ORCID Profile
0000-0002-4338-314X
Current Organisations
University College London Hospitals NHS Foundation Trust
,
Dalian Institute of Chemical Physics
,
Azienda Ospedaliero Universitaria Meyer
,
UCL Queen Square Institute of Neurology
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Publisher: Elsevier BV
Date: 06-2021
Publisher: Royal Society of Chemistry (RSC)
Date: 2019
DOI: 10.1039/C9TA03810H
Abstract: A novel channel-enhanced strategy upon atomic substitution via a dealloying process for the improved Na storage of alloying-type anodes for SIBs.
Publisher: Springer Science and Business Media LLC
Date: 20-07-2023
DOI: 10.1038/S41467-023-39539-6
Abstract: Copy number variants (CNV) are established risk factors for neurodevelopmental disorders with seizures or epilepsy. With the hypothesis that seizure disorders share genetic risk factors, we pooled CNV data from 10,590 in iduals with seizure disorders, 16,109 in iduals with clinically validated epilepsy, and 492,324 population controls and identified 25 genome-wide significant loci, 22 of which are novel for seizure disorders, such as deletions at 1p36.33, 1q44, 2p21-p16.3, 3q29, 8p23.3-p23.2, 9p24.3, 10q26.3, 15q11.2, 15q12-q13.1, 16p12.2, 17q21.31, duplications at 2q13, 9q34.3, 16p13.3, 17q12, 19p13.3, 20q13.33, and reciprocal CNVs at 16p11.2, and 22q11.21. Using genetic data from additional 248,751 in iduals with 23 neuropsychiatric phenotypes, we explored the pleiotropy of these 25 loci. Finally, in a subset of in iduals with epilepsy and detailed clinical data available, we performed phenome-wide association analyses between in idual CNVs and clinical annotations categorized through the Human Phenotype Ontology (HPO). For six CNVs, we identified 19 significant associations with specific HPO terms and generated, for all CNVs, phenotype signatures across 17 clinical categories relevant for epileptologists. This is the most comprehensive investigation of CNVs in epilepsy and related seizure disorders, with potential implications for clinical practice.
Publisher: Elsevier BV
Date: 10-2016
Publisher: Springer Science and Business Media LLC
Date: 29-10-2019
DOI: 10.1038/S41467-019-12671-Y
Abstract: Familial Adult Myoclonic Epilepsy (FAME) is characterised by cortical myoclonic tremor usually from the second decade of life and overt myoclonic or generalised tonic-clonic seizures. Four independent loci have been implicated in FAME on chromosomes (chr) 2, 3, 5 and 8. Using whole genome sequencing and repeat primed PCR, we provide evidence that chr2-linked FAME (FAME2) is caused by an expansion of an ATTTC pentamer within the first intron of STARD7 . The ATTTC expansions segregate in 158/158 in iduals typically affected by FAME from 22 pedigrees including 16 previously reported families recruited worldwide. RNA sequencing from patient derived fibroblasts shows no accumulation of the AUUUU or AUUUC repeat sequences and STARD7 gene expression is not affected. These data, in combination with other genes bearing similar mutations that have been implicated in FAME, suggest ATTTC expansions may cause this disorder, irrespective of the genomic locus involved.
Publisher: Elsevier BV
Date: 09-2015
Publisher: Wiley
Date: 23-03-2017
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 08-06-2016
Publisher: Wiley
Date: 16-07-2018
DOI: 10.1111/EPI.14516
Publisher: Oxford University Press (OUP)
Date: 03-04-2023
Abstract: Dravet syndrome is an archetypal rare severe epilepsy, considered ‘monogenic’, typically caused by loss-of-function SCN1A variants. Despite a recognizable core phenotype, its marked phenotypic heterogeneity is incompletely explained by differences in the causal SCN1A variant or clinical factors. In 34 adults with SCN1A-related Dravet syndrome, we show additional genomic variation beyond SCN1A contributes to phenotype and its ersity, with an excess of rare variants in epilepsy-related genes as a set and ex les of blended phenotypes, including one in idual with an ultra-rare DEPDC5 variant and focal cortical dysplasia. The polygenic risk score for intelligence was lower, and for longevity, higher, in Dravet syndrome than in epilepsy controls. The causal, major-effect, SCN1A variant may need to act against a broadly compromised genomic background to generate the full Dravet syndrome phenotype, whilst genomic resilience may help to ameliorate the risk of premature mortality in adult Dravet syndrome survivors.
