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Office of Neuroscience Research > Resources and Facilities > WUSTL Neuroscience Publications for the week

WUSTL Neuroscience Publications for the week

 

The publications below include authors at Washington University and were identified by Scopus search.  These are the most current publications.  For previous lists, visit the WUSTL Neuroscience publications archive.

 

April 24, 2017 

1) 

Gholipour, A.a , Rollins, C.K.b , Velasco-Annis, C.a , Ouaalam, A.a , Akhondi-Asl, A.c , Afacan, O.a , Ortinau, C.M.d , Clancy, S.a , Limperopoulos, C.e , Yang, E.a , Estroff, J.A.a , Warfield, S.K.a
A normative spatiotemporal MRI atlas of the fetal brain for automatic segmentation and analysis of early brain growth
(2017) Scientific Reports, 7 (1), art. no. 476, . 

DOI: 10.1038/s41598-017-00525-w


a Boston Children's Hospital, Harvard Medical School, Department of Radiology, Boston, MA, United States
b Boston Children's Hospital, Harvard Medical School, Department of Neurology, Boston, MA, United States
c Boston Children's Hospital, Harvard Medical School, Department of Anesthesia, Boston, MA, United States
d Washington University, School of Medicine in St. Louis, Department of Pediatrics, St. Louis, MO, United States
e Children's National Medical Center, Department of Diagnostic Imaging Radiology, Washington DC, United States


Abstract
Longitudinal characterization of early brain growth in-utero has been limited by a number of challenges in fetal imaging, the rapid change in size, shape and volume of the developing brain, and the consequent lack of suitable algorithms for fetal brain image analysis. There is a need for an improved digital brain atlas of the spatiotemporal maturation of the fetal brain extending over the key developmental periods. We have developed an algorithm for construction of an unbiased four-dimensional atlas of the developing fetal brain by integrating symmetric diffeomorphic deformable registration in space with kernel regression in age. We applied this new algorithm to construct a spatiotemporal atlas from MRI of 81 normal fetuses scanned between 19 and 39 weeks of gestation and labeled the structures of the developing brain. We evaluated the use of this atlas and additional individual fetal brain MRI atlases for completely automatic multi-atlas segmentation of fetal brain MRI. The atlas is available online as a reference for anatomy and for registration and segmentation, to aid in connectivity analysis, and for groupwise and longitudinal analysis of early brain growth. © 2017 The Author(s).


Document Type: Article
Source: Scopus

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2) 

Gangolli, M.a , Holleran, L.b , Hee Kim, J.b , Stein, T.D.c d , Alvarez, V.c d , McKee, A.C.c d , Brody, D.L.a b e
Quantitative validation of a nonlinear histology-MRI coregistration method using generalized Q-sampling imaging in complex human cortical white matter
(2017) NeuroImage, 153, pp. 152-167. 

DOI: 10.1016/j.neuroimage.2017.03.059


a Department of Biomedical Engineering, Washington University School of Medicine, St. Louis, MO, United States
b Department of Neurology, Washington University School of Medicine, St. Louis, MO, United States
c Boston University Alzheimer's Disease and CTE Center, Boston University School of Medicine, Boston, MA, United States
d VA Boston Healthcare System, Boston, MA, United States
e Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO, United States


Abstract
Advanced diffusion MRI methods have recently been proposed for detection of pathologies such as traumatic axonal injury and chronic traumatic encephalopathy which commonly affect complex cortical brain regions. However, radiological-pathological correlations in human brain tissue that detail the relationship between the multi-component diffusion signal and underlying pathology are lacking. We present a nonlinear voxel based two dimensional coregistration method that is useful for matching diffusion signals to quantitative metrics of high resolution histological images. When validated in ex vivo human cortical tissue at a 250×250×500 μm spatial resolution, the method proved robust in correlations between generalized q-sampling imaging and histologically based white matter fiber orientations, with r=0.94 for the primary fiber direction and r=0.88 for secondary fiber direction in each voxel. Importantly, however, the correlation was substantially worse with reduced spatial resolution or with fiber orientations derived using a diffusion tensor model. Furthermore, we have detailed a quantitative histological metric of white matter fiber integrity termed power coherence capable of distinguishing architecturally complex but intact white matter from disrupted white matter regions. These methods may allow for more sensitive and specific radiological-pathological correlations of neurodegenerative diseases affecting complex gray and white matter. © 2017 Elsevier Inc.


Author Keywords
Chronic Traumatic Encephalopathy;  Diffusion MRI;  Generalized Q-sampling Imaging;  Radiological-Pathological Correlations;  White Matter Injury


Document Type: Article
Source: Scopus

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3) 

Balasubramanian, P.a , Bennett, V.M.b , Pierce, L.a
The wages of dishonesty: The supply of cheating under high-powered incentives
(2017) Journal of Economic Behavior and Organization, 137, pp. 428-444. 

DOI: 10.1016/j.jebo.2017.03.022


a Washington University in St. Louis, United States
b Duke University, United States


Abstract
We use a novel design to identify how dishonesty changes through a broad reward range that, at the high end, exceeds participants’ average daily wages. Using a sample of online Indian workers who earn bonuses based on six simultaneous coin flips, we show that the relationship between dishonesty and financial rewards depends on the incentive range. We find two novel effects as incentives exceed those used in most prior research. First, dishonesty increases and reaches its maximum as rewards increase from $0.50 to $3 per reported head and as earnings reach $15, indicating that rewards can indeed motivate more cheating when large enough. More importantly, we show that dishonesty declines at the highest reward levels (up to $5 per head) as individuals appear to engage in lower magnitudes of dishonesty. We detail how our results could be explained by a reference-dependent utility with internal costs of dishonesty that are convex in the magnitude of the lie, and show survey and simulation-based evidence that support this explanation. © 2017


Author Keywords
Cheating;  Dishonesty;  Ethics;  Incentives;  Prospect theory;  Reference points


Document Type: Article
Source: Scopus

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4) 

Day, G.S., Gordon, B.A., Jackson, K., Christensen, J.J., Rosana Ponisio, M., Su, Y., Ances, B.M., Benzinger, T.L.S., Morris, J.C.
Tau-PET Binding Distinguishes Patients With Early-stage Posterior Cortical Atrophy From Amnestic Alzheimer Disease Dementia
(2017) Alzheimer Disease and Associated Disorders, . Article in Press. 

DOI: 10.1097/WAD.0000000000000196


*The Charles F and Joanne Knight Alzheimer Disease Research Center †Department of Neurology ‡Mallinckrodt Institute of Radiology §Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO


Abstract
BACKGROUND:: Flortaucipir (tau) positron emission tomography (PET) binding distinguishes individuals with clinically well-established posterior cortical atrophy (PCA) due to Alzheimer disease (AD) from cognitively normal (CN) controls. However, it is not known whether tau-PET binding patterns differentiate individuals with PCA from those with amnestic AD, particularly early in the symptomatic stages of disease. METHODS:: Flortaucipir and florbetapir (β-amyloid) PET imaging were performed in individuals with early-stage PCA (N=5), amnestic AD dementia (N=22), and CN controls (N=47). Average tau and β-amyloid deposition were quantified using standard uptake value ratios and compared at a voxelwise level, controlling for age. RESULTS:: PCA patients [median age-at-onset, 59 (51 to 61) years] were younger at symptom onset than similarly staged individuals with amnestic AD [75 (60 to 85) years] or CN controls [73 (61 to 90) years; P=0.002]. Flortaucipir uptake was higher in individuals with early-stage symptomatic PCA versus those with early-stage amnestic AD or CN controls, and greatest in posterior regions. Regional elevations in florbetapir were observed in areas of greatest tau deposition in PCA patients. CONCLUSIONS AND RELEVANCE:: Flortaucipir uptake distinguished individuals with PCA and amnestic AD dementia early in the symptomatic course. The posterior brain regions appear to be uniquely vulnerable to tau deposition in PCA, aligning with clinical deficits that define this disease subtype. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved


Document Type: Article in Press
Source: Scopus

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5) 

Saxena, A.a b , Luking, K.R.c d , Barch, D.M.b c e , Pagliaccio, D.c f
Individual differences in hedonic capacity, depressed mood, and affective states predict emotional reactivity
(2017) Motivation and Emotion, pp. 1-11. Article in Press. 

