---
_id: '7698'
abstract:
- lang: eng
  text: Motor output varies along the rostro-caudal axis of the tetrapod spinal cord.
    At limb levels, ∼60 motor pools control the alternation of flexor and extensor
    muscles about each joint, whereas at thoracic levels as few as 10 motor pools
    supply muscle groups that support posture, inspiration, and expiration. Whether
    such differences in motor neuron identity and muscle number are associated with
    segmental distinctions in interneuron diversity has not been resolved. We show
    that select combinations of nineteen transcription factors that specify lumbar
    V1 inhibitory interneurons generate subpopulations enriched at limb and thoracic
    levels. Specification of limb and thoracic V1 interneurons involves the Hox gene
    Hoxc9 independently of motor neurons. Thus, early Hox patterning of the spinal
    cord determines the identity of V1 interneurons and motor neurons. These studies
    reveal a developmental program of V1 interneuron diversity, providing insight
    into the organization of inhibitory interneurons associated with differential
    motor output.
article_processing_charge: No
article_type: original
author:
- first_name: Lora Beatrice Jaeger
  full_name: Sweeney, Lora Beatrice Jaeger
  id: 56BE8254-C4F0-11E9-8E45-0B23E6697425
  last_name: Sweeney
  orcid: 0000-0001-9242-5601
- first_name: Jay B.
  full_name: Bikoff, Jay B.
  last_name: Bikoff
- first_name: Mariano I.
  full_name: Gabitto, Mariano I.
  last_name: Gabitto
- first_name: Susan
  full_name: Brenner-Morton, Susan
  last_name: Brenner-Morton
- first_name: Myungin
  full_name: Baek, Myungin
  last_name: Baek
- first_name: Jerry H.
  full_name: Yang, Jerry H.
  last_name: Yang
- first_name: Esteban G.
  full_name: Tabak, Esteban G.
  last_name: Tabak
- first_name: Jeremy S.
  full_name: Dasen, Jeremy S.
  last_name: Dasen
- first_name: Christopher R.
  full_name: Kintner, Christopher R.
  last_name: Kintner
- first_name: Thomas M.
  full_name: Jessell, Thomas M.
  last_name: Jessell
citation:
  ama: Sweeney LB, Bikoff JB, Gabitto MI, et al. Origin and segmental diversity of
    spinal inhibitory interneurons. <i>Neuron</i>. 2018;97(2):341-355.e3. doi:<a href="https://doi.org/10.1016/j.neuron.2017.12.029">10.1016/j.neuron.2017.12.029</a>
  apa: Sweeney, L. B., Bikoff, J. B., Gabitto, M. I., Brenner-Morton, S., Baek, M.,
    Yang, J. H., … Jessell, T. M. (2018). Origin and segmental diversity of spinal
    inhibitory interneurons. <i>Neuron</i>. Elsevier. <a href="https://doi.org/10.1016/j.neuron.2017.12.029">https://doi.org/10.1016/j.neuron.2017.12.029</a>
  chicago: Sweeney, Lora B., Jay B. Bikoff, Mariano I. Gabitto, Susan Brenner-Morton,
    Myungin Baek, Jerry H. Yang, Esteban G. Tabak, Jeremy S. Dasen, Christopher R.
    Kintner, and Thomas M. Jessell. “Origin and Segmental Diversity of Spinal Inhibitory
    Interneurons.” <i>Neuron</i>. Elsevier, 2018. <a href="https://doi.org/10.1016/j.neuron.2017.12.029">https://doi.org/10.1016/j.neuron.2017.12.029</a>.
  ieee: L. B. Sweeney <i>et al.</i>, “Origin and segmental diversity of spinal inhibitory
    interneurons,” <i>Neuron</i>, vol. 97, no. 2. Elsevier, p. 341–355.e3, 2018.
  ista: Sweeney LB, Bikoff JB, Gabitto MI, Brenner-Morton S, Baek M, Yang JH, Tabak
    EG, Dasen JS, Kintner CR, Jessell TM. 2018. Origin and segmental diversity of
    spinal inhibitory interneurons. Neuron. 97(2), 341–355.e3.
  mla: Sweeney, Lora B., et al. “Origin and Segmental Diversity of Spinal Inhibitory
    Interneurons.” <i>Neuron</i>, vol. 97, no. 2, Elsevier, 2018, p. 341–355.e3, doi:<a
    href="https://doi.org/10.1016/j.neuron.2017.12.029">10.1016/j.neuron.2017.12.029</a>.
  short: L.B. Sweeney, J.B. Bikoff, M.I. Gabitto, S. Brenner-Morton, M. Baek, J.H.
    Yang, E.G. Tabak, J.S. Dasen, C.R. Kintner, T.M. Jessell, Neuron 97 (2018) 341–355.e3.
date_created: 2020-04-30T10:35:13Z
date_published: 2018-01-04T00:00:00Z
date_updated: 2024-01-31T10:13:54Z
day: '04'
doi: 10.1016/j.neuron.2017.12.029
extern: '1'
intvolume: '        97'
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 341-355.e3
publication: Neuron
publication_identifier:
  issn:
  - 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
status: public
title: Origin and segmental diversity of spinal inhibitory interneurons
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 97
year: '2018'
...
---
_id: '77'
abstract:
- lang: eng
  text: Holes confined in quantum dots have gained considerable interest in the past
    few years due to their potential as spin qubits. Here we demonstrate two-axis
    control of a spin 3/2 qubit in natural Ge. The qubit is formed in a hut wire double
    quantum dot device. The Pauli spin blockade principle allowed us to demonstrate
    electric dipole spin resonance by applying a radio frequency electric field to
    one of the electrodes defining the double quantum dot. Coherent hole spin oscillations
    with Rabi frequencies reaching 140 MHz are demonstrated and dephasing times of
    130 ns are measured. The reported results emphasize the potential of Ge as a platform
    for fast and electrically tunable hole spin qubit devices.
acknowledged_ssus:
- _id: M-Shop
- _id: NanoFab
article_processing_charge: Yes
article_type: original
author:
- first_name: Hannes
  full_name: Watzinger, Hannes
  id: 35DF8E50-F248-11E8-B48F-1D18A9856A87
  last_name: Watzinger
- first_name: Josip
  full_name: Kukucka, Josip
  id: 3F5D8856-F248-11E8-B48F-1D18A9856A87
  last_name: Kukucka
- first_name: Lada
  full_name: Vukusic, Lada
  id: 31E9F056-F248-11E8-B48F-1D18A9856A87
  last_name: Vukusic
  orcid: 0000-0003-2424-8636
- first_name: Fei
  full_name: Gao, Fei
  last_name: Gao
- first_name: Ting
  full_name: Wang, Ting
  last_name: Wang
- first_name: Friedrich
  full_name: Schäffler, Friedrich
  last_name: Schäffler
- first_name: Jian
  full_name: Zhang, Jian
  last_name: Zhang
- first_name: Georgios
  full_name: Katsaros, Georgios
  id: 38DB5788-F248-11E8-B48F-1D18A9856A87
  last_name: Katsaros
  orcid: 0000-0001-8342-202X
citation:
  ama: Watzinger H, Kukucka J, Vukušić L, et al. A germanium hole spin qubit. <i>Nature
    Communications</i>. 2018;9(3902). doi:<a href="https://doi.org/10.1038/s41467-018-06418-4">10.1038/s41467-018-06418-4</a>
  apa: Watzinger, H., Kukucka, J., Vukušić, L., Gao, F., Wang, T., Schäffler, F.,
    … Katsaros, G. (2018). A germanium hole spin qubit. <i>Nature Communications</i>.
    Nature Publishing Group. <a href="https://doi.org/10.1038/s41467-018-06418-4">https://doi.org/10.1038/s41467-018-06418-4</a>
  chicago: Watzinger, Hannes, Josip Kukucka, Lada Vukušić, Fei Gao, Ting Wang, Friedrich
    Schäffler, Jian Zhang, and Georgios Katsaros. “A Germanium Hole Spin Qubit.” <i>Nature
    Communications</i>. Nature Publishing Group, 2018. <a href="https://doi.org/10.1038/s41467-018-06418-4">https://doi.org/10.1038/s41467-018-06418-4</a>.
  ieee: H. Watzinger <i>et al.</i>, “A germanium hole spin qubit,” <i>Nature Communications</i>,
    vol. 9, no. 3902. Nature Publishing Group, 2018.
  ista: Watzinger H, Kukucka J, Vukušić L, Gao F, Wang T, Schäffler F, Zhang J, Katsaros
    G. 2018. A germanium hole spin qubit. Nature Communications. 9(3902).
  mla: Watzinger, Hannes, et al. “A Germanium Hole Spin Qubit.” <i>Nature Communications</i>,
    vol. 9, no. 3902, Nature Publishing Group, 2018, doi:<a href="https://doi.org/10.1038/s41467-018-06418-4">10.1038/s41467-018-06418-4</a>.
  short: H. Watzinger, J. Kukucka, L. Vukušić, F. Gao, T. Wang, F. Schäffler, J. Zhang,
    G. Katsaros, Nature Communications 9 (2018).
date_created: 2018-12-11T11:44:30Z
date_published: 2018-09-25T00:00:00Z
date_updated: 2023-09-08T11:44:02Z
day: '25'
ddc:
- '530'
department:
- _id: GeKa
doi: 10.1038/s41467-018-06418-4
ec_funded: 1
external_id:
  isi:
  - '000445560800010'
file:
- access_level: open_access
  checksum: e7148c10a64497e279c4de570b6cc544
  content_type: application/pdf
  creator: dernst
  date_created: 2018-12-17T10:28:30Z
  date_updated: 2020-07-14T12:48:02Z
  file_id: '5687'
  file_name: 2018_NatureComm_Watzinger.pdf
  file_size: 1063469
  relation: main_file
file_date_updated: 2020-07-14T12:48:02Z
has_accepted_license: '1'
intvolume: '         9'
isi: 1
issue: '3902 '
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
project:
- _id: 25517E86-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '335497'
  name: Towards Spin qubits and Majorana fermions in Germanium selfassembled hut-wires
- _id: 2552F888-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: Y00715
  name: Loch Spin-Qubits und Majorana-Fermionen in Germanium
publication: Nature Communications
publication_status: published
publisher: Nature Publishing Group
quality_controlled: '1'
related_material:
  record:
  - id: '7977'
    relation: popular_science
  - id: '7996'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: A germanium hole spin qubit
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 9
year: '2018'
...
---
_id: '7712'
abstract:
- lang: eng
  text: 'Male pattern baldness (MPB) is a sex-limited, age-related, complex trait.
