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WashU weekly Neuroscience publications

“Epigenetic dysregulation of enhancers in neurons is associated with Alzheimer’s disease pathology and cognitive symptoms” (2019) Nature Communications

Epigenetic dysregulation of enhancers in neurons is associated with Alzheimer’s disease pathology and cognitive symptoms
(2019) Nature Communications, 10 (1), art. no. 2246, . 

Li, P.a , Marshall, L.a , Oh, G.b , Jakubowski, J.L.a , Groot, D.b , He, Y.c , Wang, T.c , Petronis, A.b d , Labrie, V.a b e

a Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI 49503, United States
b Centre for Addiction and Mental Health, Toronto, ON M5T 1R8, Canada
c Department of Genetics, Washington University in St. Louis, St. Louis, MO 63130, United States
d Institute of Biotechnology, Life Sciences Center, Vilnius University, Vilnius, LT-10257, Lithuania
e Division of Psychiatry and Behavioral Medicine, College of Human Medicine, Michigan State University, Grand Rapids, MI 49503, United States

Abstract
Epigenetic control of enhancers alters neuronal functions and may be involved in Alzheimer’s disease (AD). Here, we identify enhancers in neurons contributing to AD by comprehensive fine-mapping of DNA methylation at enhancers, genome-wide. We examine 1.2 million CpG and CpH sites in enhancers in prefrontal cortex neurons of individuals with no/mild, moderate, and severe AD pathology (n = 101). We identify 1224 differentially methylated enhancer regions; most of which are hypomethylated at CpH sites in AD neurons. CpH methylation losses occur in normal aging neurons, but are accelerated in AD. Integration of epigenetic and transcriptomic data demonstrates a pro-apoptotic reactivation of the cell cycle in post-mitotic AD neurons. Furthermore, AD neurons have a large cluster of significantly hypomethylated enhancers in the DSCAML1 gene that targets BACE1. Hypomethylation of these enhancers in AD is associated with an upregulation of BACE1 transcripts and an increase in amyloid plaques, neurofibrillary tangles, and cognitive decline. © 2019, The Author(s).

Document Type: Article
Publication Stage: Final
Source: Scopus
Access Type: Open Access

“Aminophospholipids are signal-transducing TREM2 ligands on apoptotic cells” (2019) Scientific Reports

Aminophospholipids are signal-transducing TREM2 ligands on apoptotic cells
(2019) Scientific Reports, 9 (1), art. no. 7508, . 

Shirotani, K.a b , Hori, Y.a b , Yoshizaki, R.a , Higuchi, E.a , Colonna, M.c , Saito, T.d , Hashimoto, S.e , Saito, T.e , Saido, T.C.e , Iwata, N.a b

a Department of Genome-based Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, 852-8521, Japan
b Unit for Dementia Research and Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, 852-8521, Japan
c Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, United States
d Laboratory for Cell Signalling, Department of Immunology, RIKEN Center for Integrative Medical Sciences, Kanagawa, 230-0045, Japan
e Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama, 351-0198, Japan

Abstract
Variants of triggering receptor expressed on myeloid cells 2 (TREM2) are associated with an increased incidence of Alzheimer’s disease, as well as other neurodegenerative disorders. Using a newly developed, highly sensitive reporter cell model, consisting of Jurkat T cells stably overexpressing a reporter gene and a gene encoding TREM2DAP12 fusion protein, we show here that TREM2-dependent signal transduction in response to apoptotic Neuro2a cells is mediated by aminophospholipid ligands, phosphatidylserine and phosphatidylethanolamine, which are not exposed on the intact cell surface, but become exposed upon apoptosis. We also show that signal-transducing TREM2 ligands different from aminophospholipids, which appear to be derived from neurons, might be present in membrane fractions of mouse cerebral cortex. These results may suggest that TREM2 regulates microglial function by transducing intracellular signals from aminophospholipids on apoptotic cells, as well as unidentified ligands in the membranes of the cerebral cortex. © 2019, The Author(s).

Document Type: Article
Publication Stage: Final
Source: Scopus
Access Type: Open Access

“Cerebral aquaporin-4 expression is independent of seizures in tuberous sclerosis complex”(2019) Neurobiology of Disease

Cerebral aquaporin-4 expression is independent of seizures in tuberous sclerosis complex
(2019) Neurobiology of Disease, 129, pp. 93-101. 

Short, B.a , Kozek, L.a b , Harmsen, H.c , Zhang, B.d , Wong, M.d , Ess, K.C.a b , Fu, C.a , Naftel, R.e , Pearson, M.M.f , Carson, R.P.a b g

a Department of Pediatrics, Division of Pediatric Neurology, Vanderbilt University Medical Center, United States
b Vanderbilt Brain Institute, Vanderbilt University, United States
c Department of Pathology, Vanderbilt University Medical Center, United States
d Departments of Neurology, Pediatrics, and Neuroscience, Washington University School of Medicine, United States
e Department of Neurosurgery, Vanderbilt University Medical Center, United States
f Neurosurgery, Sacred Heart Hospital, Pensacola, FL, United States
g Department of Pharmacology, Vanderbilt University Medical Center, United States

Abstract
Astrocytes serve many functions in the human brain, many of which focus on maintenance of homeostasis. Astrocyte dysfunction in Tuberous Sclerosis Complex (TSC) has long been appreciated with activation of the mTORC1 signaling pathway resulting in gliosis and possibly contributing to the very frequent phenotype of epilepsy. We hypothesized that aberrant expression of the astrocyte protein aquaporin-4 (AQP4) may be present in TSC and contribute to disease pathology. Characterization of AQP4 expression in epileptic cortex from TSC patients demonstrated a diffuse increase in AQP4. To determine if this was due to exposure to seizures, we examined Aqp4 expression in mouse models of TSC in which Tsc1 or Tsc2 inactivation was targeted to astrocytes or glial progenitors, respectively. Loss of either Tsc1 or Tsc2 from astrocytes resulted in a marked increase in Aqp4 expression which was sensitive to mTORC1 inhibition with rapamycin. Our findings in both TSC epileptogenic cortex and in a variety of astrocyte culture models demonstrate for the first time that AQP4 expression is dysregulated in TSC. The extent to which AQP4 contributes to epilepsy in TSC is not known, though the similarities in AQP4 expression between TSC and temporal lobe epilepsy supports further studies targeting AQP4 in TSC. © 2019

Author Keywords
Aquaporin-4;  Epilepsy;  Mouse;  Tuberous sclerosis complex

Document Type: Article
Publication Stage: Final
Source: Scopus

“The accumulation of T cells within acellular nerve allografts is length-dependent and critical for nerve regeneration” (2019) Experimental Neurology

The accumulation of T cells within acellular nerve allografts is length-dependent and critical for nerve regeneration
(2019) Experimental Neurology, 318, pp. 216-231. 

Pan, D.a , Hunter, D.A.a , Schellhardt, L.a , Jo, S.a , Santosa, K.B.a , Larson, E.L.a , Fuchs, A.G.b , Snyder-Warwick, A.K.a , Mackinnon, S.E.a , Wood, M.D.a

a Division of Plastic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, MO 63110, United States
b Section of Acute and Critical Care Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, MO 63110, United States

Abstract
Repair of traumatic nerve injuries can require graft material to bridge the defect. The use of alternatives to bridge the defect, such as acellular nerve allografts (ANAs), is becoming more common and desired. Although ANAs support axon regeneration across short defects (<3 cm), axon regeneration across longer defects (>3 cm) is limited. It is unclear why alternatives, including ANAs, are functionally limited by length. After repairing Lewis rat nerve defects using short (2 cm) or long (4 cm) ANAs, we showed that long ANAs have severely reduced axon regeneration across the grafts and contain Schwann cells with a unique phenotype. But additionally, we found that long ANAs have disrupted angiogenesis and altered leukocyte infiltration compared to short ANAs as early as 2 weeks after repair. In particular, long ANAs contained fewer T cells compared to short ANAs. These outcomes were accompanied with reduced expression of select cytokines, including IFN-γ and IL-4, within long versus short ANAs. T cells within ANAs did not express elevated levels of IL-4, but expressed elevated levels of IFN-γ. We also directly assessed the contribution of T cells to regeneration across nerve grafts using athymic rats. Interestingly, T cell deficiency had minimal impact on axon regeneration across nerve defects repaired using isografts. Conversely, T cell deficiency reduced axon regeneration across nerve defects repaired using ANAs. Our data demonstrate that T cells contribute to nerve regeneration across ANAs and suggest that reduced T cells accumulation within long ANAs could contribute to limiting axon regeneration across these long ANAs. © 2019 Elsevier Inc.

Author Keywords
Acellular nerve allograft;  Peripheral nerve;  Regeneration;  Schwann cells;  T cells

Document Type: Article
Publication Stage: Final
Source: Scopus

“Patterns and predictors of family environment among adolescents at high and low risk for familial bipolar disorder” (2019) Journal of Psychiatric Research

Patterns and predictors of family environment among adolescents at high and low risk for familial bipolar disorder
(2019) Journal of Psychiatric Research, 114, pp. 153-160. 