DOI: 10.1007/s11031-017-9610-1


a Department of Psychiatry, Rush University Medical Center, Chicago, IL, United States
b Departement of Psychological and Brain Sciences, Washington University, St. Louis, MO, United States
c Neuroscience Program, Division of Biology and Biomedical Sciences, Washington University, St. Louis, MO, United States
d Department of Psychology, Stony Brook University, Stony Brook, NY, United States
e Departments of Psychiatry and Radiology, Washington University, St. Louis, MO, United States
f Section on Developmental and Affective Neuroscience, National Institute of Mental Health, Bethesda, MD, United States


Abstract
Identifying factors that contribute to inter-individual differences in emotional reactivity is central to understanding the basic mechanisms that give rise to adaptive emotion reactivity and to disruptions that may occur in psychopathology. The current study related emotional reactivity in an unselected young adult sample (N = 101) to individual difference factors relevant to emotional functioning and mood pathology, specifically anhedonia, depressed mood, and current affective state. To assess emotional reactivity, participants rated their emotional responses to 100 pictures from the International Affective Picture System. Increased self-reported anhedonia (i.e. reduced hedonic capacity) predicted blunted emotional reactivity to both positive and negative images, relative to neutral images, while elevated depressed mood predicted potentiated emotional reactivity to negative vs. neutral images. Anhedonia also accounted for far greater variance in emotional reactivity than depressed mood. Further, more positive affective state predicted potentiated reactivity to positive versus neutral images while more negative affective state predicted potentiated reactivity to negative versus neutral images beyond effects of anhedonia and depressed mood. The current study identified separable effects of anhedonia, depressed mood, and current affect on emotional reactivity. © 2017 Springer Science+Business Media New York


Author Keywords
Affect;  Anhedonia;  Depression;  Emotional reactivity;  IAPS;  Individual differences


Document Type: Article in Press
Source: Scopus

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6) 

Park, S.a , Kwon, E.b , Lee, H.c
Life course trajectories of later-life cognitive functions: Does social engagement in old age matter?
(2017) International Journal of Environmental Research and Public Health, 14 (4), art. no. 393, . 

DOI: 10.3390/ijerph14040393


a George Warren Brown School of Social Work, Washington University, 1 Brookings Drive, Saint Louis, MO, United States
b Center for Social Science, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, South Korea
c Department of Social Work, Daegu University, 201 Deagudae-ro, Gyeongsan-si, Gyeongsangbuk-do, South Korea


Abstract
This study identified differential patterns of later-life cognitive function trajectories and examined to what extent life course factors and social engagement are associated with group trajectories. Data came from seven waves of the Health and Retirement Study (HRS 1998-2010; n=7374; Observations = 41,051). Latent class growth analysis identified cognitive function trajectory groups, and multinomial logistic regression was used to examine the factors associated with group trajectories. Five heterogeneous trajectories were identified: stable high, stable moderate, stable low, high-to-moderate, and moderate-to-low. Findings suggest that, after adjusting for life course factors, individuals who became volunteers were more likely to belong to one of the two least vulnerable trajectories, stable high or high-to-moderate. Our findings suggest that, despite the cumulative life course factors vident in cognitive decline, social engagement in old age may serve as a potential protective resource. © 2017 by the authors. Licensee MDPI, Basel, Switzerland.


Author Keywords
Cognitive function;  Cumulative disadvantage;  Group trajectory;  Life-course perspective;  Social engagement


Document Type: Article
Source: Scopus

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7) 

Howard, S.P.a , Krauze, A.e , Chan, M.D.b , Tsien, C.d , Tomé, W.A.c
The evolving role for re-irradiation in the management of recurrent grade 4 glioma
(2017) Journal of Neuro-Oncology, pp. 1-8. Article in Press. 

DOI: 10.1007/s11060-017-2392-1


a Department of Human Oncology, University of Wisconsin School of Medicine and Public Health, K4/350 Clinical Science Center, 600 Highland Avenue, Madison, WI, United States
b Department of Radiation Oncology, Wake Forest School of Medicine, Winston-Salem, NC, United States
c Department of Radiation Oncology and Department of Neurology, Montefiore Medical Center and Albert Einstein College of Medicine, Bronx, NY, United States
d Department of Radiation Oncology, Washington University School of Medicine, St. Louis, MO, United States
e Radiation Oncology Branch, National Cancer Institute, Bethesda, MD, United States


Abstract
Although significant gains have been realized in the management of grade 4 glioma, the majority of these patients will ultimately suffer local recurrence within the prior field of treatment. Clearly, novel local treatment strategies are required to improve patient outcomes. Concerns of toxicity have limited enthusiasm for the utilization of re-irradiation as a treatment option. However, using modern imaging technology and precision radiotherapy delivery techniques re-irradiation has proven a feasible option achieving both a palliative benefit and prolongation of survival with low toxicity rates. The evolution of re-irradiation as a treatment modality for recurrent grade 4 glioma is reviewed. In addition, potential targeted radiosensitizers to be used in conjunction with re-irradiation are also discussed. © 2017 Springer Science+Business Media New York


Author Keywords
Central nervous system;  Radiosensitizers;  Re-irradiation;  Recurrent grade 4 glioma


Document Type: Article in Press
Source: Scopus

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8) 

Sahlholm, K.a b c , Ielacqua, G.D.a , Xu, J.b , Jones, L.A.b , Schlegel, F.a , Mach, R.H.d , Rudin, M.a e f , Schroeter, A.a e
The role of beta-arrestin2 in shaping fMRI BOLD responses to dopaminergic stimulation
(2017) Psychopharmacology, pp. 1-12. Article in Press. 

DOI: 10.1007/s00213-017-4609-6


a Institute for Biomedical Engineering, University and ETH Zurich, Wolfgang-Pauli-Str. 27, Zurich, Switzerland
b Department of Radiology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, 510 S. Kingshighway Blvd, St. Louis, MO, United States
c Department of Neuroscience, Karolinska Institutet, Retzius väg 8, Stockholm, Sweden
d Department of Radiology, Perelman School of Medicine, University of Pennsylvania, 231 S. 34th St, Philadelphia, PA, United States
e Neuroscience Center Zurich, University and ETH Zurich, Winterthurer-Str. 190, Zurich, Switzerland
f Institute of Pharmacology and Toxicology, University of Zurich, Winterthurer-Str. 190, Zurich, Switzerland


Abstract
Rationale: The dopamine D2 receptor (D2R) couples to inhibitory Gi/o proteins and is targeted by antipsychotic and antiparkinsonian drugs. Beta-arrestin2 binds to the intracellular regions of the agonist-occupied D2R to terminate G protein activation and promote internalization, but also to initiate downstream signaling cascades which have been implicated in psychosis. Functional magnetic resonance imaging (fMRI) has proven valuable for measuring dopamine receptor-mediated changes in neuronal activity, and might enable beta-arrestin2 function to be studied in vivo. Objectives: The present study examined fMRI blood oxygenation level dependent (BOLD) signal changes elicited by a dopamine agonist in wild-type (WT) and beta-arrestin2 knockout (KO) mice, to investigate whether genetic deletion of beta-arrestin2 prolongs or otherwise modifies D2R-dependent responses. Methods: fMRI BOLD data were acquired on a 9.4 T system. During scans, animals received 0.2 mg/kg apomorphine, i.v. In a subset of experiments, animals were pretreated with 2 mg/kg of the D2R antagonist, eticlopride. Results: Following apomorphine administration, BOLD signal decreases were observed in caudate/putamen of WT and KO animals. The time course of response decay in caudate/putamen was significantly slower in KO vs. WT animals. In cingulate cortex, an initial BOLD signal decrease was followed by a positive response component in WT but not in KO animals. Eticlopride pretreatment significantly reduced apomorphine-induced BOLD signal changes. Conclusions: The prolonged striatal response decay rates in KO animals might reflect impaired D2R desensitization, consistent with the known function of beta-arrestin2. Furthermore, the apomorphine-induced positive response component in cingulate cortex may depend on beta-arrestin2 signaling downstream of D2R. © 2017 The Author(s)


Author Keywords
Arrestin3;  Dopamine;  Dopamine agents;  Dopamine receptor;  Eticlopride


Document Type: Article in Press
Source: Scopus

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9) 

