---
_id: '6952'
abstract:
- lang: eng
text: 'We present a unified framework tackling two problems: class-specific 3D reconstruction
from a single image, and generation of new 3D shape samples. These tasks have
received considerable attention recently; however, most existing approaches rely
on 3D supervision, annotation of 2D images with keypoints or poses, and/or training
with multiple views of each object instance. Our framework is very general: it
can be trained in similar settings to existing approaches, while also supporting
weaker supervision. Importantly, it can be trained purely from 2D images, without
pose annotations, and with only a single view per instance. We employ meshes as
an output representation, instead of voxels used in most prior work. This allows
us to reason over lighting parameters and exploit shading information during training,
which previous 2D-supervised methods cannot. Thus, our method can learn to generate
and reconstruct concave object classes. We evaluate our approach in various settings,
showing that: (i) it learns to disentangle shape from pose and lighting; (ii)
using shading in the loss improves performance compared to just silhouettes; (iii)
when using a standard single white light, our model outperforms state-of-the-art
2D-supervised methods, both with and without pose supervision, thanks to exploiting
shading cues; (iv) performance improves further when using multiple coloured lights,
even approaching that of state-of-the-art 3D-supervised methods; (v) shapes produced
by our model capture smooth surfaces and fine details better than voxel-based
approaches; and (vi) our approach supports concave classes such as bathtubs and
sofas, which methods based on silhouettes cannot learn.'
acknowledgement: Open access funding provided by Institute of Science and Technology
(IST Austria).
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Paul M
full_name: Henderson, Paul M
id: 13C09E74-18D9-11E9-8878-32CFE5697425
last_name: Henderson
orcid: 0000-0002-5198-7445
- first_name: Vittorio
full_name: Ferrari, Vittorio
last_name: Ferrari
citation:
ama: Henderson PM, Ferrari V. Learning single-image 3D reconstruction by generative
modelling of shape, pose and shading. International Journal of Computer Vision.
2020;128:835-854. doi:10.1007/s11263-019-01219-8
apa: Henderson, P. M., & Ferrari, V. (2020). Learning single-image 3D reconstruction
by generative modelling of shape, pose and shading. International Journal of
Computer Vision. Springer Nature. https://doi.org/10.1007/s11263-019-01219-8
chicago: Henderson, Paul M, and Vittorio Ferrari. “Learning Single-Image 3D Reconstruction
by Generative Modelling of Shape, Pose and Shading.” International Journal
of Computer Vision. Springer Nature, 2020. https://doi.org/10.1007/s11263-019-01219-8.
ieee: P. M. Henderson and V. Ferrari, “Learning single-image 3D reconstruction by
generative modelling of shape, pose and shading,” International Journal of
Computer Vision, vol. 128. Springer Nature, pp. 835–854, 2020.
ista: Henderson PM, Ferrari V. 2020. Learning single-image 3D reconstruction by
generative modelling of shape, pose and shading. International Journal of Computer
Vision. 128, 835–854.
mla: Henderson, Paul M., and Vittorio Ferrari. “Learning Single-Image 3D Reconstruction
by Generative Modelling of Shape, Pose and Shading.” International Journal
of Computer Vision, vol. 128, Springer Nature, 2020, pp. 835–54, doi:10.1007/s11263-019-01219-8.
short: P.M. Henderson, V. Ferrari, International Journal of Computer Vision 128
(2020) 835–854.
date_created: 2019-10-17T13:38:20Z
date_published: 2020-04-01T00:00:00Z
date_updated: 2023-08-17T14:01:16Z
day: '01'
ddc:
- '004'
department:
- _id: ChLa
doi: 10.1007/s11263-019-01219-8
external_id:
arxiv:
- '1901.06447'
isi:
- '000491042100002'
file:
- access_level: open_access
checksum: a0f05dd4f5f64e4f713d8d9d4b5b1e3f
content_type: application/pdf
creator: dernst
date_created: 2019-10-25T10:28:29Z
date_updated: 2020-07-14T12:47:46Z
file_id: '6973'
file_name: 2019_CompVision_Henderson.pdf
file_size: 2243134
relation: main_file
file_date_updated: 2020-07-14T12:47:46Z
has_accepted_license: '1'
intvolume: ' 128'
isi: 1
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 835-854
project:
- _id: B67AFEDC-15C9-11EA-A837-991A96BB2854
name: IST Austria Open Access Fund
publication: International Journal of Computer Vision
publication_identifier:
eissn:
- 1573-1405
issn:
- 0920-5691
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Learning single-image 3D reconstruction by generative modelling of shape, pose
and shading
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 128
year: '2020'
...
