84 research outputs found
Genomic Analysis Reveals a Potential Role for Cell Cycle Perturbation in HCV-Mediated Apoptosis of Cultured Hepatocytes
- Author
- A Brazma
- A Marshall
- A Marshall
- AL Doughty
- Andrew J. Syder
- B Sainz Jr
- BD Lindenbach
- BD Lindenbach
- Bryan Paeper
- C Mayerat
- Charles M. Rice
- Deborah L. Diamond
- DR Nelson
- DR Nelson
- F Calabrese
- GK Geiss
- H Nguyen
- H Zhu
- HB Nelson
- J Gewaltig
- J Zhong
- JA Mengshol
- K Machida
- K Naka
- K Ohkawa
- KA Walters
- Kathie-Anne Walters
- KB Spurgers
- KH Baek
- KP Batts
- KY Lee
- L Deng
- LD Shostak
- M Abel
- M Korenaga
- M Okuda
- M Paiardini
- M Paiardini
- M Robinson
- Michael Farzan
- Michael G. Katze
- MJH Alter
- MV Di
- MW Smith
- N Schuster
- P Bostik
- R Teixeira
- S Bates
- S Dupont
- S Pal
- S Sarfraz
- S Wieland
- Sharon L. Lederer
- SJ Pelletier
- T Wakita
- US Park
- W Tang
- XJ Yang
- Y Sekine-Osajima
- ZQ Yao
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2009
- Field of study
The mechanisms of liver injury associated with chronic HCV infection, as well as the individual roles of both viral and host factors, are not clearly defined. However, it is becoming increasingly clear that direct cytopathic effects, in addition to immune-mediated processes, play an important role in liver injury. Gene expression profiling during multiple time-points of acute HCV infection of cultured Huh-7.5 cells was performed to gain insight into the cellular mechanism of HCV-associated cytopathic effect. Maximal induction of cell-death–related genes and appearance of activated caspase-3 in HCV-infected cells coincided with peak viral replication, suggesting a link between viral load and apoptosis. Gene ontology analysis revealed that many of the cell-death genes function to induce apoptosis in response to cell cycle arrest. Labeling of dividing cells in culture followed by flow cytometry also demonstrated the presence of significantly fewer cells in S-phase in HCV-infected relative to mock cultures, suggesting HCV infection is associated with delayed cell cycle progression. Regulation of numerous genes involved in anti-oxidative stress response and TGF-β1 signaling suggest these as possible causes of delayed cell cycle progression. Significantly, a subset of cell-death genes regulated during in vitro HCV infection was similarly regulated specifically in liver tissue from a cohort of HCV-infected liver transplant patients with rapidly progressive fibrosis. Collectively, these data suggest that HCV mediates direct cytopathic effects through deregulation of the cell cycle and that this process may contribute to liver disease progression. This in vitro system could be utilized to further define the cellular mechanism of this perturbation
Capture of MicroRNA–Bound mRNAs Identifies the Tumor Suppressor miR-34a as a Regulator of Growth Factor Signaling
- Author
- A Bagchi
- A Grimson
- A Ichimura
- A Lal
- A Lal
- Aaron Deutsch
- Andrea Ventura
- AR Pico
- Ashish Lal
- B Vanhaesebroeck
- BP Lewis
- BP Lewis
- C Gjerdrum
- C Liu
- C Shin
- C Welch
- Carla Concepcion
- CD Johnson
- D Baek
- Danielle K. Rajani
- DG Zisoulis
- DP Bartel
- DS Rao
- Elizabeth O'Day
- F Navarro
- F Sun
- Francisco Navarro
- G Mudduluru
- Gabriel Altschuler
- GT Bommer
- H Tazawa
- I Elcheva
- Jerome Thiery
- JS Wei
- Judy Lieberman
- L He
- L He
- L Salmena
- M Hafner
- M Kaller
- M Kanehisa
- M Kertesz
- M Thomas
- M Vogt
- M Yamakuchi
- Marshall P. Thomas
- Michael T. McManus
- N Li
- N Rajewsky
- N Raver-Shapira
- NR Christoffersen
- Oliver Hofmann
- P Alexiou
- P Shannon
- PJ Roberts
- Q-R Chen
- R Garzon
- RC Friedman
- RMA Linger
- RTK Pang
- S Takagi
- S Vasudevan
- S Whittaker
- SD Weeraratne
- ST Hashimi
- SW Chi
- T-C Chang
- UA Ørom
- UA Ørom
- Winston Hide
- Xiao Ling Li
- Y Li
- Y Tay
- Yoon-Chi Han
- Publication venue
- Public Library of Science
- Publication date
- 01/11/2011
- Field of study
