Complex psychiatry最新文献

{"title":"Contents Vol. 7, 2021","authors":"","doi":"10.1159/000521008","DOIUrl":"https://doi.org/10.1159/000521008","url":null,"abstract":"Elizabeth G. Atkinson – Broad Institute of MIT and Harvard, Boston, MA, USA Dimitrios Avramopoulos – Johns Hopkins University, Baltimore, MD, USA Mounira Banasr – University of Toronto, Toronto, ON, Canada Cathy L. Barr – Toronto Western Research Institute, Toronto, ON, Canada Kristen Brennand – Icahn School of Medicine at Mount Sinai, New York, NY, USA William Byerley – University of California, San Francisco, CA, USA Karmel W. Choi – Massachusetts General Hospital, Boston, MA, USA Jonathan R.I. Coleman – King’s College London, London, United Kingdom Kelly Cosgrove – Yale University, New Haven, CT, USA Shareefa Dalvie – University of Cape Town, Cape Town, South Africa Lea K. Davis – Vanderbilt University, Nashville, Nashville, TN, USA Jubao Duan – University of Chicago, Chicago, IL, USA Howard J. Edenberg – Indiana University, Indianapolis, IN, USA Joshua Gordon – National Institute of Mental Health, Bethesda, MD, USA Jeremy Hall – Cardiff University, Cardiff, United Kingdom Steven E. Hyman – Harvard University, Cambridge, MA, USA Emma C. Johnson – Washington University, St. Louis, MO, USA James L. Kennedy – Centre for Addiction and Mental Health, Toronto, ON, Canada John Krystal – Yale School of Medicine, New Haven, CT, USA Ming Li – Kunming Institute of Zoology, Kunming, China Brady Maher – Lieber Institute, Baltimore, MD, USA Anil K. Malhotra – The Zucker Hillside Hospital, Glen Oaks, NY, USA Daniel Martins-de-Souza – University of Campinas, Campinas, Brazil Janitza L. Montalvo-Ortiz – Yale University, West Haven, CT, USA Daniel J. Mueller – Centre for Addiction and Mental Health, Toronto, ON, Canada Roseann E. Peterson – Virginia Commonwealth University, Richmond, VA, USA Konasale M. Prasad – University of Pittsburgh, Pittsburgh, PA, USA Sandra Roige-Sanchez – University of California San Diego, La Jolla, CA, USA Christopher A. Ross – John Hopkins University, Baltimore, MD, USA Takeshi Sakurai – Kyoto University, Kyoto, Japan Dorothy Sit – Northwestern University, Chicago, IL, USA Hang Zhou – Yale University, West Haven, CT, USA Complex Psychiatry","PeriodicalId":72654,"journal":{"name":"Complex psychiatry","volume":"27 1","pages":"I - IV"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74117766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ankyrin-G Heterozygous Knockout Mice Display Increased Sensitivity to Social Defeat Stress.","authors":"Zachary A Cordner, Seva G Khambadkone, Shanshan Zhu, Justin Bai, R Rasadokht Forti, Ethan Goodman, Kellie L K Tamashiro, Christopher A Ross","doi":"10.1159/000518819","DOIUrl":"10.1159/000518819","url":null,"abstract":"<p><p>The <i>ANK3</i> locus has been repeatedly found to confer an increased risk for bipolar disorder. <i>ANK3</i> codes for Ankyrin-G (Ank-G), a scaffold protein concentrated at axon initial segments, nodes of Ranvier, and dendritic spines, where it organizes voltage-gated sodium and potassium channels and cytoskeletal proteins. Mice with homozygous conditional knockout of Ank-G in the adult forebrain display hyperactivity and reduced anxiety-like behaviors, responsive to mood stabilizers. Their behavior switches to a depression-like phenotype when exposed to chronic social defeat stress (SDS), and then spontaneously reverts to baseline hyperactivity. Ank-G heterozygous conditional knockouts (Ank-G Het cKO) have not previously been characterized. Here, we describe the behavior of Ank-G Het cKO mice compared to littermate controls in the open field, elevated plus maze, and forced swim test, under both unstressed and stressed conditions. We found that Ank-G Het cKO is not significantly different from controls at baseline or after chronic SDS. The chronic stress-induced \"depression-like\" behavioral phenotype is persistent for at least 28 days and is responsive to fluoxetine. Strikingly, Ank-G Het cKO mice display increased sensitivity to a short duration SDS, which does not affect controls. The heterozygous Ank-G genetic model may provide novel insights into the role of Ank-G in the pathophysiology of stress sensitivity and \"depression-like\" phenotypes and could be useful for studying Ank-G-related gene-environment interactions.</p>","PeriodicalId":72654,"journal":{"name":"Complex psychiatry","volume":" ","pages":"71-79"},"PeriodicalIF":0.0,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8740233/pdf/cxp-0007-0071.