Stapp, E.K.a b , Musci, R.J.a , Fullerton, J.M.c d , Glowinski, A.L.e , McInnis, M.f , Mitchell, P.B.g h , Hulvershorn, L.A.i , Ghaziuddin, N.f , Roberts, G.M.P.g h , Merikangas, K.R.b , Nurnberger, J.I., Jr.i j , Wilcox, H.C.a k

a Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, United States
b National Institute of Mental Health, Bethesda, MD, United States
c Neuroscience Research Australia, Randwick, Sydney, NSW, Australia
d School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia
e Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, United States
f Department of Psychiatry and Depression Center, University of Michigan, Ann Arbor, MI, United States
g School of Psychiatry, University of New South Wales, Sydney, NSW, Australia
h Black Dog Institute, Sydney, NSW, Australia
i Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN, United States
j Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, United States
k Johns Hopkins School of Medicine, Baltimore, MD, United States

Abstract
Children’s perceptions are important to understanding family environment in the bipolar disorder (BD)high-risk context. Our objectives were to empirically derive patterns of offspring-perceived family environment, and to test the association of family environment with maternal or paternal BD accounting for offspring BD and demographic characteristics. Participants aged 12–21 years (266 offspring of a parent with BD, 175 offspring of a parent with no psychiatric history)were recruited in the US and Australia. We modeled family environment using latent profile analysis based on offspring reports on the Conflict Behavior Questionnaire, Family Adaptability and Cohesion Evaluation Scales, and Home Environment Interview for Children. Parent diagnoses were based on the Diagnostic Interview for Genetic Studies and offspring diagnoses were based on the Schedule for Affective Disorders and Schizophrenia for School-Aged Children. Latent class regression was used to test associations of diagnosis and family environment. Two-thirds of all offspring perceived well-functioning family environment, characterized by nurturance, flexibility, and low conflict. Two ‘conflict classes’ perceived family environments low in flexibility and cohesion, with substantial separation based on high conflict with the father (High Paternal Conflict), or very high conflict and rigidity and low warmth with the mother (High Maternal Conflict). Maternal BD was associated with offspring perceiving High Maternal Conflict (OR 2.8, p = 0.025). Clinical care and psychosocial supports for mothers with BD should address family functioning, with attention to offspring perceptions of their wellbeing. More research is needed on the effect of paternal BD on offspring and family dynamics. © 2019

Author Keywords
Bipolar disorder;  Father-child relations;  Latent profile analysis;  Mood disorders;  Mother-child relations;  Risk factors

Document Type: Article
Publication Stage: Final
Source: Scopus

“The Neuroimmune Axis in Skin Sensation, Inflammation, and Immunity” (2019) Journal of Immunology (Baltimore, Md. : 1950)

The Neuroimmune Axis in Skin Sensation, Inflammation, and Immunity
(2019) Journal of Immunology (Baltimore, Md. : 1950), 202 (10), pp. 2829-2835.

Trier, A.M.a b , Mack, M.R.a b , Kim, B.S.b c d e  

a Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO 63110, United States
b Division of Dermatology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, United States
c Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO 63110;
d Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110; and
e Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, United States

Abstract
Although connections between the immune and nervous systems have long been recognized, the precise mechanisms that underlie this relationship are just starting to be elucidated. Advances in sensory biology have unveiled novel mechanisms by which inflammatory cytokines promote itch and pain sensations to coordinate host-protective behavioral responses. Conversely, new evidence has emphasized the importance of immune cell regulation by sensory neurons. By focusing on itch biology and how it has been informed by the more established field of pain research, we highlight recent interdisciplinary studies that demonstrate how novel neuroimmune interactions underlie a diversity of sensory, inflammatory, and infectious diseases. Copyright © 2019 by The American Association of Immunologists, Inc.

Document Type: Review
Publication Stage: Final
Source: Scopus

“Fibril Self-Assembly of Amyloid-Spider Silk Block Polypeptides” (2019) Biomacromolecules

Fibril Self-Assembly of Amyloid-Spider Silk Block Polypeptides
(2019) Biomacromolecules, 20 (5), pp. 2015-2023. 

Dai, B.a , Sargent, C.J.b , Gui, X.d , Liu, C.d , Zhang, F.a b c

a Department of Energy, Environmental and Chemical Engineering, Washington University in St. Louis, St. Louis, MO 63130, United States
b Division of Biological and Biomedical Sciences, Washington University in St. Louis, St. Louis, MO 63130, United States
c Institute of Materials Science and Engineering, Washington University in St. Louis, St. Louis, MO 63130, United States
d Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, 201210, China

Abstract
Because of their association with debilitating diseases and their potential applications in developing novel bionanomaterials, highly ordered amyloid fibrils have recently received considerable attention. While many studies have thus far focused on amyloid fibrils made with short peptides containing just one steric zipper-forming segment of native amyloid proteins, the self-assembly of proteins containing multiple steric zipper-forming segments has been rarely explored. Here we develop a strategy to create four block polypeptides, each containing 16 repeats of a zipper-forming segment from four different amyloid morphological classes. All four block polypeptides self-assemble into fibrils that display the cross-β structure characteristic of amyloids. These amyloid-spider silk block polypeptides displayed fast self-assembly kinetics, and their fibrils exhibited high thermal stability. These novel synthetic amyloids provide insights into the self-assembly of proteins containing multiple zipper-forming segments, and our approach of creating block polypeptide fibrils could be used to expand the capability of amyloid-based bionanomaterials. © 2019 American Chemical Society.

Document Type: Article
Publication Stage: Final
Source: Scopus

“CNS myelination and remyelination depend on fatty acid synthesis by oligodendrocytes” (2019) eLife

CNS myelination and remyelination depend on fatty acid synthesis by oligodendrocytes
(2019) eLife, 8, . 

Dimas, P.a , Montani, L.a , Pereira, J.A.a , Moreno, D.a , Trötzmüller, M.b , Gerber, J.a , Semenkowich, C.F.c , Köfeler, H.C.b , Suter, U.a

a Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, ETH Zürich, Zürich, Switzerland
b Center for Medical Research, Medical University of Graz, Graz, Austria
c Division of Endocrinology, Metabolism and Lipid Research, Washington University Medical School, St. Louis, United States

Abstract
Oligodendrocytes (OLs) support neurons and signal transmission in the central nervous system (CNS) by enwrapping axons with myelin, a lipid-rich membrane structure. We addressed the significance of fatty acid (FA) synthesis in OLs by depleting FA synthase (FASN) from OL progenitor cells (OPCs) in transgenic mice. While we detected no effects in proliferation and differentiation along the postnatal OL lineage, we found that FASN is essential for accurate myelination, including myelin growth. Increasing dietary lipid intake could partially compensate for the FASN deficiency. Furthermore, FASN contributes to correct myelin lipid composition and stability of myelinated axons. Moreover, we depleted FASN specifically in adult OPCs to examine its relevance for remyelination. Applying lysolecithin-induced focal demyelinating spinal cord lesions, we found that FA synthesis is essential to sustain adult OPC-derived OLs and efficient remyelination. We conclude that FA synthesis in OLs plays key roles in CNS myelination and remyelination. © 2019, Dimas et al.

Author Keywords
fatty acid synthesis;  high fat diet;  mouse;  myelin lipids;  myelination;  neuroscience;  oligodendrocytes;  remyelination

Document Type: Article
Publication Stage: Final
Source: Scopus
Access Type: Open Access

“Recent advances in preventing and managing postoperative delirium” (2019) F1000Research

Recent advances in preventing and managing postoperative delirium
(2019) F1000Research, 8, . 

Vlisides, P.a b , Avidan, M.c

a Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, MI, United States
b Center for Consciousness Science, University of Michigan Medical School, Ann Arbor, MI, United States
c Department of Anesthesiology, Washington University School of Medicine, Saint Louis, MO, United States

Abstract
Postoperative delirium is a common and harrowing complication in older surgical patients. Those with cognitive impairment or dementia are at especially high risk for developing postoperative delirium; ominously, it is hypothesized that delirium can accelerate cognitive decline and the onset of dementia, or worsen the severity of dementia. Awareness of delirium has grown in recent years as various medical societies have launched initiatives to prevent postoperative delirium and alleviate its impact. Unfortunately, delirium pathophysiology is not well understood and this likely contributes to the current state of low-quality evidence that informs perioperative guidelines. Along these lines, recent prevention trials involving ketamine and dexmedetomidine have demonstrated inconsistent findings. Non-pharmacologic multicomponent initiatives, such as the Hospital Elder Life Program, have consistently reduced delirium incidence and burden across various hospital settings. However, a substantial portion of delirium occurrences are still not prevented, and effective prevention and management strategies are needed to complement such multicomponent non-pharmacologic therapies. In this narrative review, we examine the current understanding of delirium neurobiology and summarize the present state of prevention and management efforts. © 2019 Vlisides P and Avidan M.

Author Keywords
Anesthesia;  Cognitive dysfunction;  Cognitive reserve;  Delirium;  Neurocognitive;  Neurophysiology;  Postoperative;  Surgery

Document Type: Review
Publication Stage: Final
Source: Scopus
Access Type: Open Access

“Continuation therapies after successful treatment with electroconvulsive therapy in major depressive disorder” (2019) Psychiatric Annals

Continuation therapies after successful treatment with electroconvulsive therapy in major depressive disorder
(2019) Psychiatric Annals, 49 (4), pp. 164-168. 

O’Connor, B.J., Conway, C.R.

Department of Psychiatry, Washington University School of Medicine in St. Louis, United States

Abstract
Although the use of electroconvulsive therapy (ECT) predates the use of any other biologic treatment for major depressive disorder (MDD) available today, it remains the most effective treatment for the illness. Unlike antidepressant medications, ECT is commonly discontinued upon resolution of the acute depressive episode. However, relapse rates after an acute course of ECT for MDD are extremely high, and some form of continuation therapy is indicated to prevent relapse. We present findings from a literature review on various forms of continuation treatment after a successful acute course of ECT for patients with MDD. These include various forms of pharmacotherapy, ECT, and the combination of the two. © SLACK Incorporated.

Document Type: Article
Publication Stage: Final
Source: Scopus

“Effect of tDCS on aberrant functional network connectivity in refractory hallucinatory schizophrenia: A pilot study” (2019) Psychiatry Investigation

Effect of tDCS on aberrant functional network connectivity in refractory hallucinatory schizophrenia: A pilot study
(2019) Psychiatry Investigation, 16 (3), pp. 244-248. 

Yoon, Y.B.a b c , Kim, M.d , Lee, J.d , Cho, K.I.K.a b , Kwak, S.a , Lee, T.Y.d , Kwon, J.S.a b d

a Department of Brain and Cognitive Sciences, Seoul National University, Seoul, South Korea
b Institute of Human Behavioral Medicine, SNU-MRC, Seoul, South Korea
c Department of Psychiatry, Washington University, St. Louis, MO, United States
d Department of Psychiatry, Seoul National University College of Medicine, Seoul, South Korea

Abstract
We aim to investigate the effect of fronto-temporal transcranial direct current stimulation (tDCS) on the interactions among functional networks and its association with psychotic symptoms. In this pilot study, we will determine possible candidate functional networks and an adequate sample size for future research. Seven schizophrenia patients with treatment-refractory auditory hallucinations underwent tDCS twice daily for 5 days. Resting-state fMRI data and measures of the severity of psychotic symptoms were acquired at baseline and after completion of the tDCS sessions. At baseline, decreased functional network interaction was negatively correlated with increased hallucinatory behavior. After tDCS, the previously reduced functional network connectivity significantly increased. Our results showed that fronto-temporal tDCS could possibly remediate aberrant hallucination-related functional network interactions in patients with schizophrenia. © 2019 Korean Neuropsychiatric Association.