A simple biochemical method to isolate mRNAs pulled down with a transfected, biotinylated microRNA was used to identify direct target genes of miR-34a, a tumor suppressor gene. The method reidentified most of the known miR-34a regulated genes expressed in K562 and HCT116 cancer cell lines. Transcripts for 982 genes were enriched in the pull-down with miR-34a in both cell lines. Despite this large number, validation experiments suggested that ∼90% of the genes identified in both cell lines can be directly regulated by miR-34a. Thus miR-34a is capable of regulating hundreds of genes. The transcripts pulled down with miR-34a were highly enriched for their roles in growth factor signaling and cell cycle progression. These genes form a dense network of interacting gene products that regulate multiple signal transduction pathways that orchestrate the proliferative response to external growth stimuli. Multiple candidate miR-34a–regulated genes participate in RAS-RAF-MAPK signaling. Ectopic miR-34a expression reduced basal ERK and AKT phosphorylation and enhanced sensitivity to serum growth factor withdrawal, while cells genetically deficient in miR-34a were less sensitive. Fourteen new direct targets of miR-34a were experimentally validated, including genes that participate in growth factor signaling (ARAF and PIK3R2) as well as genes that regulate cell cycle progression at various phases of the cell cycle (cyclins D3 and G2, MCM2 and MCM5, PLK1 and SMAD4). Thus miR-34a tempers the proliferative and pro-survival effect of growth factor stimulation by interfering with growth factor signal transduction and downstream pathways required for cell division
Airway Microbiota and Pathogen Abundance in Age-Stratified Cystic Fibrosis Patients
- Author
- A Amadori
- Adam J. Ratner
- B Kerem
- B Stecher
- Brian Wu
- Byron Taylor
- C Lupp
- C Palmer
- CD Sibley
- CM Bowman
- CO Webb
- CO Webb
- CO Webb
- CR Jackson
- D Tilman
- DA Antonopoulos
- DA Wardle
- Dennis Nielson
- Diem Tran
- DJ Lane
- DL Hahn
- E Bruzzese
- EC Pielou
- EH Meyer
- EL Brodie
- EL Brodie
- Eoin L. Brodie
- F Armougom
- F Bittar
- F Bittar
- Gary L. Andersen
- GB Rogers
- GB Rogers
- GB Rogers
- GB Rogers
- GS Zhang
- HA Souza
- HU Jahn
- I Letunic
- I Sekirov
- J Oksanen
- J Qin
- J Zabner
- JD Storey
- JH Connell
- JH Widdicombe
- JK Harris
- JL Flanagan
- JL Flanagan
- Jonathan Koff
- Kei E. Fujimura
- KS Pollard
- L Saiman
- M Hamady
- M Hogardt
- M Kolak
- M Martinez-Medina
- Marshall S. Baek
- Martin Allgaier
- Mary Ellen Kleinhenz
- MG van der Heijden
- Michael J. Cox
- MM Tunney
- MN Price
- MO Hill
- N Hoiby
- P McKenna
- PS Kumar
- PS Kumar
- RC Gentleman
- RC Roberts
- RE Ley
- Rebecca A. Daly
- Ronald Brown
- S Kembel
- S Marcante
- S Razvi
- SR Gill
- Susan V. Lynch
- T Coenye
- T Huber
- TD Lawley
- TD Lawley
- TF Murphy
- TP Atkinson
- TZ DeSantis
- TZ DeSantis
- Ulas Karaoz
- W Ludwig
- Y Benjamini
- Y Song
- YE Shen
- Yvonne J. Huang
- Publication venue
- Public Library of Science
- Publication date
- 01/06/2010
- Field of study
Bacterial communities in the airways of cystic fibrosis (CF) patients are, as in other ecological niches, influenced by autogenic and allogenic factors. However, our understanding of microbial colonization in younger versus older CF airways and the association with pulmonary function is rudimentary at best. Using a phylogenetic microarray, we examine the airway microbiota in age stratified CF patients ranging from neonates (9 months) to adults (72 years). From a cohort of clinically stable patients, we demonstrate that older CF patients who exhibit poorer pulmonary function possess more uneven, phylogenetically-clustered airway communities, compared to younger patients. Using longitudinal samples collected form a subset of these patients a pattern of initial bacterial community diversification was observed in younger patients compared with a progressive loss of diversity over time in older patients. We describe in detail the distinct bacterial community profiles associated with young and old CF patients with a particular focus on the differences between respective “early” and “late” colonizing organisms. Finally we assess the influence of Cystic Fibrosis Transmembrane Regulator (CFTR) mutation on bacterial abundance and identify genotype-specific communities involving members of the Pseudomonadaceae, Xanthomonadaceae, Moraxellaceae and Enterobacteriaceae amongst others. Data presented here provides insights into the CF airway microbiota, including initial diversification events in younger patients and establishment of specialized communities of pathogens associated with poor pulmonary function in older patient populations
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)
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- A. -G. Wu
- A. C. Ma
- A. K. Au
- Abdel-Aziz A. K.