---
_id: '7148'
abstract:
- lang: eng
text: In the cerebellum, GluD2 is exclusively expressed in Purkinje cells, where
it regulates synapse formation and regeneration, synaptic plasticity, and motor
learning. Delayed cognitive development in humans with GluD2 gene mutations suggests
extracerebellar functions of GluD2. However, extracerebellar expression of GluD2
and its relationship with that of GluD1 are poorly understood. GluD2 mRNA and
protein were widely detected, with relatively high levels observed in the olfactory
glomerular layer, medial prefrontal cortex, cingulate cortex, retrosplenial granular
cortex, olfactory tubercle, subiculum, striatum, lateral septum, anterodorsal
thalamic nucleus, and arcuate hypothalamic nucleus. These regions were also enriched
for GluD1, and many individual neurons coexpressed the two GluDs. In the retrosplenial
granular cortex, GluD1 and GluD2 were selectively expressed at PSD‐95‐expressing
glutamatergic synapses, and their coexpression on the same synapses was shown
by SDS‐digested freeze‐fracture replica labeling. Biochemically, GluD1 and GluD2
formed coimmunoprecipitable complex formation in HEK293T cells and in the cerebral
cortex and hippocampus. We further estimated the relative protein amount by quantitative
immunoblotting using GluA2/GluD2 and GluA2/GluD1 chimeric proteins as standards
for titration of GluD1 and GluD2 antibodies. Intriguingly, the relative amount
of GluD2 was almost comparable to that of GluD1 in the postsynaptic density fraction
prepared from the cerebral cortex and hippocampus. In contrast, GluD2 was overwhelmingly
predominant in the cerebellum. Thus, we have determined the relative extracerebellar
expression of GluD1 and GluD2 at regional, neuronal, and synaptic levels. These
data provide a molecular–anatomical basis for possible competitive and cooperative
interactions of GluD family members at synapses in various brain regions.
acknowledgement: This study was supported by Grants-in-Aid for Scientific Research
to K.K. (18K06813), Y.M. (17K08503, 17H0631319), and K.S. (16H04650) and a grant
for Scientific Research on Innovative Areas to K.S (16H06276) from the Ministry
of Education, Culture, Sports, Science and Technology of Japan (MEXT). We thank
K. Akashi, I. Watanabe-Iida, Y. Suzuki, and H. Azechi for technical assistance and
advice, and H. Uchida for valuable discussions. We thank E. Kushiya,I. Yabe, C.
Ohori, Y. Mochizuki, Y. Ishikawa, and N. Ishimoto for technical assistance in generating
GluD1-KO mice.
article_processing_charge: No
article_type: original
author:
- first_name: Chihiro
full_name: Nakamoto, Chihiro
last_name: Nakamoto
- first_name: Kohtarou
full_name: Konno, Kohtarou
last_name: Konno
- first_name: Taisuke
full_name: Miyazaki, Taisuke
last_name: Miyazaki
- first_name: Ena
full_name: Nakatsukasa, Ena
last_name: Nakatsukasa
- first_name: Rie
full_name: Natsume, Rie
last_name: Natsume
- first_name: Manabu
full_name: Abe, Manabu
last_name: Abe
- first_name: Meiko
full_name: Kawamura, Meiko
last_name: Kawamura
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Miwako
full_name: Yamasaki, Miwako
last_name: Yamasaki
- first_name: Kenji
full_name: Sakimura, Kenji
last_name: Sakimura
- first_name: Masahiko
full_name: Watanabe, Masahiko
last_name: Watanabe
citation:
ama: Nakamoto C, Konno K, Miyazaki T, et al. Expression mapping, quantification,
and complex formation of GluD1 and GluD2 glutamate receptors in adult mouse brain.
