July, 2011
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Society of Biological Psychiatry
"Scientists collaborating to eliminate the the suffering of mental illness."
In This Issue
SOBP Vision Statement
Message from the Editor
2011 Annual Meeting Other HiLites
2012 Meeting Announcement
Journal Updates
Welcome New Members
Membership Renewals
Get Involved
SOBP Contact Information
SOBP Vision Statement

The vision of the Society of Biological Psychiatry is to integrate, advance, and promulgate science relevant to psychiatric disorders, in order to reduce or prevent the suffering of people with these conditions.

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In This Issue 

(A brief summary of articles in current issue)

Message from the Editor

Strakowski picture with monitor 2011 Annual Meeting Update 

On May 12, 1253 clinical and basic behavioral neuroscientists descended upon the city of San Francisco and launched the 66th Annual Meeting of our society. By any measure, this meeting was wildly successful. The lecture hall was filled for 11 plenary talks that were uniformly excellent. These talks challenged our preconceptions and pushed us to think 'outside the box' as we move our field forward. Complementing these plenary sessions were 48 symposia, five oral sessions and two workshops that spanned the entire gamut from animal behavioral genetics to psychiatric clinical trials. The most up-do-date science was presented in three 'late breaking' oral and poster sessions. Finally, the poster  sessions were packed with many of our future research stars (i.e., junior investigators) presenting 732 posters that contained novel and clever science to challenge the older attendees to stay on their toes and keep actively reviewing our assumptions. Without a doubt, this meeting was one of SOBP's finest scientific programs and we must thank the outstanding leadership and work of Helen Mayberg, Karen Berman and the Program Committee for this accomplishment. Other details about this meeting are presented elsewhere in this newsletter.    

Obviously, then, our outstanding 66th annual meeting reflects the health of a strong Society of Biological Psychiatry (SOBP).  Our membership continues to propel behavioral neuroscience forward, and we were very pleased with the large non-member participation in San Francisco. In addition to the excellent meeting attendance and high quality presentations made there, our journal Biological Psychiatry continues steadily to rise in impact factor and has become the most important behavioral neuroscience journal available. Members reading this newsletter have every reason to be proud of the Society of Biological Psychiatry. A major goal of the Society's leadership is to continue to grow SOBP to represent broadly behavioral neuroscientists and to increase the 'brain power' of our participants. Members, we ask that you discuss the meeting with others in your department, encouraging them to join our society. Nonmembers who receive this newsletter, we hope that you will consider applying for membership in SOBP - we appreciated your support for the annual meeting and hope to see you join our membership rolls to keep SOBP growing and thriving.

Best wishes to everyone and thanks for your support of SOBP

Stephen M. Strakowski, MD

Senior Associate Dean for Research, UCCOM

Vice President of Research, UC Health 

The Dr. Stanley and Mickey Kaplan Professor and Chairman

Dept. of Psychiatry, University of Cincinnati


2011 Annual Meeting - Other Hi-Lites 

The Society presented the following awards at the meeting.  Please join us in congratulating the following award recipients:


 Gold Medal Award                            George N. Thompson Award        

2011 Gold Medal Award              Geroge N. Thompson Award 

Judith L. Rapoport, MD                                        John Krystal, MD

NIMH                                                                    Yale University


A.E. Bennett Research Award             Ziskind-Somerfeld Research Award

Bennett Award              2011 Ziskind Award

Jeffrey H. Meyer, MD                                           Melissa Malvaez, MS

University of Toronto                                           University of California, Irvine  


Humanitarian Award                         

Kay Jamison, MD 


Kay Redfeld Jamison, MD                                          

Johns Hopkins                                                                                       


Travel Fellowship Awards.

At the travel award breakfast on Saturday morning, the Society awarded 12 Travel Fellowship Awards to young investigators.  These awards are another way in which the Society supports future investigators and encourages these young researchers to become involved in the Society.  


Society of Biological Psychiatry Top Poster Award

47 posters in basic and clinical/translational research were nominated for this award.  A committee reviewed and scored each of these posters during their poster presentation.  The Society is pleased to announce the following Top Poster Awards:


Top Poster - Basic Research

Angela Bongaarts - Allen Institute for Brain Science

Gene Expression Patterns in the DLPFC of Patients with Schizophrenia and Controls

Abstract #753 


Top Poster - Clinical/Translational Research

Philip Shaw - NIMH

Anomalous Development of Cortical Surfaces in Attention-Deficit/Hyperactivity Disorder 

Abstract #281 


Poster Presentations.