- Abdelfatah S.
- Abdellatif M.
- Abdoli A.
- Abel S.
- Abeliovich H.
- Abildgaard M. H.
- Abudu Y. P.
- Acevedo-Arozena A.
- Adamopoulos I. E.
- Adeli K.
- Adolph T. E.
- Adornetto A.
- Aflaki E.
- Agam G.
- Agarwal A.
- Aggarwal B. B.
- Agnello M.
- Agostinis P.
- Agrewala J. N.
- Agrotis A.
- Aguilar P. V.
- Ahmad S. T.
- Ahmed Z. M.
- Ahumada-Castro U.
- Aits S.
- Aizawa S.
- Akkoc Y.
- Akoumianaki T.
- Akpinar H. A.
- Al-Abd A. M.
- Al-Akra L.
- Al-Gharaibeh A.
- Alaoui-Jamali M. A.
- Alberti S.
- Alcocer-Gomez E.
- Alessandri C.
- Ali M.
- Alim Al-Bari M. A.
- Aliwaini S.
- Alizadeh J.
- Almacellas E.
- Almasan A.
- Alonso A.
- Alonso G. D.
- Altan-Bonnet N.
- Altieri D. C.
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- Ambrosio S.
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- Publication date
- 01/01/2021
- Field of study
Positioning mentoring as a coach development tool:Recommendations for future practice and research
- Author
- Baek-Kyoo
- Billett S.
- Bloom G. A.
- Bloom G. A.
- Cassidy T.
- Clutterbuck D.
- Collins A.
- Crutcher B. N.
- Cull J.
- Cushion C.
- Department for Education and Skills (DfES)
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- Gilbert W.
- Gilbert W.
- Green A.
- Hill J. R.
- International Council for Coaching Excellence (ICCE)
- International Council for Coaching Excellence (ICCE)
- Jones R. L.
- Kerka S.
- Klasen N.
- Kolb D. A.
- Kram K. E.
- Mallet C.
- Marshall D.
- Marsick V. J.
- Megginson D.
- Nash C.
- Nash C.
- Nursing and Midwifery Council
- Sports Coach UK
- Srivastava S.
- Teatheredge J.
- Tomlinson P.
- Vialle W.
- Vygotsky L.
- Werthner P.
- Wickman F.
- Williams S.
- Publication venue
- 'Informa UK Limited'
- Publication date
- 01/01/2015
- Field of study
Current thinking in coach education advocates mentoring as a development tool to connect theory and practice. However, little empirical evidence exists to evaluate the effectiveness of mentoring as a coach development tool. Business, education, and nursing precede the coaching industry in their mentoring practice, and research findings offered in these domains could be drawn upon to position mentoring as sports coaching development tool. Given the remote basis of some of mentor–coach relationships in sports coaching, additional learning can be drawn from mentoring conducted by virtual or electronic mediums. This article concludes with a series of reflective questions arising from research findings in other domains, designed to engage the potential coaching organization with the mentoring process
Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease
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- Yaoqing H
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- Zadionchenko V
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- Zhou H
- Zidova M
- Zielinski M
- Zieve F
- Zineldine A.
- Zirlik A
- Zucchetti C
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2017
- Field of study
Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.
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- Abdel-Aziz AK
- Abdelfatah S
- Abdellatif M
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- Zientara-Rytter K
- Zimmermann CM
- Ziviani E
- Zoladek T
- Zong W-X
- Zorov DB
- Zorzano A
- Zou W
- Zou Z
- Zou Z
- Zuryn S
- Zwerschke W
- Álvarez ÉMC
- Ávalos Y
- Önal G
- Üstün S
- Čolić M
- Đokić J
- Žerovnik E
- Publication venue
- 'Informa UK Limited'
- Publication date
- 01/01/2021
- Field of study
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field
Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors
- Author
- Abdellaoui Abdel
- Abramova Liliya
- Adams Mark
- Adams Mark J.
- Adan Roger A. H.
- Adolfsson Rolf
- Adolfsson Rolf
- Adorjan Kristina
- Agartz Ingrid
- Agartz Ingrid
- Agerbo Esben
- Agerbo Esben
- Agerbo Esben
- Aguayo Samuel
- Ahuja Sunil
- Air Tracy M.
- Air Tracy M.
- Al Eissa Mariam
- Albani Diego
- Alda Martin
- Alda Martin
- Alfredsson Lars
- Alfredsson Lars
- Alfredsson Lars
- Alliey-Rodriguez Ney
- Als Thomas D.
- Andlauer Till F. M.
- Ando Tetsuya
- Andreassen Ole A.
- Andreassen Ole A.
- Andreassen Ole A.
- Anjorin Adebayo
- Anjorin Adebayo
- Antilla Verneri
- Antoniou Anastasia
- Appadurai Vivek
- Argyres Dean P.
- Arolt Volker
- Artigas Maria Soler
- Aschauer Harald
- Ashley-Koch Allison E.
- Aslan Mihaela
- Awasthi Swapnil
- Awasthi Swapnil
- Awasthi Swapnil
- Azevedo M. Helena
- Babadjanova Gulja
- Bacanu Silviu-Alin
- Backlund Lena
- Baek Ji Hyun
- Baker Jessica H.
- Ballas Zuhair
- Bass Nicholas
- Bass Nicholas
- Bau Claiton H. D.
- Bauer Michael
- Baune Bernhard T.
- Baune Bernhard T.
- Baune Bernhard T.
- Beckham Jean
- Beckham Jean
- Beckham Jean C.
- Beekman Aartjan T. F.
- Beins Eva C.
- Bellivier Frank
- Bellivier Frank
- Bencko Vladimir
- Bengesser Susanne
- Bergen Andrew W.
- Bergen Andrew W.
- Bergen Sarah E.
- Berger Klaus
- Berger Klaus
- Berrettini Wade H.
- Berrettini Wade H.
- Berrettini Wade H.
- Bhushan Sujata
- Biernacka Joanna M.
- Biernacka Joanna M.
- Bigdeli Tim B.
- Bigdeli Tim B.
- Bigdeli Tim B.
- Binder Elisabeth B.
- Binder Elisabeth B.
- Birgegård Andreas
- Birner Armin
- Blackwood Douglas H. R.
- Boden Joseph M.
- Boehm Ilka
- Boehnke Michael
- Boehnke Michael
- Bohus Martin
- Bohus Martin
- Boks Marco P.
- Boks Marco P.
- Boni Claudette
- Boomsma Dorret I.
- Bosch Rosa
- Bosch Rosa
- Boyko Edward
- Braff David L.
- Brandt Harry
- Brandt Harry
- Breeling James
- Breen Gerome
- Breen Gerome
- Breen Gerome
- Breen Gerome
- Brewer Jessica V.
- Brophy Mary T.
- Brum Murielle
- Brumpton Ben M.
- Brunkhorst-Kanaan Nathalie
- Bryant Richard
- Bryois Julien
- Bryois Julien
- Bryois Julien
- Budde Monika
- Budde Monika
- Buehren Katharina
- Bulik Cynthia M.
- Bulik Cynthia M.
- Burghardt Roland
- Buttenschøn Henriette N.