Publisher: Wiley
Date: 16-01-2018
Abstract: The electrochemical performance of the aluminum-sulfur (Al-S) battery has very poor reversibility and a low charge/discharge current density owing to slow kinetic processes determined by an inevitable dissociation reaction from Al
Publisher: Springer Science and Business Media LLC
Date: 05-02-2019
DOI: 10.1038/S41467-019-08422-8
Abstract: Due to the high theoretical specific energy, the lithium–oxygen battery has been heralded as a promising energy storage system for applications such as electric vehicles. However, its large over-potentials during discharge–charge cycling lead to the formation of side-products, and short cycle life. Herein, we report an ionic liquid bearing the redox active 2,2,6,6-tetramethyl-1-piperidinyloxy moiety, which serves multiple functions as redox mediator, oxygen shuttle, lithium anode protector, as well as electrolyte solvent. The additive contributes a 33-fold increase of the discharge capacity in comparison to a pure ether-based electrolyte and lowers the over-potential to an exceptionally low value of 0.9 V. Meanwhile, its molecule facilitates smooth lithium plating/stripping, and promotes the formation of a stable solid electrolyte interface to suppress side-reactions. Moreover, the proportion of ionic liquid in the electrolyte influences the reaction mechanism, and a high proportion leads to the formation of amorphous lithium peroxide and a long cycling life ( 200 cycles). In particular, it enables an outstanding electrochemical performance when operated in air.
Publisher: Wiley
Date: 03-08-2021
DOI: 10.1002/ANA.26174
Abstract: Psychoses affecting people with epilepsy increase disease burden and diminish quality of life. We characterized postictal psychosis, which comprises about one quarter of epilepsy‐related psychoses, and has unknown causation. We conducted a case–control cohort study including patients diagnosed with postictal psychosis, confirmed by psychiatric assessment, with available data regarding epilepsy, treatment, psychiatric history, psychosis profile, and outcomes. After screening 3,288 epilepsy patients, we identified 83 with psychosis 49 had postictal psychosis. Controls were 98 adults, matched by age and epilepsy type, with no history of psychosis. Logistic regression was used to investigate clinical factors associated with postictal psychosis univariate associations with a p value 0.20 were used to build a multivariate model. Polygenic risk scores for schizophrenia were calculated. Cases were more likely to have seizure clustering (odds ratio [OR] = 7.59, p 0.001), seizures with a recollected aura (OR = 2.49, p = 0.013), and a family history of psychiatric disease (OR = 5.17, p = 0.022). Cases showed predominance of right temporal epileptiform discharges (OR = 4.87, p = 0.007). There was no difference in epilepsy duration, neuroimaging findings, or antiseizure treatment between cases and controls. Polygenic risk scores for schizophrenia in an extended cohort of postictal psychosis cases (n = 58) were significantly higher than in 1,366 epilepsy controls ( R 2 = 3%, p = 6 × 10 −3 ), but not significantly different from 945 independent patients with schizophrenia ( R 2 = 0.1% , p = 0.775). Postictal psychosis occurs under particular circumstances in people with epilepsy with a heightened genetic predisposition to schizophrenia, illustrating how disease biology (seizures) and trait susceptibility (schizophrenia) may interact to produce particular outcomes (postictal psychosis) in a common disease. ANN NEUROL 2021 :464–476
Publisher: Elsevier BV
Date: 03-2021
Publisher: Elsevier BV
Date: 10-2021
Publisher: Wiley
Date: 2005
Publisher: Elsevier BV
Date: 08-2023
Publisher: American Chemical Society (ACS)
Date: 16-10-2019
Abstract: Rational control of the components of noble metal alloys is paramount for achieving satisfactory electrocatalytic performances. Though transition metals are commonly used to modify noble metals, many potential elements remain to be explored. Here, we interstitially modulate hydrogen atoms into RhPd nanoparticles to boost the alkaline hydrogen evolution reaction (HER). The obtained stable RhPd-H nanoparticles exhibit pronounced alkaline HER activity with a small overpotential of 36.6 mV at 10 mA cm
Publisher: Wiley
Date: 04-04-2017
Abstract: As a new family member of room-temperature aprotic metal-O
Publisher: American Association for the Advancement of Science (AAAS)
Date: 21-01-2022
Abstract: The advancement of lithium-oxygen (Li-O 2 ) batteries has been hindered by challenges including low discharge capacity, poor energy efficiency, severe parasitic reactions, etc. We report an Li-O 2 battery operated via a new quenching/mediating mechanism that relies on the direct chemical reactions between a versatile molecule and superoxide radical/Li 2 O 2 . The battery exhibits a 46-fold increase in discharge capacity, a low charge overpotential of 0.7 V, and an ultralong cycle life cycles. Featuring redox-active 2,2,6,6-tetramethyl-1-piperidinyloxy moieties bridged by a quenching-active perylene diimide backbone, the tailor-designed molecule acts as a redox mediator to catalyze discharge/charge reactions and serves as a reusable superoxide quencher to chemically react with superoxide species generated during battery operation. The all-in-one molecule can simultaneously tackle issues of parasitic reactions associated with superoxide radicals, singlet oxygen, high overpotentials, and lithium corrosion. The molecular design of multifunctional additives combining various capabilities opens a new avenue for developing high-performance Li-O 2 batteries.
