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Article: Differential effects of antiseizure medications on neurogenesis: Evidence from cells to animals.

Alavi, Mohaddeseh Sadat / Al-Asady, Abdulridha Mohammed / Fanoudi, Sahar / Sadeghnia, Hamid R

2024 Volume 10, Issue 4, Page(s) e26650

Abstract: Neurogenesis, the process of generating functionally integrated neurons from neural stem and progenitor cells, is involved in brain development during embryonic stages but continues throughout life. Adult neurogenesis plays essential roles in many brain ... ...

Abstract	Neurogenesis, the process of generating functionally integrated neurons from neural stem and progenitor cells, is involved in brain development during embryonic stages but continues throughout life. Adult neurogenesis plays essential roles in many brain functions such as cognition, brain plasticity, and repair. Abnormalities in neurogenesis have been described in many neuropsychiatric and neurological disorders, including epilepsy. While sharing a common property of suppressing seizures, accumulating evidence has shown that some antiseizure medications (ASM) exhibit neuroprotective potential in the non-epileptic models including Parkinson's disease, Alzheimer's disease, cerebral ischemia, or traumatic brain injury. ASM are a heterogeneous group of medications with different mechanisms of actions. Therefore, it remains to be revealed whether neurogenesis is a class effect or related to them all. In this comprehensive literature study, we reviewed the literature data on the influence of ASM on the neurogenesis process during brain development and also in the adult brain under physiological or pathological conditions. Meanwhile, we discussed the underlying mechanisms associated with the neurogenic effects of ASM by linking the reported
Language	English
Publishing date	2024-02-17
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2024.e26650
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Article ; Online: Zirconium dioxide nanoparticles induced cytotoxicity in rat cerebral cortical neurons and apoptosis in neuron-like N2a and PC12 cell lines.

Alavi, Mohaddeseh Sadat / Asadpour, Elham / Boroushaki, Mohammad Taher / Fakharzadeh Moghadam, Omid / Sadeghnia, Hamid R

Toxicology and industrial health

2024 Volume 40, Issue 4, Page(s) 145–155

Abstract: During recent decades, the application of zirconium dioxide nanoparticles ( ... ...

Abstract	During recent decades, the application of zirconium dioxide nanoparticles (ZrO
MeSH term(s)	Rats ; Male ; Animals ; Caspase 3 ; bcl-2-Associated X Protein/metabolism ; Rats, Wistar ; PC12 Cells ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Apoptosis ; Nanoparticles ; Neurons ; Cell Survival ; Zirconium
Chemical Substances	Caspase 3 (EC 3.4.22.-) ; zirconium oxide (S38N85C5G0) ; bcl-2-Associated X Protein ; Proto-Oncogene Proteins c-bcl-2 ; Zirconium (C6V6S92N3C)
Language	English
Publishing date	2024-01-24
Publishing country	England
Document type	Journal Article
ZDB-ID	56831-4
ISSN	1477-0393 ; 0748-2337
ISSN (online)	1477-0393
ISSN	0748-2337
DOI	10.1177/07482337241228622
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Article ; Online: Fibroblast Growth Factors as Tools in the Management of Neuropathic Pain Disorders.

Forouzanfar, Fatemeh / Sadeghnia, Hamid R

Current drug targets

2020 Volume 21, Issue 10, Page(s) 1034–1043

Abstract: Neuropathic pain is caused by a damage to or dysfunction of the somatosensory nervous system. The main mechanisms underlying neuropathic pain include ectopic activity in nociceptive nerves, peripheral and central sensitization, impaired inhibitory ... ...

