-Radosavljevic, M. Trauner, T. Reiberger
Journal: Journal of Hepatology (2017)
Afatinib (A) vs gefitinib (G) in patients with EGFR mutation-positive (EGFRm+) NSCLC: Updated OS data from the phase IIb trial LUX-Lung 7 (LL7)
Authors: J. Corral, K. Park, J.C.-H. Yang, T. Mok, E.-H. Tan, K. O'Byrne, V. Hirsh, M. Boyer, J. Fan, L. Zhang
Journal: Annals of Oncology (2017)
Pre-emptive post-liver transplant hepatitis C virus treatment with daas: proof of concept from a pilot study
Authors: L. Pasulo, C. Mazzarelli, C. Iegri, L. De Carlis, R. Viganò, F. Donato, P. Burra, M. Gambato, S. Fagiuoli, L. Belli
Journal: Journal of Hepatology (2017)
Single Cell Signaling Pharmacodynamics in a Phase 1b Trial of the Axl Inhibitor BGB324 in Acute Myeloid Leukemia
Authors: Monica Hellesøy, Stein-Erik Gullaksen, Benedicte Sjo Tislevoll, Oda Helen Eck Fagerholt, Hakon Reikvam, Sonja Loges, Jorge Cortes, Michael Heuser, Jörg Chromik, Jørn Skavland, André Sulen, Øystein Bruserud, Jim Lorens, Gro Gausdal, David Micklem, Bjorn T. Gjertsen
Journal: Blood (2016)
Resistant bacterial infections in cirrhosis: a French observational prospective multicentre nationwide study (RESIST study)
Authors: A. Pauwels, L. Meunier, G. Boivineau, T. Martin, I. Touze, F. Zuberbuhler, M. Allaire, W. Margos, N. Carbonell, B. Lambare, A. Mumana, C. Bureau, G. Macaigne, B. Ould-Ahmed, M. Mallet, M.-L. Rabilloud, C. Koudougou, D. Konstantinou, A. Chény, T. Broussier, M.A. Masmoudi, F. Skinazi, J.-F. Cadranel, L. Defour
Journal: Journal of Hepatology (2017)
Evaluation of a sequence-based method for hepatitis C genotyping (Deepchek ® SingleRound PCR and NS5B/5’UTR sequencing) and comparison with VERSANT HCV Genotype 2.0 assay (InnoLiPA)
Authors: G. Boland, W. Nijhuis, A. Rissewijck, R. Schuurman
Journal: Journal of Hepatology (2017)
Treatment outcomes of patients with chronic hepatitis C receiving sofosbuvir-based combination therapy within national hepatitis C elimination program in the country of Georgia
Authors: T. Tsertsvadze, A. Gamkrelidze, M. Nasrullah, L. Sharvadze, J. Morgan, L. Gvinjilia, G. Kamkamidze, D. Metreveli, V. Kerashvili, M. Butsashvili, J. Zarkua, N. Chkhartishvili, A. Abutidze, D. Baliashvili, V. Kvaratskhelia, F. Averhoff
Journal: Journal of Hepatology (2017)
Allogeneic Hematopoietic Cell Transplantation (HCT) for Acute Leukemia in First Relapse or Second Remission.