This year, the Society invited all poster presenters to deposit their poster with FACULTY of 1000 (F1000), an open access repository of conference posters and oral presentations. Many of our poster presenters have deposited their posters and one poster presented at the meeting was selected by the FACULTY of 1000 for the coveted Poster of the Week.


Mentor/Mentee Program

The Society of Biological Psychiatry recognizes the importance of mentoring to the professional development of its members. This mentoring program provides opportunities for early-career biological psychiatrists and neuroscientists to benefit from access to more experienced professionals while giving mentors the opportunity to contribute to the future of the neuroscience profession.  This year, the Society hosted 16 Mentor/Mentees at the 2011 meeting.  If you are interested in becoming a mentee or mentor for the 2012 meeting in Philadelphia, apply now.  


View the Program Materials   

You may view the entire program by using the On-Line Program Planner. 


You may download the abstract book to your ebook or smart phone so you can search for information, mark abstracts, and make notes using the Ebook technology.  Click here to download instructions for a variety of devices.


Find us on Facebook 

Visit us on Facebook to view additional pictures from the meeting.


Mark Your Calendars Now

2012 Annual Meeting in Philadelphia

May 3-5, 2012



2012 Annual Meeting Announcement 


Society of Biological Psychiatry's 67th Annual Meeting

May 3-5, 2012

Sheraton Philadelphia Downtown Hotel

Philadelphia, Pennsylvania


"Systems Neuroscience:  Applications to Psychiatric Illnesses"  


Plan now to submit an abstract and attend the annual meeting in Philadelphia.  


Important Dates:

September 1, 2011 - Abstract Submission Opens
October 24, 2011 - Overall Symposium Proposal Due
October 31, 2011 - Individual Symposium Abstracts Due
December 12, 2011 - Oral and Poster Abstracts Due 

January 9, 2012 - Hotel and Meeting Registration Opens

February 20, 2012 - Late Breaking Abstract Submission Opens*

March 16, 2012 - Late Breaking Abstracts Due*

April 20, 2012 - Registration Closes


*Tentative Dates - Subject to Change


Brochure and other meeting information will be available September 1, 2011.   

Check back frequently at www.sobp.org

For questions, email sobp@sobp.org


Journal Updates


Biological Psychiatry Cover Picture

By Caleb M. Adler, MD

Important findings published in Biological Psychiatry



March 15, 2011  


Commentary by Jordan W. Smoller

Mui˝os-Gimeno M, Espinosa-Parrilla Y, Guidi M, et al (2011).  

Human microRNAs miR-22, miR-138-2, miR-148a, and miR-488 are associated with panic disorder and regulate several anxiety candidate genes and related pathways. Biol Psychiatry;69:526-533    


Ernst C, Wanner B, Brezo J, et al (2011). A deletion in tropomyosin-related kinase B and the development of human anxiety. Biol Psychiatry;69:604-607


Despite increasing knowledge of the underlying neurophysiology of anxiety disorders, relatively few studies of the genetics of these disorders have been done. In this issue, two studies examining genetic aspects of anxiety disorders are reported. Muinos-Gimeno and colleagues identified single-nucleotide polymorphisms (SNPs) to be associated with panic disorder and related phenotypes; though the replication was not significant after controlling for multiple  comparisons. Further studies showed that some of the relevant SNPs were involved in regulating candidate genes for anxiety disorders. Ernst and colleagues reported on a relatively rare, eleven base pair deletion in a candidate gene for mood and anxiety disorders that is associated with increased anxiety symptoms in children and the appearance of adult anxiety disorders. Although these reports are limited in power, they suggest the need for large-scale, collaborative follow-up studies.


Commentary by Natalina Salmaso and Flora M. Vaccarino

Eren-Košak E, Turner CA, Watson SJ, et al (2011). Short-hairpin RNA silencing of endogenous fibroblast growth factor 2 in rat hippocampus increases anxiety behavior. Biol Psychiatry;69:534-540


Anxiety disorders affect almost 20% of Americans. Although pharmacological approaches have shown considerable efficacy, significant clinical limitations remain. Recent studies have suggested that fibroblast growth factor 2 (FGF2) may play a role in anxiety and mood disorders. In this issue, Eren-Košak and colleagues report data that suggest that hippocampal levels of FGF2 correlate to individuals' vulnerability and resilience with respect to anxiety and mood disorders. These findings represent some of the first experimental evidence that FGF2 is involved in the development of anxiety.