Author Keywords
Auditory hallucinations;  Neuroimaging;  Resting-state fMRI;  Schizophrenia and psychotic disorder;  Transcranial direct current stimulation

Document Type: Article
Publication Stage: Final
Source: Scopus
Access Type: Open Access

“Excitability and irritability in preschoolers predicts later psychopathology: The importance of positive and negative emotion dysregulation” (2019) Development and Psychopathology

Excitability and irritability in preschoolers predicts later psychopathology: The importance of positive and negative emotion dysregulation
(2019) Development and Psychopathology, . 

Vogel, A.C.a , Jackson, J.J.b , Barch, D.M.a b , Tillman, R.a , Luby, J.L.a

a Department of Psychiatry, Washington University, St. Louis School of Medicine, St. Louis, MO, United States
b Department of Psychological and Brain Sciences, Washington University in St. Louis, St. Louis, MO, United States

Abstract
Emotion dysregulation is a risk factor for the development of a variety of psychopathologic outcomes. In children, irritability, or dysregulated negative affect, has been the primary focus, as it predicts later negative outcomes even in very young children. However, dysregulation of positive emotion is increasingly recognized as a contributor to psychopathology. Here we used an exploratory factor analysis and defined four factors of emotion dysregulation: irritability, excitability, sadness, and anhedonia, in the preschool-age psychiatric assessment collected in a sample of 302 children ages 3-5 years enriched for early onset depression. The irritability and excitability factor scores defined in preschoolers predicted later diagnosis of mood and externalizing disorders when controlling for other factor scores, social adversity, maternal history of mood disorders, and externalizing diagnoses at baseline. The preschool excitability factor score predicted emotion lability in late childhood and early adolescence when controlling for other factor scores, social adversity, and maternal history. Both excitability and irritability factor scores in preschoolers predicted global functioning into the teen years and early adolescence, respectively. These findings underscore the importance of positive, as well as negative, affect dysregulation as early as the preschool years in predicting later psychopathology, which deserves both further study and clinical consideration. Copyright © Cambridge University Press 2019.

Author Keywords
depression;  emotion dysregulation;  exploratory factor analysis;  mood lability;  preschool

Document Type: Article
Publication Stage: Article in Press
Source: Scopus

“Chronic pain and chronic opioid use after intensive care discharge – Is it time to change practice?” (2019) Frontiers in Pharmacology

Chronic pain and chronic opioid use after intensive care discharge – Is it time to change practice?
(2019) Frontiers in Pharmacology, 10 (febuary), art. no. 23, . 

Stamenkovic, D.M.a b , Laycock, H.c , Karanikolas, M.d , Ladjevic, N.G.e f , Neskovic, V.a b , Bantel, C.g h

a Department of Anesthesiology and Intensive Care, Military Medical Academy, Belgrade, Serbia
b Medical Faculty, University of Defense, Belgrade, Serbia
c Imperial College London, Chelsea and Westminster Hospital, NHS Foundation Trust, London, United Kingdom
d Department of Anesthesiology, Washington University, School of Medicine, St. Louis, MO, United States
e Center for Anesthesia, Clinical Center of Serbia, Belgrade, Serbia
f School of Medicine, University of Belgrade, Belgrade, Serbia
g Universitätsklinik für Anästhesiologie, Intensivmedizin, Notfallmedizin, und Schmerztherapie, Universität Oldenburg, Klinikum Oldenburg, Oldenburg, Germany
h Imperial College London, Chelsea and Westminster Hospital, NHS Foundation Trust, London, United Kingdom

Abstract
Almost half of patients treated on intensive care unit (ICU) experience moderate to severe pain. Managing pain in the critically ill patient is challenging, as their pain is complex with multiple causes. Pharmacological treatment often focuses on opioids, and over a prolonged admission this can represent high cumulative doses which risk opioid dependence at discharge. Despite analgesia the incidence of chronic pain after treatment on ICU is high ranging from 33-73%. Measures need to be taken to prevent the transition from acute to chronic pain, whilst avoiding opioid overuse. This narrative review discusses preventive measures for the development of chronic pain in ICU patients. It considers a number of strategies that can be employed including non-opioid analgesics, regional analgesia, and non-pharmacological methods. We reason that individualized pain management plans should become the cornerstone for critically ill patients to facilitate physical and psychological well being after discharge from critical care and hospital. Copyright © 2019 Stamenkovic, Laycock, Karanikolas, Ladjevic, Neskovic and Bantel.

Author Keywords
Analgesics;  Chronic pain;  Critical care;  Opioids;  Pain

Document Type: Review
Publication Stage: Final
Source: Scopus
Access Type: Open Access

“Ciftify: A framework for surface-based analysis of legacy MR acquisitions” (2019) NeuroImage

Ciftify: A framework for surface-based analysis of legacy MR acquisitions
(2019) NeuroImage, . 

Dickie, E.W.a , Anticevic, A.b c d e , Smith, D.E.a , Coalson, T.S.f , Manogaran, M.a , Calarco, N.a , Viviano, J.D.a , Glasser, M.F.f g , Van Essen, D.C.f , Voineskos, A.N.a h

a Kimel Family Translational Imaging-Genetics Laboratory, Campbell Family Mental Health Research Institute, Centre of Addiction and Mental Health, Toronto, Canada
b Department of Psychiatry, Yale University School of Medicine, New Haven, CT, United States
c Division of Neurocognition, Neurocomputation, & Neurogenetics (N3), Yale University School of Medicine, New Haven, CT, United States
d Interdepartmental Neuroscience Program, Yale University, New Haven, CT, United States
e Department of Psychology, Yale University, New Haven, CT, United States
f Departments of Radiology and Neuroscience, Washington University School of Medicine, St Louis, United States
g St. Luke’s Hospital, Chesterfield, MO, United States
h Department of Psychiatry, University of Toronto, Toronto, Canada

Abstract
The preprocessing pipelines of the Human Connectome Project (HCP) were made publicly available for the neuroimaging community to apply the HCP analytic approach to data from non-HCP sources. The HCP analytic approach is surface-based for the cerebral cortex, uses the CIFTI “grayordinate” file format, provides greater statistical sensitivity than traditional volume-based analysis approaches, and allows for a more neuroanatomically-faithful representation of data. However, the HCP pipelines require the acquisition of specific images (namely T2w and field map) that historically have often not been acquired. Massive amounts of this ‘legacy’ data could benefit from the adoption of HCP-style methods. However, there is currently no published framework, to our knowledge, for adapting HCP preprocessing to “legacy” data. Here we present the ciftify project, a parsimonious analytic framework for adapting key modules from the HCP pipeline into existing structural workflows using FreeSurfer’s recon_all structural and existing functional preprocessing workflows. Within this framework, any functional dataset with an accompanying (i.e. T1w) anatomical data can be analyzed in CIFTI format. To simplify usage for new data, the workflow has been bundled with fMRIPrep following the BIDS-app framework. Finally, we present the package and comment on future neuroinformatics advances that may accelerate the movement to a CIFTI-based grayordinate framework. © 2019 Elsevier Inc.

Document Type: Article
Publication Stage: Article in Press
Source: Scopus

“Maximizing the Benefit of Life-Saving Treatments for Pompe Disease, Spinal Muscular Atrophy, and Duchenne Muscular Dystrophy Through Newborn Screening: Essential Steps” (2019) JAMA Neurology

Maximizing the Benefit of Life-Saving Treatments for Pompe Disease, Spinal Muscular Atrophy, and Duchenne Muscular Dystrophy Through Newborn Screening: Essential Steps
(2019) JAMA Neurology, . 

Baker, M.a , Griggs, R.b , Byrne, B.c , Connolly, A.M.d , Finkel, R.e , Grajkowska, L.f , Haidet-Phillips, A.f , Hagerty, L.f , Ostrander, R.g , Orlando, L.f , Swoboda, K.h , Watson, M.i , Howell, R.R.j

a University of Wisconsin, School of Medicine, Madison, United States
b University of Rochester, School of Medicine, Rochester, NY, United States
c University of Florida, Gainesville, United States
d Washington University, School of Medicine in St Louis, St Louis, MO, United States
e Nemours Children’s Hospital, Orlando, FL, United States
f Muscular Dystrophy Association, New York, NY, United States
g State University of New York, Upstate Medical University, Rushville, United States
h Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States
i American College of Medical Genetics and Genomics, Bethesda, MD, United States
j University of Miami Miller, School of Medicine, Miami, FL, United States

Abstract
Importance: Newborn screening (NBS) identifies infants with specific congenital disorders for which earlier intervention cannot only prevent a lifetime of chronic disability but also, most importantly, save lives. In this article, we discuss complexities associated with NBS processes in the United States, with a focus on challenges in neuromuscular disorders. Observations: As new interventions for neuromuscular disorders become available, the clinical community must prepare to overcome the challenges of adding new diseases to screening panels and understand the rigorous evidence review at the federal level and the complex process of state-level implementation. In this regard, NBS programs for Pompe disease and spinal muscular atrophy can guide the path of Duchenne muscular dystrophy and other neuromuscular disorders as future candidates for NBS. Conclusions and Relevance: The availability of advanced screening methods, the emergence of effective treatment, and the support of professional organizations may facilitate the expansion of NBS, such that an increasing number of infants can be identified in the newborn period who will benefit from life-saving interventions. © 2019 American Medical Association. All rights reserved.

Document Type: Article
Publication Stage: Article in Press
Source: Scopus

“The case for a medication first approach to the treatment of opioid use disorder” (2019) American Journal of Drug and Alcohol Abuse

The case for a medication first approach to the treatment of opioid use disorder
(2019) American Journal of Drug and Alcohol Abuse, . 