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40670821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Improved Framework for Content- and Link-Based Web-Spam Detection: A Combined Approach","authors":"A. Shahzad, Nazri M. Nawi, M. Z. Rehman, Abdullah Khan","doi":"10.1155/2021/6625739","DOIUrl":"https://doi.org/10.1155/2021/6625739","url":null,"abstract":"In this modern era, people utilise the web to share information and to deliver services and products. The information seekers use different search engines (SEs) such as Google, Bing, and Yahoo as tools to search for products, services, and information. However, web spamming is one of the most significant issues encountered by SEs because it dramatically affects the quality of SE results. Web spamming’s economic impact is enormous because web spammers index massive free advertising data on SEs to increase the volume of web traffic on a targeted website. Spammers trick an SE into ranking irrelevant web pages higher than relevant web pages in the search engine results pages (SERPs) using different web-spamming techniques. Consequently, these high-ranked unrelated web pages contain insufficient or inappropriate information for the user. To detect the spam web pages, several researchers from industry and academia are working. No efficient technique that is capable of catching all spam web pages on the World Wide Web (WWW) has been presented yet. This research is an attempt to propose an improved framework for content- and link-based web-spam identification. The framework uses stopwords, keywords’ frequency, part of speech (POS) ratio, spam keywords database, and copied-content algorithms for content-based web-spam detection. For link-based web-spam detection, we initially exposed the relationship network behind the link-based web spamming and then used the paid-link database, neighbour pages, spam signals, and link-farm algorithms. Finally, we combined all the content- and link-based spam identification algorithms to identify both types of spam. To conduct experiments and to obtain threshold values, WEBSPAM-UK2006 and WEBSPAM-UK2007 datasets were used. A promising F-measure of 79.6% with 81.2% precision shows the applicability and effectiveness of the proposed approach.","PeriodicalId":72654,"journal":{"name":"Complex psychiatry","volume":"48 1","pages":"6625739:1-6625739:18"},"PeriodicalIF":0.0,"publicationDate":"2021-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77676861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Constructing Multiple-Objective Portfolio Selection for Green Innovation and Dominating Green Innovation Indexes","authors":"Meng Li, Kezhi Liao, Y. Qi, Tong Liu","doi":"10.17632/4YKNHCK825.1","DOIUrl":"https://doi.org/10.17632/4YKNHCK825.1","url":null,"abstract":"Green innovation investments have rapidly grown since 2000. Green innovation indexes play important roles and are typically constructed by screening and indexing. However, Nobel Laureate Markowitz emphasizes portfolio selection instead of security selection and accentuates that “A good portfolio is more than a long list of good stocks.” Moreover, the screening-indexing strategies ignore that investors can take green innovation as an additional objective and thus gain additional utility. We consequently construct 3-objective portfolio selection for green innovation in addition to variance and expected return. An efficient frontier of portfolio selection then extends to an efficient surface which is a panorama of the optimal variance, expected return, and expected green innovation. Investors thus fully envisage the trade-offs and enjoy the freedom of choosing preferred portfolios on the surface. In contrast, the screening-indexing strategies inflexibly leave investors with only one point (i.e., the green innovation index). As the originality, we prove in a theorem that there typically exists a curve on the efficient surface so all portfolios on the curve dominate the green innovation index. We test the dominance by component stocks of China Securities Index 300 and obtain affirmative results out of sample. The results still hold in robustness tests. At last, we classify green innovation into categories, further model the categories by general \u0000 \u0000 k\u0000 \u0000 -objective portfolio selection, and still illustrate the dominance. Consequently, investors can consider and control each category.","PeriodicalId":72654,"journal":{"name":"Complex psychiatry","volume":"74 1","pages":"8263720:1-8263720:19"},"PeriodicalIF":0.0,"publicationDate":"2021-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79605456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Galantamine-Memantine Combination and Kynurenine Pathway Enzyme Inhibitors in the Treatment of Neuropsychiatric Disorders.","authors":"Michael Y Bai,&nbsp;David B Lovejoy,&nbsp;Gilles J Guillemin,&nbsp;Rouba Kozak,&nbsp;Trevor W Stone,&nbsp;Maju Mathew Koola","doi":"10.1159/000515066","DOIUrl":"10.1159/000515066","url":null,"abstract":"<p><p>The kynurenine pathway (KP) is a major route for L-tryptophan (L-TRP) metabolism, yielding a variety of bioactive compounds including kynurenic acid (KYNA), 3-hydroxykynurenine (3-HK), quinolinic acid (QUIN), and picolinic acid (PIC). These tryptophan catabolites are involved in the pathogenesis of many neuropsychiatric disorders, particularly when the KP becomes dysregulated. Accordingly, the enzymes that regulate the KP