Commentary by James W. Murrough and Dennis S. Charney


Pluess M , Velders FP, Belsky J, et al (2011). Serotonin Transporter polymorphism moderates effects of prenatal maternal anxiety on infant negative emotionality. Biol Psychiatry;69:520-525


Montag C, Fiebach CJ, Kirsch P, et al (2011). Interaction of 5-HTTLPR and a variation on the

oxytocin receptor gene influences negative emotionality. Biol Psychiatry;69:601-603


Homberg JR, Lesch K-P (2011). Looking on the bright side of serotonin transporter gene variation. Biol Psychiatry;69:513-519


Despite the enormous promise of genetic research, little progress has been made in identifying specific gene variants in patients with psychiatric disorders. One approach might be to focus on links between candidate genes and intermediate phenotypes, rather than more complicated, DSM-IV diagnoses. Pleuss and colleagues report that the 5-HTTLPR short allele is associated with a link between prenatal maternal anxiety and increased negative emotionality in infants. Montag and colleagues showed an interaction between the 5-HTTLPR long allele and a variant of a single nucleotide polymorphism on the oxytocin receptor gene. Individuals homozygous for both showed an effect on personality assessments, suggesting an interaction between serotonergic and oxytocinergic systems in the expression of personality. Homberg and Lesch place these studies in further perspective in their review of recent findings suggesting that the 5-HTTLPR short allele may confer situational advantages related to enhanced reactivity of the corticolimbic neural circuitry.


April 1, 2011 


Commentary by Theodora Duka

Andrews MM, Meda SA, Thomas AD, et al (2011). Individuals family history positive for alcoholism show functional magnetic resonance imaging differences in reward sensitivity that are related to impulsivity factors. Biol Psychiatry;69:675-683


Drug and alcohol abuse has been associated with both a reward deficiency syndrome and increased impulsivity. In this issue, Andrews and colleagues used fMRI to demonstrate blunted activation of the nucleus accumbens (NAcc) during performance of a monetary incentive delay task in subjects with a family history of alcoholism, as well as altered activation in other areas associated with reward. NAcc activity was inversely correlated with elements of impulsivity, linking these two constructs.


Commentary by Hitoshi Morikawa and R. Adron Harris

Mulholland PJ, Becker HC, Woodward JJ, et al (2011). Small conductance calcium-activated potassium type 2 channels regulate alcohol-associated plasticity of glutamatergic synapses. Biol Psychiatry;69:625-632


Hopf FW, Simms JA, Chang S-J, et al (2011). Chlorzoxazone, an SK-type potassium channel

activator used in humans, reduces excessive alcohol intake in rats. Biol Psychiatry;69:618-624


Several lines of recent evidence suggest that calcium-activated potassium (SK) channels might represent a target for novel therapeutics targeting alcohol use disorders. In this issue, Mulholland and colleagues report on data suggesting that alcohol exposure disrupts the SK channel-NMDA receptor feedback loop in the hippocampus of a Sprague-Dawley rat model. In addition, chronic alcohol exposure increased expression of NMDA receptor subunits, supporting suggestions that changes in SK channels and NMDA receptors are related to ethanol-related plasticity. In a related study, Hopf  and colleagues examined whether the positive SK modulator, chlorzoxazone (CZX) would reduce alcohol consumption in a group of Wistar rats. Systemic injection of CZX into rats with intermittent access to alcohol (IAA) was associated with reduced alcohol preference and less initial alcohol consumption; these effects were not seen in rats with continuous access. CZX was also associated with enhanced excitability and increased CZX inhibition of core neurons in the nucleus accumbens, particularly in rats with IAA. Together these studies support suggestions that SK channel activators such as CZX might eventually be employed to treat alcohol withdrawal and decrease consumption in patients with alcohol use disorders.