    We study MPB genetics in 205,327 European males from the UK Biobank. Here we show
    that MPB is strongly heritable and polygenic, with pedigree-heritability of 0.62
    (SE = 0.03) estimated from close relatives, and SNP-heritability of 0.39 (SE = 0.01)
    from conventionally-unrelated males. We detect 624 near-independent genome-wide
    loci, contributing SNP-heritability of 0.25 (SE = 0.01), of which 26 X-chromosome
    loci explain 11.6%. Autosomal genetic variance is enriched for common variants
    and regions of lower linkage disequilibrium. We identify plausible genetic correlations
    between MPB and multiple sex-limited markers of earlier puberty, increased bone
    mineral density (rg = 0.15) and pancreatic β-cell function (rg = 0.12). Correlations
    with reproductive traits imply an effect on fitness, consistent with an estimated
    linear selection gradient of -0.018 per MPB standard deviation. Overall, we provide
    genetic insights into MPB: a phenotype of interest in its own right, with value
    as a model sex-limited, complex trait.'
article_number: '5407'
article_processing_charge: No
article_type: original
author:
- first_name: Chloe X.
  full_name: Yap, Chloe X.
  last_name: Yap
- first_name: Julia
  full_name: Sidorenko, Julia
  last_name: Sidorenko
- first_name: Yang
  full_name: Wu, Yang
  last_name: Wu
- first_name: Kathryn E.
  full_name: Kemper, Kathryn E.
  last_name: Kemper
- first_name: Jian
  full_name: Yang, Jian
  last_name: Yang
- first_name: Naomi R.
  full_name: Wray, Naomi R.
  last_name: Wray
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
- first_name: Peter M.
  full_name: Visscher, Peter M.
  last_name: Visscher
citation:
  ama: Yap CX, Sidorenko J, Wu Y, et al. Dissection of genetic variation and evidence
    for pleiotropy in male pattern baldness. <i>Nature Communications</i>. 2018;9.
    doi:<a href="https://doi.org/10.1038/s41467-018-07862-y">10.1038/s41467-018-07862-y</a>
  apa: Yap, C. X., Sidorenko, J., Wu, Y., Kemper, K. E., Yang, J., Wray, N. R., …
    Visscher, P. M. (2018). Dissection of genetic variation and evidence for pleiotropy
    in male pattern baldness. <i>Nature Communications</i>. Springer Nature. <a href="https://doi.org/10.1038/s41467-018-07862-y">https://doi.org/10.1038/s41467-018-07862-y</a>
  chicago: Yap, Chloe X., Julia Sidorenko, Yang Wu, Kathryn E. Kemper, Jian Yang,
    Naomi R. Wray, Matthew Richard Robinson, and Peter M. Visscher. “Dissection of
    Genetic Variation and Evidence for Pleiotropy in Male Pattern Baldness.” <i>Nature
    Communications</i>. Springer Nature, 2018. <a href="https://doi.org/10.1038/s41467-018-07862-y">https://doi.org/10.1038/s41467-018-07862-y</a>.
  ieee: C. X. Yap <i>et al.</i>, “Dissection of genetic variation and evidence for
    pleiotropy in male pattern baldness,” <i>Nature Communications</i>, vol. 9. Springer
    Nature, 2018.
  ista: Yap CX, Sidorenko J, Wu Y, Kemper KE, Yang J, Wray NR, Robinson MR, Visscher
    PM. 2018. Dissection of genetic variation and evidence for pleiotropy in male
    pattern baldness. Nature Communications. 9, 5407.
  mla: Yap, Chloe X., et al. “Dissection of Genetic Variation and Evidence for Pleiotropy
    in Male Pattern Baldness.” <i>Nature Communications</i>, vol. 9, 5407, Springer
    Nature, 2018, doi:<a href="https://doi.org/10.1038/s41467-018-07862-y">10.1038/s41467-018-07862-y</a>.
  short: C.X. Yap, J. Sidorenko, Y. Wu, K.E. Kemper, J. Yang, N.R. Wray, M.R. Robinson,
    P.M. Visscher, Nature Communications 9 (2018).
date_created: 2020-04-30T10:41:19Z
date_published: 2018-12-20T00:00:00Z
date_updated: 2021-01-12T08:15:02Z
day: '20'
doi: 10.1038/s41467-018-07862-y
extern: '1'
intvolume: '         9'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1038/s41467-018-07862-y
month: '12'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Dissection of genetic variation and evidence for pleiotropy in male pattern
  baldness
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2018'
...
---
_id: '7713'
abstract:
- lang: eng
  text: There are mean differences in complex traits among global human populations.
    We hypothesize that part of the phenotypic differentiation is due to natural selection.
    To address this hypothesis, we assess the differentiation in allele frequencies
    of trait-associated SNPs among African, Eastern Asian, and European populations
    for ten complex traits using data of large sample size (up to ~405,000). We show
    that SNPs associated with height (P=2.46×10−5), waist-to-hip ratio (P=2.77×10−4),
    and schizophrenia (P=3.96×10−5) are significantly more differentiated among populations
    than matched “control” SNPs, suggesting that these trait-associated SNPs have
    undergone natural selection. We further find that SNPs associated with height
    (P=2.01×10−6) and schizophrenia (P=5.16×10−18) show significantly higher variance
    in linkage disequilibrium (LD) scores across populations than control SNPs. Our
    results support the hypothesis that natural selection has shaped the genetic differentiation
    of complex traits, such as height and schizophrenia, among worldwide populations.
article_number: '1865'
article_processing_charge: No
article_type: original
author:
- first_name: Jing
  full_name: Guo, Jing
  last_name: Guo
- first_name: Yang
  full_name: Wu, Yang
  last_name: Wu
- first_name: Zhihong
  full_name: Zhu, Zhihong
  last_name: Zhu
- first_name: Zhili
  full_name: Zheng, Zhili
  last_name: Zheng
- first_name: Maciej
  full_name: Trzaskowski, Maciej
  last_name: Trzaskowski
- first_name: Jian
  full_name: Zeng, Jian
  last_name: Zeng
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
- first_name: Peter M.
  full_name: Visscher, Peter M.
  last_name: Visscher
- first_name: Jian
  full_name: Yang, Jian
  last_name: Yang
citation:
  ama: Guo J, Wu Y, Zhu Z, et al. Global genetic differentiation of complex traits
    shaped by natural selection in humans. <i>Nature Communications</i>. 2018;9. doi:<a
    href="https://doi.org/10.1038/s41467-018-04191-y">10.1038/s41467-018-04191-y</a>
  apa: Guo, J., Wu, Y., Zhu, Z., Zheng, Z., Trzaskowski, M., Zeng, J., … Yang, J.
    (2018). Global genetic differentiation of complex traits shaped by natural selection
    in humans. <i>Nature Communications</i>. Springer Nature. <a href="https://doi.org/10.1038/s41467-018-04191-y">https://doi.org/10.1038/s41467-018-04191-y</a>
  chicago: Guo, Jing, Yang Wu, Zhihong Zhu, Zhili Zheng, Maciej Trzaskowski, Jian
    Zeng, Matthew Richard Robinson, Peter M. Visscher, and Jian Yang. “Global Genetic
    Differentiation of Complex Traits Shaped by Natural Selection in Humans.” <i>Nature
    Communications</i>. Springer Nature, 2018. <a href="https://doi.org/10.1038/s41467-018-04191-y">https://doi.org/10.1038/s41467-018-04191-y</a>.
  ieee: J. Guo <i>et al.</i>, “Global genetic differentiation of complex traits shaped
    by natural selection in humans,” <i>Nature Communications</i>, vol. 9. Springer
    Nature, 2018.
  ista: Guo J, Wu Y, Zhu Z, Zheng Z, Trzaskowski M, Zeng J, Robinson MR, Visscher
    PM, Yang J. 2018. Global genetic differentiation of complex traits shaped by natural
    selection in humans. Nature Communications. 9, 1865.
  mla: Guo, Jing, et al. “Global Genetic Differentiation of Complex Traits Shaped
    by Natural Selection in Humans.” <i>Nature Communications</i>, vol. 9, 1865, Springer
    Nature, 2018, doi:<a href="https://doi.org/10.1038/s41467-018-04191-y">10.1038/s41467-018-04191-y</a>.
  short: J. Guo, Y. Wu, Z. Zhu, Z. Zheng, M. Trzaskowski, J. Zeng, M.R. Robinson,
    P.M. Visscher, J. Yang, Nature Communications 9 (2018).
date_created: 2020-04-30T10:41:36Z
date_published: 2018-05-14T00:00:00Z
date_updated: 2021-01-12T08:15:02Z
day: '14'
doi: 10.1038/s41467-018-04191-y
extern: '1'
intvolume: '         9'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1038/s41467-018-04191-y
month: '05'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Global genetic differentiation of complex traits shaped by natural selection
  in humans
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2018'
...
---
_id: '7714'
abstract:
- lang: eng
  text: Health risk factors such as body mass index (BMI) and serum cholesterol are
    associated with many common diseases. It often remains unclear whether the risk
    factors are cause or consequence of disease, or whether the associations are the
    result of confounding. We develop and apply a method (called GSMR) that performs
    a multi-SNP Mendelian randomization analysis using summary-level data from genome-wide
    association studies to test the causal associations of BMI, waist-to-hip ratio,
    serum cholesterols, blood pressures, height, and years of schooling (EduYears)
    with common diseases (sample sizes of up to 405,072). We identify a number of
    causal associations including a protective effect of LDL-cholesterol against type-2
    diabetes (T2D) that might explain the side effects of statins on T2D, a protective
    effect of EduYears against Alzheimer’s disease, and bidirectional associations
    with opposite effects (e.g., higher BMI increases the risk of T2D but the effect
    of T2D on BMI is negative).
article_number: '224'
article_processing_charge: No
article_type: original
author:
- first_name: Zhihong
  full_name: Zhu, Zhihong
  last_name: Zhu
- first_name: Zhili
  full_name: Zheng, Zhili
  last_name: Zheng
- first_name: Futao
  full_name: Zhang, Futao
  last_name: Zhang
- first_name: Yang
  full_name: Wu, Yang
  last_name: Wu
- first_name: Maciej
  full_name: Trzaskowski, Maciej
  last_name: Trzaskowski
- first_name: Robert
  full_name: Maier, Robert
  last_name: Maier
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
- first_name: John J.
  full_name: McGrath, John J.
  last_name: McGrath
- first_name: Peter M.
  full_name: Visscher, Peter M.
  last_name: Visscher
- first_name: Naomi R.
  full_name: Wray, Naomi R.
  last_name: Wray
- first_name: Jian
  full_name: Yang, Jian
  last_name: Yang
citation:
  ama: Zhu Z, Zheng Z, Zhang F, et al. Causal associations between risk factors and
    common diseases inferred from GWAS summary data. <i>Nature Communications</i>.
    2018;9. doi:<a href="https://doi.org/10.1038/s41467-017-02317-2">10.1038/s41467-017-02317-2</a>
  apa: Zhu, Z., Zheng, Z., Zhang, F., Wu, Y., Trzaskowski, M., Maier, R., … Yang,
    J. (2018). Causal associations between risk factors and common diseases inferred
    from GWAS summary data. <i>Nature Communications</i>. Springer Nature. <a href="https://doi.org/10.1038/s41467-017-02317-2">https://doi.org/10.1038/s41467-017-02317-2</a>
  chicago: Zhu, Zhihong, Zhili Zheng, Futao Zhang, Yang Wu, Maciej Trzaskowski, Robert
    Maier, Matthew Richard Robinson, et al. “Causal Associations between Risk Factors
    and Common Diseases Inferred from GWAS Summary Data.” <i>Nature Communications</i>.
    Springer Nature, 2018. <a href="https://doi.org/10.1038/s41467-017-02317-2">https://doi.org/10.1038/s41467-017-02317-2</a>.
  ieee: Z. Zhu <i>et al.</i>, “Causal associations between risk factors and common
    diseases inferred from GWAS summary data,” <i>Nature Communications</i>, vol.
    9. Springer Nature, 2018.
  ista: Zhu Z, Zheng Z, Zhang F, Wu Y, Trzaskowski M, Maier R, Robinson MR, McGrath
    JJ, Visscher PM, Wray NR, Yang J. 2018. Causal associations between risk factors
    and common diseases inferred from GWAS summary data. Nature Communications. 9,
    224.
  mla: Zhu, Zhihong, et al. “Causal Associations between Risk Factors and Common Diseases
    Inferred from GWAS Summary Data.” <i>Nature Communications</i>, vol. 9, 224, Springer
    Nature, 2018, doi:<a href="https://doi.org/10.1038/s41467-017-02317-2">10.1038/s41467-017-02317-2</a>.
  short: Z. Zhu, Z. Zheng, F. Zhang, Y. Wu, M. Trzaskowski, R. Maier, M.R. Robinson,
    J.J. McGrath, P.M. Visscher, N.R. Wray, J. Yang, Nature Communications 9 (2018).
date_created: 2020-04-30T10:41:55Z
date_published: 2018-01-15T00:00:00Z
date_updated: 2021-01-12T08:15:03Z
day: '15'
doi: 10.1038/s41467-017-02317-2
extern: '1'
intvolume: '         9'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1038/s41467-017-02317-2
month: '01'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Causal associations between risk factors and common diseases inferred from
  GWAS summary data
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2018'
...
