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Article ; Online: Shisa7-Dependent Regulation of GABA

Castellano, David / Wu, Kunwei / Keramidas, Angelo / Lu, Wei

The Journal of neuroscience : the official journal of the Society for Neuroscience

2022 Volume 42, Issue 47, Page(s) 8758–8766

Abstract: ... ...

Abstract	GABA
MeSH term(s)	Humans ; Receptors, GABA-A/metabolism ; Kinetics ; HEK293 Cells ; Membrane Proteins/metabolism ; Carrier Proteins/metabolism ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Receptors, GABA-A ; Membrane Proteins ; Carrier Proteins ; gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2022-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.0510-22.2022
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Article: Use of Chalcogenide-Semiconductor-Sensitized Titania to Directly Charge a Vanadium Redox Battery.

Santos Andrade, Tatiana / Keramidas, Anastasios / Lianos, Panagiotis

Nanomaterials (Basel, Switzerland)

2020 Volume 10, Issue 6

Abstract: Unmediated charging of a battery using solar radiation is a very attractive project of solar energy conversion and storage. In the present work, solar energy was converted into electricity using a photocatalytic fuel cell operating with a chalcogenide- ... ...

Abstract	Unmediated charging of a battery using solar radiation is a very attractive project of solar energy conversion and storage. In the present work, solar energy was converted into electricity using a photocatalytic fuel cell operating with a chalcogenide-semiconductor-sensitized nanoparticulate titania photoanode and an air-cathode functioning by oxygen reduction. This cell produced sufficient energy to directly charge a vanadium redox battery functioning with a VOSO
Language	English
Publishing date	2020-06-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662255-5
ISSN	2079-4991
ISSN	2079-4991
DOI	10.3390/nano10061137
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Article: The development and initial validation of the White Fragility Scale.

Langrehr, Kimberly J / Watson, Laurel B / Keramidas, Alexa / Middleton, Sarah

Journal of counseling psychology

2021 Volume 68, Issue 4, Page(s) 404–417

Abstract: Over the last couple of years, the topic of White fragility has garnered a considerable degree of attention. White fragility is considered a state in which even a minimum amount of racial stress can become intolerable and trigger a range of emotional and ...

Abstract	Over the last couple of years, the topic of White fragility has garnered a considerable degree of attention. White fragility is considered a state in which even a minimum amount of racial stress can become intolerable and trigger a range of emotional and behavioral reactions intended to restore a sense of racial comfort (DiAngelo, White fragility: Why it's so hard for White people to talk about racism, 2018, Beacon Press). In effort to measure the expression of White fragility, we developed and evaluated the psychometric properties of the 21-item White Fragility Scale (WFS). Data consisted of two independent samples of White participants recruited from M-Turk (327) and a Midwest University's Psychpool (234). Results from exploratory and confirmatory factor analyses provided evidence for a bifactor model consisting of one general White fragility factor and three specific factors of Emotional Defensiveness, Accommodation of Safety, and Exceptionism. Ancillary bifactor indices supported treating the WFS as a unidimensional measure of White fragility yet also revealed meaningful utility of the Accommodation of Safety subscale. Concurrent validity evidence for the WFS was established through significant associations with modern racism, general and specific dimensions of colorblind racial attitudes, and social dominance orientation. In addition, nonsignificant, near-zero correlations with social desirability provided support for divergent validity. Recommendations for future research involving the WFS are provided as well as practical implications for professionals whose work requires a certain degree of racial stamina. (PsycInfo Database Record (c) 2021 APA, all rights reserved).
MeSH term(s)	Factor Analysis, Statistical ; Humans ; Psychometrics ; Racism ; Reproducibility of Results ; Surveys and Questionnaires
Language	English
Publishing date	2021-05-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2066555-6
ISSN	1939-2168 ; 0022-0167
ISSN (online)	1939-2168
ISSN	0022-0167
DOI	10.1037/cou0000483
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Article ; Online: Design and Modulation of Selectivity toward Vanadium(V) and Uranium(VI) Ions: Coordination Properties and Affinity of Hydroxylamino-Triazine Siderophores.

Amoiridis, Angelos / Papanikolaou, Michael / Vlasiou, Manolis / Bandeira, Nuno A G / Miras, Haralampos N / Kabanos, Themistoklis / Keramidas, Anastasios

Inorganic chemistry

2023 Volume 62, Issue 49, Page(s) 19971–19985

Abstract: Based on the strong binding and high selectivity properties of 2,6-bis[hydroxy(methyl)amino]-4-morpholino-1,3,5-triazine ( ... ...