Abstract	Neuropathic pain is caused by a damage to or dysfunction of the somatosensory nervous system. The main mechanisms underlying neuropathic pain include ectopic activity in nociceptive nerves, peripheral and central sensitization, impaired inhibitory modulation, and microglial activation. Fibroblast growth factors (FGFs) make up a large family of growth factors that mediate neural development, metabolism, and function through three main key signaling pathways, including RAS/MAP kinase pathway, PI3 kinase/Akt pathway, and PLCγ. An association between the members of the FGF system and the improvement of neuropathic pain has become evident, recently. These signaling molecules may be expected to provide new drug targets for the treatment of neuropathic pain. To the best of our knowledge, it is the first study that reviews the relationship between some members of the FGF system and neuropathic pain.
Language	English
Publishing date	2020-06-08
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2064859-5
ISSN	1873-5592 ; 1389-4501
ISSN (online)	1873-5592
ISSN	1389-4501
DOI	10.2174/1389450121666200423084205
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Article ; Online: Beneficial effects of levetiracetam in streptozotocin-induced rat model of Alzheimer's disease.

Alavi, Mohaddeseh Sadat / Fanoudi, Sahar / Hosseini, Mahmoud / Sadeghnia, Hamid R

Metabolic brain disease

2022 Volume 37, Issue 3, Page(s) 689–700

Abstract: Alzheimer's disease (AD) is the most common neurodegenerative disorder among the elderly. In the light of increasing AD prevalence and lack of effective treatment, new strategies to prevent or reverse this condition are needed. Levetiracetam (LEV) is a ... ...

Abstract	Alzheimer's disease (AD) is the most common neurodegenerative disorder among the elderly. In the light of increasing AD prevalence and lack of effective treatment, new strategies to prevent or reverse this condition are needed. Levetiracetam (LEV) is a newer antiepileptic drug that is commonly used to treat certain types of seizures. Researches indicated that LEV has several other pharmacological activities, including improvement of cognitive function. In this study, the recovery effects of chronic (28 days) administration of LEV (50, 100, and 150 mg/kg, ip) on cognitive deficits caused by the intracerebroventricular (icv) injection of streptozotocin (STZ), as a model for sporadic AD, were evaluated in rats. We also considered the protective effects of LEV against hippocampal cell loss, oxidative damage, acetylcholinesterase (AChE) activity, neuroinflammation, and tauopathy caused by STZ. LEV (100 and 150 mg/kg) significantly attenuated the STZ-induced learning and memory impairments in the passive avoidance and Morris water maze (MWM) tasks. In addition, LEV suppressed STZ-induced hippocampal neuronal loss, while restored alterations in the redox status (lipid peroxides and glutathione), AChE activity, proinflammatory cytokines (IL-1β, IL-6, TNF-α), and hyperphosphorylation of tau linked to STZ administration. In conclusion, our study demonstrated that LEV alleviated hippocampal cell death and memory deficits in STZ-AD rats, through mitigating oxidative damage, suppression of proinflammatory cytokines expression, and inhibition of abnormal tau hyperphosphorylation.
MeSH term(s)	Acetylcholinesterase/metabolism ; Alzheimer Disease/chemically induced ; Alzheimer Disease/drug therapy ; Animals ; Disease Models, Animal ; Levetiracetam/adverse effects ; Maze Learning ; Oxidative Stress ; Rats ; Streptozocin/toxicity
Chemical Substances	Levetiracetam (44YRR34555) ; Streptozocin (5W494URQ81) ; Acetylcholinesterase (EC 3.1.1.7)
Language	English
Publishing date	2022-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632824-6
ISSN	1573-7365 ; 0885-7490
ISSN (online)	1573-7365
ISSN	0885-7490
DOI	10.1007/s11011-021-00888-0
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Article ; Online: Everolimus attenuates glutamate-induced PC12 cells death.

Alavi, Mohaddeseh Sadat / Fanoudi, Sahar / Hosseini, Azar / Jalili-Nik, Mohammad / Bagheri, Amirbehzad / Sadeghnia, Hamid R

The International journal of neuroscience

2023 Volume 133, Issue 4, Page(s) 457–466

Abstract: Background: Glutamate-induced neuronal cell death plays a key role in neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. Some recent studies reported the potential immunomodulatory and neuroprotective properties of inhibitors of ... ...

