Prodynorphin gene promoter polymorphism and temporal lobe epilepsy: A meta-analysis

Zhang, Na; Ouyang, Taohui; Zhou, Qing; Hj, Kang; Zhu, Suiqiang

doi:10.1007/s11596-015-1482-6

Cited by 6 publications

(4 citation statements)

References 26 publications

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“…This result was not replicated in four independent studies of the Caucasian population for TLE [ 134 , 188 , 207 , 208 ]. However, a meta-analysis suggested that the L-allele variant of this promoter polymorphism might contribute as a risk factor for familial-TLE suggesting that further studies are required for acquiring discrete results [ 209 ].…”

Section: Genetic Studies Of Common Epilepsiesmentioning

confidence: 99%

Genetic Landscape of Common Epilepsies: Advancing towards Precision in Treatment

Thakran

Guin

Singh

et al. 2020

IJMS

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Epilepsy, a neurological disease characterized by recurrent seizures, is highly heterogeneous in nature. Based on the prevalence, epilepsy is classified into two types: common and rare epilepsies. Common epilepsies affecting nearly 95% people with epilepsy, comprise generalized epilepsy which encompass idiopathic generalized epilepsy like childhood absence epilepsy, juvenile myoclonic epilepsy, juvenile absence epilepsy and epilepsy with generalized tonic-clonic seizure on awakening and focal epilepsy like temporal lobe epilepsy and cryptogenic focal epilepsy. In 70% of the epilepsy cases, genetic factors are responsible either as single genetic variant in rare epilepsies or multiple genetic variants acting along with different environmental factors as in common epilepsies. Genetic testing and precision treatment have been developed for a few rare epilepsies and is lacking for common epilepsies due to their complex nature of inheritance. Precision medicine for common epilepsies require a panoramic approach that incorporates polygenic background and other non-genetic factors like microbiome, diet, age at disease onset, optimal time for treatment and other lifestyle factors which influence seizure threshold. This review aims to comprehensively present a state-of-art review of all the genes and their genetic variants that are associated with all common epilepsy subtypes. It also encompasses the basis of these genes in the epileptogenesis. Here, we discussed the current status of the common epilepsy genetics and address the clinical application so far on evidence-based markers in prognosis, diagnosis, and treatment management. In addition, we assessed the diagnostic predictability of a few genetic markers used for disease risk prediction in individuals. A combination of deeper endo-phenotyping including pharmaco-response data, electro-clinical imaging, and other clinical measurements along with genetics may be used to diagnose common epilepsies and this marks a step ahead in precision medicine in common epilepsies management.

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Section: Genetic Studies Of Common Epilepsiesmentioning

confidence: 99%

Genetic Landscape of Common Epilepsies: Advancing towards Precision in Treatment

Thakran

Guin

Singh

et al. 2020

IJMS

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“…Genetic variants related to ion channels (e.g., SCN1A), calcium signaling (e.g., CALHM1), or neurotransmitter actions (e.g., GABBR1, 5-HTT) have all been linked to common epilepsies, including TLE [ 7 ]. Similarly, SNPs of key neuroregulatory genes were associated with TLE, including known epilepsy-associated genes NRG1 , BDNF , or the PDYN promoter (prodynorphin; [ 159 , 160 , 161 , 162 ]). Furthermore, psychiatric comorbidities increase the risk of acquiring epilepsy, suggesting common dysregulated molecular pathways involved in the pathogenesis of both [ 146 ].…”

Section: Genetic Predispositionmentioning

confidence: 99%

Molecular Genetics of Acquired Temporal Lobe Epilepsy

Neumann,

Britsch

2024

Biomolecules

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An epilepsy diagnosis reduces a patient’s quality of life tremendously, and it is a fate shared by over 50 million people worldwide. Temporal lobe epilepsy (TLE) is largely considered a nongenetic or acquired form of epilepsy that develops in consequence of neuronal trauma by injury, malformations, inflammation, or a prolonged (febrile) seizure. Although extensive research has been conducted to understand the process of epileptogenesis, a therapeutic approach to stop its manifestation or to reliably cure the disease has yet to be developed. In this review, we briefly summarize the current literature predominately based on data from excitotoxic rodent models on the cellular events proposed to drive epileptogenesis and thoroughly discuss the major molecular pathways involved, with a focus on neurogenesis-related processes and transcription factors. Furthermore, recent investigations emphasized the role of the genetic background for the acquisition of epilepsy, including variants of neurodevelopmental genes. Mutations in associated transcription factors may have the potential to innately increase the vulnerability of the hippocampus to develop epilepsy following an injury—an emerging perspective on the epileptogenic process in acquired forms of epilepsy.

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“…The steady-state procedure focuses on the open-water performance and steady-state structural deformation of the composite propeller in a uniform flow field. Shuai Zhang et al [3] used CFD (computational fluid dynamics) method to calculate the open-water performance of 438X (X = 1,2,3) series composite propellers. The pitch changed due to elastic deformation, which mainly affected the hydrodynamic performance.…”

Section: Introductionmentioning

confidence: 99%

The Scale Effect Study on the Transient Fluid–Structure Coupling Performance of Composite Propellers

Huang

Chen

Zhang

et al. 2022

JMSE

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In order to predict the fluid–structure coupling performance of a full-scale composite propeller under a wake flow field behind a full ship, a bidirectional transient fluid–structure coupling algorithm was established. The performance includes the transient fluid–structure coupling deformation, structural natural frequency, and unsteady hydrodynamic performance. The results showed that the circumferential non-uniform wake flow field can cause periodic pulsation of the propeller’s hydrodynamic force. The average values of thrust and torque coefficient increase, while the pulsation ratio decreases with the increase in scale. The maximum deformation ratio of fluid–structure coupling is linearly related to the scale ratio. Due to the influence of fluid-added stiffness, the maximum deformation ratio needs to be modified by 3% based on the cantilever plate deflection formula. The first five natural frequencies of dry mode and wet mode decrease with the increasing scale, and the wet natural frequencies of each order decrease by 60~68% compared with dry mode. The fluid–structure coupling hydrodynamic performance still show a periodic pulsation with the phase angle, and its average value increases linearly with the scale ratio, while the pulsation ratio decreases with the power relationship of the scale ratio.

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Prodynorphin gene promoter polymorphism and temporal lobe epilepsy: A meta-analysis

Cited by 6 publications

References 26 publications

Genetic Landscape of Common Epilepsies: Advancing towards Precision in Treatment

Genetic Landscape of Common Epilepsies: Advancing towards Precision in Treatment

Molecular Genetics of Acquired Temporal Lobe Epilepsy

The Scale Effect Study on the Transient Fluid–Structure Coupling Performance of Composite Propellers

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