9 research outputs found
Description of diffusive and propagative behavior on fractals
- Author
- Publication venue
- 'American Physical Society (APS)'
- Publication date
- 01/01/2004
- Field of study
The known properties of diffusion on fractals are reviewed in order to give a general outlook of these dynamic processes. After that, we propose a description developed in the context of the intrinsic metric of fractals, which leads us to a differential equation able to describe diffusion in real fractals in the asymptotic regime. We show that our approach has a stronger physical justification than previous works on this field. The most important result we present is the introduction of a dependence on time and space for the conductivity in fractals, which is deduced by scaling arguments and supported by computer simulations. Finally, the diffusion equation is used to introduce the possibility of reaction-diffusion processes on fractals and analyze their properties. Specifically, an analytic expression for the speed of the corresponding travelling fronts, which can be of great interest for application purposes, is derived
Genome-wide analysis of 944 133 individuals provides insights into the etiology of haemorrhoidal disease
- Author
- Banasik K.
- Becker T.
- Beyder A.
- Bokelmann F.
- Brunak S.
- Buch S.
- Burmeister G.
- Chen S.
- Clausnitzer H.
- Cossais F.
- D'Amato M.
- Datz C.
- Degenhardt F.
- Doniec M.
- Ellinghaus D.
- Erikstrup C.
- Esko T.
- Farrugia G.
- Forster M.
- Franke A.
- Frey N.
- Fritsche L.
- Gabrielsen M.
- Gross J.
- Gräßle T.
- Gsur A.
- Hampe J.
- Hemmrich-Stanisak G.
- Hendricks A.
- Hinz S.
- Hveem K.
- Ito G.
- Jongen J.
- Junker R.
- Juzenas S.
- Jørgensen I.
- Kahlke V.
- Karlsen T.
- Kruis W.
- Kupcinskas J.
- Laubert T.
- Laudes M.
- Leendertz F.
- Lieb W.
- Limperger V.
- Margetis N.
- Mayr G.
- Mätz-Rensing K.
- Ness-Jensen E.
- Noblin E.
- Nowak-Göttl U.
- Németh C.
- Pandit A.
- Pedersen O.
- Peleikis H.
- Peuker K.
- Rodriguez C.
- Rosenstiel P.
- Röcken C.
- Rühlemann M.
- Sazonova O.
- Schafmayer C.
- Schniewind B.
- Schulzky M.
- Skieceviciene J.
- Skogholt A.
- Strege P.
- Teder-Laving M.
- Tepel J.
- Thomas L.
- Uellendahl-Werth F.
- Ullum H.
- Vacic V.
- Vanderwerff B.
- Vogel I.
- Volzke H.
- von Fersen L.
- von Schönfels W.
- Wedel T.
- Wilking J.
- Wittig M.
- Zawistowski M.
- Zeissig S.
- Zheng T.
- Zobel M.
- Publication venue
- 'BMJ'
- Publication date
- 01/01/2021
- Field of study
Random Walks on Fractals
- Author
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2006
- Field of study
Mapping the human genetic architecture of COVID-19
- Author
- Abdelrazik M.
- Abdullah T.
- Abe R.
- Abe S.
- Abecasis G. R.
- Abel L.
- Abernathy C.
- Abraheem A.
- Abul-Husn N. S.
- Acosta-Herrera M.
- Acquilini D.
- Adachi T.
- Adachi Y.
- Adams C.
- Adams K.
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- Adeniji K.
- Adra D.
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- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2021
- Field of study
The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease
Genome-wide analysis of 944 133 individuals provides insights into the etiology of haemorrhoidal disease
- Author
- Banasik Karina
- Becker Thomas
- Beyder Arthur
- Birger Pedersen Ole
- Bokelmann Frank
- Brunak Søren
- Buch Stephan
- Burmeister Greta
- Chen Sisi
- Clausnitzer Hartmut
- Cossais François
- D'Amato Mauro
- Datz Christian
- DBDS Consortium
- Degenhardt Frauke
- Doniec Marek
- Ellinghaus David
- Elvestad Gabrielsen Maiken
- Erikstrup Christian
- Esko Tõnu
- Farrugia Gianrico
- Forster Michael
- Franke Andre
- Frey Norbert
- Fritsche Lars G.
- Gross Justus
- Gräßle Tobias
- Gsur Andrea
- Hampe Jochen
- Hemmrich-Stanisak Georg
- Hendricks Alexander
- Hinz Sebastian
- Hveem Kristian
- Ito Go
- Jongen Johannes
- Junker Ralf
- Juzenas Simonas
- Jørgensen Isabella Friis
- Kahlke Volker
- Karlsen Tom Hemming
- Kruis Wolfgang
- Kupcinskas Jouzas
- Laubert Tilman
- Laudes Matthias
- Leendertz Fabian H.