Journal of Comparative Neurology. 2020;528(6):1003-1027. doi:10.1002/cne.24792
apa: Nakamoto, C., Konno, K., Miyazaki, T., Nakatsukasa, E., Natsume, R., Abe, M.,
… Watanabe, M. (2020). Expression mapping, quantification, and complex formation
of GluD1 and GluD2 glutamate receptors in adult mouse brain. Journal of Comparative
Neurology. Wiley. https://doi.org/10.1002/cne.24792
chicago: Nakamoto, Chihiro, Kohtarou Konno, Taisuke Miyazaki, Ena Nakatsukasa, Rie
Natsume, Manabu Abe, Meiko Kawamura, et al. “Expression Mapping, Quantification,
and Complex Formation of GluD1 and GluD2 Glutamate Receptors in Adult Mouse Brain.”
Journal of Comparative Neurology. Wiley, 2020. https://doi.org/10.1002/cne.24792.
ieee: C. Nakamoto et al., “Expression mapping, quantification, and complex
formation of GluD1 and GluD2 glutamate receptors in adult mouse brain,” Journal
of Comparative Neurology, vol. 528, no. 6. Wiley, pp. 1003–1027, 2020.
ista: Nakamoto C, Konno K, Miyazaki T, Nakatsukasa E, Natsume R, Abe M, Kawamura
M, Fukazawa Y, Shigemoto R, Yamasaki M, Sakimura K, Watanabe M. 2020. Expression
mapping, quantification, and complex formation of GluD1 and GluD2 glutamate receptors
in adult mouse brain. Journal of Comparative Neurology. 528(6), 1003–1027.
mla: Nakamoto, Chihiro, et al. “Expression Mapping, Quantification, and Complex
Formation of GluD1 and GluD2 Glutamate Receptors in Adult Mouse Brain.” Journal
of Comparative Neurology, vol. 528, no. 6, Wiley, 2020, pp. 1003–27, doi:10.1002/cne.24792.
short: C. Nakamoto, K. Konno, T. Miyazaki, E. Nakatsukasa, R. Natsume, M. Abe, M.
Kawamura, Y. Fukazawa, R. Shigemoto, M. Yamasaki, K. Sakimura, M. Watanabe, Journal
of Comparative Neurology 528 (2020) 1003–1027.
date_created: 2019-12-04T16:09:29Z
date_published: 2020-04-01T00:00:00Z
date_updated: 2023-08-17T14:06:50Z
day: '01'
ddc:
- '571'
- '599'
department:
- _id: RySh
doi: 10.1002/cne.24792
external_id:
isi:
- '000496410200001'
pmid:
- '31625608'
has_accepted_license: '1'
intvolume: ' 528'
isi: 1
issue: '6'
language:
- iso: eng
month: '04'
oa_version: None
page: 1003-1027
pmid: 1
publication: Journal of Comparative Neurology
publication_identifier:
eissn:
- 1096-9861
issn:
- 0021-9967
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Expression mapping, quantification, and complex formation of GluD1 and GluD2
glutamate receptors in adult mouse brain
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 528
year: '2020'
...
---
_id: '7033'
abstract:
- lang: eng
text: Removal of the Bax gene from mice completely protects the somas of retinal
ganglion cells (RGCs) from apoptosis following optic nerve injury. This makes
BAX a promising therapeutic target to prevent neurodegeneration. In this study,
Bax+/− mice were used to test the hypothesis that lowering the quantity of BAX
in RGCs would delay apoptosis following optic nerve injury. RGCs were damaged
by performing optic nerve crush (ONC) and then immunostaining for phospho-cJUN,
and quantitative PCR were used to monitor the status of the BAX activation mechanism
in the months following injury. The apoptotic susceptibility of injured cells
was directly tested by virally introducing GFP-BAX into Bax−/− RGCs after injury.
The competency of quiescent RGCs to reactivate their BAX activation mechanism
was tested by intravitreal injection of the JNK pathway agonist, anisomycin. Twenty-four
weeks after ONC, Bax+/− mice had significantly less cell loss in their RGC layer
than Bax+/+ mice 3 weeks after ONC. Bax+/− and Bax+/+ RGCs exhibited similar patterns
of nuclear phospho-cJUN accumulation immediately after ONC, which persisted in
Bax+/− RGCs for up to 7 weeks before abating. The transcriptional activation of
BAX-activating genes was similar in Bax+/− and Bax+/+ RGCs following ONC. Intriguingly,
cells deactivated their BAX activation mechanism between 7 and 12 weeks after
crush. Introduction of GFP-BAX into Bax−/− cells at 4 weeks after ONC showed that
these cells had a nearly normal capacity to activate this protein, but this capacity
was lost 8 weeks after crush. Collectively, these data suggest that 8–12 weeks
after crush, damaged cells no longer displayed increased susceptibility to BAX
activation relative to their naïve counterparts. In this same timeframe, retinal
glial activation and the signaling of the pro-apoptotic JNK pathway also abated.
Quiescent RGCs did not show a timely reactivation of their JNK pathway following
intravitreal injection with anisomycin. These findings demonstrate that lowering
the quantity of BAX in RGCs is neuroprotective after acute injury. Damaged RGCs
enter a quiescent state months after injury and are no longer responsive to an
apoptotic stimulus. Quiescent RGCs will require rejuvenation to reacquire functionality.
acknowledgement: This work was supported by National Eye Institute grants R01 EY012223
(RWN), R01 EY030123 (RWN), T32 EY027721 (Department of Ophthalmology and Visual
Sciences, University of Wisconsin-Madison), and a Vision Science Core grant P30
EY016665 (Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison),
an unrestricted funding grant from Research to Prevent Blindness (Department of
Ophthalmology and Visual Sciences, University of Wisconsin-Madison), the Frederick
A. Davis Endowment (RWN), and the Mr. and Mrs. George Taylor Foundation (RWN).
article_processing_charge: No
article_type: original
author:
- first_name: RJ
full_name: Donahue, RJ
last_name: Donahue
- first_name: Margaret E
full_name: Maes, Margaret E
id: 3838F452-F248-11E8-B48F-1D18A9856A87
last_name: Maes
orcid: 0000-0001-9642-1085
- first_name: JA
full_name: Grosser, JA
last_name: Grosser
- first_name: RW
full_name: Nickells, RW
last_name: Nickells
citation:
ama: Donahue R, Maes ME, Grosser J, Nickells R. BAX-depleted retinal ganglion cells
survive and become quiescent following optic nerve damage. Molecular Neurobiology.
2020;57(2):1070–1084. doi:10.1007/s12035-019-01783-7
apa: Donahue, R., Maes, M. E., Grosser, J., & Nickells, R. (2020). BAX-depleted
retinal ganglion cells survive and become quiescent following optic nerve damage.
Molecular Neurobiology. Springer Nature. https://doi.org/10.1007/s12035-019-01783-7
chicago: Donahue, RJ, Margaret E Maes, JA Grosser, and RW Nickells. “BAX-Depleted
Retinal Ganglion Cells Survive and Become Quiescent Following Optic Nerve Damage.”
Molecular Neurobiology. Springer Nature, 2020. https://doi.org/10.1007/s12035-019-01783-7.
ieee: R. Donahue, M. E. Maes, J. Grosser, and R. Nickells, “BAX-depleted retinal
ganglion cells survive and become quiescent following optic nerve damage,” Molecular
Neurobiology, vol. 57, no. 2. Springer Nature, pp. 1070–1084, 2020.
ista: Donahue R, Maes ME, Grosser J, Nickells R. 2020. BAX-depleted retinal ganglion
cells survive and become quiescent following optic nerve damage. Molecular Neurobiology.
57(2), 1070–1084.
mla: Donahue, RJ, et al. “BAX-Depleted Retinal Ganglion Cells Survive and Become
Quiescent Following Optic Nerve Damage.” Molecular Neurobiology, vol. 57,
no. 2, Springer Nature, 2020, pp. 1070–1084, doi:10.1007/s12035-019-01783-7.
short: R. Donahue, M.E. Maes, J. Grosser, R. Nickells, Molecular Neurobiology 57
(2020) 1070–1084.
date_created: 2019-11-18T14:18:39Z
date_published: 2020-02-01T00:00:00Z
date_updated: 2023-08-17T14:05:48Z
day: '01'
department:
- _id: SaSi
doi: 10.1007/s12035-019-01783-7
external_id:
isi:
- '000493754200001'
pmid:
- '31673950'
intvolume: ' 57'
isi: 1
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7035206/
month: '02'
oa: 1
oa_version: Submitted Version
page: 1070–1084
pmid: 1
publication: Molecular Neurobiology
publication_identifier:
eissn:
- 1559-1182
issn:
- 0893-7648
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: BAX-depleted retinal ganglion cells survive and become quiescent following
optic nerve damage
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 57
year: '2020'
...
---
_id: '6997'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Yuzhou
full_name: Zhang, Yuzhou
id: 3B6137F2-F248-11E8-B48F-1D18A9856A87
last_name: Zhang
orcid: 0000-0003-2627-6956
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Zhang Y, Friml J. Auxin guides roots to avoid obstacles during gravitropic
growth. New Phytologist. 2020;225(3):1049-1052. doi:10.1111/nph.16203
apa: Zhang, Y., & Friml, J. (2020). Auxin guides roots to avoid obstacles during
gravitropic growth. New Phytologist. Wiley. https://doi.org/10.1111/nph.16203
chicago: Zhang, Yuzhou, and Jiří Friml. “Auxin Guides Roots to Avoid Obstacles during
Gravitropic Growth.” New Phytologist. Wiley, 2020. https://doi.org/10.1111/nph.16203.
ieee: Y. Zhang and J. Friml, “Auxin guides roots to avoid obstacles during gravitropic
growth,” New Phytologist, vol. 225, no. 3. Wiley, pp. 1049–1052, 2020.
ista: Zhang Y, Friml J. 2020. Auxin guides roots to avoid obstacles during gravitropic
growth. New Phytologist. 225(3), 1049–1052.
mla: Zhang, Yuzhou, and Jiří Friml. “Auxin Guides Roots to Avoid Obstacles during
Gravitropic Growth.” New Phytologist, vol. 225, no. 3, Wiley, 2020, pp.
1049–52, doi:10.1111/nph.16203.
short: Y. Zhang, J. Friml, New Phytologist 225 (2020) 1049–1052.
date_created: 2019-11-12T11:41:32Z
date_published: 2020-02-01T00:00:00Z
date_updated: 2023-08-17T14:01:49Z
day: '01'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.1111/nph.16203
ec_funded: 1
external_id:
isi:
- '000489638800001'
pmid:
- '31603260'
file:
- access_level: open_access
checksum: cd42ffdb381fd52812b9583d4d407139
content_type: application/pdf
creator: dernst
date_created: 2020-11-18T16:42:48Z
date_updated: 2020-11-18T16:42:48Z
file_id: '8772'
file_name: 2020_NewPhytologist_Zhang.pdf
file_size: 717345
relation: main_file
success: 1
file_date_updated: 2020-11-18T16:42:48Z
has_accepted_license: '1'
intvolume: ' 225'
isi: 1
issue: '3'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 1049-1052
pmid: 1
project:
- _id: 261099A6-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742985'
name: Tracing Evolution of Auxin Transport and Polarity in Plants
- _id: 26538374-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03630
name: Molecular mechanisms of endocytic cargo recognition in plants
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
publication: New Phytologist
publication_identifier:
eissn:
- 1469-8137
issn:
- 0028-646x
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Auxin guides roots to avoid obstacles during gravitropic growth
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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 225
year: '2020'
...
---
_id: '7149'
abstract:
- lang: eng
text: In recent years, many genes have been associated with chromatinopathies classified
as “Cornelia de Lange Syndrome‐like.” It is known that the phenotype of these
patients becomes less recognizable, overlapping to features characteristic of
other syndromes caused by genetic variants affecting different regulators of chromatin
structure and function. Therefore, Cornelia de Lange syndrome diagnosis might
be arduous due to the seldom discordance between unexpected molecular diagnosis
and clinical evaluation. Here, we review the molecular features of Cornelia de
Lange syndrome, supporting the hypothesis that “CdLS‐like syndromes” are part
of a larger “rare disease family” sharing multiple clinical features and common
disrupted molecular pathways.
acknowledgement: ' Dipartimento DiSS, Università degli Studi di Milano, Grant/Award
Number: Linea 2; Fondazione Cariplo, Grant/Award Number: 2015-0783; German Federal
Ministry of Education and Research (BMBF), Grant/Award Number: CHROMATIN-Net; Medical
Faculty of the University of Lübeck, Grant/Award Number: J09-2017; Nickel & Co S.p.A.;
Università degli Studi di Milano, Grant/Award Numbers: Molecular & Translational
Medicine PhD Scholarship, Translational Medicine PhD Scholarship'
article_processing_charge: No
article_type: review
author:
- first_name: Laura
full_name: Avagliano, Laura
last_name: Avagliano
- first_name: Ilaria
full_name: Parenti, Ilaria
id: D93538B0-5B71-11E9-AC62-02EBE5697425
last_name: Parenti
- first_name: Paolo
full_name: Grazioli, Paolo
last_name: Grazioli
- first_name: Elisabetta
full_name: Di Fede, Elisabetta
last_name: Di Fede
- first_name: Chiara
full_name: Parodi, Chiara
last_name: Parodi
- first_name: Milena
full_name: Mariani, Milena
last_name: Mariani
- first_name: Frank J.
full_name: Kaiser, Frank J.
last_name: Kaiser
- first_name: Angelo
full_name: Selicorni, Angelo
last_name: Selicorni
- first_name: Cristina
full_name: Gervasini, Cristina
last_name: Gervasini
- first_name: Valentina
full_name: Massa, Valentina
last_name: Massa
citation:
ama: 'Avagliano L, Parenti I, Grazioli P, et al. Chromatinopathies: A focus on Cornelia
de Lange syndrome. Clinical Genetics. 2020;97(1):3-11. doi:10.1111/cge.13674'
apa: 'Avagliano, L., Parenti, I., Grazioli, P., Di Fede, E., Parodi, C., Mariani,
M., … Massa, V. (2020). Chromatinopathies: A focus on Cornelia de Lange syndrome.
Clinical Genetics. Wiley. https://doi.org/10.1111/cge.13674'
chicago: 'Avagliano, Laura, Ilaria Parenti, Paolo Grazioli, Elisabetta Di Fede,
Chiara Parodi, Milena Mariani, Frank J. Kaiser, Angelo Selicorni, Cristina Gervasini,
and Valentina Massa. “Chromatinopathies: A Focus on Cornelia de Lange Syndrome.”
Clinical Genetics. Wiley, 2020. https://doi.org/10.1111/cge.13674.'
ieee: 'L. Avagliano et al., “Chromatinopathies: A focus on Cornelia de Lange
syndrome,” Clinical Genetics, vol. 97, no. 1. Wiley, pp. 3–11, 2020.'
ista: 'Avagliano L, Parenti I, Grazioli P, Di Fede E, Parodi C, Mariani M, Kaiser
FJ, Selicorni A, Gervasini C, Massa V. 2020. Chromatinopathies: A focus on Cornelia
de Lange syndrome. Clinical Genetics. 97(1), 3–11.'
mla: 'Avagliano, Laura, et al. “Chromatinopathies: A Focus on Cornelia de Lange
Syndrome.” Clinical Genetics, vol. 97, no. 1, Wiley, 2020, pp. 3–11, doi:10.1111/cge.13674.'
short: L. Avagliano, I. Parenti, P. Grazioli, E. Di Fede, C. Parodi, M. Mariani,
F.J. Kaiser, A. Selicorni, C. Gervasini, V. Massa, Clinical Genetics 97 (2020)
3–11.
date_created: 2019-12-04T16:10:59Z
date_published: 2020-01-01T00:00:00Z
date_updated: 2023-08-17T14:06:20Z
day: '01'
department:
- _id: GaNo
doi: 10.1111/cge.13674
external_id:
isi:
- '000562561800001'
pmid:
- '31721174'
intvolume: ' 97'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 3-11
pmid: 1
publication: Clinical Genetics
publication_identifier:
eissn:
- 1399-0004
issn:
- 0009-9163
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Chromatinopathies: A focus on Cornelia de Lange syndrome'
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 97
year: '2020'
...