---
_id: '7715'
abstract:
- lang: eng
  text: Preference for mates with similar phenotypes; that is, assortative mating,
    is widely observed in humans1,2,3,4,5 and has evolutionary consequences6,7,8.
    Under Fisher's classical theory6, assortative mating is predicted to induce a
    signature in the genome at trait-associated loci that can be detected and quantified.
    Here, we develop and apply a method to quantify assortative mating on a specific
    trait by estimating the correlation (θ) between genetic predictors of the trait
    from single nucleotide polymorphisms on odd- versus even-numbered chromosomes.
    We show by theory and simulation that the effect of assortative mating can be
    quantified in the presence of population stratification. We applied this approach
    to 32 complex traits and diseases using single nucleotide polymorphism data from
    ~400,000 unrelated individuals of European ancestry. We found significant evidence
    of assortative mating for height (θ = 3.2%) and educational attainment (θ = 2.7%),
    both of which were consistent with theoretical predictions. Overall, our results
    imply that assortative mating involves multiple traits and affects the genomic
    architecture of loci that are associated with these traits, and that the consequence
    of mate choice can be detected from a random sample of genomes.
article_processing_charge: No
article_type: original
author:
- first_name: Loic
  full_name: Yengo, Loic
  last_name: Yengo
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
- first_name: Matthew C.
  full_name: Keller, Matthew C.
  last_name: Keller
- first_name: Kathryn E.
  full_name: Kemper, Kathryn E.
  last_name: Kemper
- first_name: Yuanhao
  full_name: Yang, Yuanhao
  last_name: Yang
- first_name: Maciej
  full_name: Trzaskowski, Maciej
  last_name: Trzaskowski
- first_name: Jacob
  full_name: Gratten, Jacob
  last_name: Gratten
- first_name: Patrick
  full_name: Turley, Patrick
  last_name: Turley
- first_name: David
  full_name: Cesarini, David
  last_name: Cesarini
- first_name: Daniel J.
  full_name: Benjamin, Daniel J.
  last_name: Benjamin
- first_name: Naomi R.
  full_name: Wray, Naomi R.
  last_name: Wray
- first_name: Michael E.
  full_name: Goddard, Michael E.
  last_name: Goddard
- first_name: Jian
  full_name: Yang, Jian
  last_name: Yang
- first_name: Peter M.
  full_name: Visscher, Peter M.
  last_name: Visscher
citation:
  ama: Yengo L, Robinson MR, Keller MC, et al. Imprint of assortative mating on the
    human genome. <i>Nature Human Behaviour</i>. 2018;2(12):948-954. doi:<a href="https://doi.org/10.1038/s41562-018-0476-3">10.1038/s41562-018-0476-3</a>
  apa: Yengo, L., Robinson, M. R., Keller, M. C., Kemper, K. E., Yang, Y., Trzaskowski,
    M., … Visscher, P. M. (2018). Imprint of assortative mating on the human genome.
    <i>Nature Human Behaviour</i>. Springer Nature. <a href="https://doi.org/10.1038/s41562-018-0476-3">https://doi.org/10.1038/s41562-018-0476-3</a>
  chicago: Yengo, Loic, Matthew Richard Robinson, Matthew C. Keller, Kathryn E. Kemper,
    Yuanhao Yang, Maciej Trzaskowski, Jacob Gratten, et al. “Imprint of Assortative
    Mating on the Human Genome.” <i>Nature Human Behaviour</i>. Springer Nature, 2018.
    <a href="https://doi.org/10.1038/s41562-018-0476-3">https://doi.org/10.1038/s41562-018-0476-3</a>.
  ieee: L. Yengo <i>et al.</i>, “Imprint of assortative mating on the human genome,”
    <i>Nature Human Behaviour</i>, vol. 2, no. 12. Springer Nature, pp. 948–954, 2018.
  ista: Yengo L, Robinson MR, Keller MC, Kemper KE, Yang Y, Trzaskowski M, Gratten
    J, Turley P, Cesarini D, Benjamin DJ, Wray NR, Goddard ME, Yang J, Visscher PM.
    2018. Imprint of assortative mating on the human genome. Nature Human Behaviour.
    2(12), 948–954.
  mla: Yengo, Loic, et al. “Imprint of Assortative Mating on the Human Genome.” <i>Nature
    Human Behaviour</i>, vol. 2, no. 12, Springer Nature, 2018, pp. 948–54, doi:<a
    href="https://doi.org/10.1038/s41562-018-0476-3">10.1038/s41562-018-0476-3</a>.
  short: L. Yengo, M.R. Robinson, M.C. Keller, K.E. Kemper, Y. Yang, M. Trzaskowski,
    J. Gratten, P. Turley, D. Cesarini, D.J. Benjamin, N.R. Wray, M.E. Goddard, J.
    Yang, P.M. Visscher, Nature Human Behaviour 2 (2018) 948–954.
date_created: 2020-04-30T10:42:12Z
date_published: 2018-11-26T00:00:00Z
date_updated: 2021-01-12T08:15:03Z
day: '26'
doi: 10.1038/s41562-018-0476-3
extern: '1'
intvolume: '         2'
issue: '12'
language:
- iso: eng
month: '11'
oa_version: None
page: 948-954
publication: Nature Human Behaviour
publication_identifier:
  issn:
  - 2397-3374
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Imprint of assortative mating on the human genome
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 2
year: '2018'
...
---
_id: '7716'
abstract:
- lang: eng
  text: Genomic prediction has the potential to contribute to precision medicine.
    However, to date, the utility of such predictors is limited due to low accuracy
    for most traits. Here theory and simulation study are used to demonstrate that
    widespread pleiotropy among phenotypes can be utilised to improve genomic risk
    prediction. We show how a genetic predictor can be created as a weighted index
    that combines published genome-wide association study (GWAS) summary statistics
    across many different traits. We apply this framework to predict risk of schizophrenia
    and bipolar disorder in the Psychiatric Genomics consortium data, finding substantial
    heterogeneity in prediction accuracy increases across cohorts. For six additional
    phenotypes in the UK Biobank data, we find increases in prediction accuracy ranging
    from 0.7% for height to 47% for type 2 diabetes, when using a multi-trait predictor
    that combines published summary statistics from multiple traits, as compared to
    a predictor based only on one trait.
article_number: '989'
article_processing_charge: No
article_type: original
author:
- first_name: Robert M.
  full_name: Maier, Robert M.
  last_name: Maier
- first_name: Zhihong
  full_name: Zhu, Zhihong
  last_name: Zhu
- first_name: Sang Hong
  full_name: Lee, Sang Hong
  last_name: Lee
- first_name: Maciej
  full_name: Trzaskowski, Maciej
  last_name: Trzaskowski
- first_name: Douglas M.
  full_name: Ruderfer, Douglas M.
  last_name: Ruderfer
- first_name: Eli A.
  full_name: Stahl, Eli A.
  last_name: Stahl
- first_name: Stephan
  full_name: Ripke, Stephan
  last_name: Ripke
- first_name: Naomi R.
  full_name: Wray, Naomi R.
  last_name: Wray
- first_name: Jian
  full_name: Yang, Jian
  last_name: Yang
- first_name: Peter M.
  full_name: Visscher, Peter M.
  last_name: Visscher
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
citation:
  ama: Maier RM, Zhu Z, Lee SH, et al. Improving genetic prediction by leveraging
    genetic correlations among human diseases and traits. <i>Nature Communications</i>.
    2018;9. doi:<a href="https://doi.org/10.1038/s41467-017-02769-6">10.1038/s41467-017-02769-6</a>
  apa: Maier, R. M., Zhu, Z., Lee, S. H., Trzaskowski, M., Ruderfer, D. M., Stahl,
    E. A., … Robinson, M. R. (2018). Improving genetic prediction by leveraging genetic
    correlations among human diseases and traits. <i>Nature Communications</i>. Springer
    Nature. <a href="https://doi.org/10.1038/s41467-017-02769-6">https://doi.org/10.1038/s41467-017-02769-6</a>
  chicago: Maier, Robert M., Zhihong Zhu, Sang Hong Lee, Maciej Trzaskowski, Douglas
    M. Ruderfer, Eli A. Stahl, Stephan Ripke, et al. “Improving Genetic Prediction
    by Leveraging Genetic Correlations among Human Diseases and Traits.” <i>Nature
    Communications</i>. Springer Nature, 2018. <a href="https://doi.org/10.1038/s41467-017-02769-6">https://doi.org/10.1038/s41467-017-02769-6</a>.
  ieee: R. M. Maier <i>et al.</i>, “Improving genetic prediction by leveraging genetic
    correlations among human diseases and traits,” <i>Nature Communications</i>, vol.
    9. Springer Nature, 2018.
  ista: Maier RM, Zhu Z, Lee SH, Trzaskowski M, Ruderfer DM, Stahl EA, Ripke S, Wray
    NR, Yang J, Visscher PM, Robinson MR. 2018. Improving genetic prediction by leveraging
    genetic correlations among human diseases and traits. Nature Communications. 9,
    989.
  mla: Maier, Robert M., et al. “Improving Genetic Prediction by Leveraging Genetic
    Correlations among Human Diseases and Traits.” <i>Nature Communications</i>, vol.
    9, 989, Springer Nature, 2018, doi:<a href="https://doi.org/10.1038/s41467-017-02769-6">10.1038/s41467-017-02769-6</a>.
  short: R.M. Maier, Z. Zhu, S.H. Lee, M. Trzaskowski, D.M. Ruderfer, E.A. Stahl,
    S. Ripke, N.R. Wray, J. Yang, P.M. Visscher, M.R. Robinson, Nature Communications
    9 (2018).
date_created: 2020-04-30T10:42:29Z
date_published: 2018-03-07T00:00:00Z
date_updated: 2021-01-12T08:15:03Z
day: '07'
doi: 10.1038/s41467-017-02769-6
extern: '1'
intvolume: '         9'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1038/s41467-017-02769-6
month: '03'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Improving genetic prediction by leveraging genetic correlations among human
  diseases and traits
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2018'
...
---
_id: '7717'
abstract:
- lang: eng
  text: "Background: DNA methylation levels change along with age, but few studies
    have examined the variation in the rate of such changes between individuals.\r\nMethods:
    We performed a longitudinal analysis to quantify the variation in the rate of
    change of DNA methylation between individuals using whole blood DNA methylation
    array profiles collected at 2–4 time points (N = 2894) in 954 individuals (67–90
    years).\r\nResults: After stringent quality control, we identified 1507 DNA methylation
    CpG sites (rsCpGs) with statistically significant variation in the rate of change
    (random slope) of DNA methylation among individuals in a mixed linear model analysis.
    Genes in the vicinity of these rsCpGs were found to be enriched in Homeobox transcription
    factors and the Wnt signalling pathway, both of which are related to ageing processes.
    Furthermore, we investigated the SNP effect on the random slope. We found that
    4 out of 1507 rsCpGs had one significant (P < 5 × 10−8/1507) SNP effect and 343
    rsCpGs had at least one SNP effect (436 SNP-probe pairs) reaching genome-wide
    significance (P < 5 × 10−8). Ninety-five percent of the significant (P < 5 × 10−8)
    SNPs are on different chromosomes from their corresponding probes.\r\nConclusions:
    We identified CpG sites that have variability in the rate of change of DNA methylation
    between individuals, and our results suggest a genetic basis of this variation.