Winograd, R.P.a , Presnall, N.b , Stringfellow, E.a , Wood, C.a , Horn, P.a , Duello, A.a , Green, L.a , Rudder, T.c

a Missouri Institute of Mental Health, University of Missouri, St. Louis, United States
b Clayton Behavioral, Washington University, St. Louis, United States
c Missouri Department of Mental Health, Jefferson, MO, United States

Abstract
Background: The opioid addiction and overdose crisis continues to ravage communities across the U.S. Maintenance pharmacotherapy using buprenorphine or methadone is the most effective intervention for Opioid Use Disorder (OUD), yet few have immediate and sustained access to these medications. Objectives: To address lack of medication access for people with OUD, the Missouri Department of Mental Health began implementing a Medication First (Med First) treatment approach in its publicly-funded system of comprehensive substance use disorder treatment programs. Methods: This Perspective describes the four principles of Med First, which are based on evidence-based guidelines. It draws conceptual comparisons between the Housing First approach to chronic homelessness and the Med First approach to pharmacotherapy for OUD, and compares state certification standards for substance use disorder (SUD) treatment (the traditional approach) to Med First guidelines for OUD treatment. Finally, the Perspective details how Med First principles have been practically implemented. Results: Med First principles emphasize timely access to maintenance pharmacotherapy without requiring psychosocial services or discontinuation for any reason other than harm to the client. Early results regarding medication utilization and treatment retention are promising. Feedback from providers has been largely favorable, though clinical- and system-level obstacles to effective OUD treatment remain. Conclusion: Like the Housing First model, Medication First is designed to decrease human suffering and activate the strengths and capacities of people in need. It draws on decades of research and facilitates partnerships between psychosocial and medical treatment providers to offer effective and life-saving care to persons with OUD. © 2019, © 2019 Taylor & Francis Group, LLC.

Author Keywords
buprenorphine;  housing first;  low-barrier;  medication first;  Opioid use disorder;  treatment approach

Document Type: Article
Publication Stage: Article in Press
Source: Scopus

“CXCL13/CXCR5 signaling contributes to diabetes-induced tactile allodynia via activating pERK, pSTAT3, pAKT pathways and pro-inflammatory cytokines production in the spinal cord of male mice” (2019) Brain, Behavior, and Immunity

CXCL13/CXCR5 signaling contributes to diabetes-induced tactile allodynia via activating pERK, pSTAT3, pAKT pathways and pro-inflammatory cytokines production in the spinal cord of male mice
(2019) Brain, Behavior, and Immunity, . 

Liu, S.a , Liu, X.c , Xiong, H.a , Wang, W.a , Liu, Y.b , Yin, L.a , Tu, C.a , Wang, H.b , Xiang, X.a , Xu, J.a , Duan, B.a , Tao, A.c , Zhao, Z.d e , Mei, Z.a

a School of Pharmaceutical Sciences, South-Central University for Nationalities, Wuhan, China
b College of Life Science, South-Central University for Nationalities, Wuhan, China
c The Second Afliated Hospital, The State Key Laboratory of Respiratory Disease, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, Guangzhou Medical University, Guangzhou, 510260, China
d Center for the Study of Itch, Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO, United States
e Barnes-Jewish Hospital, St. Louis, MO, United States

Abstract
Painful diabetic neuropathy (PDN) is a severely debilitating chronic pain syndrome. Spinal chemokine CXCL13 and its receptor CXCR5 were recently demonstrated to play a pivotal role in the pathogenesis of chronic pain induced by peripheral tissue inflammation or nerve injury. In this study we investigated whether CXCL13/CXCR5 mediates PDN and the underlying spinal mechanisms. We used the db/db type 2 diabetes mice, which showed obvious hyperglycemia and obese, long-term mechanical allodynia, and increased expression of CXCL13, CXCR5 as well as pro-inflammatory cytokines TNF-α and IL-6 in the spinal cord. Furthermore, in the spinal cord of db/db mice there is significantly increased gliosis and upregulated phosphorylation of cell signaling kinases, including pERK, pAKT and pSTAT3. Mechanical allodynia and upregulated pERK, pAKT and pSTAT3 as well as production of TNF-α and IL-6 were all attenuated by the noncompetitive NMDA receptor antagonist MK-801. If spinal giving U0126 (a selective MEK inhibitor) or AG490 (a Janus kinase (JAK)-STAT inhibitor) to db/db mice, both of them can decrease the mechanical allodynia, but only inhibit pERK (by U0126) or pSTAT3 (by AG490) respectively. Acute administration of CXCL13 in C57BL/6J mice resulted in exacerbated thermal hyperalgesia and mechanical allodynia, activation of the pERK, pAKT and pSTAT3 pathways and increased production of pro-inflammatory cytokines (IL-1β, TNF-α and IL-6), which were all attenuated by knocking out of Cxcr5. In all, our work showed that chemokine CXCL13 and its receptor CXCR5 in spinal cord contribute to the pathogenesis of PDN and may help develop potential novel therapeutic approaches for patients afflicted with PDN. © 2019 Elsevier Inc.

Author Keywords
CXCL13;  CXCR5;  Diabetic neuropathy;  Neuroinflammation;  Pain behavior;  Spinal cord

Document Type: Article
Publication Stage: Article in Press
Source: Scopus

“Niemann-Pick Type C Disease Reveals a Link between Lysosomal Cholesterol and PtdIns(4,5)P 2 That Regulates Neuronal Excitability” (2019) Cell Reports

Niemann-Pick Type C Disease Reveals a Link between Lysosomal Cholesterol and PtdIns(4,5)P 2 That Regulates Neuronal Excitability
(2019) Cell Reports, 27 (9), pp. 2636-2648.e4. 

Vivas, O.a , Tiscione, S.A.a , Dixon, R.E.a , Ory, D.S.b , Dickson, E.J.a

a Department of Physiology and Membrane Biology, University of California, Davis, Davis, CA 95616, United States
b Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, United States

Abstract
There is increasing evidence that the lysosome is involved in the pathogenesis of a variety of neurodegenerative disorders. Thus, mechanisms that link lysosome dysfunction to the disruption of neuronal homeostasis offer opportunities to understand the molecular underpinnings of neurodegeneration and potentially identify specific therapeutic targets. Here, using a monogenic neurodegenerative disorder, NPC1 disease, we demonstrate that reduced cholesterol efflux from lysosomes aberrantly modifies neuronal firing patterns. The molecular mechanism linking alterations in lysosomal cholesterol egress to intrinsic tuning of neuronal excitability is a transcriptionally mediated upregulation of the ABCA1 transporter, whose PtdIns(4,5)P 2 -floppase activity decreases plasma membrane PtdIns(4,5)P 2 . The consequence of reduced PtdIns(4,5)P 2 is a parallel decrease in a key regulator of neuronal excitability, the voltage-gated KCNQ2/3 potassium channel, which leads to hyperexcitability in NPC1 disease neurons. Thus, cholesterol efflux from lysosomes regulates PtdIns(4,5)P 2 to shape the electrical and functional identity of the plasma membrane of neurons in health and disease. © 2019 The Author(s)

NPC1 disease is a neurodegenerative disorder that occurs due to mutations in the lysosomal NPC1 cholesterol transporter. Vivas et al. define steps in the pathogenic cascade, downstream of lysosomal cholesterol accumulation, that lead to hyperexcitability in NPC1 disease neurons. © 2019 The Author(s)

Author Keywords
ABCA1;  cholesterol;  excitability;  KCNQ2/3 channels;  neurodegeneration;  NPC1;  NPC1 disease;  phosphoinositides;  PtdIns(4,5)P 2

Document Type: Article
Publication Stage: Final
Source: Scopus

“Publisher Correction: Gene expression imputation across multiple brain regions provides insights into schizophrenia risk (Nature Genetics, (2019), 51, 4, (659-674), 10.1038/s41588-019-0364-4)” (2019) Nature Genetics

Publisher Correction: Gene expression imputation across multiple brain regions provides insights into schizophrenia risk (Nature Genetics, (2019), 51, 4, (659-674), 10.1038/s41588-019-0364-4)
(2019) Nature Genetics, . 