Commentary by Joel Gelernter

Ducci F, Kaakinen M, Pouta A, et al (2011). TTC12-ANKK1-DRD2 and CHRNA5-CHRNA3-CHRNB4 influence different pathways leading to smoking behavior from adolescence to mid-adulthood. Biol Psychiatry;69:650-660


Several single nucleotide polymorphisms in gene clusters associated with smoking behavior were found to be associated with smoking. Carriers of three or more risk alleles had increased odds of smoking regularly, compared to individuals with no risk alleles. Some effects appeared to be mediated by early influence on smoking habits and others by novelty seeking, while some of these effects appeared to be more direct.


April 15, 2011 


Commentary by James W. Murrough and Alexander Neumeister

McDevitt RA, Hiroi R, Mackenzie SM, et al (2011). Serotonin 1B autoreceptors originating in the caudal dorsal raphe nucleus reduce expression of fear and depression-like behavior. Biol Psychiatry;69:780-787


The 5HT1B serotonin receptor is being increasingly viewed as playing a potentially important role in depressive and anxiety disorders, raising the possibility of new treatments targeting this receptor. In this issue, McDevitt and colleagues report their findings that overexpression of

5HT1B through viral mediated gene transfer in the caudal dorsal raphe nucleus impacted expressions of helplessness and fear in Sprague-Dawley rats without affecting evidence of anxiety. They also observed decreased freezing behavior with administration of the 5HT1B agonist CP-94,253. Potential therapeutic applications are complicated however, by the functional disparities between subpopulations of the 5HT1B receptor.


Commentary by Jennifer A. Bartz

Bilderbeck AC, McCabe C, Wakeley J, et al (2011). Serotonergic activity influences the cognitive appraisal of close intimate relationships in healthy adults. Biol Psychiatry;69:720-725


Potential neurochemical mediators of human intimacy have recently come under increasing research focus. As part of this research, serotonin has been widely associated with effects on a variety of mood states. In this issue, Bilderbeck and colleagues report that tryptophan-depleted adults viewing pictures of couples judged them to be less "intimate" and "romantic" than did adults who had ingested a tryptophan-containing drink prior to testing. In addition, tryptophan depleted women viewed men as more dominant in the relationships pictured, and described couples pictured touching each other to be more able to resolve their conflicts. These findings emphasize the role that serotonin has been suggested to play in interpersonal relationships, and highlights the possible connection between serotonin dysfunction in numerous psychiatric disorders and interpersonal difficulties often associated with these disorders.


Commentary by Pedro L. Delgado

Feder A, Skipper J, Blair JR,, et al (2011). Tryptophan depletion and emotional processing in healthy volunteers at high risk for depression. Biol Psychiatry;69:804-807


Tryptophan depletion has previously been associated with depression in high-risk individuals. In this issue, Feder and colleagues show that tryptophan depletion in adolescents at high risk for major depressive disorder is associated with increased rates of inappropriate responses to sad distractors in an affective go/no-go task. In contrast, there was no effect on emotionally neutral decision making. They conclude that serotonin might be more closely linked to affective processing than to mood state.

May 1, 2011 


Commentary by Matthew W. State

Stein MB, Yang BZ, Chavira DA, et al (2011). A common genetic variant in the neurexin superfamily member CNTNAP2 is associated with increased risk for selective mutism and social anxiety-related traits. Biol Psychiatry;69:825-831


Stein and colleagues report an association between a variation in the neuronal adhesion molecule, Contactin-Associated Protein-like 2 (CNTNAP2) which has been implicated in autism, and risk for selective mutism. These findings suggest some commonalities between autism spectrum disorders and social anxiety. In a larger context, these findings highlight the potentially pleiotropic effects of individual genes.


Commentary by Robert R. Ring

Sala M, Braida D, Lentini D, et al (2011). Pharmacologic rescue of impaired cognitive flexibility, social deficits, increased aggression, and seizure susceptibility in oxytocin receptor null mice: a neurobehavioral model of autism. Biol Psychiatry;69:875-882


Autism spectrum disorders (ASD) are attracting increasing attention and funding as public awareness of these disorders grows. This growth has also fueled increased interest on the part of the pharmaceutical industry and emerging recognition of potential neurophysiological overlap between ASD and other psychiatric disorders such as schizophrenia. In this issue, Sala and colleagues show that oxytocin receptor null mice exhibit autistic-like behaviors including cognitive inflexibility that are alleviated by the intracerebral administration of oxytocin and vasopressin. Their increased seizure activity, also often observed in ASD, similarly responded to oxytocin administration. The authors suggest that in the absence of the oxytocin receptor activity is mediated through an arginine vasopressin receptor (V1a). In a linked finding, the authors note that hippocampal neurons from oxytocin receptor null mice showed decreased GABA-ergic synapses. They suggest that oxytocin receptor null mice might serve as a useful model for studying treatment of ASD.


Commentary by Clyde Franks

Recent studies have implicated a novel group of genes coding for a group of synaptic adhesion proteins, termed the  leucine-rich repeat transmembrane neuronal family (LRRTM) in a range of psychiatric pathology. These studies suggest that LRRTMs may play a role in "fine tuning" synapse function. While the precise role of LRRTMs in the manifestation of psychiatric disorders remains unclear, hypotheses include effects on laterality, glutamatergic synaptic transmission, and synaptic pruning. Future studies will need to include epigenetic studies of the LRRTM gene family and examine the effects of these genes on cognition and other potential phenotypic expressions.


May 15, 2011 


Commentary by Maria Jalbrzikowski and Carrie E. Bearden

Kates WR, Antshel KM, Faraone SV, et al (2011). Neuroanatomic predictors to prodromal psychosis in velocardiofacial syndrome (22q11.2 deletion syndrome): a longitudinal study. Biol Psychiatry;69:945-952


Recent evidence suggests that schizophrenia is associated with greater genetic heterogeneity than was previously thought, indicating a need to focus on rare, highly penetrant genetic variants. Velocardiofacial syndrome (VCFS) results from one such rare variant; while it accounts for only one to two percent of schizophrenic patients, almost one third of these individuals will go on to develop schizophrenia. In this issue, Kates and colleagues report increased frontal gray and white matter volumes, as well as increased amygdala and lateral ventricle in patients with VCFS. Over time, total schizophrenia prodromal symptoms were predicted by alterations in multiple brain regions, while decrements in temporal gray matter and verbal IQ were predicative of the development of positive prodromal symptoms. These findings are interpreted in light of previous studies of non-VCFS individuals at risk for schizophrenia.


Commentary by Heike Tost and Andreas Meyer-Lindenberg

Nixon DC, Prust MJ, Sambataro F, et al (2011). Interactive effects of DAOA (G72) and catechol-O-methyltransferase on neurophysiology in prefrontal cortex. Biol Psychiatry;69:1006-1008


Schizophrenia research has long focused on two  neurotransmitters, dopamine and glutamate. More recent evidence suggests extensive interactions between the two systems at both cellular and network levels. Using fMRI, Nixon and colleagues report a functional epistasis in healthy individuals, of D-amino acid oxidase activator (DAOA) by catechol-O-methyltransferase (COMT) manifested by effects on efficiency within the dorsolateral prefrontal cortex during performance of a working memory task. This study uses working memory as an intermediate phenotype to provide a functional confirmation of an epistasis suggested to impact schizophrenia risk.

June 1, 2011 


Commentary by Eisuke Koya and Bruce T. Hope

Kim J, Park BH, Lee JH, et al (2011). Cell type-specific alterations in the nucleus accumbens by repeated exposures to cocaine. Biol Psychiatry;69:1026-1034


Rothwell PE, Kourrich S, Thomas MJ (2011). Synaptic adaptations in the nucleus accumbens caused by experiences linked to relapse. Biol Psychiatry;69:1124-1126


Dopamine receptors in the nucleus accumbens have long been implicated in substance use disorders. Little is known however, about differences in cocaine related synaptic changes between D1 receptors (D1R) and D2 receptors (D2R). In this issue, Kim and colleagues analyzed the effects of injected cocaine on D1R and D2R medium spiny neurons of the nucleus accumbens of transgenic mice. They found that D1R neurons demonstrated increased spine density, coupled with decreased membrane excitability and increased frequency of miniature excitatory post-synaptic currents after repeated cocaine injections. In contrast, D2R showed decreased excitatory post-synaptic current and no change in membrane excitability. Miniature inhibitory post-synaptic currents were decreased in D1R neurons but unchanged in D2R neurons. In a complementary study, Rothwell and colleagues found that experiences associated with reinstatement, a rodent model of drug relapse are linked to reduced excitatory synaptic strength in the nucleus accumbens shell, as are stress and drug re-exposure. These findings suggest that this change in the nucleus accumbens represents a common synaptic modification associated with drug relapse. Together, these studies support the role of synaptic changes in the nucleus accumbens in substance use disorders.