    Genes around these CpG sites have been reported to be involved in the ageing process."
article_number: '75'
article_processing_charge: No
article_type: original
author:
- first_name: Qian
  full_name: Zhang, Qian
  last_name: Zhang
- first_name: Riccardo E
  full_name: Marioni, Riccardo E
  last_name: Marioni
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
- first_name: Jon
  full_name: Higham, Jon
  last_name: Higham
- first_name: Duncan
  full_name: Sproul, Duncan
  last_name: Sproul
- first_name: Naomi R
  full_name: Wray, Naomi R
  last_name: Wray
- first_name: Ian J
  full_name: Deary, Ian J
  last_name: Deary
- first_name: Allan F
  full_name: McRae, Allan F
  last_name: McRae
- first_name: Peter M
  full_name: Visscher, Peter M
  last_name: Visscher
citation:
  ama: Zhang Q, Marioni RE, Robinson MR, et al. Genotype effects contribute to variation
    in longitudinal methylome patterns in older people. <i>Genome Medicine</i>. 2018;10(1).
    doi:<a href="https://doi.org/10.1186/s13073-018-0585-7">10.1186/s13073-018-0585-7</a>
  apa: Zhang, Q., Marioni, R. E., Robinson, M. R., Higham, J., Sproul, D., Wray, N.
    R., … Visscher, P. M. (2018). Genotype effects contribute to variation in longitudinal
    methylome patterns in older people. <i>Genome Medicine</i>. Springer Nature. <a
    href="https://doi.org/10.1186/s13073-018-0585-7">https://doi.org/10.1186/s13073-018-0585-7</a>
  chicago: Zhang, Qian, Riccardo E Marioni, Matthew Richard Robinson, Jon Higham,
    Duncan Sproul, Naomi R Wray, Ian J Deary, Allan F McRae, and Peter M Visscher.
    “Genotype Effects Contribute to Variation in Longitudinal Methylome Patterns in
    Older People.” <i>Genome Medicine</i>. Springer Nature, 2018. <a href="https://doi.org/10.1186/s13073-018-0585-7">https://doi.org/10.1186/s13073-018-0585-7</a>.
  ieee: Q. Zhang <i>et al.</i>, “Genotype effects contribute to variation in longitudinal
    methylome patterns in older people,” <i>Genome Medicine</i>, vol. 10, no. 1. Springer
    Nature, 2018.
  ista: Zhang Q, Marioni RE, Robinson MR, Higham J, Sproul D, Wray NR, Deary IJ, McRae
    AF, Visscher PM. 2018. Genotype effects contribute to variation in longitudinal
    methylome patterns in older people. Genome Medicine. 10(1), 75.
  mla: Zhang, Qian, et al. “Genotype Effects Contribute to Variation in Longitudinal
    Methylome Patterns in Older People.” <i>Genome Medicine</i>, vol. 10, no. 1, 75,
    Springer Nature, 2018, doi:<a href="https://doi.org/10.1186/s13073-018-0585-7">10.1186/s13073-018-0585-7</a>.
  short: Q. Zhang, R.E. Marioni, M.R. Robinson, J. Higham, D. Sproul, N.R. Wray, I.J.
    Deary, A.F. McRae, P.M. Visscher, Genome Medicine 10 (2018).
date_created: 2020-04-30T10:42:50Z
date_published: 2018-10-22T00:00:00Z
date_updated: 2021-01-12T08:15:04Z
day: '22'
doi: 10.1186/s13073-018-0585-7
extern: '1'
intvolume: '        10'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1186/s13073-018-0585-7
month: '10'
oa: 1
oa_version: Published Version
publication: Genome Medicine
publication_identifier:
  issn:
  - 1756-994X
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Genotype effects contribute to variation in longitudinal methylome patterns
  in older people
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 10
year: '2018'
...
---
_id: '7718'
abstract:
- lang: eng
  text: Flores Island, Indonesia, was inhabited by the small-bodied hominin species
    Homo floresiensis, which has an unknown evolutionary relationship to modern humans.
    This island is also home to an extant human pygmy population. Here we describe
    genome-scale single-nucleotide polymorphism data and whole-genome sequences from
    a contemporary human pygmy population living on Flores near the cave where H.
    floresiensis was found. The genomes of Flores pygmies reveal a complex history
    of admixture with Denisovans and Neanderthals but no evidence for gene flow with
    other archaic hominins. Modern individuals bear the signatures of recent positive
    selection encompassing the FADS (fatty acid desaturase) gene cluster, likely related
    to diet, and polygenic selection acting on standing variation that contributed
    to their short-stature phenotype. Thus, multiple independent instances of hominin
    insular dwarfism occurred on Flores.
article_processing_charge: No
article_type: original
author:
- first_name: Serena
  full_name: Tucci, Serena
  last_name: Tucci
- first_name: Samuel H.
  full_name: Vohr, Samuel H.
  last_name: Vohr
- first_name: Rajiv C.
  full_name: McCoy, Rajiv C.
  last_name: McCoy
- first_name: Benjamin
  full_name: Vernot, Benjamin
  last_name: Vernot
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
- first_name: Chiara
  full_name: Barbieri, Chiara
  last_name: Barbieri
- first_name: Brad J.
  full_name: Nelson, Brad J.
  last_name: Nelson
- first_name: Wenqing
  full_name: Fu, Wenqing
  last_name: Fu
- first_name: Gludhug A.
  full_name: Purnomo, Gludhug A.
  last_name: Purnomo
- first_name: Herawati
  full_name: Sudoyo, Herawati
  last_name: Sudoyo
- first_name: Evan E.
  full_name: Eichler, Evan E.
  last_name: Eichler
- first_name: Guido
  full_name: Barbujani, Guido
  last_name: Barbujani
- first_name: Peter M.
  full_name: Visscher, Peter M.
  last_name: Visscher
- first_name: Joshua M.
  full_name: Akey, Joshua M.
  last_name: Akey
- first_name: Richard E.
  full_name: Green, Richard E.
  last_name: Green
citation:
  ama: Tucci S, Vohr SH, McCoy RC, et al. Evolutionary history and adaptation of a
    human pygmy population of Flores Island, Indonesia. <i>Science</i>. 2018;361(6401):511-516.
    doi:<a href="https://doi.org/10.1126/science.aar8486">10.1126/science.aar8486</a>
  apa: Tucci, S., Vohr, S. H., McCoy, R. C., Vernot, B., Robinson, M. R., Barbieri,
    C., … Green, R. E. (2018). Evolutionary history and adaptation of a human pygmy
    population of Flores Island, Indonesia. <i>Science</i>. American Association for
    the Advancement of Science. <a href="https://doi.org/10.1126/science.aar8486">https://doi.org/10.1126/science.aar8486</a>
  chicago: Tucci, Serena, Samuel H. Vohr, Rajiv C. McCoy, Benjamin Vernot, Matthew
    Richard Robinson, Chiara Barbieri, Brad J. Nelson, et al. “Evolutionary History
    and Adaptation of a Human Pygmy Population of Flores Island, Indonesia.” <i>Science</i>.
    American Association for the Advancement of Science, 2018. <a href="https://doi.org/10.1126/science.aar8486">https://doi.org/10.1126/science.aar8486</a>.
  ieee: S. Tucci <i>et al.</i>, “Evolutionary history and adaptation of a human pygmy
    population of Flores Island, Indonesia,” <i>Science</i>, vol. 361, no. 6401. American
    Association for the Advancement of Science, pp. 511–516, 2018.
  ista: Tucci S, Vohr SH, McCoy RC, Vernot B, Robinson MR, Barbieri C, Nelson BJ,
    Fu W, Purnomo GA, Sudoyo H, Eichler EE, Barbujani G, Visscher PM, Akey JM, Green
    RE. 2018. Evolutionary history and adaptation of a human pygmy population of Flores
    Island, Indonesia. Science. 361(6401), 511–516.
  mla: Tucci, Serena, et al. “Evolutionary History and Adaptation of a Human Pygmy
    Population of Flores Island, Indonesia.” <i>Science</i>, vol. 361, no. 6401, American
    Association for the Advancement of Science, 2018, pp. 511–16, doi:<a href="https://doi.org/10.1126/science.aar8486">10.1126/science.aar8486</a>.
  short: S. Tucci, S.H. Vohr, R.C. McCoy, B. Vernot, M.R. Robinson, C. Barbieri, B.J.
    Nelson, W. Fu, G.A. Purnomo, H. Sudoyo, E.E. Eichler, G. Barbujani, P.M. Visscher,
    J.M. Akey, R.E. Green, Science 361 (2018) 511–516.
date_created: 2020-04-30T10:43:24Z
date_published: 2018-08-03T00:00:00Z
date_updated: 2021-01-12T08:15:04Z
day: '03'
doi: 10.1126/science.aar8486
extern: '1'
external_id:
  pmid:
  - '30072539'
intvolume: '       361'
issue: '6401'
language:
- iso: eng
month: '08'
oa_version: None
page: 511-516
pmid: 1
publication: Science
publication_identifier:
  issn:
  - 0036-8075
  - 1095-9203
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
status: public
title: Evolutionary history and adaptation of a human pygmy population of Flores Island,
  Indonesia
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 361
year: '2018'
...
---
_id: '7721'
abstract:
- lang: eng
  text: 'The availability of genome-wide genetic data on hundreds of thousands of
    people has led to an equally rapid growth in methodologies available to analyse
    these data. While the motivation for undertaking genome-wide association studies
    (GWAS) is identification of genetic markers associated with complex traits, once
    generated these data can be used for many other analyses. GWAS have demonstrated
    that complex traits exhibit a highly polygenic genetic architecture, often with
    shared genetic risk factors across traits. New methods to analyse data from GWAS
    are increasingly being used to address a diverse set of questions about the aetiology
    of complex traits and diseases, including psychiatric disorders. Here, we give
    an overview of some of these methods and present examples of how they have contributed
    to our understanding of psychiatric disorders. We consider: (i) estimation of
    the extent of genetic influence on traits, (ii) uncovering of shared genetic control
    between traits, (iii) predictions of genetic risk for individuals, (iv) uncovering
    of causal relationships between traits, (v) identifying causal single-nucleotide
    polymorphisms and genes or (vi) the detection of genetic heterogeneity. This classification
    helps organise the large number of recently developed methods, although some could
    be placed in more than one category. While some methods require GWAS data on individual
    people, others simply use GWAS summary statistics data, allowing novel well-powered
    analyses to be conducted at a low computational burden.'
article_processing_charge: No
article_type: original
author:
- first_name: R. M.
  full_name: Maier, R. M.
  last_name: Maier
- first_name: P. M.
  full_name: Visscher, P. M.
  last_name: Visscher
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
- first_name: N. R.
  full_name: Wray, N. R.
  last_name: Wray
citation:
  ama: 'Maier RM, Visscher PM, Robinson MR, Wray NR. Embracing polygenicity: A review
    of methods and tools for psychiatric genetics research. <i>Psychological Medicine</i>.
    2018;48(7):1055-1067. doi:<a href="https://doi.org/10.1017/s0033291717002318">10.1017/s0033291717002318</a>'
  apa: 'Maier, R. M., Visscher, P. M., Robinson, M. R., &#38; Wray, N. R. (2018).
    Embracing polygenicity: A review of methods and tools for psychiatric genetics
    research. <i>Psychological Medicine</i>. Cambridge University Press. <a href="https://doi.org/10.1017/s0033291717002318">https://doi.org/10.1017/s0033291717002318</a>'
  chicago: 'Maier, R. M., P. M. Visscher, Matthew Richard Robinson, and N. R. Wray.
    “Embracing Polygenicity: A Review of Methods and Tools for Psychiatric Genetics
    Research.” <i>Psychological Medicine</i>. Cambridge University Press, 2018. <a
    href="https://doi.org/10.1017/s0033291717002318">https://doi.org/10.1017/s0033291717002318</a>.'
  ieee: 'R. M. Maier, P. M. Visscher, M. R. Robinson, and N. R. Wray, “Embracing polygenicity:
    A review of methods and tools for psychiatric genetics research,” <i>Psychological
    Medicine</i>, vol. 48, no. 7. Cambridge University Press, pp. 1055–1067, 2018.'
  ista: 'Maier RM, Visscher PM, Robinson MR, Wray NR. 2018. Embracing polygenicity:
    A review of methods and tools for psychiatric genetics research. Psychological
    Medicine. 48(7), 1055–1067.'
  mla: 'Maier, R. M., et al. “Embracing Polygenicity: A Review of Methods and Tools
    for Psychiatric Genetics Research.” <i>Psychological Medicine</i>, vol. 48, no.