Huckins, L.M.a b c d , Dobbyn, A.a b , Ruderfer, D.M.e , Hoffman, G.a d , Wang, W.a b , Pardiñas, A.F.f , Rajagopal, V.M.g h i , Als, T.D.g h i , T. Nguyen, H.a b , Girdhar, K.a b , Boocock, J.j , Roussos, P.a b c d , Fromer, M.a b , Kramer, R.k , Domenici, E.l , Gamazon, E.R.e m , Purcell, S.a b d , Johnson, J.S.a , Shah, H.R.b d , Klein, L.L.p , Dang, K.K.q , Logsdon, B.A.q , Mahajan, M.C.b d , Mangravite, L.M.q , Toyoshiba, H.s , Gur, R.E.t , Hahn, C.-G.u , Schadt, E.b d , Lewis, D.A.p , Haroutunian, V.a q v w , Peters, M.A.q , Lipska, B.K.k , Buxbaum, J.D.x y , Hirai, K.z , Perumal, T.M.q , Essioux, L.aa , Ripke, S.aj ak , Neale, B.M.aj ak al am , Corvin, A.an , Walters, J.T.R.f , Farh, K.-H.aj , Holmans, P.A.f ao , Lee, P.aj ak am , Bulik-Sullivan, B.aj ak , Collier, D.A.ap aq , Huang, H.aj al , Pers, T.H.al ar as , Agartz, I.at au av , Agerbo, E.h ae af , Albus, M.aw , Alexander, M.ax , Amin, F.ay az , Bacanu, S.A.ba , Begemann, M.bb , Belliveau, R.A., Jrak , Bene, J.bc bd , Bergen, S.E.ak be , Bevilacqua, E.ak , Bigdeli, T.B.ba , Black, D.W.bf , Bruggeman, R.bg , Buccola, N.G.bh , Buckner, R.L.bi bj bk , Byerley, W.bl , 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Hammer, C.bb , Hamshere, M.L.f , Hansen, M.di , Hansen, T.h ac , Haroutunian, V.c v x , Hartmann, A.M.db , Henskens, F.A.bo dj dk , Herms, S.cd ce dl , Hirschhorn, J.N.al as dm , Hoffmann, P.cd ce dl , Hofman, A.cd ce , Hollegaard, M.V.ai , Hougaard, D.M.ai , Ikeda, M.dn , Joa, I.do , Julia, A.dp , Kahn, R.S.bm , Kalaydjieva, L.dq dr , Karachanak-Yankova, S.ds , Karjalainen, J.cy , Kavanagh, D.f , Keller, M.C.dt , Kennedy, J.L.du dv dw , Khrunin, A.dx , Kim, Y.bz , Klovins, J.dy , Knowles, J.A.dz , Konte, B.db , Kucinskas, V.ea , Kucinskiene, Z.A.ea , Kuzelova-Ptackova, H.eb , Kahler, A.K.be , Laurent, C.ax ec , Keong, J.L.C.bv ed , Lee, S.H.dg , Legge, S.E.f , Lerer, B.ee , Li, M.bs bt ef , Li, T.eg , Liang, K.-Y.eh , Lieberman, J.ei , Limborska, S.dx , Loughland, C.M.bo ej , Lubinski, J.ek , Lonnqvist, J.el , Macek, M., Jreb , Magnusson, P.K.E.be , Maher, B.S.em , Maier, W.en , Mallet, J.eo , Marsal, S.dp , Mattheisen, M.g h i ep , Mattingsdal, M.av eq , McCarley, R.W.er es , McDonald, C.et , McIntosh, A.M.eu ev , Meier, S.cx , Meijer, C.J.dh , Melegh, B.bc bd , Melle, I.av ew , Mesholam-Gately, R.I.er ex , Metspalu, A.ey , Michie, P.T.bo ez , Milani, L.ey , Milanova, V.fa , Mokrab, Y.ap , Morris, D.W.an cj , Mors, O.h i fb , Murphy, K.C.fc , Murray, R.M.fd , Myin-Germeys, I.fe , Muller-Myhsok, B.ff fg fh , Nelis, M.ey , Nenadic, I.fi , Nertney, D.A.fj , Nestadt, G.fk , Nicodemus, K.K.fl , Nikitina-Zake, L.dy , Nisenbaum, L.fm , Nordin, A.fn , O’Callaghan, E.fo , O’Dushlaine, C.ak , O’Neill, F.A.fp , Oh, S.-Y.fq , Olincy, A.du , Olsen, L.h bk , Van Os, J.fe fr , Pantelis, C.bo fs , Papadimitriou, G.N.cg , Papiol, S.bb , Parkhomenko, E.c , Pato, M.T.dz , Paunio, T.ft fu , Pejovic-Milovancevic, M.fv , Perkins, D.O.fw , Pietiläinen, O.fu fx , Pimm, J.cb , Pocklington, A.J.f , Powell, J.fd , Price, A.al fy , Pulver, A.E.fk , Purcell, S.M.a , Quested, D.fz , Rasmussen, H.B.ac ap , Reichenberg, A.c , Reimers, M.A.ga , Richards, A.L.f , Roffman, J.L.bi bk , Roussos, P.a d , Ruderfer, D.M.a e f , Salomaa, V.cr , Sanders, A.R.ck cl , Schall, U.bo ej , Schubert, C.R.gb , Schulze, T.G.cx gc , Schwab, S.G.gd , Scolnick, E.M.ak , Scott, R.J.bo ge gf , Seidman, L.J.em ex , Shi, J.gg , Sigurdsson, E.gh , Silagadze, T.gi , Silverman, J.M.c gj , Sim, K.bv , Slominsky, P.dx , Smoller, J.W.ak am , So, H.-C.bs , Spencer, C.C.A.gk , Stahl, E.A.a b c d , Stefansson, H.gl , Steinberg, S.gl , Stogmann, E.gm , Straub, R.E.gn , Strengman, E.bm go , Strohmaier, J.cx , Stroup, T.S.ei , Subramaniam, M.bv , Suvisaari, J.el , Svrakic, D.M.bw , Szatkiewicz, J.P.bz , Soderman, E.at , Thirumalai, S.gp , Toncheva, D.ds , Tosato, S.gq , Veijola, J.gr gs , Waddington, J.gt , Walsh, D.gu , Wang, D.df , Wang, Q.eg , Webb, B.T.ba , Weiser, M.cc , Wildenauer, D.B.gv , Williams, N.M.f , Williams, S.bz , Witt, S.H.cx , Wolen, A.R.ga , Wong, E.H.M.bs , Wormley, B.K.ba , Xi, H.S.gw , Zai, C.C.du dv , Zheng, X.gx , Zimprich, F.gm , Wray, N.R.dg , Stefansson, K.gl , Visscher, P.M.dg , Adolfsson, R.fn , Andreassen, O.A.av ew , Blackwood, D.H.R.ev , Bramon, E.gy , Buxbaum, J.D.b c w x , Børglum, A.D.g h i fb , Cichon, S.cd ce dl gz , Darvasi, A.ha , Domenici, E.hb , Ehrenreich, H.bb , Esko, T.al as dm ey , Gejman, P.V.ck cl , Gill, M.an , Gurling, H.cb , Hultman, C.M.be , Iwata, N.dn , Jablensky, A.V.bo dr gv hc , Jonsson, E.G.at av , Kendler, K.S.hd , Kirov, G.f , Knight, J.dt dv dw , Lencz, T.he hf hg , Levinson, D.F.ax , Li, Q.S.df , Liu, J.gx hh , Malhotra, A.K.he hf hg , McCarroll, S.A.ak dm , McQuillin, A.cb , Moran, J.L.ak , Mortensen, P.B.h ae af , Mowry, B.J.dg hi , Nothen, M.M.cd ce , Ophoff, R.A.j bm cz , Owen, M.J.f ao , Palotie, A.ak am fx , Pato, C.N.dz , Petryshen, T.L.ak er hj , Posthuma, D.hk hl hm , Rietschel, M.cx , Riley, B.P.hd , Rujescu, D.db dc , Sham, P.C.bs bt ef , Sklar, P.a b c d x , Clair, D.S.hn , Weinberger, D.R.gn ho , Wendland, J.R.gb , Werge, T.h ac hp , Daly, M.J.aj ak al , Sullivan, P.F.be bz fw , O’Donovan, M.C.f ao , Børglum, A.D.g h i , Demontis, D.g h i , Rajagopal, V.M.g h i , Als, T.D.g h i , Mattheisen, M.g h i , Grove, J.g h i ab , Werge, T.h ac ad , Mortensen, P.B.g h ae af , Pedersen, C.B.h ae af , Agerbo, E.h ae af , Pedersen, M.G.h ae af , Mors, O.h ag , Nordentoft, M.h ah , Hougaard, D.M.h ai , Bybjerg-Grauholm, J.h ai , Bækvad-Hansen, M.h ai , Hansen, C.S.h ai , Demontis, D.g h i , Børglum, A.D.g h i , Walters, J.T.R.f , O’Donovan, M.C.f , Sullivan, P.n o , Owen, M.J.f , Devlin, B.p , Sieberts, S.K.q , Cox, N.J.e , Im, H.K.r , Sklar, P.a b c d , Stahl, E.A.a b c d , CommonMind Consortiumhq , The Schizophrenia Working Group of the Psychiatric Genomics Consortiumhq , iPSYCH-GEMS Schizophrenia Working Grouphq