- Lieb Wolfgang
- Limperger Verena
- Margetis Nikolaos
- Mayr Gabriele
- Mätz-Rensing Kerstin
- Ness-Jensen Eivind
- Noblin Elizabeth S.
- Nowak-Göttl Ulrike
- Németh Christopher Georg
- Pandit Anita
- Peleikis Hans Günter
- Peuker Kenneth
- Rodriguez Cristina Leal
- Rosenstiel Philip C.
- Röcken Christoph
- Rühlemann Malte Christoph
- Sazonova Olga
- Schafmayer Clemens
- Schniewind Bodo
- Schulzky Martin
- Skieceviciene Jurgita
- Skogholt Anne Heidi
- Strege Peter R.
- Teder-Laving Maris
- Tepel Jürgen
- The 23andMe Research Team
- Thomas Laurent
- Uellendahl-Werth Florian
- Ullum Henrik
- Vacic Vladimir
- Vanderwerff Brett
- Vogel Ilka
- Volzke Henry
- von Fersen Lorenzo
- von Schönfels Witigo
- Wedel Thilo
- Wilking Julia
- Wittig Michael
- Zawistowski Matthew
- Zeissig Sebastian
- Zheng Tenghao
- Zobel Myrko
- Publication venue
- 'BMJ'
- Publication date
- 01/01/2021
- Field of study
Objective Haemorrhoidal disease (HEM) affects a large and silently suffering fraction of the population but its aetiology, including suspected genetic predisposition, is poorly understood. We report the first genome-wide association study (GWAS) meta-analysis to identify genetic risk factors for HEM to date. Design We conducted a GWAS meta-analysis of 218 920 patients with HEM and 725 213 controls of European ancestry. Using GWAS summary statistics, we performed multiple genetic correlation analyses between HEM and other traits as well as calculated HEM polygenic risk scores (PRS) and evaluated their translational potential in independent datasets. Using functional annotation of GWAS results, we identified HEM candidate genes, which differential expression and coexpression in HEM tissues were evaluated employing RNA-seq analyses. The localisation of expressed proteins at selected loci was investigated by immunohistochemistry. Results We demonstrate modest heritability and genetic correlation of HEM with several other diseases from the GI, neuroaffective and cardiovascular domains. HEM PRS validated in 180 435 individuals from independent datasets allowed the identification of those at risk and correlated with younger age of onset and recurrent surgery. We identified 102 independent HEM risk loci harbouring genes whose expression is enriched in blood vessels and GI tissues, and in pathways associated with smooth muscles, epithelial and endothelial development and morphogenesis. Network transcriptomic analyses highlighted HEM gene coexpression modules that are relevant to the development and integrity of the musculoskeletal and epidermal systems, and the organisation of the extracellular matrix. Conclusion HEM has a genetic component that predisposes to smooth muscle, epithelial and connective tissue dysfunction
Genomewide Association Study of Severe Covid-19 with Respiratory Failure.
- Author
- Acosta-Herrera M
- Aghemo A
- Albillos A
- Albrecht W
- Aliberti S
- Aneli S
- Angelini C
- Asselta R
- Aziz F
- Badalamenti S
- Baldini M
- Banales JM
- Bandera A
- Baselli G
- Bettini LR
- Biondi A
- Blanco-Grau A
- Blandino Ortiz A
- Blasi F
- Bocciolone M
- Bonfanti P
- Bosari S
- Braun N
- Bujanda L
- Buti M
- Caballero-Garralda A
- Cardamone G
- Carrabba M
- Carreras Nolla A
- Castro P
- Cazzaniga M
- Cea C
- Cecconi M
- Ceriotti F
- Chercoles AG
- Ciccarelli M
- Costantino G
- D'Amato M
- D'Angiò M
- de Cid R
- de Pablo R
- Degenhardt F
- Duga S
- ElAbd H
- Ellinghaus D
- Erdmann J
- Faverio P
- Fernández J
- Ferrer R
- Ferrusquía-Acosta J
- Figuera Basso ME
- Folseraas T
- Foti G
- Fracanzani AL
- Franke A
- Galván-Femenia I
- Garcia-Etxebarria K
- Garcia-Fernandez A-E
- García Sánchez F
- Gassner C
- Goerg S
- Gori A
- Grasselli G
- Grimsrud MM
- Gualtierotti R
- Hemmrich-Stanisak G
- Hernandez-Tejero M
- Hov JR
- Invernizzi P
- Izquierdo-Sanchez L
- Jiménez D
- Julià A
- Juzenas S
- Karlsen TH
- Kurihara H
- Kässens J
- Latiano A
- Lenz TL
- Lleo A
- Marsal S
- Martinelli-Boneschi F
- Martín J
- Martínez N
- Mateos B
- Matullo G
- May S
- Mesonero F
- Milani C
- Miozzo M
- Montano N
- Monzani V
- Moreira L
- Moreno V
- Muñiz-Diaz E
- My I
- Nafria Jimenez B
- Navas E
- Nieto R
- Omodei P
- Paccapelo C
- Palmieri O
- Palom A
- Paraboschi EM
- Pelusi S
- Peschuck A
- Pesenti A
- Pestaña D