    7, Cambridge University Press, 2018, pp. 1055–67, doi:<a href="https://doi.org/10.1017/s0033291717002318">10.1017/s0033291717002318</a>.'
  short: R.M. Maier, P.M. Visscher, M.R. Robinson, N.R. Wray, Psychological Medicine
    48 (2018) 1055–1067.
date_created: 2020-04-30T10:44:35Z
date_published: 2018-05-01T00:00:00Z
date_updated: 2021-01-12T08:15:05Z
day: '01'
doi: 10.1017/s0033291717002318
extern: '1'
intvolume: '        48'
issue: '7'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1017/s0033291717002318
month: '05'
oa: 1
oa_version: Published Version
page: 1055-1067
publication: Psychological Medicine
publication_identifier:
  issn:
  - 0033-2917
  - 1469-8978
publication_status: published
publisher: Cambridge University Press
quality_controlled: '1'
status: public
title: 'Embracing polygenicity: A review of methods and tools for psychiatric genetics
  research'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 48
year: '2018'
...
---
_id: '7722'
abstract:
- lang: eng
  text: We develop a Bayesian mixed linear model that simultaneously estimates single-nucleotide
    polymorphism (SNP)-based heritability, polygenicity (proportion of SNPs with nonzero
    effects), and the relationship between SNP effect size and minor allele frequency
    for complex traits in conventionally unrelated individuals using genome-wide SNP
    data. We apply the method to 28 complex traits in the UK Biobank data (N = 126,752)
    and show that on average, 6% of SNPs have nonzero effects, which in total explain
    22% of phenotypic variance. We detect significant (P < 0.05/28) signatures of
    natural selection in the genetic architecture of 23 traits, including reproductive,
    cardiovascular, and anthropometric traits, as well as educational attainment.
    The significant estimates of the relationship between effect size and minor allele
    frequency in complex traits are consistent with a model of negative (or purifying)
    selection, as confirmed by forward simulation. We conclude that negative selection
    acts pervasively on the genetic variants associated with human complex traits.
article_processing_charge: No
article_type: original
author:
- first_name: Jian
  full_name: Zeng, Jian
  last_name: Zeng
- first_name: Ronald
  full_name: de Vlaming, Ronald
  last_name: de Vlaming
- first_name: Yang
  full_name: Wu, Yang
  last_name: Wu
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
- first_name: Luke R.
  full_name: Lloyd-Jones, Luke R.
  last_name: Lloyd-Jones
- first_name: Loic
  full_name: Yengo, Loic
  last_name: Yengo
- first_name: Chloe X.
  full_name: Yap, Chloe X.
  last_name: Yap
- first_name: Angli
  full_name: Xue, Angli
  last_name: Xue
- first_name: Julia
  full_name: Sidorenko, Julia
  last_name: Sidorenko
- first_name: Allan F.
  full_name: McRae, Allan F.
  last_name: McRae
- first_name: Joseph E.
  full_name: Powell, Joseph E.
  last_name: Powell
- first_name: Grant W.
  full_name: Montgomery, Grant W.
  last_name: Montgomery
- first_name: Andres
  full_name: Metspalu, Andres
  last_name: Metspalu
- first_name: Tonu
  full_name: Esko, Tonu
  last_name: Esko
- first_name: Greg
  full_name: Gibson, Greg
  last_name: Gibson
- first_name: Naomi R.
  full_name: Wray, Naomi R.
  last_name: Wray
- first_name: Peter M.
  full_name: Visscher, Peter M.
  last_name: Visscher
- first_name: Jian
  full_name: Yang, Jian
  last_name: Yang
citation:
  ama: Zeng J, de Vlaming R, Wu Y, et al. Signatures of negative selection in the
    genetic architecture of human complex traits. <i>Nature Genetics</i>. 2018;50(5):746-753.
    doi:<a href="https://doi.org/10.1038/s41588-018-0101-4">10.1038/s41588-018-0101-4</a>
  apa: Zeng, J., de Vlaming, R., Wu, Y., Robinson, M. R., Lloyd-Jones, L. R., Yengo,
    L., … Yang, J. (2018). Signatures of negative selection in the genetic architecture
    of human complex traits. <i>Nature Genetics</i>. Springer Nature. <a href="https://doi.org/10.1038/s41588-018-0101-4">https://doi.org/10.1038/s41588-018-0101-4</a>
  chicago: Zeng, Jian, Ronald de Vlaming, Yang Wu, Matthew Richard Robinson, Luke
    R. Lloyd-Jones, Loic Yengo, Chloe X. Yap, et al. “Signatures of Negative Selection
    in the Genetic Architecture of Human Complex Traits.” <i>Nature Genetics</i>.
    Springer Nature, 2018. <a href="https://doi.org/10.1038/s41588-018-0101-4">https://doi.org/10.1038/s41588-018-0101-4</a>.
  ieee: J. Zeng <i>et al.</i>, “Signatures of negative selection in the genetic architecture
    of human complex traits,” <i>Nature Genetics</i>, vol. 50, no. 5. Springer Nature,
    pp. 746–753, 2018.
  ista: Zeng J, de Vlaming R, Wu Y, Robinson MR, Lloyd-Jones LR, Yengo L, Yap CX,
    Xue A, Sidorenko J, McRae AF, Powell JE, Montgomery GW, Metspalu A, Esko T, Gibson
    G, Wray NR, Visscher PM, Yang J. 2018. Signatures of negative selection in the
    genetic architecture of human complex traits. Nature Genetics. 50(5), 746–753.
  mla: Zeng, Jian, et al. “Signatures of Negative Selection in the Genetic Architecture
    of Human Complex Traits.” <i>Nature Genetics</i>, vol. 50, no. 5, Springer Nature,
    2018, pp. 746–53, doi:<a href="https://doi.org/10.1038/s41588-018-0101-4">10.1038/s41588-018-0101-4</a>.
  short: J. Zeng, R. de Vlaming, Y. Wu, M.R. Robinson, L.R. Lloyd-Jones, L. Yengo,
    C.X. Yap, A. Xue, J. Sidorenko, A.F. McRae, J.E. Powell, G.W. Montgomery, A. Metspalu,
    T. Esko, G. Gibson, N.R. Wray, P.M. Visscher, J. Yang, Nature Genetics 50 (2018)
    746–753.
date_created: 2020-04-30T10:44:57Z
date_published: 2018-04-16T00:00:00Z
date_updated: 2021-01-12T08:15:06Z
day: '16'
doi: 10.1038/s41588-018-0101-4
extern: '1'
intvolume: '        50'
issue: '5'
language:
- iso: eng
month: '04'
oa_version: None
page: 746-753
publication: Nature Genetics
publication_identifier:
  issn:
  - 1061-4036
  - 1546-1718
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Signatures of negative selection in the genetic architecture of human complex
  traits
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 50
year: '2018'
...
---
_id: '7723'
abstract:
- lang: eng
  text: Genome-wide association studies (GWAS) have identified thousands of loci that
    are robustly associated with complex diseases. The use of linear mixed model (LMM)
    methodology for GWAS is becoming more prevalent due to its ability to control
    for population structure and cryptic relatedness and to increase power. The odds
    ratio (OR) is a common measure of the association of a disease with an exposure
    (e.g., a genetic variant) and is readably available from logistic regression.
    However, when the LMM is applied to all-or-none traits it provides estimates of
    genetic effects on the observed 0–1 scale, a different scale to that in logistic
    regression. This limits the comparability of results across studies, for example
    in a meta-analysis, and makes the interpretation of the magnitude of an effect
    from an LMM GWAS difficult. In this study, we derived transformations from the
    genetic effects estimated under the LMM to the OR that only rely on summary statistics.
    To test the proposed transformations, we used real genotypes from two large, publicly
    available data sets to simulate all-or-none phenotypes for a set of scenarios
    that differ in underlying model, disease prevalence, and heritability. Furthermore,
    we applied these transformations to GWAS summary statistics for type 2 diabetes
    generated from 108,042 individuals in the UK Biobank. In both simulation and real-data
    application, we observed very high concordance between the transformed OR from
    the LMM and either the simulated truth or estimates from logistic regression.
    The transformations derived and validated in this study improve the comparability
    of results from prospective and already performed LMM GWAS on complex diseases
    by providing a reliable transformation to a common comparative scale for the genetic
    effects.
article_processing_charge: No
article_type: original
author:
- first_name: Luke R.
  full_name: Lloyd-Jones, Luke R.
  last_name: Lloyd-Jones
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
- first_name: Jian
  full_name: Yang, Jian
  last_name: Yang
- first_name: Peter M.
  full_name: Visscher, Peter M.
  last_name: Visscher
citation:
  ama: Lloyd-Jones LR, Robinson MR, Yang J, Visscher PM. Transformation of summary
    statistics from linear mixed model association on all-or-none traits to odds ratio.
    <i>Genetics</i>. 2018;208(4):1397-1408. doi:<a href="https://doi.org/10.1534/genetics.117.300360">10.1534/genetics.117.300360</a>
  apa: Lloyd-Jones, L. R., Robinson, M. R., Yang, J., &#38; Visscher, P. M. (2018).
    Transformation of summary statistics from linear mixed model association on all-or-none
    traits to odds ratio. <i>Genetics</i>. Genetics Society of America. <a href="https://doi.org/10.1534/genetics.117.300360">https://doi.org/10.1534/genetics.117.300360</a>
  chicago: Lloyd-Jones, Luke R., Matthew Richard Robinson, Jian Yang, and Peter M.
    Visscher. “Transformation of Summary Statistics from Linear Mixed Model Association
    on All-or-None Traits to Odds Ratio.” <i>Genetics</i>. Genetics Society of America,
    2018. <a href="https://doi.org/10.1534/genetics.117.300360">https://doi.org/10.1534/genetics.117.300360</a>.
  ieee: L. R. Lloyd-Jones, M. R. Robinson, J. Yang, and P. M. Visscher, “Transformation
    of summary statistics from linear mixed model association on all-or-none traits
    to odds ratio,” <i>Genetics</i>, vol. 208, no. 4. Genetics Society of America,
    pp. 1397–1408, 2018.
  ista: Lloyd-Jones LR, Robinson MR, Yang J, Visscher PM. 2018. Transformation of
    summary statistics from linear mixed model association on all-or-none traits to
    odds ratio. Genetics. 208(4), 1397–1408.
  mla: Lloyd-Jones, Luke R., et al. “Transformation of Summary Statistics from Linear
    Mixed Model Association on All-or-None Traits to Odds Ratio.” <i>Genetics</i>,
    vol. 208, no. 4, Genetics Society of America, 2018, pp. 1397–408, doi:<a href="https://doi.org/10.1534/genetics.117.300360">10.1534/genetics.117.300360</a>.
  short: L.R. Lloyd-Jones, M.R. Robinson, J. Yang, P.M. Visscher, Genetics 208 (2018)
    1397–1408.
date_created: 2020-04-30T10:45:19Z
date_published: 2018-04-01T00:00:00Z
date_updated: 2021-01-12T08:15:06Z
day: '01'
doi: 10.1534/genetics.117.300360
extern: '1'
intvolume: '       208'
issue: '4'
language:
- iso: eng
month: '04'
oa_version: None
page: 1397-1408
publication: Genetics
publication_identifier:
  issn:
  - 0016-6731
  - 1943-2631
publication_status: published
publisher: Genetics Society of America
quality_controlled: '1'
status: public
title: Transformation of summary statistics from linear mixed model association on
  all-or-none traits to odds ratio
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 208
year: '2018'
...