Abstract	Background: Glutamate-induced neuronal cell death plays a key role in neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. Some recent studies reported the potential immunomodulatory and neuroprotective properties of inhibitors of serine-threonine kinase, mTOR (mammalian target of rapamycin). However, no study was conducted about the neuroprotective potential of everolimus (EVR), a selective and potent mTOR inhibitor. Therefore, this study was planned to investigate whether EVR has protective effects against glutamate-induced toxicity in PC12 cells, which are used as model for neurons injury, and to elucidate the underlying mechanism. Methods: PC12 cells were concurrently treated with glutamate (8 mM) and EVR (0-40 nM) for 24 h. Then, the cells viability, apoptosis rate, and apoptosis-related proteins (caspase-3, bax and bcl-2) were measured using MTT, annexin V/PI and immunoblotting assays. Results: Analyzing the protective effect of different concentrations of EVR (0-40 nM) against glutamate-induced cytotoxicity revealed a significant increase in cell viability in co-treatment regimen ( Conclusion: The results demonstrated, for the first time, that EVR could protect against glutamate-mediated PC12 cell death
MeSH term(s)	Rats ; Animals ; Glutamic Acid/toxicity ; Caspase 3/metabolism ; bcl-2-Associated X Protein/metabolism ; bcl-2-Associated X Protein/pharmacology ; Everolimus/pharmacology ; PC12 Cells ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Proto-Oncogene Proteins c-bcl-2/pharmacology ; Apoptosis/physiology ; Apoptosis Regulatory Proteins ; Cell Survival ; Neuroprotective Agents/pharmacology ; Mammals/metabolism
Chemical Substances	Glutamic Acid (3KX376GY7L) ; Caspase 3 (EC 3.4.22.-) ; bcl-2-Associated X Protein ; Everolimus (9HW64Q8G6G) ; Proto-Oncogene Proteins c-bcl-2 ; Apoptosis Regulatory Proteins ; Neuroprotective Agents
Language	English
Publishing date	2023-02-02
Publishing country	England
Document type	Journal Article
ZDB-ID	3061-2
ISSN	1563-5279 ; 1543-5245 ; 0020-7454
ISSN (online)	1563-5279 ; 1543-5245
ISSN	0020-7454
DOI	10.1080/00207454.2021.1929210
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Article: Levetiracetam promoted rat embryonic neurogenesis via NMDA receptor-mediated mechanism in vitro

Alavi, Mohaddeseh Sadat / Negah, Sajad Sahab / Ghorbani, Ahmad / Hosseini, Azar / Sadeghnia, Hamid R.

Life sciences. 2021 Nov. 01, v. 284

2021

Abstract: Levetiracetam (LEV) is a broad-spectrum antiepileptic drug with neuroprotective properties and novel mechanisms of action. Some evidence suggests that LEV may impact adult neurogenesis, but the results are controversial. The present study was aimed to ... ...

