Evidence map›Paper›PMID 37103687›Full record

ArticleMolecular neurobiology2023

Aberrant adenosine signaling in patients with focal cortical dysplasia.

Mengyi Guo, Jing Zhang, Jing Wang, Xiongfei Wang, Qing Gao, Chongyang Tang, Jiahui Deng, Zhonghua Xiong, Xiangru Kong, Yuguang Guan and 4 more

Open access · greenAbstract read
In one paragraph

Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

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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

14 authors at 2 institutions in 2 countries.

Mengyi Guo *Department of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Jing Zhang *Department of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Jing Wang *Department of Neurology, Center of Epilepsy, Beijing Institute for Brain Disorders, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Xiongfei WangDepartment of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Qing GaoDepartment of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Chongyang TangDepartment of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Jiahui DengDepartment of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Zhonghua XiongDepartment of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Xiangru KongDepartment of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Yuguang GuanDepartment of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Jian ZhouDepartment of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China.
Detlev BoisonDepartment of Neurosurgery, Robert Wood Johnson & New Jersey Medical Schools, Rutgers University, Piscataway, NJ, 08854, USA.
Guoming LuanDepartment of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China. luangm@ccmu.edu.cn.ORCID http://orcid.org/0000-0002-9674-6549
Tianfu LiDepartment of Brain Institute, Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing Key Laboratory of Epilepsy Research, Sanbo Brain Hospital, Capital Medical University, Beijing, 100093, China. tianfuli@ccmu.edu.cn.ORCID http://orcid.org/0000-0002-0883-4988
Capital Medical University · CNRutgers, The State University of New Jersey · US

Funding

The Role of Adenosine in Ketogenic Diet TherapyR01NS065957 · NINDS · TRINITY COLLEGE · PI BOISON, DETLEV, GEIGER, JONATHAN DAVID · 2010 to 2021
$3.9M
Therapies for Epilepsy Prevention - Focus on AdenosineR01NS127846 · NINDS · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI Detlev Boison · 2022 to 2026
$2.1M
Adenosine receptor mediated therapies for SUDEPR01NS103740 · NINDS · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI BOISON, DETLEV · 2018 to 2022
$1.7M
NINDS NIH HHS R01 NS065957NINDS NIH HHS R01 NS103740NINDS NIH HHS R01 NS127846
6 · The paper itself

Abstract

Focal cortical dysplasia (FCD), a common malformation of cortical development, is frequently associated with pharmacoresistant epilepsy in both children and adults. Adenosine is an inhibitory modulator of brain activity and a prospective anti-seizure agent with potential for clinical translation. Our previous results demonstrated that the major adenosine-metabolizing enzyme adenosine kinase (ADK) was upregulated in balloon cells (BCs) within FCD type IIB lesions, suggesting that dysfunction of the adenosine system is implicated in the pathophysiology of FCD. In our current study, we therefore performed a comprehensive analysis of adenosine signaling in surgically resected cortical specimens from patients with FCD type I and type II via immunohistochemistry and immunoblot analysis. Adenosine enzyme signaling was assessed by quantifying the levels of the key enzymes of adenosine metabolism, i.e., ADK, adenosine deaminase (ADA), and ecto-5'-nucleotidase (CD73). Adenosine receptor signaling was assessed by quantifying the levels of adenosine A

Indexed as

EpilepsyFocal Cortical DysplasiaMalformations of Cortical DevelopmentMalformations of Cortical Development, Group IAdultChildHumansSignal TransductionTOR Serine-Threonine KinasesTOR Serine-Threonine KinasesAdenosine A2A receptorAdenosine kinaseBalloon cellEpilepsyFocal cortical dysplasia

Identifiers

PMID37103687
PMCPMC10330374
OpenAlexW4367175261

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.