Culverhouse, R.C., Saccone, N.L., Horton, A.C., Ma, Y., Anstey, K.J., Banaschewski, T., Burmeister, M., Cohen-Woods, S., Etain, B., Fisher, H.L., Goldman, N., Guillaume, S., Horwood, J., Juhasz, G., Lester, K.J., Mandelli, L., Middeldorp, C.M., Olié, E., Villafuerte, S., Air, T.M., Araya, R., Bowes, L., Burns, R., Byrne, E.M., Coffey, C., Coventry, W.L., Gawronski, K.A.B., Glei, D., Hatzimanolis, A., Hottenga, J.-J., Jaussent, I., Jawahar, C., Jennen-Steinmetz, C., Kramer, J.R., Lajnef, M., Little, K., zu Schwabedissen, H.M., Nauck, M., Nederhof, E., Petschner, P., Peyrot, W.J., Schwahn, C., Sinnamon, G., Stacey, D., Tian, Y., Toben, C., van der Auwera, S., Wainwright, N., Wang, J.-C., Willemsen, G., Anderson, I.M., Arolt, V., Åslund, C., Bagdy, G., Baune, B.T., Bellivier, F., Boomsma, D.I., Courtet, P., Dannlowski, U., de Geus, E.J.C., Deakin, J.F.W., Easteal, S., Eley, T., Fergusson, D.M., Goate, A.M., Gonda, X., Grabe, H.J., Holzman, C., Johnson, E.O., Kennedy, M., Laucht, M., Martin, N.G., Munafò, M.R., Nilsson, K.W., Oldehinkel, A.J., Olsson, C.A., Ormel, J., Otte, C., Patton, G.C., Penninx, B.W.J.H., Ritchie, K., Sarchiapone, M., Scheid, J.M., Serretti, A., Smit, J.H., Stefanis, N.C., Surtees, P.G., Völzke, H., Weinstein, M., Whooley, M., Nurnberger Jr, J.I., Breslau, N., Bierut, L.J.
Collaborative meta-analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression
(2017) Molecular Psychiatry, . Article in Press. 

DOI: 10.1038/mp.2017.44


Department of Medicine and Division of Biostatistics, Washington University in St. Louis School of Medicine, St. Louis, MO, USA


Abstract
The hypothesis that the S allele of the 5-HTTLPR serotonin transporter promoter region is associated with increased risk of depression, but only in individuals exposed to stressful situations, has generated much interest, research and controversy since first proposed in 2003. Multiple meta-analyses combining results from heterogeneous analyses have not settled the issue. To determine the magnitude of the interaction and the conditions under which it might be observed, we performed new analyses on 31 data sets containing 38 802 European ancestry subjects genotyped for 5-HTTLPR and assessed for depression and childhood maltreatment or other stressful life events, and meta-analysed the results. Analyses targeted two stressors (narrow, broad) and two depression outcomes (current, lifetime). All groups that published on this topic prior to the initiation of our study and met the assessment and sample size criteria were invited to participate. Additional groups, identified by consortium members or self-identified in response to our protocol (published prior to the start of analysis) with qualifying unpublished data, were also invited to participate. A uniform data analysis script implementing the protocol was executed by each of the consortium members. Our findings do not support the interaction hypothesis. We found no subgroups or variable definitions for which an interaction between stress and 5-HTTLPR genotype was statistically significant. In contrast, our findings for the main effects of life stressors (strong risk factor) and 5-HTTLPR genotype (no impact on risk) are strikingly consistent across our contributing studies, the original study reporting the interaction and subsequent meta-analyses. Our conclusion is that if an interaction exists in which the S allele of 5-HTTLPR increases risk of depression only in stressed individuals, then it is not broadly generalisable, but must be of modest effect size and only observable in limited situations.Molecular Psychiatry advance online publication, 4 April 2017; doi:10.1038/mp.2017.44. © 2017 Macmillan Publishers Limited, part of Springer Nature.


Document Type: Article in Press
Source: Scopus

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10) 

Lee, Y.a , Chou, T.-F.b , Pittman, S.K.a , Keith, A.L.a , Razani, B.c d , Weihl, C.C.a
Keap1/Cullin3 Modulates p62/SQSTM1 Activity via UBA Domain Ubiquitination
(2017) Cell Reports, 19 (1), pp. 188-202. 

DOI: 10.1016/j.celrep.2017.03.030


a Department of Neurology, Washington University School of Medicine, St. Louis, MO, United States
b Division of Medical Genetics, Department of Pediatrics, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, CA, United States
c Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States
d Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, United States


Abstract
p62/SQSTM1 (p62) is a scaffolding protein that facilitates the formation and degradation of ubiquitinated aggregates via its self-interaction and ubiquitin binding domains. The regulation of this process is unclear but may relate to the post-translational modification of p62. In the present study, we find that Keap1/Cullin3 ubiquitinates p62 at lysine 420 within its UBA domain. Substitution of lysine 420 with an arginine diminishes p62 sequestration and degradation activity similar what is seen when the UBA domain is deleted. Overexpression of Keap1/Cullin3 in p62-WT-expressing cells increases ubiquitinated inclusion formation and p62's association with LC3 and rescues proteotoxicity. This effect is not seen in cells expressing a mutant p62 that fails to interact with Keap1. Interestingly, p62 disease mutants have diminished or absent UBA domain ubiquitination. These data suggest that the ubiquitination of p62’s UBA domain at lysine 420 may regulate p62’s function and be disrupted in p62-associated disease. © 2017 The Author(s)


Author Keywords
aggregaphagy;  autophagy;  neurodegeneration;  SQSTM1/p62;  ubiquitin


Document Type: Article
Source: Scopus

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11) 

Sun, X.a b c , Laroche, G.d , Wang, X.b , Ågren, H.b , Bowman, G.R.c , Giguère, P.M.d , Tu, Y.b
Propagation of the Allosteric Modulation Induced by Sodium in the δ-Opioid Receptor
(2017) Chemistry - A European Journal, 23 (19), pp. 4615-4624. 

DOI: 10.1002/chem.201605575


a Pharmaceutical Research Center, School of Pharmacy, Guangzhou Medical University, 195 Dongfengxi Rd, Guangzhou, China
b Division of Theoretical Chemistry and Biology, School of Biotechnology, KTH Royal Institute of Technology, Stockholm, Sweden
c Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO, United States
d Department of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Rd, Ottawa, ON, Canada


Abstract
Allosteric sodium in the helix bundle of a G protein-coupled receptor (GPCR) can modulate the receptor activation on the intracellular side. This phenomenon has confounded the GPCR community for decades. In this work, we present a theoretical model that reveals the mechanism of the allosteric modulation induced by sodium in the δ-opioid receptor. We found that the allosteric sodium ion exploits a distinct conformation of the key residue Trp2746.48 to propagate the modulation to helices 5 and 6, which further transmits along the helices and regulates their positions on the intracellular side. This mechanism is supported by subsequent functional assays. Remarkably, our results highlight the contrast between the allosteric effects towards two GPCR partners, the G protein and β-arrestin, as indicated by the fact that the allosteric modulation initiated by the sodium ion significantly affects the β-arrestin recruitment, while it alters the G protein signaling only moderately. We believe that the mechanism revealed in this work can be used to explain allosteric effects initiated by sodium in other GPCRs since the allosteric sodium is highly conserved across GPCRs. © 2017 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim


Author Keywords
allosteric effects;  G protein-coupled receptor;  GPCR activation;  molecular dynamics;  opioid receptors


Document Type: Article
Source: Scopus

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12) 

O'Callaghan, C.
Grades of Multisensory Awareness
(2017) Mind and Language, 32 (2), pp. 155-181. 

DOI: 10.1111/mila.12137


Department of Philosophy, Washington University in St. Louis, United States


Abstract
Psychophysics and neuroscience demonstrate that different sensory systems interact and influence each other. Perceiving involves extensive cooperation and coordination among systems associated with sight, hearing, touch, smell, and taste. Nonetheless, it remains unclear in what respects conscious perceptual awareness is multisensory. This article distinguishes six differing varieties of multisensory awareness, explicates their consequences, and thereby elucidates the multisensory nature of perception. It argues on these grounds that perceptual awareness need not be exhausted by that which is associated with each of the respective sensory modalities along with whatever accrues thanks to simple co-consciousness. © 2017 John Wiley & Sons Ltd


Document Type: Article
Source: Scopus

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13) 

Smyth, M.D.a , Vellimana, A.K.a , Asano, E.b c , Sood, S.d
Corpus callosotomy—Open and endoscopic surgical techniques
(2017) Epilepsia, 58, pp. 73-79. 

DOI: 10.1111/epi.13681


a Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO, United States
b Department of Pediatrics, Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, United States
c Department of Neurology, Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, United States
d Department of Neurosurgery, Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, United States


Abstract
Corpus callosotomy is a palliative surgical procedure for patients with refractory epilepsy. It can be performed through an open approach via a standard craniotomy and the aid of an operating microscope, or alternatively via a mini-craniotomy with endoscope assistance. The extent of callosal disconnection performed varies according to indications and surgeon preference. In this article, we describe both open and endoscopic surgical techniques for anterior and complete corpus callosotomy. Wiley Periodicals, Inc. © 2017 International League Against Epilepsy


Author Keywords
Callosotomy technique;  Complete callosotomy;  Corpus callosotomy;  Endoscopic callosotomy;  Epilepsy surgery


Document Type: Article
Source: Scopus

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14) 

Pineda, J.A.a , Gill, J.b
The Road between Statistics and Clinical Decision Making Is Longer Than We Think
(2017) Pediatric Critical Care Medicine, 18 (4), pp. 388-390. 

DOI: 10.1097/PCC.0000000000001113


a Division of Critical Care Medicine, Department of Pediatrics and Neurology, Washington University, School of Medicine, St. Louis, MO, United States
b Departments of Surgery, Political Science and Biostatistics, Washington University, School of Medicine, St. Louis, MO, United States


Author Keywords
Bayesian analysis;  clinical decision making;  hypothermia;  meta-analysis;  traumatic brain injury


Document Type: Editorial
Source: Scopus

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15) 

Weiner, M.W.a b c d e u , Veitch, D.P.a , Aisen, P.S.f , Beckett, L.A.g , Cairns, N.J.h i , Green, R.C.j , Harvey, D.g , Jack, C.R., Jr.k , Jagust, W.l , Morris, J.C.f , Petersen, R.C.m , Saykin, A.J.n o , Shaw, L.M.p , Toga, A.W.q , Trojanowski, J.Q.p r s t
Recent publications from the Alzheimer's Disease Neuroimaging Initiative: Reviewing progress toward improved AD clinical trials
(2017) Alzheimer's and Dementia, 13 (4), pp. e1-e85. 

DOI: 10.1016/j.jalz.2016.11.007


a Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, United States
b Department of Radiology, University of California, San Francisco, CA, United States
c Department of Medicine, University of California, San Francisco, CA, United States
d Department of Psychiatry, University of California, San Francisco, CA, United States
e Department of Neurology, University of California, San Francisco, CA, United States
f Alzheimer's Therapeutic Research Institute, University of Southern California, San Diego, CA, United States
g Division of Biostatistics, Department of Public Health Sciences, University of California, Davis, CA, United States
h Knight Alzheimer's Disease Research Center, Washington University School of Medicine, Saint Louis, MO, United States
i Department of Neurology, Washington University School of Medicine, Saint Louis, MO, United States
j Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States
k Department of Radiology, Mayo Clinic, Rochester, MN, United States
l Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA, United States
m Department of Neurology, Mayo Clinic, Rochester, MN, United States
n Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN, United States
o Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, United States
p Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States
q Laboratory of Neuroimaging, Institute of Neuroimaging and Informatics, Keck School of Medicine of University of Southern California, Los Angeles, CA, United States
r Institute on Aging, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States
s Alzheimer's Disease Core Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States
t Udall Parkinson's Research Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States


Abstract
Introduction The Alzheimer's Disease Neuroimaging Initiative (ADNI) has continued development and standardization of methodologies for biomarkers and has provided an increased depth and breadth of data available to qualified researchers. This review summarizes the over 400 publications using ADNI data during 2014 and 2015. Methods We used standard searches to find publications using ADNI data. Results (1) Structural and functional changes, including subtle changes to hippocampal shape and texture, atrophy in areas outside of hippocampus, and disruption to functional networks, are detectable in presymptomatic subjects before hippocampal atrophy; (2) In subjects with abnormal β-amyloid deposition (Aβ+), biomarkers become abnormal in the order predicted by the amyloid cascade hypothesis; (3) Cognitive decline is more closely linked to tau than Aβ deposition; (4) Cerebrovascular risk factors may interact with Aβ to increase white-matter (WM) abnormalities which may accelerate Alzheimer's disease (AD) progression in conjunction with tau abnormalities; (5) Different patterns of atrophy are associated with impairment of memory and executive function and may underlie psychiatric symptoms; (6) Structural, functional, and metabolic network connectivities are disrupted as AD progresses. Models of prion-like spreading of Aβ pathology along WM tracts predict known patterns of cortical Aβ deposition and declines in glucose metabolism; (7) New AD risk and protective gene loci have been identified using biologically informed approaches; (8) Cognitively normal and mild cognitive impairment (MCI) subjects are heterogeneous and include groups typified not only by “classic” AD pathology but also by normal biomarkers, accelerated decline, and suspected non-Alzheimer's pathology; (9) Selection of subjects at risk of imminent decline on the basis of one or more pathologies improves the power of clinical trials; (10) Sensitivity of cognitive outcome measures to early changes in cognition has been improved and surrogate outcome measures using longitudinal structural magnetic resonance imaging may further reduce clinical trial cost and duration; (11) Advances in machine learning techniques such as neural networks have improved diagnostic and prognostic accuracy especially in challenges involving MCI subjects; and (12) Network connectivity measures and genetic variants show promise in multimodal classification and some classifiers using single modalities are rivaling multimodal classifiers. Discussion Taken together, these studies fundamentally deepen our understanding of AD progression and its underlying genetic basis, which in turn informs and improves clinical trial design. © 2017


Author Keywords
Alzheimer's disease;  Amyloid;  Biomarker;  Disease progression;  Mild cognitive impairment;  Tau


Document Type: Review
Source: Scopus

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16) 

Song, X.D.a , Garnett, R.b , Barbour, D.L.c
Psychometric function estimation by probabilistic classification
(2017) Journal of the Acoustical Society of America, 141 (4), pp. 2513-2525. 

DOI: 10.1121/1.4979594


a Laboratory of Sensory Neuroscience and Neuroengineering, Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, Missouri, United States
b Department of Computer Science and Engineering, Washington University in St. Louis, St. Louis, Missouri, United States
c Laboratory of Sensory Neuroscience and Neuroengineering, Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, Missouri, United States


Abstract
Conventional psychometric function (PF) estimation involves fitting a parametric, unidimensional sigmoid to binary subject responses, which is not readily extendible to higher order PFs. This study presents a nonparametric, Bayesian, multidimensional PF estimator that also relies upon traditional binary subject responses. This technique is built upon probabilistic classification (PC), which attempts to ascertain the subdomains corresponding to each subject response as a function of multiple independent variables. Increased uncertainty in the location of class boundaries results in a greater spread in the PF estimate, which is similar to a parametric PF estimate with a lower slope. PC was evaluated on both one-dimensional (1D) and two-dimensional (2D) simulated auditory PFs across a variety of function shapes and sample numbers. In the 1D case, PC demonstrated equivalent performance to conventional maximum likelihood regression for the same number of simulated responses. In the 2D case, where the responses were distributed across two independent variables, PC accuracy closely matched the accuracy of 1D maximum likelihood estimation at discrete values of the second variable. The flexibility and scalability of the PC formulation make this an excellent option for estimating traditional PFs as well as more complex PFs, which have traditionally lacked rigorous estimation procedures. © 2017 Acoustical Society of America.


Document Type: Article
Source: Scopus

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17) 

Wildburger, N.C.
MALDI-imaging mass spectrometry of brain lipids
(2017) Neuromethods, 125, pp. 45-59. 

DOI: 10.1007/978-1-4939-6946-3_4


Department of Neurology, Washington University School of Medicine, 660 South Euclid Ave, St. Louis, MO, United States


Abstract
Advances in mass spectrometry (MS) over the past two decades have made MS an invaluable tool for the detection and characterization of biomolecules. One such biomolecule, lipids, is an important, but often times challenging species to analyze. Here, we describe the matrix-assisted laser desorption/ionization imaging mass spectrometry (MALDI-IMS) of lipids and glycolipids from mammalian brain in an untargeted and high-throughput approach. © Springer Science+Business Media LLC 2017.


Author Keywords
Brain;  Cryo-sectioning;  ITO slides;  MALDI-IMS;  Mass spectrometry;  Shotgun lipidomics;  Sublimation


Document Type: Book Chapter
Source: Scopus

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18) 

Sorensen, C.J.a , Hastings, M.K.a b , Lang, C.E.a c d , McGill, J.B.e , Clark, B.R.a d , Bohnert, K.L.a , Mueller, M.J.a f
Relationship of shoulder activity and skin intrinsic fluorescence with low level shoulder pain and disability in people with type 2 diabetes
(2017) Journal of Diabetes and its Complications, . Article in Press. 