- Bybjerg-Grauholm Jonas
- Bybjerg-Grauholm Jonas
- Byerley William
- Byrne Enda M.
- Byrne Enda M.
- Bækvad-Hansen Marie
- Bækvad-Hansen Marie
- Bøen Erlend
- Børglum Anders D.
- Børglum Anders D.
- Børglum Anders D.
- Børte Sigrid
- Cahn Wiepke
- Cai Na
- Cairns Murray
- Campos Adrian I.
- Carlberg Laura
- Carr Vaughan J.
- Carter Bruce W.
- Casas Miguel
- Casas Miquel
- Cassina Matteo
- Castelao Enrique
- Castelao Enrique
- Catts Stanley
- Cervantes Pablo
- Cervilla Jorge A.
- Chang Kyong-Mi
- Chang Xiao
- Charney Alexander W.
- Chaumette Boris
- Chen Hsi-Chung
- Chen Wei J.
- Cho Kelly
- Cho Kelly
- Christensen Jane Hvarregaard
- Cichon Sven
- Cichon Sven
- Cichon Sven
- Cichon Sven
- Clarke Toni-Kim
- Clarke Toni-Kim
- Clementi Maurizio
- Cohen David
- Coleman Jonathan R. I.
- Coleman Jonathan R. I.
- Coleman Jonathan R. I.
- Coleman Jonathan R. I.
- Colodro-Conde Lucía
- Cone Roger D.
- Connor Todd
- Constans Joseph
- Coombes Brandon
- Coon Hilary
- Corvin Aiden
- Corvin Aiden
- Courtet Philippe
- Couvy-Duchesne Baptiste
- Craddock Nicholas
- Craddock Nicholas
- Craddock Nick
- Craig David
- Crawford Gregory E.
- Crawford Steven
- Crawford Steven
- Crivelli Silvia
- Crow Scott
- Crow Scott
- Crowley James J.
- Cruceanu Cristiana
- Cuellar-Barboza Alfredo
- Cunningham Julie
- Curtis David
- Czerski Piotr M.
- Dahmen Norbert
- Dale Anders M.
- Dalkner Nina
- Danner Unna N.
- Dannlowski Udo
- Dannlowski Udo
- David Friederike S.
- Davies Gail
- Davis Oliver S. P.
- de Geus E. J. C.
- de Zwaan Martina
- Dedoussis George
- Degenhardt Franziska
- Degenhardt Franziska
- Degenhardt Franziska
- Degortes Daniela
- Dellitalia Louis
- Demontis Ditte
- Dennis Michelle F.
- Depaulo J. Raymond
- DePaulo J. Raymond
- der Auwera Sandra Van
- Derks Eske M.
- DeSocio Janiece E.
- Di Florio Arianna
- DiBlasi Emily
- Dick Danielle M.
- Dietl Lydie
- Dikeos Dimitris
- Dikeos Dimitris
- Dina Christian
- Direk Nese
- Djurovic Srdjan
- Djurovic Srdjan
- Dmitrzak-Weglarz Monika
- Do Nhan
- Dobbyn Amanda L.
- Docherty Anna R.
- Dolan Conor V.
- Domenici Enrico
- Domschke Katharina
- Douzenis Athanassios
- Drange Ole Kristian
- Duncan Laramie E.
- Dunn Erin C.
- Duriez Philibert
- Edenberg Howard J.
- Edenberg Howard J.
- Edwards Alexis C.
- Egberts Karin
- Ehrlich Stefan
- Eley Thalia C.
- Elvsåshagen Torbjørn
- Erlangsen Annette
- Escaramís Geòrgia
- Escott-Price Valentina
- Escott-Price Valentina
- Esko Tõnu
- Esko Tõnu
- Esko Tõnu
- Esko Tõnu
- Espeseth Thomas
- Estivill Xavier
- Etain Bruno
- Fanous Ayman H.
- Farmer Anne
- Favaro Angela
- Fayad Joseph
- Ferentinos Panagiotis
- Fernández-Aranda Fernando
- Fernández-Aranda Fernando
- Ferrier I. Nicol
- Fichter Manfred M.
- Fichter Manfred M.
- Finucane Hilary K.
- Fiorentino Alessia
- Fischer Krista
- Florez Hermes
- Floyd James A. B.
- Foo Jerome C.
- Foo Jerome C.
- Foretova Lenka
- Foroud Tatiana M.
- Forstner Andreas J.
- Forstner Andreas J.
- Forstner Andreas J.
- Forstner Andreas J.
- Forty Liz
- Forzan Monica
- Frank Josef
- Frank Josef
- Frank Josef
- Franklin Christopher S.
- Frei Oleksandr
- Freimer Nelson B.
- Frisén Louise
- Frye Mark
- Frye Mark
- Fullerton Janice M.
- Fullerton Janice M.
- Föcker Manuel
- Gaddy Melinda
- Gade Katrin
- Galfalvy Hanga
- Gallinger Steven
- Gallinger Steven
- Gambaro Giovanni
- Gandal Michael
- Gandal Michael J.
- Gappy Saib
- Garnham Julie
- Gaspar Héléna A.
- Gaspar Héléna A.
- Gatt Justine M.
- Gawlik Micha
- Gaziano J. Michael
- Gaziano J. Michael
- Gejman Pablo V.
- Gelernter Joel
- Gelernter Joel
- Gershon Elliot S.
- Gibson Gretchen
- Giegling Ina
- Giegling Ina
- Gill Michael
- Giuranna Johanna
- Giusti-Rodríquez Paola
- Gizer Ian R.
- Glatt Stephen J.
- Godschalk Michael
- Goes Fernando S.
- Goes Fernando S.
- Gonidakis Fragiskos
- Gordon Scott
- Gordon Scott D.
- Gordon Scott D.
- Gordon-Smith Katherine
- Gorwood Philip
- Gorwood Philip
- Grabe Hans J.
- Grabe Hans J.
- Greco Jennifer
- Green Melissa J.
- Green Melissa J.
- Greenwood Tiffany A.
- Grevet Eugenio H.
- Grigoroiu-Serbanescu Maria
- Grigoroiu-Serbanescu Maria
- Grove Jakob
- Grove Jakob
- Grove Jakob
- Guillaume Sébastien
- Guo Yiran
- Guo Yiran
- Gupta Samir
- Gutierrez Blanca
- Gutierrez Salvador
- Guzman-Parra Jose
- Guzman-Parra José
- Ha Kyooseob
- Hafferty Jonathan D.
- Hagenaars Saskia P.
- Hakonarson Hakon
- Hakonarson Hakon
- Hall Lynsey S.
- Halmi Katherine A.
- Halmi Katherine A.
- Hamilton Steven P.
- Hamilton Steven P.
- Hammer Kimberly
- Hamner Mark
- Hamshere Marian L.
- Hanscombe Ken B.
- Hansen Christine Søholm
- Hansen Christine Søholm
- Hansen Thomas F.
- Haraldsson Magnus
- Harley John
- Hartmann Annette
- Harvey Phillip D.
- Hassan Kiadeh Farnush Farhadi
- Hatzikotoulas Konstantinos
- Hauser Elizabeth
- Hauser Elizabeth R.
- Hauser Joanna
- Hauser Joanna
- Hauser Joanna
- Hauser Michael A.
- Hautzinger Martin
- Hayward Caroline
- Heath Andrew C.
- Hebebrand Johannes
- Heilbronner Urs
- Heilmann-Heimbach Stefanie
- Helder Sietske G.
- Hellgren Dennis
- Henders Anjali K.
- Henskens Frans
- Herms Stefan
- Herms Stefan
- Herms Stefan
- Herpertz-Dahlmann Beate
- Herzog Wolfgang
- Hickie Ian B.
- Hillert Jan
- Hinney Anke
- Hishimoto Akitoyo
- Hoffmann Per
- Hoffmann Per
- Hoffmann Per
- Holmans Peter A.
- Homuth Georg
- Hong Kyung Sue
- Horn Carsten
- Horwood L. John
- Hottenga Jouke-Jan
- Hougaard David M.
- Hougaard David M.
- Hougaard David M.
- Howard David M.
- Huang Grant
- Huckins Laura
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- Zipfel Stephan
- Zwart John-Anker
- Świątkowska Beata
- Świątkowska Beata
- Świątkowska Beata
- Publication venue
- Publication date
- 01/01/2021
- Field of study
Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe
The United States COVID-19 Forecast Hub dataset
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- Abu-Mostafa Yaser
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- Rodríguez Alexander
- Romberg Justin
- Rosenstrom Erik T.