---
_id: '7724'
abstract:
- lang: eng
  text: Modern molecular genetic datasets, primarily collected to study the biology
    of human health and disease, can be used to directly measure the action of natural
    selection and reveal important features of contemporary human evolution. Here
    we leverage the UK Biobank data to test for the presence of linear and nonlinear
    natural selection in a contemporary population of the United Kingdom. We obtain
    phenotypic and genetic evidence consistent with the action of linear/directional
    selection. Phenotypic evidence suggests that stabilizing selection, which acts
    to reduce variance in the population without necessarily modifying the population
    mean, is widespread and relatively weak in comparison with estimates from other
    species.
article_processing_charge: No
article_type: original
author:
- first_name: Jaleal S.
  full_name: Sanjak, Jaleal S.
  last_name: Sanjak
- first_name: Julia
  full_name: Sidorenko, Julia
  last_name: Sidorenko
- first_name: Matthew Richard
  full_name: Robinson, Matthew Richard
  id: E5D42276-F5DA-11E9-8E24-6303E6697425
  last_name: Robinson
  orcid: 0000-0001-8982-8813
- first_name: Kevin R.
  full_name: Thornton, Kevin R.
  last_name: Thornton
- first_name: Peter M.
  full_name: Visscher, Peter M.
  last_name: Visscher
citation:
  ama: Sanjak JS, Sidorenko J, Robinson MR, Thornton KR, Visscher PM. Evidence of
    directional and stabilizing selection in contemporary humans. <i>Proceedings of
    the National Academy of Sciences</i>. 2018;115(1):151-156. doi:<a href="https://doi.org/10.1073/pnas.1707227114">10.1073/pnas.1707227114</a>
  apa: Sanjak, J. S., Sidorenko, J., Robinson, M. R., Thornton, K. R., &#38; Visscher,
    P. M. (2018). Evidence of directional and stabilizing selection in contemporary
    humans. <i>Proceedings of the National Academy of Sciences</i>. Proceedings of
    the National Academy of Sciences. <a href="https://doi.org/10.1073/pnas.1707227114">https://doi.org/10.1073/pnas.1707227114</a>
  chicago: Sanjak, Jaleal S., Julia Sidorenko, Matthew Richard Robinson, Kevin R.
    Thornton, and Peter M. Visscher. “Evidence of Directional and Stabilizing Selection
    in Contemporary Humans.” <i>Proceedings of the National Academy of Sciences</i>.
    Proceedings of the National Academy of Sciences, 2018. <a href="https://doi.org/10.1073/pnas.1707227114">https://doi.org/10.1073/pnas.1707227114</a>.
  ieee: J. S. Sanjak, J. Sidorenko, M. R. Robinson, K. R. Thornton, and P. M. Visscher,
    “Evidence of directional and stabilizing selection in contemporary humans,” <i>Proceedings
    of the National Academy of Sciences</i>, vol. 115, no. 1. Proceedings of the National
    Academy of Sciences, pp. 151–156, 2018.
  ista: Sanjak JS, Sidorenko J, Robinson MR, Thornton KR, Visscher PM. 2018. Evidence
    of directional and stabilizing selection in contemporary humans. Proceedings of
    the National Academy of Sciences. 115(1), 151–156.
  mla: Sanjak, Jaleal S., et al. “Evidence of Directional and Stabilizing Selection
    in Contemporary Humans.” <i>Proceedings of the National Academy of Sciences</i>,
    vol. 115, no. 1, Proceedings of the National Academy of Sciences, 2018, pp. 151–56,
    doi:<a href="https://doi.org/10.1073/pnas.1707227114">10.1073/pnas.1707227114</a>.
  short: J.S. Sanjak, J. Sidorenko, M.R. Robinson, K.R. Thornton, P.M. Visscher, Proceedings
    of the National Academy of Sciences 115 (2018) 151–156.
date_created: 2020-04-30T10:45:43Z
date_published: 2018-01-02T00:00:00Z
date_updated: 2021-01-12T08:15:07Z
day: '02'
doi: 10.1073/pnas.1707227114
extern: '1'
intvolume: '       115'
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 151-156
publication: Proceedings of the National Academy of Sciences
publication_identifier:
  issn:
  - 0027-8424
  - 1091-6490
publication_status: published
publisher: Proceedings of the National Academy of Sciences
quality_controlled: '1'
related_material:
  link:
  - relation: erratum
    url: https://doi.org/10.1073/pnas.1806837115
status: public
title: Evidence of directional and stabilizing selection in contemporary humans
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 115
year: '2018'
...
---
_id: '7754'
abstract:
- lang: eng
  text: Creating a selective gel that filters particles based on their interactions
    is a major goal of nanotechnology, with far-reaching implications from drug delivery
    to controlling assembly pathways. However, this is particularly difficult when
    the particles are larger than the gel’s characteristic mesh size because such
    particles cannot passively pass through the gel. Thus, filtering requires the
    interacting particles to transiently reorganize the gel’s internal structure.
    While significant advances, e.g., in DNA engineering, have enabled the design
    of nano-materials with programmable interactions, it is not clear what physical
    principles such a designer gel could exploit to achieve selective permeability.
    We present an equilibrium mechanism where crosslink binding dynamics are affected
    by interacting particles such that particle diffusion is enhanced. In addition
    to revealing specific design rules for manufacturing selective gels, our results
    have the potential to explain the origin of selective permeability in certain
    biological materials, including the nuclear pore complex.
article_number: '4348'
article_processing_charge: No
article_type: original
author:
- first_name: Carl Peter
  full_name: Goodrich, Carl Peter
  id: EB352CD2-F68A-11E9-89C5-A432E6697425
  last_name: Goodrich
  orcid: 0000-0002-1307-5074
- first_name: Michael P.
  full_name: Brenner, Michael P.
  last_name: Brenner
- first_name: Katharina
  full_name: Ribbeck, Katharina
  last_name: Ribbeck
citation:
  ama: Goodrich CP, Brenner MP, Ribbeck K. Enhanced diffusion by binding to the crosslinks
    of a polymer gel. <i>Nature Communications</i>. 2018;9. doi:<a href="https://doi.org/10.1038/s41467-018-06851-5">10.1038/s41467-018-06851-5</a>
  apa: Goodrich, C. P., Brenner, M. P., &#38; Ribbeck, K. (2018). Enhanced diffusion
    by binding to the crosslinks of a polymer gel. <i>Nature Communications</i>. Springer
    Nature. <a href="https://doi.org/10.1038/s41467-018-06851-5">https://doi.org/10.1038/s41467-018-06851-5</a>
  chicago: Goodrich, Carl Peter, Michael P. Brenner, and Katharina Ribbeck. “Enhanced
    Diffusion by Binding to the Crosslinks of a Polymer Gel.” <i>Nature Communications</i>.
    Springer Nature, 2018. <a href="https://doi.org/10.1038/s41467-018-06851-5">https://doi.org/10.1038/s41467-018-06851-5</a>.
  ieee: C. P. Goodrich, M. P. Brenner, and K. Ribbeck, “Enhanced diffusion by binding
    to the crosslinks of a polymer gel,” <i>Nature Communications</i>, vol. 9. Springer
    Nature, 2018.
  ista: Goodrich CP, Brenner MP, Ribbeck K. 2018. Enhanced diffusion by binding to
    the crosslinks of a polymer gel. Nature Communications. 9, 4348.
  mla: Goodrich, Carl Peter, et al. “Enhanced Diffusion by Binding to the Crosslinks
    of a Polymer Gel.” <i>Nature Communications</i>, vol. 9, 4348, Springer Nature,
    2018, doi:<a href="https://doi.org/10.1038/s41467-018-06851-5">10.1038/s41467-018-06851-5</a>.
  short: C.P. Goodrich, M.P. Brenner, K. Ribbeck, Nature Communications 9 (2018).
date_created: 2020-04-30T11:38:01Z
date_published: 2018-10-19T00:00:00Z
date_updated: 2021-01-12T08:15:18Z
day: '19'
doi: 10.1038/s41467-018-06851-5
extern: '1'
intvolume: '         9'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1038/s41467-018-06851-5
month: '10'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
  issn:
  - 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Enhanced diffusion by binding to the crosslinks of a polymer gel
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2018'
...
---
_id: '456'
abstract:
- lang: eng
  text: 'Inhibition of the endoplasmic reticulum stress pathway may hold the key to
    Zika virus-associated microcephaly treatment. '
article_number: eaar7514
author:
- first_name: Gaia
  full_name: Novarino, Gaia
  id: 3E57A680-F248-11E8-B48F-1D18A9856A87
  last_name: Novarino
  orcid: 0000-0002-7673-7178
citation:
  ama: 'Novarino G. Zika-associated microcephaly: Reduce the stress and race for the
    treatment. <i>Science Translational Medicine</i>. 2018;10(423). doi:<a href="https://doi.org/10.1126/scitranslmed.aar7514">10.1126/scitranslmed.aar7514</a>'
  apa: 'Novarino, G. (2018). Zika-associated microcephaly: Reduce the stress and race
    for the treatment. <i>Science Translational Medicine</i>. American Association
    for the Advancement of Science. <a href="https://doi.org/10.1126/scitranslmed.aar7514">https://doi.org/10.1126/scitranslmed.aar7514</a>'
  chicago: 'Novarino, Gaia. “Zika-Associated Microcephaly: Reduce the Stress and Race
    for the Treatment.” <i>Science Translational Medicine</i>. American Association
    for the Advancement of Science, 2018. <a href="https://doi.org/10.1126/scitranslmed.aar7514">https://doi.org/10.1126/scitranslmed.aar7514</a>.'
  ieee: 'G. Novarino, “Zika-associated microcephaly: Reduce the stress and race for
    the treatment,” <i>Science Translational Medicine</i>, vol. 10, no. 423. American
    Association for the Advancement of Science, 2018.'
  ista: 'Novarino G. 2018. Zika-associated microcephaly: Reduce the stress and race
    for the treatment. Science Translational Medicine. 10(423), eaar7514.'
  mla: 'Novarino, Gaia. “Zika-Associated Microcephaly: Reduce the Stress and Race
    for the Treatment.” <i>Science Translational Medicine</i>, vol. 10, no. 423, eaar7514,
    American Association for the Advancement of Science, 2018, doi:<a href="https://doi.org/10.1126/scitranslmed.aar7514">10.1126/scitranslmed.aar7514</a>.'
  short: G. Novarino, Science Translational Medicine 10 (2018).
date_created: 2018-12-11T11:46:34Z
date_published: 2018-01-10T00:00:00Z
date_updated: 2021-01-12T07:59:42Z
day: '10'
department:
- _id: GaNo
doi: 10.1126/scitranslmed.aar7514
intvolume: '        10'
issue: '423'
language:
- iso: eng
month: '01'
oa_version: None
publication: Science Translational Medicine
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7365'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Zika-associated microcephaly: Reduce the stress and race for the treatment'
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 10
year: '2018'
...
---
_id: '457'
abstract:
- lang: eng
  text: Temperate bacteriophages integrate in bacterial genomes as prophages and represent
    an important source of genetic variation for bacterial evolution, frequently transmitting
    fitness-augmenting genes such as toxins responsible for virulence of major pathogens.
    However, only a fraction of bacteriophage infections are lysogenic and lead to
    prophage acquisition, whereas the majority are lytic and kill the infected bacteria.
    Unless able to discriminate lytic from lysogenic infections, mechanisms of immunity
    to bacteriophages are expected to act as a double-edged sword and increase the
    odds of survival at the cost of depriving bacteria of potentially beneficial prophages.
    We show that although restriction-modification systems as mechanisms of innate
    immunity prevent both lytic and lysogenic infections indiscriminately in individual
    bacteria, they increase the number of prophage-acquiring individuals at the population
    level. We find that this counterintuitive result is a consequence of phage-host
    population dynamics, in which restriction-modification systems delay infection
    onset until bacteria reach densities at which the probability of lysogeny increases.