Publisher: Wiley
Date: 03-05-2022
DOI: 10.1111/EPI.17237
Abstract: Epilepsy syndromes have been recognized for >50 years, as distinct electroclinical phenotypes with therapeutic and prognostic implications. Nonetheless, no formally accepted International League Against Epilepsy (ILAE) classification of epilepsy syndromes has existed. The ILAE Task Force on Nosology and Definitions was established to reach consensus regarding which entities fulfilled criteria for an epilepsy syndrome and to provide definitions for each syndrome. We defined an epilepsy syndrome as "a characteristic cluster of clinical and electroencephalographic features, often supported by specific etiological findings (structural, genetic, metabolic, immune, and infectious)." The diagnosis of a syndrome in an in idual with epilepsy frequently carries prognostic and treatment implications. Syndromes often have age-dependent presentations and a range of specific comorbidities. This paper describes the guiding principles and process for syndrome identification in both children and adults, and the template of clinical data included for each syndrome. We ided syndromes into typical age at onset, and further characterized them based on seizure and epilepsy types and association with developmental and/or epileptic encephalopathy or progressive neurological deterioration. Definitions for each specific syndrome are contained within the corresponding position papers.
Publisher: Elsevier BV
Date: 08-2019
Publisher: Springer Science and Business Media LLC
Date: 07-2016
DOI: 10.1038/AM.2016.91
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 10-09-2020
DOI: 10.1212/WNL.0000000000010794
Abstract: To define the risks and consequences of cardiac abnormalities in ATP1A3 -related syndromes. Patients meeting clinical diagnostic criteria for rapid-onset dystonia-parkinsonism (RDP), alternating hemiplegia of childhood (AHC), and cerebellar ataxia, areflexia, pes cavus, optic atrophy, and sensorineural hearing loss (CAPOS) with ATP1A3 genetic analysis and at least 1 cardiac assessment were included. We evaluated the cardiac phenotype in an Atp1a3 knock-in mouse (Mashl +/− ) to determine the sequence of events in seizure-related cardiac death. Ninety-eight patients with AHC, 9 with RDP, and 3 with CAPOS (63 female, mean age 17 years) were included. Resting ECG abnormalities were found in 52 of 87 (60%) with AHC, 2 of 3 (67%) with CAPOS, and 6 of 9 (67%) with RDP. Serial ECGs showed dynamic changes in 10 of 18 patients with AHC. The first Holter ECG was abnormal in 24 of 65 (37%) cases with AHC and RDP with either repolarization or conduction abnormalities. Echocardiography was normal. Cardiac intervention was required in 3 of 98 (≈3%) patients with AHC. In the mouse model, resting ECGs showed intracardiac conduction delay during induced seizures, heart block or complete sinus arrest led to death. We found increased prevalence of ECG dynamic abnormalities in all ATP1A3 -related syndromes, with a risk of life-threatening cardiac rhythm abnormalities equivalent to that in established cardiac channelopathies (≈3%). Sudden cardiac death due to conduction abnormality emerged as a seizure-related outcome in murine Atp1a3 -related disease. ATP1A3 -related syndromes are cardiac diseases and neurologic diseases. We provide guidance to identify patients potentially at higher risk of sudden cardiac death who may benefit from insertion of a pacemaker or implantable cardioverter-defibrillator.
Publisher: Elsevier BV
Date: 05-2004
Publisher: Oxford University Press (OUP)
Date: 22-06-2020
Abstract: Cytogenic testing is routinely applied in most neurological centres for severe paediatric epilepsies. However, which characteristics of copy number variants (CNVs) confer most epilepsy risk and which epilepsy subtypes carry the most CNV burden, have not been explored on a genome-wide scale. Here, we present the largest CNV investigation in epilepsy to date with 10 712 European epilepsy cases and 6746 ancestry-matched controls. Patients with genetic generalized epilepsy, lesional focal epilepsy, non-acquired focal epilepsy, and developmental and epileptic encephalopathy were included. All s les were processed with the same technology and analysis pipeline. All investigated epilepsy types, including lesional focal epilepsy patients, showed an increase in CNV burden in at least one tested category compared to controls. However, we observed striking differences in CNV burden across epilepsy types and investigated CNV categories. Genetic generalized epilepsy patients have the highest CNV burden in all categories tested, followed by developmental and epileptic encephalopathy patients. Both epilepsy types also show association for deletions covering genes intolerant for truncating variants. Genome-wide CNV breakpoint association showed not only significant loci for genetic generalized and developmental and epileptic encephalopathy patients but also for lesional focal epilepsy patients. With a 34-fold risk for developing genetic generalized epilepsy, we show for the first time that the established epilepsy-associated 15q13.3 deletion represents the strongest risk CNV for genetic generalized epilepsy across the whole genome. Using the human interactome, we examined the largest connected component of the genes overlapped by CNVs in the four epilepsy types. We observed that genetic generalized epilepsy and non-acquired focal epilepsy formed disease modules. In summary, we show that in all common epilepsy types, 1.5–3% of patients carry epilepsy-associated CNVs. The characteristics of risk CNVs vary tremendously across and within epilepsy types. Thus, we advocate genome-wide genomic testing to identify all disease-associated types of CNVs.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Zhangquan Peng.