DOI: 10.1016/j.jdiacomp.2017.03.005


a Program in Physical Therapy, Washington University School of Medicine in St. Louis, St. Louis, MO
b Orthopaedic Surgery, Washington University School of Medicine in St. Louis, St. Louis, MO
c Program in Occupational Therapy, Washington University School of Medicine in St. Louis, St. Louis, MO
d Department of Neurology, Washington University School of Medicine in St. Louis, St. Louis, MO
e Division of Endocrinology, Metabolism, and Lipid Research, Washington University School of Medicine in St. Louis, St. Louis, MO
f Department of Radiology, Washington University School of Medicine in St. Louis, St. Louis, MO


Abstract
Aim: People with type 2 diabetes (T2DM) have a high incidence of musculoskeletal disorders thought to be influenced by high non-enzymatic advanced glycated end-products (AGEs). The goals of this study were to determine differences in shoulder activity level and AGEs in people with T2DM compared to matched controls, and to determine factors associated with shoulder pain and disability. Methods: Eighty-one participants, T2DM (n = 52) and controls (n = 29), were examined for magnitude and duration of shoulder activity (measured using accelerometers), skin intrinsic florescence (SIF) as a surrogate measure of AGE level, and the Shoulder Pain and Disability Index (SPADI) as a self-report of shoulder pain and disability. Results: Compared with controls, T2DM participants had 23% less shoulder activity (p = 0.01), greater SIF level (3.6. ±. 1.7 vs 2.7. ±. 0.6. AU, p = 0.01), less shoulder strength (p. <. 0.05), and the duration of their shoulder activity was moderately associated (r = 0.40; p. <. 0.01) with reported shoulder pain and disability. Shoulder pain and disability were not related to SIF level. Conclusions: Persons with T2DM have higher SIF levels and shoulder symptoms and disability indices than controls. Research is needed to determine if a shoulder mobility intervention to increase strength and mobility can help decrease shoulder pain and disability. © 2017 Elsevier Inc.


Author Keywords
Accelerometers;  Advanced glycation end products;  Shoulder limited joint mobility;  Skin intrinsic fluorescence;  Type 2 diabetes


Document Type: Article in Press
Source: Scopus

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19) 

Lenze, S.N.
Early Childhood Mental Health. Starting Early with the Pregnant Mother
(2017) Child and Adolescent Psychiatric Clinics of North America, . Article in Press. 

DOI: 10.1016/j.chc.2017.02.001


Department of Psychiatry, Washington University School of Medicine, Campus Box 8504, 660 South Euclid Avenue, St Louis, MO 63110, USA


Abstract
Perinatal mental health has important implications for maternal and child outcomes. Most women with psychiatric disorders during pregnancy go undiagnosed and untreated, despite widespread initiatives for early identification. Universal screening for psychiatric disorders, particularly depression and anxiety, has been implemented in obstetric and primary care settings. However, there is little evidence regarding the effectiveness on psychiatric symptom reduction or prevention of adverse outcomes in children. Recently, comprehensive screening and follow-up programs integrated within obstetric or primary care settings have shown promising results in improving maternal mental health outcomes. Further work is needed to determine best clinical and most cost-effective practices. © 2017 Elsevier Inc.


Author Keywords
Anxiety;  Depression;  Perinatal;  Pregnancy;  Screening


Document Type: Article in Press
Source: Scopus

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20) 

Adkins, A.E.a b ai aj , Hack, L.M.a b , Bigdeli, T.B.b , Williamson, V.S.a b , Mcmichael, G.O.a b , Mamdani, M.a b , Edwards, A.C.a b , Aliev, F.a b ai , Chan, R.F.a c , Bhandari, P.c , Raabe, R.C.d , Alaimo, J.T.d , Blackwell, G.G.d , Moscati, A.a b , Poland, R.S.b , Rood, B.b , Patterson, D.G.e , Walsh, D.f , Whitfield, J.B.g , Zhu, G.g , Montgomery, G.W.g , Henders, A.K.g , Martin, N.G.g , Heath, A.C.h , Madden, P.A.h , Frank, J.i , Ridinger, M.k , Wodarz, N.k , Soyka, M.l m , Zill, P.m , Ising, M.n , Nöthen, M.M.o p q , Kiefer, F.j , Rietschel, M.i , Gelernter, J.r s t v , Sherva, R.z , Koesterer, R.z , Almasy, L.w , Zhao, H.t u , Kranzler, H.R.x y , Farrer, L.A.v z aa ab ac ad , Maher, B.S.ae , Prescott, C.A.af , Dick, D.M.a b c ai aj , Bacanu, S.A.a b , Mathies, L.D.d , Davies, A.G.a d , Vladimirov, V.I.a b ag ah , Grotewiel, M.a c , Bowers, M.S.a b d ak , Bettinger, J.C.a d , Webb, B.T.a b , Miles, M.F.a c d , Kendler, K.S.a b c , Riley, B.P.a b c
Genomewide Association Study of Alcohol Dependence Identifies Risk Loci Altering Ethanol-Response Behaviors in Model Organisms
(2017) Alcoholism: Clinical and Experimental Research, . Article in Press. 

DOI: 10.1111/acer.13362


a Virginia Commonwealth University Alcohol Research Center Virginia Commonwealth University Richmond, Virginia
b Department of Psychiatry Virginia Commonwealth University Richmond, Virginia
c Department of Human and Molecular Genetics Virginia Commonwealth University Richmond, Virginia
d Department of Pharmacology and Toxicology Virginia Commonwealth University Richmond, Virginia
e Shaftesbury Square Hospital Belfast United Kingdom
f Health Research Board Dublin 2 Ireland
g Genetic Epidemiology QIMR Berghofer Medical Research Institute Royal Brisbane and Women's Hospital Brisbane, Qld Australia
h Department of Psychiatry Washington University School of Medicine St. Louis, Missouri
i Department of Genetic Epidemiology in Psychiatry Central Institute of Mental Health Medical Faculty Mannheim/Heidelberg University Mannheim Germany
j Department of Addictive Behavior and Addiction Medicine Central Institute of Mental Health Medical Faculty Mannheim/Heidelberg University Mannheim Germany
k Department of Psychiatry University Hospital Regensburg University of Regensburg Regensburg Germany
l Privatklinik Meiringen Meiringen Switzerland
m Department of Psychiatry and Psychotherapy University of Munich Munich Germany
n Department of Molecular Psychology Max-Planck-Institute of Psychiatry Munich Germany
o Department of Genomics Life and Brain Center University of Bonn Bonn Germany
p Institute of Human Genetics University of Bonn Bonn Germany
q German Center for Neurodegenerative Diseases (DZNE) University of Bonn Bonn Germany
r Department of Psychiatry Yale University School of Medicine New Haven, Connecticut
s Department of Neurobiology Yale University School of Medicine New Haven, Connecticut
t Department of Genetics Yale University School of Medicine New Haven, Connecticut
u Department of Biostatistics Yale University School of Medicine New Haven, Connecticut
v Department of Psychiatry VA CT Healthcare Center West Haven, Connecticut
w Department of Genetics Texas Biomedical Research Institute San Antonio, Texas
x Department of Psychiatry Treatment Research Center University of Pennsylvania Perelman School of Medicine Philadelphia, Pennsylvania
y Philadelphia VA Medical Center VISN 4 MIRECC Philadelphia, Pennsylvania
z Department of Medicine (Biomedical Genetics) Boston University School of Medicine Boston, Massachusetts
aa Department of Neurology Boston University School of Medicine Boston, Massachusetts
ab Department of Ophthalmology Boston University School of Medicine Boston, Massachusetts
ac Department of Epidemiology Boston University School of Public Health Boston, Massachusetts
ad Department of Biostatistics Boston University School of Public Health Boston, Massachusetts
ae Department of Mental Health Johns Hopkins Bloomberg School of Public Health Baltimore, Maryland
af Department of Psychology University of Southern California Los Angeles California
ag Lieber Institute for Brain Development Johns Hopkins University Baltimore, Maryland
ah Center for Biomarker Research and Personalized Medicine School of Pharmacy Virginia Commonwealth University Richmond, Virginia
ai Department of Psychology Virginia Commonwealth University PO Box 842018 Richmond 23284-2018VA
aj College Behavioral and Emotional Health Institute Virginia Commonwealth University PO Box 842018 Richmond 23284-2018VA
ak Faulk Center for Molecular Therapeutics Department of Biomedical Engineering Northwestern University 1801 Maple Ave Evanston 60201IL