- Peter W
- Peyvandi F
- Prati D
- Preatoni P
- Protti A
- Pumarola T
- Quereda C
- Rimoldi V
- Riveiro-Barciela M
- Roade L
- Rodrigues PM
- Rodriguez-Frias F
- Rodríguez-Gandía M
- Romero-Gómez M
- Rühlemann MC
- Sacchi N
- Sandoval E
- Santoro L
- Schaefer M
- Schulzky M
- Scudeller L
- Severe Covid-19 GWAS Group
- Solier A
- Sumoy L
- Tanck A
- Tentorio P
- Terranova L
- Téllez L
- Uellendahl-Werth F
- Valenti L
- Valsecchi MG
- Voza A
- Wendorff M
- Wesse T
- Wienbrandt L
- Wittig M
- Yi X
- Zanella A
- Zheng T
- Özer O
- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2020
- Field of study
BACKGROUND: There is considerable variation in disease behavior among patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (Covid-19). Genomewide association analysis may allow for the identification of potential genetic factors involved in the development of Covid-19. METHODS: We conducted a genomewide association study involving 1980 patients with Covid-19 and severe disease (defined as respiratory failure) at seven hospitals in the Italian and Spanish epicenters of the SARS-CoV-2 pandemic in Europe. After quality control and the exclusion of population outliers, 835 patients and 1255 control participants from Italy and 775 patients and 950 control participants from Spain were included in the final analysis. In total, we analyzed 8,582,968 single-nucleotide polymorphisms and conducted a meta-analysis of the two case-control panels. RESULTS: We detected cross-replicating associations with rs11385942 at locus 3p21.31 and with rs657152 at locus 9q34.2, which were significant at the genomewide level (P<5×10-8) in the meta-analysis of the two case-control panels (odds ratio, 1.77; 95% confidence interval [CI], 1.48 to 2.11; P = 1.15×10-10; and odds ratio, 1.32; 95% CI, 1.20 to 1.47; P = 4.95×10-8, respectively). At locus 3p21.31, the association signal spanned the genes SLC6A20, LZTFL1, CCR9, FYCO1, CXCR6 and XCR1. The association signal at locus 9q34.2 coincided with the ABO blood group locus; in this cohort, a blood-group-specific analysis showed a higher risk in blood group A than in other blood groups (odds ratio, 1.45; 95% CI, 1.20 to 1.75; P = 1.48×10-4) and a protective effect in blood group O as compared with other blood groups (odds ratio, 0.65; 95% CI, 0.53 to 0.79; P = 1.06×10-5). CONCLUSIONS: We identified a 3p21.31 gene cluster as a genetic susceptibility locus in patients with Covid-19 with respiratory failure and confirmed a potential involvement of the ABO blood-group system. (Funded by Stein Erik Hagen and others.)
Genome-wide analysis of 944 133 individuals provides insights into the etiology of haemorrhoidal disease
- Publication venue
- Publication date
- 01/01/2021
- Field of study
Objective Haemorrhoidal disease (HEM) affects a large and silently
suffering fraction of the population but its aetiology, including
suspected genetic predisposition, is poorly understood. We report the
first genome-wide association study (GWAS) meta-analysis to identify
genetic risk factors for HEM to date. Design We conducted a GWAS
meta-analysis of 218 920 patients with HEM and 725 213 controls of
European ancestry. Using GWAS summary statistics, we performed multiple
genetic correlation analyses between HEM and other traits as well as
calculated HEM polygenic risk scores (PRS) and evaluated their
translational potential in independent datasets. Using functional
annotation of GWAS results, we identified HEM candidate genes, which
differential expression and coexpression in HEM tissues were evaluated
employing RNA-seq analyses. The localisation of expressed proteins at
selected loci was investigated by immunohistochemistry. Results We
demonstrate modest heritability and genetic correlation of HEM with
several other diseases from the GI, neuroaffective and cardiovascular
domains. HEM PRS validated in 180 435 individuals from independent
datasets allowed the identification of those at risk and correlated with
younger age of onset and recurrent surgery. We identified 102
independent HEM risk loci harbouring genes whose expression is enriched
in blood vessels and GI tissues, and in pathways associated with smooth
muscles, epithelial and endothelial development and morphogenesis.