- Rowland Michael A.
- Rumack Aaron
- Sagun Levent
- Salekin Asif
- Sarker Arnab
- Schrader Chris
- Schwarz Tom
- Scott James G.
- Sen Pei
- Serban Nicoleta
- Shah Apurv
- Shah Devavrat
- Shah Sam
- Shakhnovich Elizabeth
- Shaman Jeffrey
- Sharma Rakshith
- Sheldon Daniel
- Sherratt Katharine
- Shi Yunfeng
- Shin Lauren
- Shingi Siddhant
- Shrivastav Monika
- Siegel Daniel
- Simon Noah
- Singhvi Divya
- Sinha Deeksha
- Sinha Rajarishi
- Slayton Rachel B.
- Smith Claire P.
- Soni Saksham
- Soohoo Connor
- Spaeder Jeffrey
- Spantidakis Ioannis
- Spatz Ryan
- Srivastava Ajitesh
- Stage Steven A.
- Stark Ariane
- Stiefeling Chris
- Suchoski Bradley T.
- Sumner Timothy
- Sun Jimeng
- Sun Tao
- Sundar Saketh
- Swann Julie L.
- Tabassum Anika
- Tallaksen Katharine
- Tec Mauricio
- Thanou Dorina
- Thayaparan Leann
- Tibshirani Rob
- Tibshirani Ryan J.
- Tirumala Kushal
- Tiwari Avtansh
- Tomar Vishal
- Tran Quoc
- Truelove Shaun A.
- Trump Benjamin D.
- Tsai Thomas
- Tseng Albert
- Tsiourvas Asterios
- Turner Stephen D.
- Turtle James
- US COVID-19 Forecast Hub Consortium
- Vahedi Behzad
- Van Bussel Frank
- van de Walle Axel
- Varadarajan Vignesh
- Venkatramanan Srinivasan
- Ventura Valerie
- Vespignani Alessandro
- Vytheeswaran Jagath
- Walker Jo W.
- Walraven Robert
- Wang Christopher
- Wang Dongdong
- Wang Dongliang
- Wang Guannan
- Wang Lijing
- Wang Lily
- Wang Lingxiao
- Wang Liqiang
- Wang Qinxia
- Wang Yijin
- Wang Yu-Xiang
- Wang Yuanjia
- Wang Yueying
- Wang Zhongying
- Wasserman Larry
- Wattanchit Nutcha
- Weisberg Shane
- White Jerome
- Wilde Joshua
- Wilkinson Barrie
- Wills Josh
- Wilson Austin
- Wilson Daniel
- Wilson Shelby
- Wolffram Daniel
- Wolfinger Russ
- Wong Alexander
- Woody Spencer
- Wu Dongxia
- Xiao Cao
- Xiao Jade
- Xie Jiajia
- Xie Shanghong
- Xie Xing
- Xiong Xinyue
- Xu Pan
- Xu Tianjian
- Yamana Teresa K.
- Yan Xifeng
- Yeluri Akshay
- Yeung Dit-Yan
- Yoder Nate
- Yogurtcu Osman N.
- Yoon Jinsung
- You Jialu
- Yu Rose
- Yu Shan
- Yurk Dominic
- Zeng Donglin
- Zhang Leyou
- Zhang Michael
- Zhang Shun
- Zhang Shunpu
- Zhang Weitong
- Zhang-James Yanli
- Zhao Yanting
- Zheng Andrew
- Zheng Shun
- Zhou Mingyuan
- Zimmerman Peter
- Zlokapa Alexander
- Zoraghein Hamidreza
- Zorn Martha W.