Abstract
Background: Alcohol dependence (AD) shows evidence for genetic liability, but genes influencing risk remain largely unidentified. Methods: We conducted a genomewide association study in 706 related AD cases and 1,748 unscreened population controls from Ireland. We sought replication in 15,496 samples of European descent. We used model organisms (MOs) to assess the role of orthologous genes in ethanol (EtOH)-response behaviors. We tested 1 primate-specific gene for expression differences in case/control postmortem brain tissue. Results: We detected significant association in COL6A3 and suggestive association in 2 previously implicated loci, KLF12 and RYR3. None of these signals are significant in replication. A suggestive signal in the long noncoding RNA LOC339975 is significant in case:control meta-analysis, but not in a population sample. Knockdown of a COL6A3 ortholog in Caenorhabditis elegans reduced EtOH sensitivity. Col6a3 expression correlated with handling-induced convulsions in mice. Loss of function of the KLF12 ortholog in C. elegans impaired development of acute functional tolerance (AFT). Klf12 expression correlated with locomotor activation following EtOH injection in mice. Loss of function of the RYR3 ortholog reduced EtOH sensitivity in C. elegans and rapid tolerance in Drosophila. The ryanodine receptor antagonist dantrolene reduced motivation to self-administer EtOH in rats. Expression of LOC339975 does not differ between cases and controls but is reduced in carriers of the associated rs11726136 allele in nucleus accumbens (NAc). Conclusions: We detect association between AD and COL6A3, KLF12, RYR3, and LOC339975. Despite nonreplication of COL6A3, KLF12, and RYR3 signals, orthologs of these genes influence behavioral response to EtOH in MOs, suggesting potential involvement in human EtOH response and AD liability. The associated LOC339975 allele may influence gene expression in human NAc. Although the functions of long noncoding RNAs are poorly understood, there is mounting evidence implicating these genes in multiple brain functions and disorders. © 2017 Research Society on Alcoholism.


Author Keywords
COL6A3;  KLF12;  LOC339975;  RYR3;  Alcohol Dependence


Document Type: Article in Press
Source: Scopus

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21) 

Zhou, Y.a b , Liu, J.c , Driesen, N.c , Womer, F.d , Chen, K.a , Wang, Y.e , Jiang, X.a , Zhou, Q.a , Bai, C.f , Wang, D.a , Tang, Y.a b , Wang, F.a f
White Matter Integrity in Genetic High-Risk Individuals and First-Episode Schizophrenia Patients: Similarities and Disassociations
(2017) BioMed Research International, 2017, art. no. 3107845, . 

DOI: 10.1155/2017/3107845


a Department of Psychiatry, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, China
b Department of Geriatrics, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, China
c Department of Psychiatry, Yale University, School of Medicine, New Haven, CT, United States
d Department of Psychiatry, Washington University, School of Medicine, St. Louis, MO, United States
e Mental Health Center of Shenyang, Shenyang, Liaoning, China
f Department of Radiology, First Affiliated Hospital, China Medical University, Shenyang, Liaoning, China


Abstract
White matter (WM) neuroimaging studies have shown varied findings at different stages of schizophrenia (SZ). Understanding these variations may elucidate distinct markers of genetic vulnerability and conversion to psychosis. To examine the similarities and differences in WM connectivity between those at-risk for and in early stages of SZ, a cross-sectional diffusion tensor imaging study of 48 individuals diagnosed with first-episode SZ (FE-SZ), 37 nonpsychotic individuals at a high genetic risk of SZ (GHR-SZ), and 67 healthy controls (HC) was conducted. Decreased fractional anisotropy (FA) in the corpus callosum (CC), anterior cingulum (AC), and uncinate fasciculus (UF) was observed in both the GHR-SZ and FE-SZ groups, while decreased FAs in the superior longitudinal fasciculus (SLF) and the fornix were only seen in the FE-SZ participants. Additionally, both GHR-SZ and FE-SZ showed worse executive performance than HC. The left SLF III FA was significantly positively correlated with hallucinations, and right SLF II was positively correlated with thought disorder. The presence of shared WM deficits in both FE-SZ and GHR-SZ individuals may reflect the genetic liability to SZ, while the disparate FA changes in the FE-SZ group may represent symptom-generating circuitry that mediates perceptual and cognitive disturbances of SZ and ultimately culminates in the onset of psychotic episodes. © 2017 Yifang Zhou et al.


Document Type: Article
Source: Scopus

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22) 

Jovanovic, M.D.a , Svrakic, D.b
Integrative treatment of personality disorder. part i: Psychotherapy
(2017) Psychiatria Danubina, 29 (1), pp. 2-3. 


a Department of Psychology, Faculty of Media and Communications, Karaoreva 65, Belgrade, Serbia
b Department of Psychiatry, Washington University School of Medicine in St Louis, St Louis, United States


Abstract
In this paper, we outline the concept of integrative therapy of borderline personality, also referred to as fragmented personality, which we consider to be the core psychopathology underlying all clinical subtypes of personality disorder. Hence, the terms borderline personality, borderline disorder, fragmented personality, and personality disorder are used interchangeably, as synonyms. Our integrative approach combines pharmacotherapy and psychotherapy, each specifically tailored to accomplish a positive feedback modulation of their respective effects. We argue that pharmacotherapy and psychotherapy of personality disorder complement each other. Pharmacological control of disruptive affects clears the stage, in some cases builds the stage, for the psychotherapeutic process to take place. In turn, psychotherapy promotes integration of personality fragments into more cohesive structures of self and identity, ultimately establishing self-regulation of mood and anxiety. We introduce our original method of psychotherapy, called reconstructive interpersonal therapy (RIT). The RIT integrates humanistic-existential and psychodynamic paradigms, and is thereby designed to accomplish a deep reconstruction of core psychopathology within the setting of high structure. We review and comment the current literature on the strategies, goals, therapy process, priorities, and phases of psychotherapy of borderline disorders, and describe in detail the fundamental principles of RIT.


Author Keywords
Borderline personality;  Integrative treatment;  Personality disorder;  Psychotherapy;  Reconstructive interpersonal therapy


Document Type: Review
Source: Scopus

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23) 

Kozower, B.D.
Pain, pain, go away: The importance of measuring patient-reported outcomes
(2017) Journal of Thoracic and Cardiovascular Surgery, . Article in Press. 

DOI: 10.1016/j.jtcvs.2017.03.031


Washington University School of Medicine, St Louis, Mo


Document Type: Article in Press
Source: Scopus

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24) 

Hanley, D.a , Prichep, L.S.b c , Bazarian, J.d , Huff, J.S.e , Naunheim, R.f , Garrett, J.g , Jones, E.B.h , Wright, D.W.i , O'Neill, J.j , Badjatia, N.k , Gandhi, D.l , Curley, K.C.m n , Chiacchierini, R.o , O'Neil, B.p , Hack, D.C.q
Emergency Department Triage of Traumatic Head Injury Using a Brain Electrical Activity Biomarker: A Multisite Prospective Observational Validation Trial
(2017) Academic Emergency Medicine, . Article in Press. 

DOI: 10.1111/acem.13175


a Brain Injury Outcomes The Johns Hopkins Medical Institutions Baltimore, MD
b Department of Psychiatry New York University School of Medicine New York, NY
c BrainScope Co., Inc. Bethesda, MD
d University of Rochester Medical Center Rochester, NY
e University of Virginia Health System Charlottesville, VA
f Washington University Barnes Jewish Medical Center St. Louis, MO
g Baylor University Medical Center Dallas, TX
h University of Texas Memorial Hermann Hospital Houston, TX
i Emory University School of Medicine and Grady Memorial Hospital Atlanta, GA
j Allegheny General Hospital Pittsburgh, PA
k R. Adams Cowley Shock Trauma Center Baltimore, MD
l Department of Radiology University of Maryland Baltimore, MD
m Iatrikos Research and Development Strategies LLC Tampa, FL
n Department of Surgery Uniformed Services University of the Health Sciences Bethesda, MD
o R. P. Chiacchierini Consulting LLC Gaithersburg, MD
p Detroit Receiving Hospital Detroit, MI
q Brain Health Harpers Ferry, WV


Abstract
Objectives: A brain electrical activity biomarker for identifying traumatic brain injury (TBI) in emergency department (ED) patients presenting with high Glasgow Coma Scale (GCS) after sustaining a head injury has shown promise for objective, rapid triage. The main objective of this study was to prospectively evaluate the efficacy of an automated classification algorithm to determine the likelihood of being computed tomography (CT) positive, in high-functioning TBI patients in the acute state. Methods: Adult patients admitted to the ED for evaluation within 72 hours of sustaining a closed head injury with GCS 12 to 15 were candidates for study. A total of 720 patients (18-85 years) meeting inclusion/exclusion criteria were enrolled in this observational, prospective validation trial, at 11 U.S. EDs. GCS was 15 in 97%, with the first and third quartiles being 15 (interquartile range = 0) in the study population at the time of the evaluation. Standard clinical evaluations were conducted and 5 to 10 minutes of electroencephalogram (EEG) was acquired from frontal and frontal-temporal scalp locations. Using an a priori derived EEG-based classification algorithm developed on an independent population and applied to this validation population prospectively, the likelihood of each subject being CT+ was determined, and performance metrics were computed relative to adjudicated CT findings. Results: Sensitivity of the binary classifier (likely CT+ or CT-) was 92.3% (95% confidence interval [CI] = 87.8%-95.5%) for detection of any intracranial injury visible on CT (CT+), with specificity of 51.6% (95% CI = 48.1%-55.1%) and negative predictive value (NPV) of 96.0% (95% CI = 93.2%-97.9%). Using ternary classification (likely CT+, equivocal, likely CT-) demonstrated enhanced sensitivity to traumatic hematomas (≥1 mL of blood), 98.6% (95% CI = 92.6%-100.0%), and NPV of 98.2% (95% CI = 95.5%-99.5%). Conclusion: Using an EEG-based biomarker high accuracy of predicting the likelihood of being CT+ was obtained, with high NPV and sensitivity to any traumatic bleeding and to hematomas. Specificity was significantly higher than standard CT decision rules. The short time to acquire results and the ease of use in the ED environment suggests that EEG-based classifier algorithms have potential to impact triage and clinical management of head-injured patients. © 2017 Society for Academic Emergency Medicine.


Document Type: Article in Press
Source: Scopus

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25) 

Wegscheid, M.L., Anastasaki, C., Gutmann, D.H.
Human stem cell modeling in neurofibromatosis type 1 (NF1)
(2017) Experimental Neurology, . Article in Press. 

DOI: 10.1016/j.expneurol.2017.04.001


Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, United States


Abstract
The future of precision medicine is heavily reliant on the use of human tissues to identify the key determinants that account for differences between individuals with the same disorder. This need is exemplified by the neurofibromatosis type 1 (NF1) neurogenetic condition. As such, individuals with NF1 are born with a germline mutation in the NF1 gene, but may develop numerous distinct neurological problems, ranging from autism and attention deficit to brain and peripheral nerve sheath tumors. Coupled with accurate preclinical mouse models, the availability of NF1 patient-derived induced pluripotent stem cells (iPSCs) provides new opportunities to define the critical factors that underlie NF1-associated nervous system disease pathogenesis and progression. In this review, we discuss the generation and potential applications of iPSC technology to the study of NF1. © 2017 Elsevier Inc.


Author Keywords
IPSC;  Microglia;  Neurodevelopment;  Neurofibroma;  NF1;  Optic pathway glioma;  Retinal ganglion cell;  Stem cell;  Tumor


Document Type: Article in Press
Source: Scopus

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26) 

Shen, M.D.a b c d e f g h i j k l , Kim, S.H.a b c d e f g h i j k l , McKinstry, R.C.a b c d e f g h i j k l , Gu, H.a b c d e f g h i j k l , Hazlett, H.C.a b c d e f g h i j k l , Nordahl, C.W.a b c d e f g h i j k l , Emerson, R.W.a b c d e f g h i j k l , Shaw, D.a b c d e f g h i j k l , Elison, J.T.a b c d e f g h i j k l , Swanson, M.R.a b c d e f g h i j k l , Fonov, V.S.a b c d e f g h i j k l , Gerig, G.a b c d e f g h i j k l , Dager, S.R.a b c d e f g h i j k l , Botteron, K.N.a b c d e f g h i j k l , Paterson, S.a b c d e f g h i j k l , Schultz, R.T.a b c d e f g h i j k l , Evans, A.C.a b c d e f g h i j k l , Estes, A.M.a b c d e f g h i j k l , Zwaigenbaum, L.a b c d e f g h i j k l , Styner, M.A.a b c d e f g h i j k l , Amaral, D.G.a b c d e f g h i j k l , Piven, J.a b c d e f g h i j k l , Piven, J.m n o p q r , Hazlett, H.C.m n o p q r , Chappell, C.m n o p q r , Dager, S.m n o p q r , Estes, A.m n o p q r , Shaw, D.m n o p q r , Botteron, K.m n o p q r , McKinstry, R.m n o p q r , Constantino, J.m n o p q r , Pruett, J.m n o p q r , Schultz, R.m n o p q r , Zwaigenbaum, L.m n o p q r , Elison, J.m n o p q r , Evans, A.C.m n o p q r , Collins, D.L.m n o p q r , Pike, G.B.m n o p q r , Fonov, V.m n o p q r , Kostopoulos, P.m n o p q r , Das, S.m n o p q r , Gerig, G.m n o p q r , Styner, M.m n o p q r , Gu, H.m n o p q r
Increased Extra-axial Cerebrospinal Fluid in High-Risk Infants Who Later Develop Autism
(2017) Biological Psychiatry, . Article in Press. 

DOI: 10.1016/j.biopsych.2017.02.1095


a Carolina Institute for Developmental Disabilities and Department of Psychiatry, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina
b Department of Biostatistics, School of Global Public Health, University of North Carolina at Chapel Hill School of Global Public Health, Chapel Hill, North Carolina
c MIND Institute and Department of Psychiatry and Behavioral Sciences, University of California, Davis, School of Medicine, Sacramento, California
d Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, Missourt
e Department of Radiology, University of Washington Medical Center, Seattle, Washington
f Department of Speech and Hearing Science, University of Washington, Seattle, Washington
g Institute of Child Development, University of Minnesota, Minneapolis, Minnesota
h Montreal Neurological Institute, McGill University, Montreal, Quebec
i Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada
j Computer Science and Engineering, New York University Tandon School of Engineering, New York, New York
k Department of Psychology, Temple University, Philadelphia, Pennsylvania
l Center for Autism Research, Children's Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania
m Clinical sites-University of North Carolina
n Children's Hospital of Philadelphia
o Data Coordinating Center-Montreal Neurological Institute
p Image Processing Core-New York University
q University of North Carolina
r Statistical Analysis Core-University of North Carolina


Abstract
Background: We previously reported that infants who developed autism spectrum disorder (ASD) had increased cerebrospinal fluid (CSF) in the subarachnoid space (i.e., extra-axial CSF) from 6 to 24 months of age. We attempted to confirm and extend this finding in a larger independent sample. Methods: A longitudinal magnetic resonance imaging study of infants at risk for ASD was carried out on 343 infants, who underwent neuroimaging at 6, 12, and 24 months. Of these infants, 221 were at high risk for ASD because of an older sibling with ASD, and 122 were at low risk with no family history of ASD. A total of 47 infants were diagnosed with ASD at 24 months and were compared with 174 high-risk and 122 low-risk infants without ASD. Results: Infants who developed ASD had significantly greater extra-axial CSF volume at 6 months compared with both comparison groups without ASD (18% greater than high-risk infants without ASD; Cohen's d = 0.54). Extra-axial CSF volume remained elevated through 24 months (d = 0.46). Infants with more severe autism symptoms had an even greater volume of extra-axial CSF from 6 to 24 months (24% greater at 6 months, d = 0.70; 15% greater at 24 months, d = 0.70). Extra-axial CSF volume at 6 months predicted which high-risk infants would be diagnosed with ASD at 24 months with an overall accuracy of 69% and corresponding 66% sensitivity and 68% specificity, which was fully cross-validated in a separate sample. Conclusions: This study confirms and extends previous findings that increased extra-axial CSF is detectable at 6 months in high-risk infants who develop ASD. Future studies will address whether this anomaly is a contributing factor to the etiology of ASD or an early risk marker for ASD. © 2017 Society of Biological Psychiatry.


Author Keywords
Autism;  Brain development;  CSF;  Extra-axial fluid;  Infancy;  MRI


Document Type: Article in Press
Source: Scopus

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27) 

Hudson, D.L.
Quality Over Quantity: Integrating Mental Health Assessment Tools into Primary Care Practice
(2016) The Permanente journal, 20 (3), pp. 90-92. 

DOI: 10.7812/TPP/15-148


Assistant Professor at the Brown School of Social Work at Washington University in St Louis, MO


Abstract
Depression is one of the most common, costly, and debilitating psychiatric disorders in the US. There are also strong associations between depression and physical health outcomes, particularly chronic diseases such as diabetes mellitus. Yet, mental health services are underutilized throughout the US. Recent policy changes have encouraged depression screening in primary care settings. However, there is not much guidance about how depression screeners are administered. There are people suffering from depression who are not getting the treatment they need. It is important to consider whether enough care is being taken when administering depression screeners in primary care settings.


Document Type: Article
Source: Scopus

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28) 

Reisman, M.D.a , Bauer, A.Q.b , Markow, Z.c , Culver, J.P.a b c
Non-invasive functional neuroimaging in the mouse using diffuse optical tomography
(2016) Optics InfoBase Conference Papers, Part F17-OTS 2016, p. 3. 

DOI: 10.1364/OTS.2016.OM4C.7


a Departments of Physics, Washington University, St. Louis, MO, United States
b Departments of Radiology, Washington University, St. Louis, MO, United States
c Departments of Biomedical Engineering, Washington University, St. Louis, MO, United States


Abstract
We present a new technique expanding on previous minimally invasive optical intrinsic signal (OIS) imaging methods to perform non-invasive functional neuroimaging in mice using Structured Illumination combined with Diffuse Optical Tomography. © OSA 2016.


Document Type: Conference Paper
Source: Scopus

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29) 

Eggebrecht, A.T.a , Culver, J.P.a b c
Imaging brain function in children with autism spectrum disorder with diffuse optical tomography
(2016) Optics InfoBase Conference Papers, Part F19-Translational 2016, 3 p. 

DOI: 10.1364/TRANSLATIONAL.2016.JW3A.25


a Department of Radiology, St. Louis, MO, United States
b Department of Physics, St. Louis, MO, United States
c Department of Biomedical Engineering, Washington University School of Medicine, St. Louis, MO, United States


Abstract
We present a feasibility study on applying diffuse optical tomography to school-aged children with autism. Feasibility is tested via assessments of raw data quality and functional activations to language processing and social-perception paradigms. © OSA 2016.


Document Type: Conference Paper
Source: Scopus

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30) 

Orukari, I.a , Bauer, A.Q.b , Baxter, G.A.b , Rubin, J.B.c , Culver, J.P.a b
Alterations in resting state networks in a mouse model of glioma growth
(2016) Optics InfoBase Conference Papers, Part F17-OTS 2016, p. 3. 


a Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, MO, United States
b Department of Radiology, Washington University School of Medicine, St. Louis, MO, United States
c Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, United States


Abstract
The relationship between brain tumor growth and alterations in resting state networks is poorly understood. Functional connectivity optical intrinsic imaging enables assessment of resting state alterations in a mouse model of glioma growth. © OSA 2016.


Document Type: Conference Paper
Source: Scopus

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31) 

Orukari, I.a , Bauer, A.Q.b , Baxter, G.A.b , Rubin, J.B.c , Culver, J.P.a b
Alterations in resting state networks in a mouse model of glioma growth
(2016) Optics InfoBase Conference Papers, Part F19-Translational 2016, 3 p. 

DOI: 10.1364/TRANSLATIONAL.2016.JM3A.45


a Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, MO, United States
b Department of Radiology, Washington University School of Medicine, St. Louis, MO, United States
c Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, United States


Abstract
The relationship between brain tumor growth and alterations in resting state networks is poorly understood. Functional connectivity optical intrinsic imaging enables assessment of resting state alterations in a mouse model of glioma growth. © OSA 2016.


Document Type: Conference Paper
Source: Scopus

https://www.scopus.com/static/images/s.gif


32) 

Eggebrecht, A.T.a , Culver, J.P.a b c
Imaging brain function in children with autism spectrum disorder with diffuse optical tomography
(2016) Optics InfoBase Conference Papers, Part F17-OTS 2016, p. 3. 


a Department of Radiology, Washington University School of Medicine, St. Louis, MI, United States
b Department of Physics, Washington University School of Medicine, St. Louis, MI, United States
c Department of Biomedical Engineering, Washington University School of Medicine, St. Louis, MI, United States


Abstract
We present a feasibility study on applying diffuse optical tomography to school-aged children with autism. Feasibility is tested via assessments of raw data quality and functional activations to language processing and social-perception paradigms. © OSA 2016.


Document Type: Conference Paper
Source: Scopus

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33) 

Karch, C.M.a , Ezerskiy, L.b , Redaelli, V.c , Giovagnoli, A.R.c , Tiraboschi, P.c , Pelliccioni, G.d , Pelliccioni, P.d , Kapetis, D.e , D'Amato, I.c , Piccoli, E.c , Ferretti, M.G.c , Tagliavini, F.c , Rossi, G.c
Missense mutations in progranulin gene associated with frontotemporal lobar degeneration: study of pathogenetic features
(2016) Neurobiology of aging, 38, pp. 215.e1-12. 

DOI: 10.1016/j.neurobiolaging.2015.10.029


a Department of Psychiatry, Washington University School of Medicine, St Louis, MO, USA; Hope Center Program on Protein Aggregation and Neurodegeneration, Washington University School of Medicine, St Louis, MO, USA
b Department of Psychiatry, Washington University School of Medicine, St Louis, MO, USA
c Division of Neurology V and Neuropathology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milano, Italy
d Division of Neurology, Geriatric Hospital, INRCA-IRCCS, Ancona, Italy
e Bioinformatics Unit, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milano, Italy


Abstract
GRN, the gene coding for the progranulin (PGRN) protein, was recognized as a gene linked to frontotemporal lobar degeneration (FTLD). The first mutations identified were null mutations giving rise to haploinsufficiency. Missense mutations were subsequently detected, but only a small subset has been functionally investigated. We identified missense mutations (C105Y, A199V, and R298H) in FTLD cases with family history and/or with low plasma PGRN levels. The aim of this study was to determine their pathogenicity. We performed functional studies, analyzing PGRN expression, secretion, and cleavage by elastase. GRN C105Y affected both secretion and elastase cleavage, likely representing a pathogenic mutation. GRN A199V did not alter the physiological properties of PGRN and GRN R298H produced only moderate effects on PGRN secretion, indicating that their pathogenicity is uncertain. In the absence of strong segregation data and neuropathological examinations, genetic, biomarker, and functional studies can be applied to an algorithm to assess the likelihood of pathogenicity for a mutation. This information can improve our understanding of the complex mechanisms by which GRN mutations lead to FTLD. Copyright © 2016 Elsevier Inc. All rights reserved.


Author Keywords
Frontotemporal lobar degeneration;  Functional analysis;  GRN;  Mutation;  Pathogenetic;  Progranulin


Document Type: Article
Source: Scopus

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34) 

Perrino, C.M.a , Zynger, D.L.b
Adrenal neuroendocrine tumors: Pheochromocytoma and neuroblastic tumors
(2016) Neuroendocrine Tumors: Review of Pathology, Molecular and Therapeutic Advances, pp. 323-357. 

DOI: 10.1007/978-1-4939-3426-3_17


a Department of Pathology and Immunology Campus, Washington University, St. Louis, MO, United States
b Department of Pathology, The Ohio State University Wexner Medical Center, Columbus, OH, United States


Abstract
The adrenal medulla forms from sympathetic ganglion arising from the neural crest. Primitive sympathecoblasts mature into chromaffin cells which produce catecholamines. Pheochromocytomas are tumors arising from the chromaffin cells within the adrenal gland. These tumors are termed paraganglioma if arising from chromaffin cells outside of the adrenal. In embryonic development, sympathecoblasts form clusters which during embryogenesis can remain in or nearby the adrenal. These primitive clusters are hypothesized to be the source of neuroblastic tumors, such as neuroblastoma, and can arise throughout the sympathoadrenal neuroendocrine system. © Springer Science+Business Media, LLC 2016.


Author Keywords
Ganglioneuroblastoma;  Ganglioneuroma;  Neuroblastic tumors;  Neuroblastoma;  Pheochromocytoma


Document Type: Book Chapter
Source: Scopus