Authors: Je-Hwan Lee, Seong-Jun Choi, Jung-Hee Lee, Young-Shin Lee, SungCheol Yun, Sung-Soo Yoon, Inho Kim, Seonyang Park, Byoung Kook Kim, Chul Won Jung, Kihyun Kim, Jin Seok Ahn, Kyoo-Hyung Lee
Journal: Blood (2005)
Clonal History and Genetic Predictors of Transformation Into Small-Cell Carcinomas From Lung Adenocarcinomas
Authors: June-Koo Lee, Junehawk Lee, Sehui Kim, Soyeon Kim, Jeonghwan Youk, Seongyeol Park, Yohan An, Bhumsuk Keam, Dong-Wan Kim, Dae Seog Heo, Young Tae Kim, Jin-Soo Kim, Se Hyun Kim, Jong Seok Lee, Se-Hoon Lee, Keunchil Park, Ja-Lok Ku, Yoon Kyung Jeon, Doo Hyun Chung, Peter J. Park, Joon Kim, Tae Min Kim, Young Seok Ju
Journal: Journal of Clinical Oncology (2017)

Purpose Histologic transformation of EGFR mutant lung adenocarcinoma (LADC) into small-cell lung cancer (SCLC) has been described as one of the major resistant mechanisms for epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). However, the molecular pathogenesis is still unclear. Methods We investigated 21 patients with advanced EGFR-mutant LADCs that were transformed into EGFR TKI-resistant SCLCs. Among them, whole genome sequencing was applied for nine tumors acquired at various time points from four patients to reconstruct their clonal evolutionary history and to detect genetic predictors for small-cell transformation. The findings were validated by immunohistochemistry in 210 lung cancer tissues. Results We identified that EGFR TKI-resistant LADCs and SCLCs share a common clonal origin and undergo branched evolutionary trajectories. The clonal divergence of SCLC ancestors from the LADC cells occurred before the first EGFR TKI treatments, and the complete inactivation of both RB1 and TP53 were observed from the early LADC stages in sequenced tumors. We extended the findings by immunohistochemistry in the early-stage LADC tissues of 75 patients treated with EGFR TKIs; inactivation of both Rb and p53 was strikingly more frequent in the small-cell-transformed group than in the nontransformed group (82% v 3%; odds ratio, 131; 95% CI, 19.9 to 859). Among patients registered in a predefined cohort (n = 65), an EGFR mutant LADC that harbored completely inactivated Rb and p53 had a 43× greater risk of small-cell transformation (relative risk, 42.8; 95% CI, 5.88 to 311). Branch-specific mutational signature analysis revealed that apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC)-induced hypermutation was frequent in the branches toward small-cell transformation. Conclusion EGFR TKI-resistant SCLCs are branched out early from the LADC clones that harbor completely inactivated RB1 and TP53. The evaluation of RB1 and TP53 status in EGFR TKI-treated LADCs is informative in predicting small-cell transformation.
A critique of the “ultra‐high risk” and “transition” paradigm
Authors: Jim van Os, Sinan Guloksuz
Journal: World Psychiatry (2017)

The transdiagnostic expression of psychotic experiences in common mental disorder (anxiety/depression/substance use disorder) is associated with a poorer prognosis, and a small minority of people may indeed develop a clinical picture that meets criteria for schizophrenia. However, it appears neither useful nor valid to observe early states of multidimensional psychopathology in young people through the “schizo”‐prism, and apply misleadingly simple, unnecessary and inefficient binary concepts of “risk” and “transition”. A review of the “ultra‐high risk” (UHR) or “clinical high risk” (CHR) literature indicates that UHR/CHR samples are highly heterogeneous and represent individuals diagnosed with common mental disorder (anxiety/depression/substance use disorder) and a degree of psychotic experiences. Epidemiological research has shown that psychotic experiences are a (possibly non‐causal) marker of the severity of multidimensional psychopathology, driving poor outcome, yet notions of “risk” and “transition” in UHR/CHR research are restrictively defined on the basis of positive psychotic phenomena alone, ignoring how baseline differences in multidimensional psychopathology may differentially impact course and outcome. The concepts of “risk” and “transition” in UHR/CHR research are measured on the same dimensional scale, yet are used to produce artificial diagnostic shifts. In fact, “transition” in UHR/CHR research occurs mainly as a function of variable sample enrichment strategies rather than the UHR/CHR “criteria” themselves. Furthermore, transition rates in UHR/CHR research are inflated as they do not exclude false positives associated with the natural fluctuation of dimensional expression of psychosis. Biological associations with “transition” thus likely represent false positive findings, as was the initial claim of strong effects of omega‐3 polyunsatured fatty acids in UHR samples. A large body of UHR/CHR intervention research has focused on the questionable outcome of “transition”, which shows lack of correlation with functional outcome. It may be more productive to consider the full range of person‐specific psychopathology in all young individuals who seek help for mental health problems, instead of “policing” youngsters for the transdiagnostic dimension of psychosis. Instead of the relatively inefficient medical high‐risk approach, a public health perspective, focusing on improved access to a low‐stigma, high‐hope, small scale and youth‐specific environment with acceptable language and interventions may represent a more useful and efficient strategy.