- Zou Difan
- Zou Zihang
- Publication venue
- Nature Research
- Publication date
- 17/08/2022
- Field of study
Academic researchers, government agencies, industry groups, and individuals have produced forecasts at an unprecedented scale during the COVID-19 pandemic. To leverage these forecasts, the United States Centers for Disease Control and Prevention (CDC) partnered with an academic research lab at the University of Massachusetts Amherst to create the US COVID-19 Forecast Hub. Launched in April 2020, the Forecast Hub is a dataset with point and probabilistic forecasts of incident cases, incident hospitalizations, incident deaths, and cumulative deaths due to COVID-19 at county, state, and national, levels in the United States. Included forecasts represent a variety of modeling approaches, data sources, and assumptions regarding the spread of COVID-19. The goal of this dataset is to establish a standardized and comparable set of short-term forecasts from modeling teams. These data can be used to develop ensemble models, communicate forecasts to the public, create visualizations, compare models, and inform policies regarding COVID-19 mitigation. These open-source data are available via download from GitHub, through an online API, and through R packages
Host-directed therapy targeting the Mycobacterium tuberculosis granuloma: a review
- Author
- A Arce-Mendoza
- A Dorhoi
- A Kubler
- A Lenaerts
- A Michelucci
- A Singhal
- A Zumla
- AG Rosas-Taraco
- AH Alzeer
- AP Yim
- B Hirshberg
- B Prideaux
- B Sloan
- B Yi
- BA Boone
- BG Marshall
- BK Podell
- Brendan K. Podell
- BS Somashekar
- BS Somashekar
- C Braian
- C Liang
- C Othieno
- C Xiong
- CA Behling
- CD Sohaskey
- CJ Fox
- CL Strelko
- CW Ong
- CW Ong
- DC Klonoff
- DF Ackart
- DF Ackart
- DG Russell
- Dilara Kiran
- DM Tobin
- DM Tobin
- E Hrabec
- E Peresi
- E Pienaar
- EJ Munoz-Elias
- F Alatas
- F Polet
- F Shemirani
- FG Schmid
- G Basta
- G Canetti
- G Canetti
- G Vanham
- GJ Canetti
- H Bruns
- H Bruns
- H Cho
- H Eoh
- H Rachman
- H Salamon
- H Tomioka
- HI Boshoff
- HM Algood
- HM Lander
- HP Windish
- I Pernicova
- I Preez du
- I Rosenkrands
- IM Orme
- IM Orme
- J Barbi
- J Bentley
- J Daniel
- J Folkman
- J Marrero
- J Zhang
- J Zhao
- JA Armstrong
- JA Critchley
- JC Batten
- JC Batten
- JH Helderman
- JO Olobo
- JP Lanoix
- K Patel
- KJ Seung
- KJ Welsh
- KN Aronis
- L Cudkowicz
- L Cudkowicz
- L Zheng
- LE Via
- LE Via
- LG Bekker
- LG Wayne
- LH Ly
- LH Ly
- LH Ly
- M Arai
- M Datta
- M Fabri
- M MacFarlane
- M Seiscento
- M Sitkovsky
- MA Matty
- MA Richardson
- MA Zoelen van
- Mark Chambers
- MC Kjellsson
- MC Tsai
- MJ Kim
- MM Delmastro-Greenwood
- N Ahmed
- N Ahmed
- N Kapoor
- N Lewin
- NF Walker
- NJ Garton
- NJ Maciver
- P Brassard
- P Elkington
- P Lint Van
- P Morgenstern
- P Peyron
- PC Drobac
- PT Elkington
- PT Elkington
- PT Elkington
- Q Zhang
- R Madansein
- R Singh
- R Sivangala
- R Tadokera
- R Vashisht
- R Visse
- Randall J. Basaraba
- RE Rojas
- RJ Napier
- RL Hunter
- RS Wallis
- RT Robinson
- RW Manthei
- S Aly
- S Aly
- S Clark
- S Ehlers
- S Hahn
- S Nhamoyebonde
- S Sundararajan
- S Tan
- S Watanabe
- SD Chakravarty
- SD Stowe
- SH Baek
- SH Lee
- SH Oehlers
- SM Irwin
- SR Jacobs
- SS Allen
- T Niimi
- T Roberts
- T Sathyamoorthy
- T Sathyamoorthy
- T Shimazaki
- T Wang
- TD Bold
- TM Zielonka
- V Clifford
- V Dartois
- V Jakus
- V Ramos-Kichik
- V Singh
- W Lee
- W Matsuyama
- WR Barclay
- WR Barclay
- WS Chung
- X Cun
- Y Abe
- Y Ishibashi
- Z Ahmad
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
- …