Abstract	Levetiracetam (LEV) is a broad-spectrum antiepileptic drug with neuroprotective properties and novel mechanisms of action. Some evidence suggests that LEV may impact adult neurogenesis, but the results are controversial. The present study was aimed to evaluate the effects of LEV on the proliferation and differentiation of rat embryonic neural stem cells (NSCs) and to explore the role of GABAB or NMDA receptors.NSCs were isolated from rat fetal ganglionic eminence at embryonic day 14.5. The effects of LEV on viability, proliferation, neurosphere formation, and neuronal or astroglial differentiation of NSCs were assessed using resazurin, BrdU incorporation, immunocytochemistry, quantitative real-time PCR, and western blotting. Additionally, we addressed the relationship between treatment with NMDA and GABAB receptor antagonists (MK801 and saclofen, respectively) in combination with LEV on these parameters.The data showed that LEV (50 μM) significantly increased the number (p < 0.01) and diameter of neurospheres (p < 0.05), enhanced proliferation (p < 0.01), and promoted neuronal differentiation, as revealed by significantly increased expressions of DCX and NeuN. The expressions of astroglial markers, GFAP and Olig2, were markedly reduced. The addition of MK801 (10 μM) significantly diminished neurospheres growth (p < 0.001), decreased the number of proliferating cells (p < 0.01), and reduced the number of new neurons (p < 0.001) but increased the astroglial cells (p < 0.001) induced by LEV. Co-treatment with saclofen (25 μM) did not significantly affect LEV-induced NSCs proliferation and differentiation.Our findings suggest that LEV may enhance rat embryonic neurogenesis mainly through an NMDA receptor-mediated mechanism.
Keywords	adults ; anticonvulsants ; immunocytochemistry ; neurogenesis ; neurons ; quantitative polymerase chain reaction ; rats ; viability
Language	English
Dates of publication	2021-1101
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.119923
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Levetiracetam promoted rat embryonic neurogenesis via NMDA receptor-mediated mechanism in vitro.

Alavi, Mohaddeseh Sadat / Negah, Sajad Sahab / Ghorbani, Ahmad / Hosseini, Azar / Sadeghnia, Hamid R

Life sciences

2021 Volume 284, Page(s) 119923

Abstract: Aims: Levetiracetam (LEV) is a broad-spectrum antiepileptic drug with neuroprotective properties and novel mechanisms of action. Some evidence suggests that LEV may impact adult neurogenesis, but the results are controversial. The present study was ... ...

Abstract	Aims: Levetiracetam (LEV) is a broad-spectrum antiepileptic drug with neuroprotective properties and novel mechanisms of action. Some evidence suggests that LEV may impact adult neurogenesis, but the results are controversial. The present study was aimed to evaluate the effects of LEV on the proliferation and differentiation of rat embryonic neural stem cells (NSCs) and to explore the role of GABA Main methods: NSCs were isolated from rat fetal ganglionic eminence at embryonic day 14.5. The effects of LEV on viability, proliferation, neurosphere formation, and neuronal or astroglial differentiation of NSCs were assessed using resazurin, BrdU incorporation, immunocytochemistry, quantitative real-time PCR, and western blotting. Additionally, we addressed the relationship between treatment with NMDA and GABA Key findings: The data showed that LEV (50 μM) significantly increased the number (p < 0.01) and diameter of neurospheres (p < 0.05), enhanced proliferation (p < 0.01), and promoted neuronal differentiation, as revealed by significantly increased expressions of DCX and NeuN. The expressions of astroglial markers, GFAP and Olig2, were markedly reduced. The addition of MK801 (10 μM) significantly diminished neurospheres growth (p < 0.001), decreased the number of proliferating cells (p < 0.01), and reduced the number of new neurons (p < 0.001) but increased the astroglial cells (p < 0.001) induced by LEV. Co-treatment with saclofen (25 μM) did not significantly affect LEV-induced NSCs proliferation and differentiation. Significance: Our findings suggest that LEV may enhance rat embryonic neurogenesis mainly through an NMDA receptor-mediated mechanism.
MeSH term(s)	Animals ; Baclofen/analogs & derivatives ; Baclofen/pharmacology ; Biomarkers/metabolism ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Dizocilpine Maleate/pharmacology ; Doublecortin Protein ; Embryo, Mammalian/physiology ; Female ; Levetiracetam/pharmacology ; Male ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Neural Stem Cells/cytology ; Neural Stem Cells/drug effects ; Neural Stem Cells/metabolism ; Neurogenesis/drug effects ; Neurons/cytology ; Neurons/drug effects ; Neurons/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/metabolism ; Spheroids, Cellular/cytology ; Spheroids, Cellular/drug effects ; Rats
Chemical Substances	Biomarkers ; Dcx protein, rat ; Doublecortin Protein ; Nerve Tissue Proteins ; RNA, Messenger ; Receptors, N-Methyl-D-Aspartate ; Levetiracetam (44YRR34555) ; Dizocilpine Maleate (6LR8C1B66Q) ; Baclofen (H789N3FKE8) ; saclofen (LRZ36BCQ1Y)
Language	English
Publishing date	2021-09-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.119923
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Article ; Online: Nigella sativa and thymoquinone attenuate oxidative stress and cognitive impairment following cerebral hypoperfusion in rats.