    These results underscore the importance of population-level dynamics as a key
    factor modulating costs and benefits of immunity to temperate bacteriophages
article_processing_charge: No
author:
- first_name: Maros
  full_name: Pleska, Maros
  id: 4569785E-F248-11E8-B48F-1D18A9856A87
  last_name: Pleska
  orcid: 0000-0001-7460-7479
- first_name: Moritz
  full_name: Lang, Moritz
  id: 29E0800A-F248-11E8-B48F-1D18A9856A87
  last_name: Lang
- first_name: Dominik
  full_name: Refardt, Dominik
  last_name: Refardt
- first_name: Bruce
  full_name: Levin, Bruce
  last_name: Levin
- first_name: Calin C
  full_name: Guet, Calin C
  id: 47F8433E-F248-11E8-B48F-1D18A9856A87
  last_name: Guet
  orcid: 0000-0001-6220-2052
citation:
  ama: Pleska M, Lang M, Refardt D, Levin B, Guet CC. Phage-host population dynamics
    promotes prophage acquisition in bacteria with innate immunity. <i>Nature Ecology
    and Evolution</i>. 2018;2(2):359-366. doi:<a href="https://doi.org/10.1038/s41559-017-0424-z">10.1038/s41559-017-0424-z</a>
  apa: Pleska, M., Lang, M., Refardt, D., Levin, B., &#38; Guet, C. C. (2018). Phage-host
    population dynamics promotes prophage acquisition in bacteria with innate immunity.
    <i>Nature Ecology and Evolution</i>. Springer Nature. <a href="https://doi.org/10.1038/s41559-017-0424-z">https://doi.org/10.1038/s41559-017-0424-z</a>
  chicago: Pleska, Maros, Moritz Lang, Dominik Refardt, Bruce Levin, and Calin C Guet.
    “Phage-Host Population Dynamics Promotes Prophage Acquisition in Bacteria with
    Innate Immunity.” <i>Nature Ecology and Evolution</i>. Springer Nature, 2018.
    <a href="https://doi.org/10.1038/s41559-017-0424-z">https://doi.org/10.1038/s41559-017-0424-z</a>.
  ieee: M. Pleska, M. Lang, D. Refardt, B. Levin, and C. C. Guet, “Phage-host population
    dynamics promotes prophage acquisition in bacteria with innate immunity,” <i>Nature
    Ecology and Evolution</i>, vol. 2, no. 2. Springer Nature, pp. 359–366, 2018.
  ista: Pleska M, Lang M, Refardt D, Levin B, Guet CC. 2018. Phage-host population
    dynamics promotes prophage acquisition in bacteria with innate immunity. Nature
    Ecology and Evolution. 2(2), 359–366.
  mla: Pleska, Maros, et al. “Phage-Host Population Dynamics Promotes Prophage Acquisition
    in Bacteria with Innate Immunity.” <i>Nature Ecology and Evolution</i>, vol. 2,
    no. 2, Springer Nature, 2018, pp. 359–66, doi:<a href="https://doi.org/10.1038/s41559-017-0424-z">10.1038/s41559-017-0424-z</a>.
  short: M. Pleska, M. Lang, D. Refardt, B. Levin, C.C. Guet, Nature Ecology and Evolution
    2 (2018) 359–366.
date_created: 2018-12-11T11:46:35Z
date_published: 2018-02-01T00:00:00Z
date_updated: 2023-09-15T12:04:57Z
day: '01'
department:
- _id: CaGu
- _id: GaTk
doi: 10.1038/s41559-017-0424-z
ec_funded: 1
external_id:
  isi:
  - '000426516400027'
intvolume: '         2'
isi: 1
issue: '2'
language:
- iso: eng
month: '02'
oa_version: None
page: 359 - 366
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
- _id: 251BCBEC-B435-11E9-9278-68D0E5697425
  grant_number: RGY0079/2011
  name: Multi-Level Conflicts in Evolutionary Dynamics of Restriction-Modification
    Systems (HFSP Young investigators' grant)
- _id: 251D65D8-B435-11E9-9278-68D0E5697425
  grant_number: '24210'
  name: Effects of Stochasticity on the Function of Restriction-Modi cation Systems
    at the Single-Cell Level (DOC Fellowship)
publication: Nature Ecology and Evolution
publication_status: published
publisher: Springer Nature
publist_id: '7364'
quality_controlled: '1'
related_material:
  record:
  - id: '202'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Phage-host population dynamics promotes prophage acquisition in bacteria with
  innate immunity
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 2
year: '2018'
...
---
_id: '458'
abstract:
- lang: eng
  text: We consider congruences of straight lines in a plane with the combinatorics
    of the square grid, with all elementary quadrilaterals possessing an incircle.
    It is shown that all the vertices of such nets (we call them incircular or IC-nets)
    lie on confocal conics. Our main new results are on checkerboard IC-nets in the
    plane. These are congruences of straight lines in the plane with the combinatorics
    of the square grid, combinatorially colored as a checkerboard, such that all black
    coordinate quadrilaterals possess inscribed circles. We show how this larger class
    of IC-nets appears quite naturally in Laguerre geometry of oriented planes and
    spheres and leads to new remarkable incidence theorems. Most of our results are
    valid in hyperbolic and spherical geometries as well. We present also generalizations
    in spaces of higher dimension, called checkerboard IS-nets. The construction of
    these nets is based on a new 9 inspheres incidence theorem.
acknowledgement: DFG Collaborative Research Center TRR 109 “Discretization in Geometry
  and Dynamics”; People Programme (Marie Curie Actions) of the European Union’s Seventh
  Framework Programme (FP7/2007-2013) REA grant agreement n◦[291734]
article_processing_charge: No
author:
- first_name: Arseniy
  full_name: Akopyan, Arseniy
  id: 430D2C90-F248-11E8-B48F-1D18A9856A87
  last_name: Akopyan
  orcid: 0000-0002-2548-617X
- first_name: Alexander
  full_name: Bobenko, Alexander
  last_name: Bobenko
citation:
  ama: Akopyan A, Bobenko A. Incircular nets and confocal conics. <i>Transactions
    of the American Mathematical Society</i>. 2018;370(4):2825-2854. doi:<a href="https://doi.org/10.1090/tran/7292">10.1090/tran/7292</a>
  apa: Akopyan, A., &#38; Bobenko, A. (2018). Incircular nets and confocal conics.
    <i>Transactions of the American Mathematical Society</i>. American Mathematical
    Society. <a href="https://doi.org/10.1090/tran/7292">https://doi.org/10.1090/tran/7292</a>
  chicago: Akopyan, Arseniy, and Alexander Bobenko. “Incircular Nets and Confocal
    Conics.” <i>Transactions of the American Mathematical Society</i>. American Mathematical
    Society, 2018. <a href="https://doi.org/10.1090/tran/7292">https://doi.org/10.1090/tran/7292</a>.
  ieee: A. Akopyan and A. Bobenko, “Incircular nets and confocal conics,” <i>Transactions
    of the American Mathematical Society</i>, vol. 370, no. 4. American Mathematical
    Society, pp. 2825–2854, 2018.
  ista: Akopyan A, Bobenko A. 2018. Incircular nets and confocal conics. Transactions
    of the American Mathematical Society. 370(4), 2825–2854.
  mla: Akopyan, Arseniy, and Alexander Bobenko. “Incircular Nets and Confocal Conics.”
    <i>Transactions of the American Mathematical Society</i>, vol. 370, no. 4, American
    Mathematical Society, 2018, pp. 2825–54, doi:<a href="https://doi.org/10.1090/tran/7292">10.1090/tran/7292</a>.
  short: A. Akopyan, A. Bobenko, Transactions of the American Mathematical Society
    370 (2018) 2825–2854.
date_created: 2018-12-11T11:46:35Z
date_published: 2018-04-01T00:00:00Z
date_updated: 2023-09-11T14:19:12Z
day: '01'
department:
- _id: HeEd
doi: 10.1090/tran/7292
ec_funded: 1
external_id:
  isi:
  - '000423197800019'
intvolume: '       370'
isi: 1
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1602.04637
month: '04'
oa: 1
oa_version: Preprint
page: 2825 - 2854
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '291734'
  name: International IST Postdoc Fellowship Programme
publication: Transactions of the American Mathematical Society
publication_status: published
publisher: American Mathematical Society
publist_id: '7363'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Incircular nets and confocal conics
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 370
year: '2018'
...
---
_id: '46'
abstract:
- lang: eng
  text: We analyze a disordered central spin model, where a central spin interacts
    equally with each spin in a periodic one-dimensional (1D) random-field Heisenberg
    chain. If the Heisenberg chain is initially in the many-body localized (MBL) phase,
    we find that the coupling to the central spin suffices to delocalize the chain
    for a substantial range of coupling strengths. We calculate the phase diagram
    of the model and identify the phase boundary between the MBL and ergodic phase.
    Within the localized phase, the central spin significantly enhances the rate of
    the logarithmic entanglement growth and its saturation value. We attribute the
    increase in entanglement entropy to a nonextensive enhancement of magnetization
    fluctuations induced by the central spin. Finally, we demonstrate that correlation
    functions of the central spin can be utilized to distinguish between MBL and ergodic
    phases of the 1D chain. Hence, we propose the use of a central spin as a possible
    experimental probe to identify the MBL phase.
acknowledgement: F.P. acknowledges the sup- port of the DFG Research Unit FOR 1807
  through Grants No. PO 1370/2-1 and No. TRR80, the Nanosystems Initiative Munich
  (NIM) by the German Excellence Initiative, and the European Research Council (ERC)
  under the European Union’s Horizon 2020 research and innovation programme (Grant
  Agreement No. 771537). N.Y.Y. acknowledges support from the NSF (PHY-1654740), the
  ARO STIR program, and a Google research award.
article_number: '161122'
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: Daniel
  full_name: Hetterich, Daniel
  last_name: Hetterich
- first_name: Norman
  full_name: Yao, Norman
  last_name: Yao
- first_name: Maksym
  full_name: Serbyn, Maksym
  id: 47809E7E-F248-11E8-B48F-1D18A9856A87
  last_name: Serbyn
  orcid: 0000-0002-2399-5827
- first_name: Frank
  full_name: Pollmann, Frank
  last_name: Pollmann
- first_name: Björn
  full_name: Trauzettel, Björn
  last_name: Trauzettel
citation:
  ama: Hetterich D, Yao N, Serbyn M, Pollmann F, Trauzettel B. Detection and characterization
    of many-body localization in central spin models. <i>Physical Review B</i>. 2018;98(16).
    doi:<a href="https://doi.org/10.1103/PhysRevB.98.161122">10.1103/PhysRevB.98.161122</a>
  apa: Hetterich, D., Yao, N., Serbyn, M., Pollmann, F., &#38; Trauzettel, B. (2018).
    Detection and characterization of many-body localization in central spin models.
    <i>Physical Review B</i>. American Physical Society. <a href="https://doi.org/10.1103/PhysRevB.98.161122">https://doi.org/10.1103/PhysRevB.98.161122</a>
  chicago: Hetterich, Daniel, Norman Yao, Maksym Serbyn, Frank Pollmann, and Björn
    Trauzettel. “Detection and Characterization of Many-Body Localization in Central
    Spin Models.” <i>Physical Review B</i>. American Physical Society, 2018. <a href="https://doi.org/10.1103/PhysRevB.98.161122">https://doi.org/10.1103/PhysRevB.98.161122</a>.
  ieee: D. Hetterich, N. Yao, M. Serbyn, F. Pollmann, and B. Trauzettel, “Detection
    and characterization of many-body localization in central spin models,” <i>Physical
    Review B</i>, vol. 98, no. 16. American Physical Society, 2018.
  ista: Hetterich D, Yao N, Serbyn M, Pollmann F, Trauzettel B. 2018. Detection and
    characterization of many-body localization in central spin models. Physical Review
    B. 98(16), 161122.
  mla: Hetterich, Daniel, et al. “Detection and Characterization of Many-Body Localization
    in Central Spin Models.” <i>Physical Review B</i>, vol. 98, no. 16, 161122, American
    Physical Society, 2018, doi:<a href="https://doi.org/10.1103/PhysRevB.98.161122">10.1103/PhysRevB.98.161122</a>.
  short: D. Hetterich, N. Yao, M. Serbyn, F. Pollmann, B. Trauzettel, Physical Review
    B 98 (2018).
date_created: 2018-12-11T11:44:20Z
date_published: 2018-10-15T00:00:00Z
date_updated: 2023-09-11T12:55:03Z
day: '15'
department:
- _id: MaSe
doi: 10.1103/PhysRevB.98.161122
external_id:
  arxiv:
  - '1806.08316'
  isi:
  - '000448596500002'
intvolume: '        98'
isi: 1
issue: '16'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1806.08316
month: '10'
oa: 1
oa_version: Preprint
publication: Physical Review B
publication_status: published
publisher: American Physical Society
publist_id: '8008'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Detection and characterization of many-body localization in central spin models
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 98
year: '2018'
...
---
_id: '461'
abstract:
- lang: eng
  text: Turbulence is the major cause of friction losses in transport processes and
    it is responsible for a drastic drag increase in flows over bounding surfaces.
    While much effort is invested into developing ways to control and reduce turbulence
    intensities, so far no methods exist to altogether eliminate turbulence if velocities
    are sufficiently large. We demonstrate for pipe flow that appropriate distortions
    to the velocity profile lead to a complete collapse of turbulence and subsequently
    friction losses are reduced by as much as 90%. Counterintuitively, the return
    to laminar motion is accomplished by initially increasing turbulence intensities
    or by transiently amplifying wall shear. Since neither the Reynolds number nor
    the shear stresses decrease (the latter often increase), these measures are not
    indicative of turbulence collapse. Instead, an amplification mechanism                      measuring
    the interaction between eddies and the mean shear is found to set a threshold
    below which turbulence is suppressed beyond recovery.
acknowledgement: We acknowledge the European Research Council under the European Union’s
  Seventh Framework Programme (FP/2007-2013)/ERC Grant Agreement 306589, the European
  Research Council (ERC) under the European Union’s Horizon 2020 research and innovation
  programme (grant agreement no. 737549) and the Deutsche Forschungsgemeinschaft (Project
  No. FOR 1182) for financial support. We thank our technician P. Maier for providing
  highly valuable ideas and greatly supporting us in all technical aspects. We thank
  M. Schaner for technical drawings, construction and design. We thank M. Schwegel
  for a Matlab code to post-process experimental data.
article_processing_charge: No
author:
- first_name: Jakob
  full_name: Kühnen, Jakob
  id: 3A47AE32-F248-11E8-B48F-1D18A9856A87
  last_name: Kühnen
  orcid: 0000-0003-4312-0179
- first_name: Baofang
  full_name: Song, Baofang
  last_name: Song
- first_name: Davide
  full_name: Scarselli, Davide
  id: 40315C30-F248-11E8-B48F-1D18A9856A87
  last_name: Scarselli
  orcid: 0000-0001-5227-4271
- first_name: Nazmi B
  full_name: Budanur, Nazmi B
  id: 3EA1010E-F248-11E8-B48F-1D18A9856A87
  last_name: Budanur
  orcid: 0000-0003-0423-5010
- first_name: Michael
  full_name: Riedl, Michael
  id: 3BE60946-F248-11E8-B48F-1D18A9856A87
  last_name: Riedl
  orcid: 0000-0003-4844-6311
- first_name: Ashley
  full_name: Willis, Ashley
  last_name: Willis
- first_name: Marc
  full_name: Avila, Marc
  last_name: Avila
- first_name: Björn
  full_name: Hof, Björn
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
citation:
  ama: Kühnen J, Song B, Scarselli D, et al. Destabilizing turbulence in pipe flow.
    <i>Nature Physics</i>. 2018;14:386-390. doi:<a href="https://doi.org/10.1038/s41567-017-0018-3">10.1038/s41567-017-0018-3</a>
  apa: Kühnen, J., Song, B., Scarselli, D., Budanur, N. B., Riedl, M., Willis, A.,
    … Hof, B. (2018). Destabilizing turbulence in pipe flow. <i>Nature Physics</i>.
    Nature Publishing Group. <a href="https://doi.org/10.1038/s41567-017-0018-3">https://doi.org/10.1038/s41567-017-0018-3</a>
  chicago: Kühnen, Jakob, Baofang Song, Davide Scarselli, Nazmi B Budanur, Michael
    Riedl, Ashley Willis, Marc Avila, and Björn Hof. “Destabilizing Turbulence in
    Pipe Flow.” <i>Nature Physics</i>. Nature Publishing Group, 2018. <a href="https://doi.org/10.1038/s41567-017-0018-3">https://doi.org/10.1038/s41567-017-0018-3</a>.
  ieee: J. Kühnen <i>et al.</i>, “Destabilizing turbulence in pipe flow,” <i>Nature
    Physics</i>, vol. 14. Nature Publishing Group, pp. 386–390, 2018.
  ista: Kühnen J, Song B, Scarselli D, Budanur NB, Riedl M, Willis A, Avila M, Hof
    B. 2018. Destabilizing turbulence in pipe flow. Nature Physics. 14, 386–390.
  mla: Kühnen, Jakob, et al. “Destabilizing Turbulence in Pipe Flow.” <i>Nature Physics</i>,
    vol. 14, Nature Publishing Group, 2018, pp. 386–90, doi:<a href="https://doi.org/10.1038/s41567-017-0018-3">10.1038/s41567-017-0018-3</a>.
  short: J. Kühnen, B. Song, D. Scarselli, N.B. Budanur, M. Riedl, A. Willis, M. Avila,
    B. Hof, Nature Physics 14 (2018) 386–390.
date_created: 2018-12-11T11:46:36Z
date_published: 2018-01-08T00:00:00Z
date_updated: 2024-03-25T23:30:20Z
day: '08'
department:
- _id: BjHo
doi: 10.1038/s41567-017-0018-3
ec_funded: 1
external_id:
  isi:
  - '000429434100020'
intvolume: '        14'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1711.06543
month: '01'
oa: 1
oa_version: Preprint
page: 386-390
project:
- _id: 25152F3A-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '306589'
  name: Decoding the complexity of turbulence at its origin
- _id: 25104D44-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '737549'
  name: Eliminating turbulence in oil pipelines
publication: Nature Physics
publication_status: published
publisher: Nature Publishing Group
publist_id: '7360'
quality_controlled: '1'
related_material:
  record:
  - id: '12726'
    relation: dissertation_contains
    status: public
  - id: '14530'
    relation: dissertation_contains
    status: public
  - id: '7258'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Destabilizing turbulence in pipe flow
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 14
year: '2018'
...
---
_id: '462'
abstract:
- lang: eng
  text: 'AtNHX5 and AtNHX6 are endosomal Na+,K+/H+ antiporters that are critical for
    growth and development in Arabidopsis, but the mechanism behind their action remains
    unknown. Here, we report that AtNHX5 and AtNHX6, functioning as H+ leak, control
    auxin homeostasis and auxin-mediated development. We found that nhx5 nhx6 exhibited
    growth variations of auxin-related defects. We further showed that nhx5 nhx6 was
    affected in auxin homeostasis. Genetic analysis showed that AtNHX5 and AtNHX6
    were required for the function of the ER-localized auxin transporter PIN5. Although
    AtNHX5 and AtNHX6 were co-localized with PIN5 at ER, they did not interact directly.
    Instead, the conserved acidic residues in AtNHX5 and AtNHX6, which are essential
    for exchange activity, were required for PIN5 function. AtNHX5 and AtNHX6 regulated
    the pH in ER. Overall, AtNHX5 and AtNHX6 may regulate auxin transport across the
    ER via the pH gradient created by their transport activity. H+-leak pathway provides
    a fine-tuning mechanism that controls cellular auxin fluxes. '
acknowledgement: 'This work was supported by the National Natural Science Foundation
  of China (31571464, 31371438 and 31070222 to Q.S.Q.), the National Basic Research
  Program of China (973 project, 2013CB429904 to Q.S.Q.), the Research Fund for the
  Doctoral Program of Higher Education of China (20130211110001 to Q.S.Q.), the Ministry
  of Education, Youth and Sports of the Czech Republic (the National Program for Sustainability
  I, LO1204), and The Czech Science Foundation GAČR (GA13–40637S) to JF. We thank
  Dr. Tom J. Guilfoyle for DR5::GUS line and Dr. Jia Li for pBIB‐RFP vector and DR5::GFP
  line. We thank Liping Guan and Yang Zhao for their help with the confocal microscope
  assay. '
article_processing_charge: No
article_type: original
author:
- first_name: Ligang
  full_name: Fan, Ligang
  last_name: Fan
- first_name: Lei
  full_name: Zhao, Lei
  last_name: Zhao
- first_name: Wei
  full_name: Hu, Wei
  last_name: Hu
- first_name: Weina
  full_name: Li, Weina
  last_name: Li
- first_name: Ondřej
  full_name: Novák, Ondřej
  last_name: Novák
- first_name: Miroslav
  full_name: Strnad, Miroslav
  last_name: Strnad
- first_name: Sibu
  full_name: Simon, Sibu
  id: 4542EF9A-F248-11E8-B48F-1D18A9856A87
  last_name: Simon
  orcid: 0000-0002-1998-6741
- first_name: Jirí
  full_name: Friml, Jirí
  id: 4159519E-F248-11E8-B48F-1D18A9856A87
  last_name: Friml
  orcid: 0000-0002-8302-7596
- first_name: Jinbo
  full_name: Shen, Jinbo
  last_name: Shen
- first_name: Liwen
  full_name: Jiang, Liwen
  last_name: Jiang
- first_name: Quan
  full_name: Qiu, Quan
  last_name: Qiu
citation:
  ama: Fan L, Zhao L, Hu W, et al. NHX antiporters regulate the pH of endoplasmic
    reticulum and auxin-mediated development. <i>Plant, Cell and Environment</i>.
    2018;41:850-864. doi:<a href="https://doi.org/10.1111/pce.13153">10.1111/pce.13153</a>
  apa: Fan, L., Zhao, L., Hu, W., Li, W., Novák, O., Strnad, M., … Qiu, Q. (2018).
    NHX antiporters regulate the pH of endoplasmic reticulum and auxin-mediated development.
    <i>Plant, Cell and Environment</i>. Wiley-Blackwell. <a href="https://doi.org/10.1111/pce.13153">https://doi.org/10.1111/pce.13153</a>
  chicago: Fan, Ligang, Lei Zhao, Wei Hu, Weina Li, Ondřej Novák, Miroslav Strnad,
    Sibu Simon, et al. “NHX Antiporters Regulate the PH of Endoplasmic Reticulum and
    Auxin-Mediated Development.” <i>Plant, Cell and Environment</i>. Wiley-Blackwell,
    2018. <a href="https://doi.org/10.1111/pce.13153">https://doi.org/10.1111/pce.13153</a>.
  ieee: L. Fan <i>et al.</i>, “NHX antiporters regulate the pH of endoplasmic reticulum
    and auxin-mediated development,” <i>Plant, Cell and Environment</i>, vol. 41.
    Wiley-Blackwell, pp. 850–864, 2018.
  ista: Fan L, Zhao L, Hu W, Li W, Novák O, Strnad M, Simon S, Friml J, Shen J, Jiang
    L, Qiu Q. 2018. NHX antiporters regulate the pH of endoplasmic reticulum and auxin-mediated
    development. Plant, Cell and Environment. 41, 850–864.
  mla: Fan, Ligang, et al. “NHX Antiporters Regulate the PH of Endoplasmic Reticulum
    and Auxin-Mediated Development.” <i>Plant, Cell and Environment</i>, vol. 41,
    Wiley-Blackwell, 2018, pp. 850–64, doi:<a href="https://doi.org/10.1111/pce.13153">10.1111/pce.13153</a>.
  short: L. Fan, L. Zhao, W. Hu, W. Li, O. Novák, M. Strnad, S. Simon, J. Friml, J.
    Shen, L. Jiang, Q. Qiu, Plant, Cell and Environment 41 (2018) 850–864.
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