such as indoleamine 2,3-dioxygenase (IDO)/tryptophan 2,3-dioxygenase, kynurenine aminotransferases (KATs), and kynurenine 3-monooxygenase (KMO) represent potential drug targets as enzymatic inhibition can favorably rebalance KP metabolite concentrations. In addition, the galantamine-memantine combination, through its modulatory effects at the alpha7 nicotinic acetylcholine receptors and N-methyl-D-aspartate receptors, may counteract the effects of KYNA. The aim of this review is to highlight the effectiveness of IDO-1, KAT II, and KMO inhibitors, as well as the galantamine-memantine combination in the modulation of different KP metabolites. KAT II inhibitors are capable of decreasing the KYNA levels in the rat brain by a maximum of 80%. KMO inhibitors effectively reduce the central nervous system (CNS) levels of 3-HK, while markedly boosting the brain concentration of KYNA. Emerging data suggest that the galantamine-memantine combination also lowers L-TRP, kynurenine, KYNA, and PIC levels in humans. Presently, there are only 2 pathophysiological mechanisms (cholinergic and glutamatergic) that are FDA approved for the treatment of cognitive dysfunction for which purpose the galantamine-memantine combination has been designed for clinical use against Alzheimer's disease. The alpha7 nicotinic-NMDA hypothesis targeted by the galantamine-memantine combination has been implicated in the pathophysiology of various CNS diseases. Similarly, KYNA is well capable of modulating the neuropathophysiology of these disorders. This is known as the KYNA-centric hypothesis, which may be implicated in the management of certain neuropsychiatric conditions. In line with this hypothesis, KYNA may be considered as the \"conductor of the orchestra\" for the major pathophysiological mechanisms underlying CNS disorders. Therefore, there is great opportunity to further explore and compare the biological effects of these therapeutic modalities in animal models with a special focus on their effects on KP metabolites in the CNS and with the ultimate goal of progressing to clinical trials for many neuropsychiatric diseases.</p>","PeriodicalId":72654,"journal":{"name":"Complex psychiatry","volume":"7 1-2","pages":"19-33"},"PeriodicalIF":0.0,"publicationDate":"2021-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000515066","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39905714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Front & Back Matter","authors":"","doi":"10.1159/000518991","DOIUrl":"https://doi.org/10.1159/000518991","url":null,"abstract":"","PeriodicalId":72654,"journal":{"name":"Complex psychiatry","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76111753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Validity of Brief Phenotyping in Population Biobanks for Psychiatric Genome-Wide Association Studies on the Biobank Scale.","authors":"Jonathan R I Coleman","doi":"10.1159/000516837","DOIUrl":"10.1159/000516837","url":null,"abstract":"","PeriodicalId":72654,"journal":{"name":"Complex psychiatry","volume":"7 1-2","pages":"11-15"},"PeriodicalIF":0.0,"publicationDate":"2021-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8443942/pdf/cxp-0007-0011.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39706298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perspective on Beyond Statistical Significance: Finding Meaningful Effects","authors":"H. Edenberg","doi":"10.1159/000517237","DOIUrl":"https://doi.org/10.1159/000517237","url":null,"abstract":"Genome-wide association studies (GWASs) in psychiatry have recently identified many loci that affect a wide variety of disorders and related traits, although the number of associated loci varies widely among psychiatric and substance-use traits. The successes of GWAS have triggered thoughts about how to move beyond identification of loci (which contain a very large number of variants), to identification of the functional variants within them that actually contribute to the risk for the traits, and from there to identifying the genes, pathways, and mechanisms involved. The hope is that knowledge of the key genes and pathways will lead to better diagnosis, treatment, and prevention of these complex disorders. On September 2, 2020, three institutes within the US National Institutes of Health (NIH) sponsored a virtual meeting entitled “Beyond Statistical Significance: Finding Meaningful Effects” devoted to exploring these issues. The structure of the meeting – initial presentations followed by discussion sections on 3 sets of topics through which all willing participants cycled and a general discussion as a wrap-up – allowed for lively interaction and the presentation of many ideas. Dr. Elizabeth Hoffman opened the meeting by stating its objective was “To develop best practice recommendations for identifying, analyzing, and interpreting meaningful effects by engaging researchers from a range of disciplines in discussions of meaningful science that go beyond