Fanoudi, Sahar / Alavi, Mohaddeseh S / Hosseini, Mahmoud / Sadeghnia, Hamid R

Metabolic brain disease

2019 Volume 34, Issue 4, Page(s) 1001–1010

Abstract: Nigella sativa, a plant widely used in traditional medicine, possesses anti-inflammatory, antioxidant and neuroprotective properties. In the present study, we investigated the effect of hydroalcoholic extract of N. sativa seeds (NSE) and its active ... ...

Abstract	Nigella sativa, a plant widely used in traditional medicine, possesses anti-inflammatory, antioxidant and neuroprotective properties. In the present study, we investigated the effect of hydroalcoholic extract of N. sativa seeds (NSE) and its active constituent, thymoquinone (TQ), on learning and memory deficits, hippocampal acetylcholine esterase (AChE) activity, and markers of redox status, mainly lipid peroxidation and superoxide dismutase (SOD) activity following cerebral hypoperfusion in rats. Cerebral hypoperfusion was induced by permanent occlusion of bilateral common carotid arteries (2VO). Male Wistar rats were administered either a vehicle (sham group: 10 ml/kg/day, ip), NSE (100, 200, and 400 mg/kg/day, ip), TQ (10, 20, and 40 mg/kg/day, ip), or donepezil (5 mg/kg/day, ip) for 10 days (three days before and seven days after ligation). Spatial learning and memory deficits were investigated using the Morris water maze (MWM) task. 2VO produced significant learning and memory deficits as evidenced by increased latency time to reach the hidden platform, increased swimming time, and decreased time spent in the target quadrant in the probe trial in the MWM task. There was also a significant increase in the lipid peroxidation level and AChE activity, and a significant decrease in SOD activity in the hippocampal portion of hypoperfused rats, as compared with the sham group. Treatment with NSE (400 mg/kg/day; p < 0.001) and TQ (40 mg/kg/day; p < 0.001), as well as donepezil significantly prevented learning and memory impairments and alleviated changes in the hippocampal lipid peroxide level and SOD and AChE activities in this model. In conclusion, our data suggest that N. sativa and thymoquinone have a beneficial role in cerebrovascular insufficiency states and dementia.
MeSH term(s)	Acetylcholinesterase/metabolism ; Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Benzoquinones/pharmacology ; Benzoquinones/therapeutic use ; Brain Ischemia/complications ; Brain Ischemia/metabolism ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/metabolism ; Hippocampus/drug effects ; Hippocampus/metabolism ; Lipid Peroxidation/drug effects ; Male ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Nigella sativa ; Oxidative Stress/drug effects ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Rats ; Rats, Wistar ; Seeds ; Spatial Learning/drug effects ; Spatial Memory/drug effects ; Thiobarbituric Acid Reactive Substances/metabolism
Chemical Substances	Antioxidants ; Benzoquinones ; Neuroprotective Agents ; Plant Extracts ; Thiobarbituric Acid Reactive Substances ; Acetylcholinesterase (EC 3.1.1.7) ; thymoquinone (O60IE26NUF)
Language	English
Publishing date	2019-04-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	632824-6
ISSN	1573-7365 ; 0885-7490
ISSN (online)	1573-7365
ISSN	0885-7490
DOI	10.1007/s11011-019-00394-4
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Article: Potential protective roles of phytochemicals on glutamate-induced neurotoxicity: A review.

Afshari, Amir R / Fanoudi, Sahar / Rajabian, Arezoo / Sadeghnia, Hamid R / Mollazadeh, Hamid / Hosseini, Azar

Iranian journal of basic medical sciences

2020 Volume 23, Issue 9, Page(s) 1113–1123

Abstract: Glutamate, as an essential neurotransmitter, has been thought to have different roles in the central nervous system (CNS), including nerve regeneration, synaptogenesis, and neurogenesis. Excessive glutamate causes an up-regulation of the multiple ... ...

Abstract	Glutamate, as an essential neurotransmitter, has been thought to have different roles in the central nervous system (CNS), including nerve regeneration, synaptogenesis, and neurogenesis. Excessive glutamate causes an up-regulation of the multiple signaling pathways, including phosphoinositide-3 kinase/protein kinase B (PI3K/Akt), Akt/mammalian target of rapamycin (mTOR) protein, mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK)1/2, and autophagy that are involved in neurodegenerative diseases pathophysiology. There are numerous findings on curcumin, astaxanthin, thymoquinone, and berberine, as natural products, which have outstanding effects in cell signaling far beyond their anti-oxidant activity, considering as a potential therapeutic target for glutamate excitotoxicity. Herein, we address the role of glutamate as a potential target in neurodegenerative diseases and discuss the protective effects of certain phytochemicals on glutamate-induced neurotoxicity.
Language	English
Publishing date	2020-09-09
Publishing country	Iran
Document type	Journal Article ; Review
ZDB-ID	2500485-2
ISSN	2008-3874 ; 2008-3866
ISSN (online)	2008-3874
ISSN	2008-3866
DOI	10.22038/ijbms.2020.43687.10259
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Article ; Online: Wnt/beta-catenin and PI3K/Akt/mTOR Signaling Pathways in Glioblastoma: Two Main Targets for Drug Design: A Review.

Shahcheraghi, Seyed H / Tchokonte-Nana, Venant / Lotfi, Marzieh / Lotfi, Malihe / Ghorbani, Ahmad / Sadeghnia, Hamid R

Current pharmaceutical design

2020 Volume 26, Issue 15, Page(s) 1729–1741

Abstract: Glioblastoma (GBM) is the most common and malignant astrocytic glioma, accounting for about 90% of all brain tumors with poor prognosis. Despite recent advances in understanding molecular mechanisms of oncogenesis and the improved neuroimaging ... ...

Abstract	Glioblastoma (GBM) is the most common and malignant astrocytic glioma, accounting for about 90% of all brain tumors with poor prognosis. Despite recent advances in understanding molecular mechanisms of oncogenesis and the improved neuroimaging technologies, surgery, and adjuvant treatments, the clinical prognosis of patients with GBM remains persistently unfavorable. The signaling pathways and the regulation of growth factors of glioblastoma cells are very abnormal. The various signaling pathways have been suggested to be involved in cellular proliferation, invasion, and glioma metastasis. The Wnt signaling pathway with its pleiotropic functions in neurogenesis and stem cell proliferation is implicated in various human cancers, including glioma. In addition, the PI3K/Akt/mTOR pathway is closely related to growth, metabolism, survival, angiogenesis, autophagy, and chemotherapy resistance of GBM. Understanding the mechanisms of GBM's invasion, represented by invasion and migration, is an important tool in designing effective therapeutic interventions. This review will investigate two main signaling pathways in GBM: PI3K/Akt/mTOR and Wnt/beta-catenin signaling pathways.
MeSH term(s)	Brain Neoplasms/drug therapy ; Cell Line, Tumor ; Cell Proliferation ; Drug Design ; Glioblastoma/drug therapy ; Humans ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt/metabolism ; TOR Serine-Threonine Kinases/metabolism ; beta Catenin
Chemical Substances	beta Catenin ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2020-02-12
Publishing country	United Arab Emirates
Document type	Journal Article ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/1381612826666200131100630
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