Commentary by Andrew Holmes

Nam HW, Lee MR, Zhu Y, et al (2011). Type 1 equilibrative nucleoside transporter regulates ethanol drinking through accumbal N-methyl-D-aspartate receptor signaling. Biol Psychiatry;69:1043-1051


Although pharmacologic interventions for alcohol use disorders remain limited, there have been significant advances in understanding the neuropharmacology of alcohol exposure. In this issue, Nam and colleagues report on their study of mice lacking the equilibrative nucleoside transporter gene (ENT1), which have been previously demonstrated to exhibit increased ethanol preferring behavior. Using a range of techniques, the authors demonstrated that ENT1 is involved with NMDA glutamate receptor-mediated signaling in the nucleus accumbens, and is linked to the behavioral changes in ENT negative mice. These studies may suggest future areas for treatment of alcohol use disorders.



Commentary by Stephanie S. O'Malley

Garza D, Murphy M, Tseng LJ, et al (2011). A double-blind randomized placebo-controlled pilot study of neuropsychiatric adverse events in abstinent smokers treated with varenicline or placebo. Biol Psychiatry;69:1075-1082


The characterization of neuropsychiatric adverse effects (NPAEs)  can be complicated; recent post marketing reports have suggested that varenicline may be associated with a range of NPAEs not observed in previous clinical trials. In this issue, Garza and colleagues report on a double-blind, placebo-controlled study of NPAEs in smokers receiving varenicline. They report no clinically significant differences on measures of mood, anxiety, or hostility. Efforts were made to control for potential confounds by selecting patients without existing psychiatric conditions and using a two week inpatient hospitalization to ensure comparable smoking cessation rates. The study was not however, powered to detect rare NPAEs, and did not test for the potential effects of stressful events. In addition, because smokers with a psychiatric history were excluded, these findings cannot be generalized to that large population.


June 15, 2011 


Commentary by Amy F.T. Arnsten and B.J. Casey


Understanding of the role of prefrontal cortical networks in both healthy neurophysiology and neuropathological conditions has increased significantly over the past few years, impacting research into a range of mood, psychotic and attention disorders. This special issue includes a range of studies examining different aspects of prefrontal networks in preclinical and clinical populations. Together, these studies highlight the emerging role of clinical neuroscience in our conceptualization of psychiatric illnesses- and the potential this increased understanding might play have for facilitating early identification and treatment of these illnesses.


Members of SOBP receive Biological Psychiatry as part of their membership    Click here to learn more about this prestigious journal.


Top 6 Reasons to Publish in Biological Psychiatry  
1.  High Impact Factor - 8.674
2.  4th of 126 Psychiatry Journals
3.  15th of 237 Neuroscience Journals
4.  1st Decision - 30 Days
5.  ePubs - 6 Weeks
6.  In Print - 4 Months