statistical significance.” It should not surprise anyone that one conclusion was that these questions are difficult and there are no one-size-fits-all answers. A good summary of the meeting has been posted at https://apps1.seiservices.com/meaningfuleffects/, with details of the presentations and the discussions. Some of these issues have been discussed in relation to the NIH Adolescent Brain Cognitive Development study [1] in a preprint recently posted to bioRxiv [2]. I will not recapitulate the meeting summary here, but rather provide a perspective on the key questions discussed, and potential future directions.","PeriodicalId":72654,"journal":{"name":"Complex psychiatry","volume":"24 1","pages":"1 - 8"},"PeriodicalIF":0.0,"publicationDate":"2021-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74118000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Publicly Available hiPSC Lines with Extreme Polygenic Risk Scores for Modeling Schizophrenia.","authors":"Kristina Dobrindt, Hanwen Zhang, Debamitra Das, Sara Abdollahi, Tim Prorok, Sulagna Ghosh, Sarah Weintraub, Giulio Genovese, Samuel K Powell, Anina Lund, Schahram Akbarian, Kevin Eggan, Steven McCarroll, Jubao Duan, Dimitrios Avramopoulos, Kristen J Brennand","doi":"10.1159/000512716","DOIUrl":"10.1159/000512716","url":null,"abstract":"<p><p>Schizophrenia (SZ) is a common and debilitating psychiatric disorder with limited effective treatment options. Although highly heritable, risk for this polygenic disorder depends on the complex interplay of hundreds of common and rare variants. Translating the growing list of genetic loci significantly associated with disease into medically actionable information remains an important challenge. Thus, establishing platforms with which to validate the impact of risk variants in cell-type-specific and donor-dependent contexts is critical. Towards this, we selected and characterized a collection of 12 human induced pluripotent stem cell (hiPSC) lines derived from control donors with extremely low and high SZ polygenic risk scores (PRS). These hiPSC lines are publicly available at the California Institute for Regenerative Medicine (CIRM). The suitability of these extreme PRS hiPSCs for CRISPR-based isogenic comparisons of neurons and glia was evaluated across 3 independent laboratories, identifying 9 out of 12 meeting our criteria. We report a standardized resource of publicly available hiPSCs on which we hope to perform genome engineering and generate diverse kinds of functional data, with comparisons across studies facilitated by the use of a common set of genetic backgrounds.</p>","PeriodicalId":72654,"journal":{"name":"Complex psychiatry","volume":"6 3-4","pages":"68-82"},"PeriodicalIF":0.0,"publicationDate":"2021-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7923934/pdf/cxp-0006-0068.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9974831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the Convergent Mechanisms between Major Depressive Disorder and Parkinson's Disease.","authors":"Angela A Tran,&nbsp;Myra De Smet,&nbsp;Gary D Grant,&nbsp;Tien K Khoo,&nbsp;Dean L Pountney","doi":"10.1159/000512657","DOIUrl":"https://doi.org/10.1159/000512657","url":null,"abstract":"<p><p>Major depressive disorder (MDD) affects more than cognition, having a temporal relationship with neuroinflammatory pathways of Parkinson's disease (PD). Although this association is supported by epidemiological and clinical studies, the underlying mechanisms are unclear. Microglia and astrocytes play crucial roles in the pathophysiology of both MDD and PD. In PD, these cells can be activated by misfolded forms of the protein α-synuclein to release cytokines that can interact with multiple different physiological processes to produce depressive symptoms, including monoamine transport and availability, the hypothalamus-pituitary axis, and neurogenesis. In MDD, glial cell activation can be induced by peripheral inflammatory agents that cross the blood-brain barrier and/or c-Fos signalling from neurons. The resulting neuroinflammation can cause neurodegeneration due to oxidative stress and glutamate excitotoxicity, contributing to PD pathology. Astrocytes are another major link due to their recognized role in the glymphatic clearance mechanism. Research suggesting that MDD causes astrocytic destruction or structural atrophy highlights the possibility that accumulation of α-synuclein in the brain is facilitated as the brain cannot adequately clear the protein aggregates. This review examines research into the overlapping pathophysiology of MDD and PD with particular focus on the roles of glial cells and neuroinflammation.</p>","PeriodicalId":72654,"journal":{"name":"Complex psychiatry","volume":"6 3-4","pages":"47-61"},"PeriodicalIF":0.0,"publicationDate":"2021-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000512657","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9974830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}