Network transcriptomic analyses highlighted HEM gene coexpression
modules that are relevant to the development and integrity of the
musculoskeletal and epidermal systems, and the organisation of the
extracellular matrix. Conclusion HEM has a genetic component that
predisposes to smooth muscle, epithelial and connective tissue
dysfunction
Mapping the human genetic architecture of COVID-19
- Author
- Abdelrazik M
- Abdullah T
- Abe R
- Abe S
- Abecasis GR
- Abel L
- Abernathy C
- Abraheem A
- Abul-Husn NS
- Acosta-Herrera M
- Acquilini D
- Acquilini D
- Adachi T
- Adachi Y
- Adams C
- Adams K
- Adanini O
- Adeleye O
- Adeniji K
- Adra D
- Afifi N
- Afilalo J
- Afilalo M
- Afolabi D
- Afrasiabi Z
- Afset JE
- Agasou A
- Aghemo A
- Agranoff D
- Agrawal S
- Aguirre LA
- Agwuh K
- Ahmad HF
- Ahmad N
- Ahmed A
- Ahmed C
- Ahmed KA
- Ai M
- Ail D
- Akeroyd L
- Akhtar MN
- Akhtar S
- Akinkugbe O
- Aksentijevich A
- Al Thani A
- Al-Muftah W
- Al-Sarraj Y
- Alarcon C
- Alarcon-Riquelme ME
- Alasdair F
- Alaverdian D
- Alavere H
- Albertos R
- Albillos A
- Albrecht W
- Albrich W
- Albrich WC
- Aldera EL
- Aldridge J
- Alegria A
- Alex B
- Alexander P
- Alfonso J
- Algera AG
- Ali A
- Ali IMA
- Ali S
- Aliberti S
- Allan A
- Allan E
- Allan J
- Alldis Z
- Allen L
- Allen S
- Allibone S
- Allison KS
- Allos R
- Ally SM
- Almaden-Boyle C
- Altabaibeh A
- Altmueller J
- Alvaro A
- Amar D
- Amin V
- Amitrano S
- Amiya S
- Ampuero J
- Anan R
- Anania S
- Anastasescu E
- Anderson F
- Anderson J
- Anderson M
- Anderson P
- Anderson S
- Anderson S
- Anderson T
- Ando A
- Andolfo I
- Andrade V
- Andretta F
- Andreucci E
- Andreucci E
- Andrew A
- Andrew B
- Andrew G
- Andrews E
- Andrews SJ
- Andrews SJ
- Andrews SJ
- Andrews SJ
- Andrikopoulos P
- Anedda F
- Aneli S
- Anemoli V
- Angelini C
- Angus B
- Annis A
- Antcliffe D
- Antinori A
- Antoni MD
- Anumakonda V
- Anwar M
- Anzai T
- Apetri E
- Arai D
- Arana E
- Arbane G
- Archer K
- Arciero E
- Arden T
- Arias SS
- Arif S
- Arimura K
- Armstrong J
- Armstrong JA
- Armstrong L
- Armstrong R
- Arning N
- Arnold S
- Arora J
- Artuso R
- Arumugam P
- Asakura T
- Asano K
- Aschard H
- Ascolillo S
- Ashish A
- Ashley E
- Ashraf S
- Ashraf S
- Ashton L
- Ashworth M
- Asiimwe IG
- Aslibekyan S
- Asselta R
- Atanasovska B
- Atkinson D
- Atkinson EG
- Attwood B
- Aucella F
- Augustin M
- Auld D
- Auld F
- Austin K
- Austin P
- Auton A
- Auton A
- Avendano-Ortiz J
- Awano N
- Ayers A
- Azarzar S
- Aziz F
- Azuma M
- Azuure C
- Azzolini E
- Baba R
- Baba T
- Bach B
- Bacher P
- Bachetti T
- Badalamenti S
- Badia JR
- Badji RM
- Bahmer T
- Baikady RR
- Baillie JK
- Baillie JK
- Baillie JK
- Baillie JK
- Baines B
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- Baines K
- Baird T
- Baird Y
- Bakshi S
- Bakthavatsalam D
- Balaconis MK
- Baldassarri M
- Baldini M
- Ball CA
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- Baltzell AH
- Bamford A
- Bamford P
- Banach D
- Banagan J
- Banales JM
- Bancroft H
- Band G
- Bandera A
- Bandini M
- Bandla N
- Bano S
- Baptista D
- Barada O
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- Zanelli G
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- zu Bentrup FM
- Zucchi P
- Zwinderman AHK
- Zyndorf M
- Publication venue
- Publication date
- 01/01/2021
- Field of study
The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3,4,5,6,7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease