Evidence map›Paper›PMID 34403849›Full record

ArticleBiomaterials2021

Bioengineered optogenetic model of human neuromuscular junction.

Olaia F Vila, Miguel Chavez, Stephen P Ma, Keith Yeager, Lyandysha V Zholudeva, Jennifer M Colón-Mercado, Yihuai Qu, Trevor R Nash, Carmen Lai, Carissa M Feliciano and 7 more

Open access · greenAbstract read
In one paragraph

Article in Biomaterials, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 43 citations in OpenAlex.

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  14. Optimization of Application-Driven Development ofTissue engineering. Part B, Reviews · 2022
    Review
  15. Article
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  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 1 country.

Olaia F VilaColumbia University, 622 W 168th St, New York, NY, 10032, USA; Gladstone Institutes, 1650 Owens St, San Francisco, CA, 94158, USA. Electronic address: olaia.vila@gladstone.ucsf.edu.
Miguel ChavezColumbia University, 622 W 168th St, New York, NY, 10032, USA.
Stephen P MaColumbia University, 622 W 168th St, New York, NY, 10032, USA.
Keith YeagerColumbia University, 622 W 168th St, New York, NY, 10032, USA.
Lyandysha V ZholudevaGladstone Institutes, 1650 Owens St, San Francisco, CA, 94158, USA.
Jennifer M Colón-MercadoNational Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, 20892, USA.
Yihuai QuColumbia University, 622 W 168th St, New York, NY, 10032, USA.
Trevor R NashColumbia University, 622 W 168th St, New York, NY, 10032, USA.
Carmen LaiGladstone Institutes, 1650 Owens St, San Francisco, CA, 94158, USA.
Carissa M FelicianoGladstone Institutes, 1650 Owens St, San Francisco, CA, 94158, USA; Department of Pediatrics, UCSF, 550 16th St, Floor 5, San Francisco, CA, 94143, USA.
Matthew CarterGladstone Institutes, 1650 Owens St, San Francisco, CA, 94158, USA.
Roger D KammDepartment of Mechanical Engineering and Biological Engineering, Massachusetts Institute of Technology, Cambridge MA, 02139, USA.
Luke M JudgeGladstone Institutes, 1650 Owens St, San Francisco, CA, 94158, USA; Department of Pediatrics, UCSF, 550 16th St, Floor 5, San Francisco, CA, 94143, USA.
Bruce R ConklinGladstone Institutes, 1650 Owens St, San Francisco, CA, 94158, USA.
Michael E WardNational Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD, 20892, USA.
Todd C McDevittGladstone Institutes, 1650 Owens St, San Francisco, CA, 94158, USA.
Gordana Vunjak-NovakovicColumbia University, 622 W 168th St, New York, NY, 10032, USA. Electronic address: gv2131@columbia.edu.
Gladstone Institutes · USColumbia University · USNational Institute of Neurological Disorders and Stroke · USMassachusetts Institute of Technology · US

Funding

Transcriptional Networks During Cardiac DifferentiationP01HL089707 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI SRIVASTAVA, DEEPAK · 2008 to 2017
$20.4M
Tissue Engineering Resource Center: TTDP41EB027062 · NIBIB · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Gordana Vunjak-Novakovic · 2019 to 2026
$12.6M
Multi-tissue platform for modeling systemic pathologiesUH3EB025765 · NIBIB · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI VUNJAK-NOVAKOVIC, GORDANA · 2019 to 2021
$4.0M
Multi-tissue platform for modeling systemic pathologiesUG3EB025765 · NIBIB · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI VUNJAK-NOVAKOVIC, GORDANA · 2017 to 2019
$2.8M
JAX-Gladstone, SCGE Disease Models Studies SupplementU01ES032673 · NIEHS · J. DAVID GLADSTONE INSTITUTES · PI CONKLIN, BRUCE R · 2020 to 2022
$2.4M
Protein quality control, cardiomyopathy, cardiotoxicity and human isogenic iPSCsR01HL135358 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI CONKLIN, BRUCE R · 2017 to 2020
$2.0M
NHLBI NIH HHS P01 HL089707NHLBI NIH HHS R01 HL135358NIBIB NIH HHS P41 EB027062NIBIB NIH HHS UG3 EB025765NIBIB NIH HHS UH3 EB025765NIEHS NIH HHS U01 ES032673
6 · The paper itself

Abstract

Functional human tissues engineered from patient-specific induced pluripotent stem cells (hiPSCs) hold great promise for investigating the progression, mechanisms, and treatment of musculoskeletal diseases in a controlled and systematic manner. For example, bioengineered models of innervated human skeletal muscle could be used to identify novel therapeutic targets and treatments for patients with complex central and peripheral nervous system disorders. There is a need to develop standardized and objective quantitative methods for engineering and using these complex tissues, in order increase their robustness, reproducibility, and predictiveness across users. Here we describe a standardized method for engineering an isogenic, patient specific human neuromuscular junction (NMJ) that allows for automated quantification of NMJ function to diagnose disease using a small sample of blood serum and evaluate new therapeutic modalities. By combining tissue engineering, optogenetics, microfabrication, optoelectronics and video processing, we created a novel platform for the precise investigation of the development and degeneration of human NMJ. We demonstrate the utility of this platform for the detection and diagnosis of myasthenia gravis, an antibody-mediated autoimmune disease that disrupts the NMJ function.

Indexed as

Induced Pluripotent Stem CellsOptogeneticsHumansMuscle, SkeletalNeuromuscular JunctionReproducibility of ResultsDisease modelingHuman tissue modelsiPS cellsMyasthenia gravisNeuromuscular junctionOptogenetics

Identifiers

PMID34403849
PMCPMC8439334
OpenAlexW3190440603

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.