a Pamela Sklar Division of Psychiatric Genomics, Icahn School of Medicine at Mount Sinai, New York, NY, United States
b Department of Genetics and Genomics, Icahn School of Medicine at Mount Sinai, New York, NY, United States
c Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, United States
d Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, United States
e Vanderbilt University Medical Center, Nashville, TN, United States
f MRC Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, United Kingdom
g Department of Biomedicine, Aarhus University, Aarhus, Denmark
h The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, Denmark
i Center for Integrative Sequencing, Aarhus University, Aarhus, Denmark
j Department of Human Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, United States
k Human Brain Collection Core, National Institute of Mental Health, Bethesda, MD, United States
l Laboratory of Neurogenomic Biomarkers, Centre for Integrative Biology (CIBIO), University of Trento, Trento, Italy
m Clare Hall, University of Cambridge, Cambridge, United Kingdom
n University of North Carolina at Chapel Hill, Chapel Hill, NC, United States
o Karolinska Institutet, Stockholm, Sweden
p Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, United States
q Systems Biology, Sage Bionetworks, Seattle, WA, United States
r Section of Genetic Medicine, Department of Medicine, University of Chicago, Chicago, IL, United States
s Integrated Technology Research Laboratories, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Japan
t Neuropsychiatry Section, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States
u Neuropsychiatric Signaling Program, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States
v Psychiatry, JJ Peters Virginia Medical Center, Bronx, NY, United States
w Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, New York, NY, United States
x Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States
y Seaver Autism Center for Research and Treatment, Icahn School of Medicine at Mount Sinai, New York, NY, United States
z CNS Drug Discovery Unit, Pharmaceutical Research Division, Takeda Pharmaceutical Company Limited, Fujisawa, Japan
aa F. Hoffman-La Roche Ltd, Basel, Switzerland
ab Bioinformatics Research Centre, Aarhus University, Aarhus, Denmark
ac Institute of Biological Psychiatry, MHC Sct. Hans, Mental Health Services Copenhagen, Roskilde, Denmark
ad Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark
ae National Centre for Register-Based Research, Aarhus University, Aarhus, Denmark
af Centre for Integrated Register-based Research, Aarhus University, Aarhus, Denmark
ag Psychosis Research Unit, Aarhus University Hospital, Risskov, Denmark
ah Mental Health Services in the Capital Region of Denmark, Mental Health Center Copenhagen, University of Copenhagen, Copenhagen, Denmark
ai Center for Neonatal Screening, Department for Congenital Disorders, Statens Serum Institut, Copenhagen, Denmark
aj Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, United States
ak Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA, United States
al Medical and Population Genetics Program, Broad Institute of MIT and Harvard, Cambridge, MA, United States
am Psychiatric and Neurodevelopmental Genetics Unit, Massachusetts General Hospital, Boston, MA, United States
an Neuropsychiatric Genetics Research Group, Department of Psychiatry, Trinity College Dublin, Dublin, Ireland
ao NationalCentre for Mental Health, Cardiff University, Cardiff, United Kingdom
ap Eli Lilly and Company Limited, Erl Wood Manor, Sunninghill Road, Windlesham, Surrey, United Kingdom
aq Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King’s College London, London, United Kingdom
ar Center for BiologicalSequence Analysis, Department of Systems Biology, Technical University of Denmark, Kongens Lyngby, Denmark
as Division of Endocrinology and Center for Basic and Translational Obesity Research, Boston Children’s Hospital, Boston, MA, United States
at Department of Clinical Neuroscience, Psychiatry Section, Karolinska Institutet, Stockholm, Sweden
au Department of Psychiatry, Diakonhjemmet Hospital, Oslo, Norway
av NORMENT, KG Jebsen Centre for Psychosis Research, Institute of Clinical Medicine, University of Oslo, Oslo, Norway
aw State Mental Hospital, Haar, Germany
ax Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA, United States
ay Department of Psychiatry and Behavioral Sciences, Atlanta Veterans Affairs Medical Center, Atlanta, GA, United States
az Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA, United States
ba Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, United States
bb Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Gottingen, Germany
bc Department of Medical Genetics, University of Pécs, Pécs, Hungary
bd Szentagothai Research Center, University of Pécs, Pécs, Hungary
be Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
bf Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA, United States
bg University Medical Center Groningen, Department of Psychiatry, University of Groningen, Groningen, Netherlands
bh School of Nursing, Louisiana State University Health Sciences Center, New Orleans, LA, United States
bi Athinoula A. Martinos Center, Massachusetts General Hospital, Boston, MA, United States
bj Center for Brain Science, Harvard University, Cambridge, MA, United States
bk Department of Psychiatry, Massachusetts General Hospital, Boston, MA, United States
bl Department of Psychiatry, University of California at San Francisco, San Francisco, CA, United States
bm University Medical Center Utrecht, Department of Psychiatry, Rudolf Magnus Institute of Neuroscience, Utrecht, Netherlands
bn Centre Hospitalier du Rouvray and INSERM U1079 Faculty of Medicine, Rouen, France
bo Schizophrenia Research Institute, Sydney, NSW, Australia
bp School of Psychiatry, University of New South Wales, Sydney, NSW, Australia
bq Royal Brisbane and Women’s Hospital, University of Queensland, Brisbane, QLD, Australia
br Institute of Psychology, Chinese Academy of Science, Beijing, China
bs Department of Psychiatry, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
bt State Key Laboratory for Brain and Cognitive Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
bu Castle Peak Hospital, Hong Kong, China
bv Institute of Mental Health, Singapore, Singapore
bw Department of Psychiatry, Washington University, St. Louis, MO, United States
bx Department of Child and Adolescent Psychiatry, Assistance Publique Hopitaux de Paris, Pierre and Marie Curie Faculty of Medicine and Institute for Intelligent Systems and Robotics, Paris, France
by Blue Note Biosciences, Princeton, NJ, United States
bz Department of Genetics, University of North Carolina, Chapel Hill, NC, United States
ca Department of Psychological Medicine, Queen Mary University of London, London, United Kingdom
cb Molecular Psychiatry Laboratory, Division of Psychiatry, University College London, London, United Kingdom
cc Sheba Medical Center, Tel Hashomer, Israel
cd Department of Genomics, Life and Brain Center, Bonn, Germany
ce Institute of Human Genetics, University of Bonn, Bonn, Germany
cf AppliedMolecular Genomics Unit, VIB Department of Molecular Genetics, University of Antwerp, Antwerp, Belgium
cg First Department of Psychiatry, University of Athens Medical School, Athens, Greece
ch Department of Psychiatry, University College Cork, Co, Cork, Ireland
ci Department of Medical Genetics, Oslo University Hospital, Oslo, Norway
cj Cognitive Genetics and Therapy Group, School of Psychology and Discipline of Biochemistry, National University of Ireland Galway, Co, Galway, Ireland
ck Department of Psychiatry and Behavioral Neuroscience, University of Chicago, Chicago, IL, United States
cl Department of Psychiatry and Behavioral Sciences, North Shore University Health System, Evanston, IL, United States
cm Department of Non-Communicable Disease Epidemiology, London School of Hygiene and Tropical Medicine, London, United Kingdom
cn Department of Child and Adolescent Psychiatry, University Clinic of Psychiatry, Skopje, Macedonia
co Department of Psychiatry, University of Regensburg, Regensburg, Germany
cp Department of General Practice, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland
cq Folkhälsan Research Center, Helsinki, Finland, Biomedicum Helsinki, Helsinki, Finland
cr National Institute for Health and Welfare, Helsinki, Finland
cs Translational Technologies and Bioinformatics, Pharma Research and Early Development, F. Hoffman-La Roche, Basel, Switzerland
ct Department of Psychiatry, Georgetown University School of Medicine, Washington, DC, United States
cu Department of Psychiatry, Keck School of Medicine of the University of Southern California, Los Angeles, CA, United States
cv Department of Psychiatry, Virginia Commonwealth University School of Medicine, Richmond, VA, United States
cw Mental Health Service Line, Washington VA Medical Center, Washington, DC, United States
cx Department of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, Heidelberg, Mannheim, Germany
cy Department of Genetics, University of Groningen, University Medical Centre Groningen, Groningen, Netherlands
cz Department of Psychiatry, University of Colorado Denver, Aurora, CO, United States
da Center for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, Los Angeles, CA, United States
db Department of Psychiatry, University of Halle, Halle, Germany
dc Department of Psychiatry, University of Munich, Munich, Germany
dd Departments of Psychiatry and Human and Molecular Genetics, INSERM, Institut de Myologie, Hôpital de la Pitiè-Salpêtrière, Paris, France
de Mental Health Research Centre, Russian Academy of Medical Sciences, Moscow, Russian Federation
df Neuroscience Therapeutic Area, Janssen Research and Development, Raritan, NJ, United States
dg Queensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia
dh Academic Medical Centre University of Amsterdam, Department of Psychiatry, Amsterdam, Netherlands
di Illumina, La Jolla, CA, United States
dj Priority Research Centre for Health Behaviour, University of Newcastle, Newcastle, NSW, Australia
dk School of Electrical Engineering and Computer Science, University of Newcastle, Newcastle, NSW, Australia
dl Division of Medical Genetics, Department of Biomedicine, University of Basel, Basel, Switzerland
dm Department of Genetics, Harvard Medical School, Boston, MA, United States
dn Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Japan
do Regional Centre for Clinical Researchin Psychosis, Department of Psychiatry, Stavanger University Hospital, Stavanger, Norway
dp Rheumatology Research Group, Vall d’Hebron Research Institute, Barcelona, Spain
dq Centre for Medical Research, The University of Western Australia, Perth, WA, Australia
dr The Perkins Institute for Medical Research, The University of Western Australia, Perth, WA, Australia
ds Department of Medical Genetics, Medical University, Sofia, Bulgaria
dt Department of Psychology, University of Colorado Boulder, Boulder, CO, United States
du Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada
dv Department of Psychiatry, University of Toronto, Toronto, ON, Canada
dw Institute of Medical Science, University of Toronto, Toronto, ON, Canada
dx Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, Russian Federation
dy Latvian Biomedical Research and Study Centre, Riga, Latvia
dz Department of Psychiatry and Zilkha Neurogenetics Institute, Keck School of Medicine at University of Southern California, Los Angeles, CA, United States
ea Faculty of Medicine, Vilnius University, Vilnius, Lithuania
eb Department of Biology and Medical Genetics, 2nd Faculty of Medicine and University Hospital Motol, Prague, Czech Republic
ec Department of Child and Adolescent Psychiatry, Pierre and Marie Curie Faculty of Medicine, Paris, France
ed Duke-NUS Graduate Medical School, Singapore, Singapore
ee Department of Psychiatry, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
ef Centre for Genomic Sciences, The University of Hong Kong, Hong Kong, China
eg Mental Health Centre and Psychiatric Laboratory, West China Hospital, Sichuan University, Chengdu, Sichuan, China
eh Department of Biostatistics, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, United States
ei Department of Psychiatry, Columbia University, New York, New York, NY, United States
ej Priority Centre for Translational Neuroscience and Mental Health, University of Newcastle, Newcastle, NSW, Australia
ek Department of Genetics and Pathology, International Hereditary Cancer Center, Pomeranian Medical University in Szczecin, Szczecin, Poland
el Department of Mental Health and Substance Abuse Services, National Institute for Health and Welfare, Helsinki, Finland
em Department of Mental Health, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, United States
en Department of Psychiatry, University of Bonn, Bonn, Germany
eo Centre National de la Recherche Scientifique, Laboratoire de Génétique Moléculaire de la Neurotransmission et des Processus Neurodénégératifs, Hôpital de la Pitiè-Salpêtrière, Paris, France
ep Department of Genomics Mathematics, University of Bonn, Bonn, Germany
eq Research Unit, Sørlandet Hospital, Kristiansand, Norway
er Department of Psychiatry, Harvard Medical School, Boston, MA, United States
es VA Boston Health Care System, Brockton, MA, United States
et Department of Psychiatry, National University of Ireland Galway, Co, Galway, Ireland
eu Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, United Kingdom
ev Division of Psychiatry, University of Edinburgh, Edinburgh, United Kingdom
ew Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway
ex Massachusetts Mental Health Center Public Psychiatry Division of the Beth Israel Deaconess Medical Center, Boston, MA, United States
ey Estonian Genome Center, University of Tartu, Tartu, Estonia
ez School of Psychology, University of Newcastle, Newcastle, NSW, Australia
fa First Psychiatric Clinic, Medical University, Sofia, Bulgaria
fb Department P, Aarhus University Hospital, Risskov, Denmark
fc Department of Psychiatry, Royal College of Surgeons in Ireland, Dublin, Ireland
fd King’s College London, London, United Kingdom
fe Maastricht University Medical Centre, South Limburg Mental Health Research and TeachingNetwork, EURON, Maastricht, Netherlands
ff Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom
fg Max Planck Institute of Psychiatry, Munich, Germany
fh Munich Cluster for Systems Neurology (SyNergy), Munich, Germany
fi Department of Psychiatry and Psychotherapy, Jena University Hospital, Jena, Germany
fj Department of Psychiatry, Queensland Brain Institute and Queensland Centre for Mental Health Research, University of Queensland, Brisbane, QLD, Australia
fk Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, United States
fl Department of Psychiatry, Trinity College Dublin, Dublin, Ireland
fm Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN, United States
fn Department of Clinical Sciences, Psychiatry, Umeå University, Umeå, Sweden
fo DETECT Early Intervention Service for Psychosis, Blackrock, Co, Dublin, Ireland
fp Centre for Public Health, Institute of Clinical Sciences, Queen’s University Belfast, Belfast, United Kingdom
fq Lawrence Berkeley National Laboratory, University of California at Berkeley, Berkeley, CA, United States
fr Institute of Psychiatry, King’s College London, London, United Kingdom
fs Melbourne Neuropsychiatry Centre, University of Melbourne & Melbourne Health, Melbourne, VIC, Australia
ft Department of Psychiatry, University of Helsinki, Helsinki, Finland
fu Public Health Genomics Unit, National Institute for Health and Welfare, Helsinki, Finland
fv Medical Faculty, University of Belgrade, Belgrade, Serbia
fw Department of Psychiatry, University of North Carolina, Chapel Hill, NC, United States
fx Institute for Molecular Medicine Finland, FIMM, University of Helsinki, Helsinki, Finland
fy Department of Epidemiology, Harvard School of Public Health, Boston, MA, United States
fz Department of Psychiatry, University of Oxford, Oxford, United Kingdom
ga Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, United States
gb Pharma Therapeutics Clinical Research, Pfizer Worldwide Research and Development, Cambridge, MA, United States
gc Department of Psychiatry and Psychotherapy, University of Gottingen, Göttingen, Germany
gd Psychiatry and Psychotherapy Clinic, University of Erlangen, Erlangen, Germany
ge Hunter New England Health Service, Newcastle, NSW, Australia
gf School of Biomedical Sciences, University of Newcastle, Newcastle, NSW, Australia
gg Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, United States
gh University of Iceland, Landspitali, National University Hospital, Reykjavik, Iceland
gi Department of Psychiatry and Drug Addiction, Tbilisi State Medical University (TSMU), Tbilisi, Georgia
gj Research and Development, Bronx Veterans Affairs Medical Center, New York, NY, United States
gk WellcomeTrust Centre for Human Genetics, Oxford, United Kingdom
gl deCODE Genetics, Reykjavik, Iceland
gm Department of Clinical Neurology, Medical University of Vienna, Wien, Austria
gn Lieber Institute for Brain Development, Baltimore, MD, United States
go Department of Medical Genetics, University Medical Centre Utrecht, Utrecht, Netherlands
gp Berkshire Healthcare NHS Foundation Trust, Bracknell, United Kingdom
gq Section of Psychiatry, University of Verona, Verona, Italy
gr Department of Psychiatry, University of Oulu, Oulu, Finland
gs University Hospital of Oulu, Oulu, Finland
gt Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland
gu Health Research Board, Dublin, Ireland
gv School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Perth, WA, Australia
gw Computational Sciences CoE, Pfizer Worldwide Research and Development, Cambridge, MA, United States
gx Human Genetics, Genome Institute of Singapore, A*STAR, Singapore, Singapore
gy University College London, London, United Kingdom
gz Institute of Neuroscience and Medicine (INM-1), Research Center Juelich, Juelich, Germany
ha Department of Genetics, The Hebrew University of Jerusalem, Jerusalem, Israel
hb NeuroscienceDiscovery and Translational Area, Pharma Research and Early Development, F. Hoffman-La Roche, Basel, Switzerland
hc Centre for Clinical Research in Neuropsychiatry, School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Medical Research Foundation Building, Perth, WA, Australia
hd Virginia Institute for Psychiatric and Behavioral Genetics, Departments of Psychiatry and Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA, United States
he The Feinstein Institute for Medical Research, Manhasset, NY, United States
hf The Hofstra NS-LIJ School of Medicine, Hempstead, NY, United States
hg The Zucker Hillside Hospital, Glen Oaks, NY, United States
hh Saw Swee Hock School of Public Health, National University of Singapore, Singapore, Singapore
hi Queensland Centre for Mental Health Research, University of Queensland, Brisbane, QLD, Australia
hj Center for HumanGenetic Research and Department of Psychiatry, Massachusetts General Hospital, Boston, MA, United States
hk Department of Child and Adolescent Psychiatry, Erasmus University Medical Centre, Rotterdam, Netherlands
hl Department of Complex Trait Genetics, Neuroscience Campus Amsterdam, VU University Medical Center Amsterdam, Amsterdam, Netherlands
hm Department of Functional Genomics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU University, Amsterdam, Netherlands
hn University of Aberdeen, Institute of Medical Sciences, Aberdeen, United Kingdom
ho Departments of Psychiatry, Neurology, Neuroscience and Institute of Genetic Medicine, Johns Hopkins School of Medicine, Baltimore, MD, United States
hp Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark

Abstract
In the HTML version of the article originally published, the author group ‘The Schizophrenia Working Group of the Psychiatric Genomics Consortium’ was displayed incorrectly. The error has been corrected in the HTML version of the article. © 2019, The Author(s), under exclusive licence to Springer Nature America, Inc.

Document Type: Erratum
Publication Stage: Article in Press
Source: Scopus
Access Type: Open Access

“Adding the keyword mnemonic to retrieval practice: A potent combination for foreign language vocabulary learning?” (2019) Memory and Cognition

Adding the keyword mnemonic to retrieval practice: A potent combination for foreign language vocabulary learning?
(2019) Memory and Cognition, . 

Miyatsu, T., McDaniel, M.A.

Department of Psychological and Brain Sciences, Washington University, 1 Brookings Dr., Campus Box 1125, St Louis, MO 63130, United States

Abstract
The keyword mnemonic and retrieval practice are two cognitive techniques that have each been identified to enhance foreign language vocabulary learning. However, little is known about the use of these techniques in combination. Previous demonstrations of retrieval-practice effects in foreign language vocabulary learning have tended to use several rounds of retrieval practice. In contrast, we focused on a situation in which retrieval practice was limited to twice per item. For this situation, it is unclear whether retrieval practice will be effective relative to restudying. We advance the view that the keyword mnemonic catalyzes the effectiveness of retrieval practice in this learning context. Experiment 1 (48-h delay) partially supported this view, such that there was no testing effect with retrieval practice alone, but the keyword-retrieval combination did not promote better retention than keyword alone. Experiments 2 and 3 (1-week delay) supported the catalytic view by showing that the keyword-retrieval combination was better than keyword alone, but in the absence of keyword encoding there was no retrieval practice effect (replicating Experiment 1). However, with four rounds of retrieval practice, a marginally significant testing effect emerged (Experiment 3). Moreover, the routes through which participants reached each answer were identified by asking retrieval-route questions in Experiments 2 and 3. Keyword-mediated retrieval, which was observed sometimes even in no-keyword instructed conditions, was shown to be more effective than unmediated retrieval. Our findings suggest that incorporating effective encoding techniques prior to retrieval practice could augment the effectiveness of retrieval practice, at least for vocabulary learning. © 2019, The Psychonomic Society, Inc.

Author Keywords
Foreign language vocabulary learning;  Retrieval practice;  Testing effect;  The keyword mnemonic

Document Type: Article
Publication Stage: Article in Press
Source: Scopus

“Functions of Non-Suicidal Self-Injury in Late Adolescence: A Latent Class Analysis” (2019) Archives of Suicide Research

Functions of Non-Suicidal Self-Injury in Late Adolescence: A Latent Class Analysis
(2019) Archives of Suicide Research, . 

Case, J.A.C.a , Burke, T.A.b , Siegel, D.M.c , Piccirillo, M.L.d , Alloy, L.B.e , Olino, T.M.f

a Julia A. C. Case, Department of Psychology, Temple University, Philadelphia, PA, United States
b Department of Psychology, Temple University, Philadelphia, PA, United States
c Department of Psychology, Temple University, Philadelphia, PA, United States
d Department of Psychological & Brain Sciences, Washington University in St. Louis, St. Louis, MO, United States
e Department of Psychology, Temple University, Philadelphia, PA, United States
f Department of Psychology, Temple University, Philadelphia, PA, United States

Abstract
This study employed latent class analysis utilizing an array of features of non-suicidal self-injury (NSSI) in order to identify distinct subgroups of self-injurers. Participants were 359 undergraduates with NSSI history. Indicator variables were lifetime and last year frequency rates, number of methods, scarring, pain during self-injury, and functions of NSSI. Analyses yielded mild/experimental NSSI, moderate NSSI, moderate multiple functions NSSI, and severe NSSI groups, endorsing low, moderate, moderate multiple functions, and high frequencies of self-injury and presence of functions, respectively. Following class assignment, groups differed on self-esteem, social support and belongingness, internalizing symptoms, suicidal ideation and behaviors, and additional NSSI constructs. These subtype analyses emphasize matching phenotypes of NSSI to specific interventions considering dimensions of clinical functioning. © 2019, © 2019 International Academy for Suicide Research.

Author Keywords
functions;  latent class analysis;  non-suicidal self-injury (NSSI);  scarring;  suicide

Document Type: Article
Publication Stage: Article in Press
Source: Scopus

“An inverse relationship between cortical plasticity and cognitive inhibition in late-life depression” (2019) Neuropsychopharmacology

An inverse relationship between cortical plasticity and cognitive inhibition in late-life depression
(2019) Neuropsychopharmacology, . 

Lissemore, J.I.a b , Shanks, H.R.C.a , Butters, M.A.c , Bhandari, A.a , Zomorrodi, R.a , Rajji, T.K.a b d , Karp, J.F.c e , Reynolds, C.F., IIIc , Lenze, E.J.f , Daskalakis, Z.J.a b d , Mulsant, B.H.b d , Blumberger, D.M.a b d

a Temerty Centre for Therapeutic Brain Intervention, Centre for Addiction and Mental Health, Toronto, ON M6J 1H4, Canada
b Department of Psychiatry, University of Toronto, Toronto, ON M5T 1R8, Canada
c Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States
d Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON M5T 1R8, Canada
e VAPHS, Geriatric Research Education and Clinical Center, Pittsburgh, PA, United States
f Healthy Mind Lab, Department of Psychiatry, Washington University School of Medicine, St Louis, MO, United States

Abstract
Executive dysfunction is a common and disabling component of late-life depression (LLD), yet its neural mechanisms remain unclear. In particular, it is not yet known how executive functioning in LLD relates to measures of cortical physiology that may change with age and illness, namely cortical inhibition/excitation and plasticity. Here, we used transcranial magnetic stimulation (TMS) to measure cortical inhibition/excitation (n = 51), and the potentiation of cortical activity following paired associative stimulation, which is thought to reflect long-term potentiation (LTP)-like cortical plasticity (n = 32). We assessed the correlation between these measures of cortical physiology and two measures of executive functioning: cognitive inhibition, assessed using the Delis–Kaplan Executive Function System Color-Word Interference [“Stroop”] Test, and cognitive flexibility, assessed using the Trail Making Test. Correlations with recall memory and processing speed were also performed to assess the specificity of any associations to executive functioning. A significant correlation was found between greater LTP-like cortical plasticity and poorer cognitive inhibition, a core executive function (r p = −0.56, p &lt; 0.001). We did not observe significant associations between cortical inhibition/excitation and executive functioning, or between any neurophysiological measure and cognitive flexibility, memory, or processing speed. Our finding that elevated cortical plasticity is associated with diminished cognitive inhibition emphasizes the importance of balanced synaptic strengthening to healthy cognition. More specifically, our findings suggest that hyper-excitability of cortical circuits following repeated cortical activation may promote inappropriate prepotent responses in LLD. LTP-like cortical plasticity might therefore represent a neural mechanism underlying an inhibitory control cognitive endophenotype of LLD. © 2019, American College of Neuropsychopharmacology.