Welcome New Members
Please welcome the following new members to the Society. 
NikaAdhamForest Research Institute
SchahramAkbarianUniversity of Massachusetts Medical School
MatthewAlbaughUniversity of Vermont
JorgeAlmeidaUniversity of Pittsburgh Medical Center
FelixBacigalupoUniversity of California Davis
Darrick T.BaluHarvard University
SegevBarakGallo Research Center, UCSF
Robert D. BeechYale University
AndrewBergenSRI International
Jon BernerPrivate Practice
NicholasBoloHarvard Medical School
Angela L. BongaartsAllen Institute for Brain Science
KarinBorgmann-WinterUniversity of Pennsylvania
ElisaBrietzkeUniversity of Sao Paulo
ClaudiaBussUniversity of California, Irvine
Brandon John CornejoUniversity of Wisconsin
Kathryn ReganCullenUniversity of Minnesota
Zafiris J.DaskalakisCentre for Addiction and Mental Health
RudiDe RaedtGhent University
DanielledeCampoUniversity of Rochester
MollyEmbreeEmory University
AmitEtkinStanford University
Kevin JosephFomalontEmory University
IgorGalynkerBeth Israel Medical Center
KennethGarciaLong Island College Hospital
Stephen E.GilmaHarvard School of Public Health
VinaGoghariUniversity of Calgary
James M. GoldUniversity of Maryland School of Medicine
IrvingGottesmanUniversity of Minnesota
RodrigoGrassi-OliveiraPontifical Catholic University of Rio Grande do Sul
StaciGruberMcLean Hospital - Harvard Medical School
SalvadorGuinjoanFLENI - Psychiatry and Cognitive Neurology
RubenGurUniversity of Pennsylvania
EbrahimHaroonEmory University
MaryHeitzegUniversity of Michigan
Ulrich MichaelHemmeterCanton of St. Gallen /Switzerland
AvinashHosanagarUniversity of Michigan
JosephHulihanJohnson & Johnson
Johanna M.JarchoNIH
SarahKeedyUniversity of Illinois, Chicago
David N.KennedyU. Massachusetts Medical
MichaelKiangMcMaster University
HeideKlumppUniversity of Michigan
BernatKocsisHarvard Medical School
JeffreyKoganAstellas Research Institute of America
ChristopherKyePrivate Practice
ChristineLarsonUniversity of Wisconsin-Milwaukee
ChunyuLiuUniversity of Chicago
NancyLowMcGill University
KaiMacDonald UCSD
GiovanniMarzulloPer Aspera Research Foundation
Brian J. MickeyUniversity of Michigan
MariaMorabitoUniversity of Massachusetts Medical School
YuvalNeriaNew York State Psychiatric Institute
FabianoNeryUniversity of Sao Paulo
Tuong-ViNguyenMcGill University - Montreal
Alexander B.NiculescuIndiana University School of Medicine
MargaretaNiznikiewiczHarvard Medical School
Tim F. OberlanderUniversity of British Columbia
GillianO'DriscollMcGill University
JonathanOlerUniversity of Wisconsin-Madison
ElizabethOsuchUniversity of Western Ontario
Rajeev PanguluriUniversity of Mississippi
Roy H. PerlisMGH Psychiatry Center for Experimental Drugs and Diagnostics
MarcusRonaldBristol-Myers Squibb
Roberto B.Sassi Centre for Mountain Health Services
KirtiSaxenaUT Health Science  Houston
DanielaSchillerNew York University
Michael BretSchneiderNeoStim Inc.
Steven E.SheltonUniversity of Wisconin-Madison
EdwardShortMedical University of South Carolina
Tony J. SimonUniversity of California, Davis
DorothySitUniversity of Massachusetts Medical Center
GwennSmithJohns Hopkins School of Medicine
MichaelStevensOlin Neuropsychiatry Research Center
ArdesheerTalatiNew York State Psychiatric Institute
IndiraTendolkarDonders Institute
Heidi W.ThermenosHarvard Medical School
Moriah E.ThomasonWayne State University
HeikeTostNational Institute of Mental Health
SusannahTyeDeakin University
RudolfUherKing's College London
KaterinaVelanovaUniversity of Pittsburgh
GerardoVillarrealUniversity of New Mexico
ChristopherWallMayo Clinic
Tony W. WilsonUniversity of Nebraska Medical Center
Stephen J. WoodUniversity of Birmingham

If you are interested in joining the Society please visit www.sobp.org or email sobp@sobp.org.  We will be happy to answer any questions you may have regarding the Society or find a sponsor for your application. 


Membership Renewals for 2012
2012 Membership Renewals due December 31, 2011

Stay connected and engaged - Renew your membership for 2012 now
and continue to receive your member benefits:    
  1. Subscription to our top-rated journal, Biological Psychiatry
  2. Reduced registration fees for the annual meetring
  3. Sponsor abstracts and membership applications
  4. Access to members-only on-line tools
  5. Leadership opportunities on committees or officers
  6. Recognition and affiliation with a premier organization
  7. Networking and professional development
Renew on-line at www.sobp.org.  If you need your login information or an invoice for payment email sobp@sobp.org

Renewal invoices for 2012 will be emailed to you August. 2011  If you do not receive or have questions, please let us know.  Email sobp@sobp.org
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Society of Biological Psychiatry Newsletter Editorial Staff 

Stephen M. Strakowski, MD, Editor

Editorial Board
Helen Mayberg, MD
William B. Lawson, MD, PhD
Alan H. Young, MD, PhD
Caleb M. Adler, MD
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