Abstract	Based on the strong binding and high selectivity properties of 2,6-bis[hydroxy(methyl)amino]-4-morpholino-1,3,5-triazine (H
Language	English
Publishing date	2023-11-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	1484438-2
ISSN	1520-510X ; 0020-1669
ISSN (online)	1520-510X
ISSN	0020-1669
DOI	10.1021/acs.inorgchem.3c02678
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Article ; Online: Erythromelalgia caused by the missense mutation p.Arg220Pro in an alternatively spliced exon of SCN9A (NaV1.7).

Deuis, Jennifer R / Kumble, Smitha / Keramidas, Angelo / Ragnarsson, Lotten / Simons, Cas / Pais, Lynn / White, Susan M / Vetter, Irina

Human molecular genetics

2023 Volume 33, Issue 2, Page(s) 103–109

Abstract: Erythromelalgia (EM), is a familial pain syndrome characterized by episodic 'burning' pain, warmth, and erythema. EM is caused by monoallelic variants in SCN9A, which encodes the voltage-gated sodium channel (NaV) NaV1.7. Over 25 different SCN9A ... ...

Abstract	Erythromelalgia (EM), is a familial pain syndrome characterized by episodic 'burning' pain, warmth, and erythema. EM is caused by monoallelic variants in SCN9A, which encodes the voltage-gated sodium channel (NaV) NaV1.7. Over 25 different SCN9A mutations attributed to EM have been described to date, all identified in the SCN9A transcript utilizing exon 6N. Here we report a novel SCN9A missense variant identified in seven related individuals with stereotypic episodes of bilateral lower limb pain presenting in childhood. The variant, XM_011511617.3:c.659G>C;p.(Arg220Pro), resides in the exon 6A of SCN9A, an exon previously shown to be selectively incorporated by developmentally regulated alternative splicing. The mutation is located in the voltage-sensing S4 segment of domain I, which is important for regulating channel activation. Functional analysis showed the p.Arg220Pro mutation altered voltage-dependent activation and delayed channel inactivation, consistent with a NaV1.7 gain-of-function molecular phenotype. These results demonstrate that alternatively spliced isoforms of SCN9A should be included in all genomic testing of EM.
MeSH term(s)	Humans ; Erythromelalgia/genetics ; Mutation, Missense/genetics ; NAV1.7 Voltage-Gated Sodium Channel/genetics ; Pain/genetics ; Mutation ; Exons/genetics
Chemical Substances	NAV1.7 Voltage-Gated Sodium Channel ; SCN9A protein, human
Language	English
Publishing date	2023-09-16
Publishing country	England
Document type	Journal Article
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddad152
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Article ; Online: Correlations of receptor desensitization of gain-of-function GABRB3 variants with clinical severity.

Lin, Susan X N / Ahring, Philip K / Keramidas, Angelo / Liao, Vivian W Y / Møller, Rikke S / Chebib, Mary / Absalom, Nathan L

Brain : a journal of neurology

2023 Volume 147, Issue 1, Page(s) 224–239

Abstract: Genetic variants associated with developmental and epileptic encephalopathies have been identified in the GABRB3 gene that encodes the β3 subunit of GABAA receptors. Typically, variants alter receptor sensitivity to GABA resulting in either gain- or loss- ...

Abstract	Genetic variants associated with developmental and epileptic encephalopathies have been identified in the GABRB3 gene that encodes the β3 subunit of GABAA receptors. Typically, variants alter receptor sensitivity to GABA resulting in either gain- or loss-of-function, which correlates with patient phenotypes. However, it is unclear how another important receptor property, desensitization, contributes to the greater clinical severity of gain-of-function variants. Desensitization properties of 20 gain-of-function GABRB3 variant receptors were evaluated using two-electrode voltage-clamp electrophysiology. The parameters measured included current decay rates and steady-state currents. Selected variants with increased or reduced desensitization were also evaluated using whole-cell electrophysiology in transfected mammalian cell lines. Of the 20 gain-of-function variants assessed, 13 were found to alter receptor desensitization properties. Seven variants reduced desensitization at equilibrium, which acts to worsen gain-of-function traits. Six variants accelerated current decay kinetics, which limits gain-of-function traits. All affected patients displayed severe clinical phenotypes with intellectual disability and difficult-to-treat epilepsy. Nevertheless, variants that reduced desensitization at equilibrium were associated with more severe clinical outcomes. This included younger age of first seizure onset (median 0.5 months), movement disorders (dystonia and dyskinesia), epilepsy of infancy with migrating focal seizures (EIMFS) and risk of early mortality. Variants that accelerated current decay kinetics were associated with slightly milder phenotypes with later seizure onset (median 4 months), unclassifiable developmental and epileptic encephalopathies or Lennox-Gastaut syndrome and no movement disorders. Our study reveals that gain-of-function GABRB3 variants can increase or decrease receptor desensitization properties and that there is a correlation with the degree of disease severity. Variants that reduced the desensitization at equilibrium were clustered in the transmembrane regions that constitute the channel pore and correlated with greater disease severity, while variants that accelerated current decay were clustered in the coupling loops responsible for receptor activation and correlated with lesser severity.
MeSH term(s)	Animals ; Humans ; Infant, Newborn ; Gain of Function Mutation ; Mutation/genetics ; Epilepsy/genetics ; Seizures ; Epilepsy, Generalized ; Movement Disorders ; Mammals/metabolism ; Receptors, GABA-A/genetics ; Receptors, GABA-A/metabolism
Chemical Substances	GABRB3 protein, human ; Receptors, GABA-A
Language	English
Publishing date	2023-08-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awad285
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Article ; Online: The effects of insecticides on two splice variants of the glutamate-gated chloride channel receptor of the major malaria vector, Anopheles gambiae.

Atif, Mohammed / Lynch, Joseph W / Keramidas, Angelo

British journal of pharmacology

2019 Volume 177, Issue 1, Page(s) 175–187

Abstract: Background and purpose: Between half to 1 million people die annually from malaria. Anopheles gambiae mosquitoes are major malaria vectors. Unfortunately, resistance has emerged to the agents currently used to control A. gambiae, creating a demand for ... ...

Abstract	Background and purpose: Between half to 1 million people die annually from malaria. Anopheles gambiae mosquitoes are major malaria vectors. Unfortunately, resistance has emerged to the agents currently used to control A. gambiae, creating a demand for novel control measures. The pentameric glutamate-gated chloride channel (GluCl) expressed in the muscle and nerve cells of these organisms are a potentially important biological target for malaria control. The pharmacological properties of Anophiline GluCl receptors are, however, largely unknown. Accordingly, we compared the efficacy of four insecticides (lindane, fipronil, picrotoxin, and ivermectin) on two A. gambiae GluCl receptor splice variants with the aim of providing a molecular basis for designing novel anti-malaria treatments. Experimental approach: The A. gambiae GluCl receptor b1 and c splice variants were expressed homomerically in Xenopus laevis oocytes and studied with electrophysiological techniques, using two-electrode voltage-clamp. Key results: The b1 and c GluCl receptors were activated with similar potencies by glutamate and ivermectin. Fipronil was more potent than picrotoxin and lindane at inhibiting glutamate- and ivermectin-gated currents. Importantly, b1 GluCl receptors exhibited reduced sensitivity to picrotoxin and lindane. They also recovered from these effects to a greater extent than c GluCl receptors CONCLUSIONS AND IMPLICATIONS: The two splice variant subunits exhibited differential sensitivities to multiple, structurally divergent insecticides, without accompanying changes in the sensitivity to the endogenous neurotransmitter, glutamate, implying that drug resistance may be caused by alterations in relative subunit expression levels, without affecting physiological function. Our results strongly suggest that it should be feasible to develop novel subunit-specific pharmacological agents.
MeSH term(s)	Amino Acid Sequence ; Animals ; Anopheles/genetics ; Anopheles/metabolism ; Chloride Channels/genetics ; Chloride Channels/metabolism ; Dose-Response Relationship, Drug ; Female ; Glutamic Acid/pharmacology ; Insecticides/pharmacology ; Ivermectin/pharmacology ; Mosquito Vectors/genetics ; Mosquito Vectors/metabolism ; Oocytes/drug effects ; Oocytes/metabolism ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Xenopus laevis
Chemical Substances	Chloride Channels ; Insecticides ; Protein Isoforms ; glutamate-gated chloride channels ; Glutamic Acid (3KX376GY7L) ; Ivermectin (70288-86-7)
Language	English
Publishing date	2019-10-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.14855
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Article ; Online: Effects of GluN2A and GluN2B gain-of-function epilepsy mutations on synaptic currents mediated by diheteromeric and triheteromeric NMDA receptors.

Chen, Xiumin / Keramidas, Angelo / Harvey, Robert J / Lynch, Joseph W

Neurobiology of disease

2020 Volume 140, Page(s) 104850

Abstract: Mutations in synaptic NMDA receptors (NMDARs) are associated with epilepsy and neurodevelopmental disorders. The effects of several such mutations have been investigated in recombinantly-expressed NMDARs under conditions of steady-state activation. Such ... ...

Abstract	Mutations in synaptic NMDA receptors (NMDARs) are associated with epilepsy and neurodevelopmental disorders. The effects of several such mutations have been investigated in recombinantly-expressed NMDARs under conditions of steady-state activation. Such experiments provide only limited insight into how mutations affect NMDAR-mediated excitatory synaptic currents (EPSCs). The present study aimed to characterize the effects of the GluN2A
MeSH term(s)	Animals ; Epilepsy/genetics ; Female ; Gain of Function Mutation ; HEK293 Cells ; Humans ; Male ; Neurons/physiology ; Patch-Clamp Techniques ; Rats ; Receptors, N-Methyl-D-Aspartate/genetics ; Synapses/physiology
Chemical Substances	NR2B NMDA receptor ; Receptors, N-Methyl-D-Aspartate ; N-methyl D-aspartate receptor subtype 2A (VH92ICR8HX)
Language	English
Publishing date	2020-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2020.104850
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Article: Psychiatric patient with Chilaiditi's syndrome.

Vasileiadis, P / Mavridis, G / Keramidas, A / Chardalidou, D / Pervos, I / Charalampous, C

Clinical schizophrenia & related psychoses

2018

Abstract: Background: Chilaiditi's sign is defined as the interposition of bowels between the liver and the right diaphragm. When the patient is symptomatic due to the intestinal obstruction, the case is referred to as Chilaiditi's syndrome.: Objective: To ... ...

Abstract	Background: Chilaiditi's sign is defined as the interposition of bowels between the liver and the right diaphragm. When the patient is symptomatic due to the intestinal obstruction, the case is referred to as Chilaiditi's syndrome. Objective: To emphasize the importance of accurate diagnose of Chilaiditi's syndrome in patients with psychotic disturbances. Method: A 46 years old male was admitted to our department suffering from a constant epigastric and right upper quadrant pain with radiation to the right shoulder. The pain started 10 hours before the admission of the patient and was accompanied with vomiting. Patient has a history of schizophrenia and intellectual disability. He was in a stimulatory situation and unable to give any information about his state of health. Results: Patient was afebrile, tachycardic and laboratory results were normal. The chest and abdomen x-ray showed the Chilaiditi's sign. With the ultrasound procedure the case of the pneumoperitoneum was excluded. A conservative treatment with IV fluid hydration, pain management, diet modification, laxatives and enemas, was used. After a week of hospitalization, the patient felt well, having proper diet and regular evacuations and at the Chilaiditi's sign was no more observed. Discussion: The etiology of the Chilaiditi's syndrome is multifactoral and it has been reported that it is associated with psychotropic medication and intellectual disability. Conclusions: The diagnosis of the syndrome is vital in order to avoid unnecessary and dangerous surgical interventions. Only few publications of a Chilaiditi syndrome in patients with psychosis are cited in the literature.
Language	English
Publishing date	2018-06-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2489256-7
ISSN	1941-2010 ; 1935-1232
ISSN (online)	1941-2010
ISSN	1935-1232
DOI	10.3371/CSRP.VAMA.061518
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Article ; Online: Anti-seizure mechanisms of midazolam and valproate at the β2(L51M) variant of the GABA

Kuanyshbek, Alibek / Wang, Meng / Andersson, Åsa / Tuifua, Marie / Palmer, Elizabeth E / Sachdev, Rani K / Mu, Ting-Wei / Vetter, Irina / Keramidas, Angelo

Neuropharmacology

2022 Volume 221, Page(s) 109295

Abstract: Genetic sequencing is identifying an expanding number of variants of ... ...

Abstract	Genetic sequencing is identifying an expanding number of variants of GABA
MeSH term(s)	Humans ; Receptors, GABA-A/metabolism ; Valproic Acid/pharmacology ; Valproic Acid/therapeutic use ; Midazolam/pharmacology ; Midazolam/therapeutic use ; Epilepsy/drug therapy ; gamma-Aminobutyric Acid/therapeutic use
Chemical Substances	Receptors, GABA-A ; Valproic Acid (614OI1Z5WI) ; Midazolam (R60L0SM5BC) ; gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2022-10-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2022.109295
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