Document Type: Article
Publication Stage: Article in Press
Source: Scopus

“Psychotic symptoms and suicidal ideation in child and adolescent bipolar I disorder” (2019) Bipolar Disorders

Psychotic symptoms and suicidal ideation in child and adolescent bipolar I disorder
(2019) Bipolar Disorders, . 

Duffy, M.E.a , Gai, A.R.a , Rogers, M.L.a , Joiner, T.E.a , Luby, J.L.b , Joshi, P.T.c , Wagner, K.D.d , Emslie, G.J.e f , Walkup, J.T.g , Axelson, D.h

a Department of Psychology, Florida State University, Tallahassee, FL, United States
b Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, United States
c Department of Psychiatry, University of California, Irvine, CA, United States
d Department of Psychiatry, University of Texas Medical Branch, Galveston, TX, United States
e Division of Child and Adolescent Psychiatry, Children’s Medical Center, Dallas, TX, United States
f Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, United States
g Department of Psychiatry, Ann and Robert H. Lurie Children’s Hospital of Chicago, Chicago, IL, United States
h Nationwide Children’s Hospital Research Institute, The Ohio State University College of Medicine, Columbus, OH, United States

Abstract
Objectives: The purpose of this study was to explore associations between specific types of hallucinations and delusions and suicidal ideation in a sample of children and adolescents with bipolar I disorder. Methods: Participants (N = 379) were children and adolescents aged 6-15 years (M = 10.2, SD = 2.7) with DSM-IV diagnoses of bipolar I disorder, mixed or manic phase. The study sample was 53.8% female and primarily White (73.6% White, 17.9% Black, and 8.5% Other). Presence and nature of psychotic symptoms, suicidal ideation, and functioning level were assessed through clinician-administered measures. A series of logistic regressions was performed to assess the contribution of each subtype of psychotic symptom to the presence of suicidal ideation above and beyond age, sex, socio-economic status, age at bipolar disorder onset, and global level of functioning. Results: Hallucinations overall, delusions of guilt, and number of different psychotic symptom types were uniquely associated with increased odds of suicidal ideation after accounting for covariates. Other forms of delusions (eg, grandiose) and specific types of hallucinations (eg, auditory) were not significantly uniquely associated with the presence of suicidal ideation. Conclusions: Findings of this study suggest the presence of hallucinations as a whole, delusions of guilt specifically, and having multiple concurrent types of psychotic symptoms are associated with the presence of suicidal ideation in children and adolescents with bipolar I disorder. Psychotic symptom subtypes, as opposed to psychosis as a whole, are an under-examined, potentially important, area for consideration regarding suicidal ideation in pediatric bipolar I disorder. © 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

Author Keywords
adolescent;  bipolar disorder;  child;  delusions;  hallucinations;  psychotic symptoms;  suicidal ideation

Document Type: Article
Publication Stage: Article in Press
Source: Scopus

“Common Data Element for Unruptured Intracranial Aneurysm and Subarachnoid Hemorrhage: Recommendations from Assessments and Clinical Examination Workgroup/Subcommittee” (2019) Neurocritical Care

Common Data Element for Unruptured Intracranial Aneurysm and Subarachnoid Hemorrhage: Recommendations from Assessments and Clinical Examination Workgroup/Subcommittee
(2019) Neurocritical Care, . Cited 1 time.

Damani, R.a , Mayer, S.b , Dhar, R.c , Martin, R.H.d , Nyquist, P.e , Olson, D.W.M.f , Mejia-Mantilla, J.H.g , Muehlschlegel, S.h , Jauch, E.C.i , Mocco, J.j , Mutoh, T.k , Suarez, J.I.e l , Macdonald, R.L.l , Amin-Hanjani, S.l , Brown, R.D.l , de Oliveira Manoel, A.L.l , Derdeyn, C.P.l , Etminan, N.l , Keller, E.l , LeRoux, P.D.l , Morita, A.l , Rinkel, G.l , Rufennacht, D.l , Stienen, M.N.l , Torner, J.l , Vergouwen, M.D.I.l , Wong, G.K.C.l , Brown, R.D., Jr.l , Bijlenga, P.l , Ko, N.l , McDougall, C.G.l , Mocco, J.l , Murayama, Y.l , Werner, M.J.H.l , Broderick, J.l , Jauch, E.C.l , Kirkpatrick, P.J.l , Martin, R.H.l , Olson, D.l , Mejia-Mantilla, J.H.l , van der Jagt, M.l , Bambakidis, N.l , Brophy, G.l , Bulsara, K.l , Claassen, J.l , Connolly, E.S.l , Hoffer, S.A.l , Hoh, B.L.l , Holloway, R.G.l , Kelly, A.l , Nakaji, P.l , Rabinstein, A.l , Vajkoczy, P.l , Vergouwen, M.D.I.l , Woo, H.l , Zipfel, G.J.l , Chou, S.l , Doré, S.l , Dumont, A.S.l , Gunel, M.l , Kasuya, H.l , Roederer, A.l , Ruigrok, Y.l , Vespa, P.M.l , Sarrafzadeh-Khorrasani, A.S.l , Hackenberg, K.l , Huston, J., IIIl , Krings, T.l , Lanzino, G.l , Meyers, P.M.l , Wintermark, M.l , Daly, J.l , Ogilvy, C.l , Rhoney, D.H.l , Roos, Y.l , Siddiqui, A.l , Algra, A.l , Frösen, J.l , Hasan, D.l , Juvela, S.l , Langer, D.J.l , Salman, R.A.-S.l , Hanggi, D.l , Schweizer, T.l , Visser-Meily, J.l , Amos, L.l , Ludet, C.l , Moy, C.l , Odenkirchen, J.l , Ala’i, S.l , Esterlitz, J.l , Joseph, K.l , Sheikh, M.l , the Unruptured Intracranial Aneurysms and SAH CDE Project Investigatorsl

a Department of Neurology, Baylor College of Medicine, Houston, TX, United States
b Department of Neurology, Henry Ford Hospital, Detroit, MI, United States
c Department of Neurology, Washington University School of Medicine, St Louis, MO, United States
d Department of Public Health Sciences, Medical University of South Carolina, Charleston, SC, United States
e Neurosciences Critical Care, Departments of Anesthesiology and Critical Care Medicine, Neurology, and Neurosurgery, The Johns Hopkins University School of Medicine, 1800 Orleans Street, Zayed 3014C, Baltimore, MD 21287, United States
f Department of Neurology and Neurotherapeutics, UT Southwestern Medical Center, Dallas, TX, United States
g Fundacion Valle del Lili, Cali, Colombia
h Department of Neurology, University of Massachusetts Medical School, Worcester, MA, United States
i Department of Emergency Medicine, Medical University of South Carolina, Charleston, SC, United States
j Department of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY, United States
k Department of Surgical Neurology, Research Institute for Brain and Blood Vessels, Akita, Japan

Abstract
Background: Clinical studies of subarachnoid hemorrhage (SAH) and unruptured cerebral aneurysms lack uniformity in terms of variables used for assessments and clinical examination of patients which has led to difficulty in comparing studies and performing meta-analyses. The overall goal of the National Institute of Health/National Institute of Neurological Disorders and Stroke Unruptured Intracranial Aneurysms (UIA) and subarachnoid hemorrhage (SAH) Common Data Elements (CDE) Project was to provide common definitions and terminology for future unruptured intracranial aneurysm and SAH research. Methods: This paper summarizes the recommendations of the subcommittee on SAH Assessments and Clinical Examination. The subcommittee consisted of an international and multidisciplinary panel of experts in UIA and SAH. Consensus recommendations were developed by reviewing previously published CDEs for other neurological diseases including traumatic brain injury, epilepsy and stroke, and the SAH literature. Recommendations for CDEs were classified by priority into “core,” “supplemental—highly recommended,” “supplemental” and “exploratory.” Results: We identified 248 variables for Assessments and Clinical Examination. Only the World Federation of Neurological Societies grading scale was classified as “Core.” The Glasgow Coma Scale was classified as “Supplemental—Highly Recommended.” All other Assessments and Clinical Examination variables were categorized as “Supplemental.” Conclusion: The recommended Assessments and Clinical Examination variables have been collated from a large number of potentially useful scales, history, clinical presentation, laboratory, and other tests. We hope that adherence to these recommendations will facilitate the comparison of results across studies and meta-analyses of individual patient data. © 2019, Neurocritical Care Society.

Author Keywords
Aneurysm;  Assessments;  Clinical examination;  Clinical studies;  Common data elements;  Data coding;  Data collection;  Glasgow Coma Scale;  Hemorrhagic stroke;  Standardization;  Subarachnoid hemorrhage;  World Federation of Neurological Societies

Document Type: Article
Publication Stage: Article in Press
Source: Scopus

“Surveying patients with ‘hidden hearing loss'” (2018) Hearing Journal

Surveying patients with ‘hidden hearing loss’
(2018) Hearing Journal, 71 (12), pp. 28 and 30. 

Spehar, B., Lichtenhan, J.T.

Department of Otolaryngology, Washington University, School of Medicine, St. Louis, United States

Document Type: Short Survey
Publication Stage: Final
Source: Scopus

“What is seen and what is not seen in the economy: An effect of our evolved psychology” (2018) The Behavioral and Brain Sciences

What is seen and what is not seen in the economy: An effect of our evolved psychology
(2018) The Behavioral and Brain Sciences, 41, p. e191. 

Boyer, P.a , Petersen, M.B.b

a Departments of Psychology and Anthropology, Washington University in St. Louis, St. Louis, MO, United States
b Department of Political Science and Aarhus Institute of Advanced Studies, Aarhus University, Aarhus C, 8000, Switzerland

Abstract
Specific features of our evolved cognitive architecture explain why some aspects of the economy are “seen” and others are “not seen.” Drawing from the commentaries of economists, psychologists, and other social scientists on our original proposal, we propose a more precise model of the acquisition and spread of folk-beliefs about the economy. In particular, we try to provide a clearer delimitation of the field of folk-economic beliefs (sect. R2) and to dispel possible misunderstandings of the role of variation in evolutionary psychology (sect. R3). We also comment on the difficulty of explaining folk-economic beliefs in terms of domain-general processes or biases (sect. R4), as developmental studies show how encounters with specific environments calibrate domain-specific systems (sect. R5). We offer a more detailed description of the connections between economic beliefs and political psychology (sect. R6) and of the probable causes of individual variation in that domain (sect. R7). Taken together, these arguments point to a better integration or consilience between economics and human evolution (sect. R8).

Document Type: Article
Publication Stage: Final
Source: Scopus