25 results on '"E. Annabi"'
Search Results
2. Rare cutaneous adverse effects of COVID‐19 vaccines: a case series and review of the literature
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Selim Aractingi, Sarah Guégan, Bénédicte Oulès, Nathalie Franck, B. Garel, Nicolas Dupin, E Annabi, and Pierre Sohier
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2019-20 coronavirus outbreak ,medicine.medical_specialty ,COVID-19 Vaccines ,Drug-Related Side Effects and Adverse Reactions ,Coronavirus disease 2019 (COVID-19) ,SARS-CoV-2 ,business.industry ,Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ,MEDLINE ,COVID-19 ,Dermatology ,Administration, Cutaneous ,Letter To The Editor ,Letters To The Editor ,Infectious Diseases ,medicine ,Humans ,Adverse effect ,business - Published
- 2021
3. Investigating the effects of capping layer on optical gain of nitride based semiconductor nanostructure lasers
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V. Mohadesi, Asghar Asgari, and E. Annabi Milani
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Materials science ,Nanostructure ,Semiconductor nanostructures ,02 engineering and technology ,Nitride ,01 natural sciences ,Schrödinger equation ,law.invention ,Inorganic Chemistry ,Condensed Matter::Materials Science ,symbols.namesake ,law ,0103 physical sciences ,Electrical and Electronic Engineering ,Physical and Theoretical Chemistry ,Wave function ,Spectroscopy ,010302 applied physics ,business.industry ,Organic Chemistry ,021001 nanoscience & nanotechnology ,Thermal conduction ,Laser ,Atomic and Molecular Physics, and Optics ,Electronic, Optical and Magnetic Materials ,symbols ,Optoelectronics ,0210 nano-technology ,business ,Layer (electronics) - Abstract
In this study, the effects of GaN capping layer on the behaviour of AlGaN/GaN nanostructure based laser is considered. We have employed the self-consistent solution of Poisson and Schrodinger equations for calculation of the energy levels, wave functions and conduction and valance bands profile. The impact of different thicknesses of the capping layer has been studied for sheet carrier density, then on optical gain. The results indicate that, by increasing the thickness of the cap layer, the optical gain decreases.
- Published
- 2017
4. Annular eruption with weight loss in a 47-year-old man.
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Annabi E, Lalevée S, Bettuzzi T, Demortier J, Papouin B, De Mestier Du Bourg L, Sbidian E, and Ingen-Housz-Oro S
- Abstract
Competing Interests: Competing interests: None declared.
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- 2023
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5. Improving efficiency of semitransparent organic solar cells by constructing semitransparent microcavity.
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Annabi Milani E, Piralaee M, and Asgari A
- Abstract
Semitransparent organic solar cells have become attractive recently because of their photon harvesting in the near-infrared and ultraviolet range and passing in the visible light region. Semitransparent organic solar cells with Glass/MoO3/Ag/MoO3/PBDB-T:ITIC/TiO2/Ag/PML/1DPCs structure have been studied in this work and the effects microcavity with 1-dimensional photonic crystals (1DPCs) on the solar cell performance such as the power conversion efficiency, the average visible transmittance, Light utilization efficiency (LUE), the color coordinates in the CIE color space, and CIE LAB are investigated. The analytical calculation including the density of exactions and their displacement is used to model the devices. The model shows that the presence of microcavity can improve the power conversion efficiency by about %17 in comparison with the absence of microcavity. Although the transmission is decreasing slightly, microcavity does not change the color coordinates much. The device can transmit high-quality light with a near-white sensation to the human eye., (© 2023. The Author(s).)
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- 2023
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6. Toxic epidermal necrolysis possibly associated with mogamulizumab in a patient with Sézary syndrome.
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Lazaridou I, Calvani J, Annabi E, Moins-Teisserenc H, Ta VA, Rivet J, Ram-Wolff C, Dumont M, Mahevas T, Vignon-Pennamen MD, Mourah S, Bouaziz JD, Louveau B, Bagot M, Battistella M, and de Masson A
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- Humans, Antibodies, Monoclonal, Humanized adverse effects, Sezary Syndrome drug therapy, Stevens-Johnson Syndrome etiology, Skin Neoplasms drug therapy
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- 2023
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7. Cutaneous exanthema revealing Multisystem-Inflammatory Syndrome in adults (MIS-A) in the course of SARS-CoV-2 infection.
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Pernea P, Annabi E, Walter A, Blum L, Bennacer Y, and Begon E
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- Adult, Humans, SARS-CoV-2, Systemic Inflammatory Response Syndrome complications, Systemic Inflammatory Response Syndrome diagnosis, COVID-19 complications, Exanthema etiology
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- 2023
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8. The protective effects of thymol and carvacrol against di (2-ethylhexyl) phthalate-induced cytotoxicity in HEK-293 cells.
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Amara I, Timoumi R, Annabi E, Ben Othmène Y, and Abid-Essefi S
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- Antioxidants pharmacology, Glutathione, HEK293 Cells, Humans, Kidney metabolism, Oxidative Stress, Reactive Oxygen Species, Cymenes pharmacology, Diethylhexyl Phthalate toxicity, Thymol pharmacology
- Abstract
The protective effects of thymol and carvacrol, two phenolic monoterpenes with a wide spectrum of pharmacological effects, against the oxidative stress produced by the di (2-ethylhexyl) phthalate (DEHP) in human embryonic kidney cells 293 cells (HEK-293 cells) were investigated in this study. The cytotoxicity was monitored by cell viability, while oxidative stress generation was assessed by reactive oxygen species (ROS) quantification, antioxidant enzyme activities measurement, glutathione concentration, and malondialdehyde (MDA) quantification. The genotoxicity was evaluated by the measurement of DNA fragmentation through the Comet assay. Our results demonstrated that the pretreatment of HEK-293 cells with thymol or carvacrol, 2 h before DEHP exposure, significantly increased the cell viability, decreased the ROS overproduction, modulated catalase (CAT), and superoxide dismutase (SOD) activities, restored the reduced glutathione content, and reduced the MDA level. The DNA fragmentation was also decreased by thymol and carvacrol pretreatment. These findings suggest that thymol and carvacrol could protect HEK-293 cells from DEHP-induced oxidative stress., (© 2022 Wiley Periodicals LLC.)
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- 2022
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9. Rare cutaneous adverse effects of COVID-19 vaccines: a case series and review of the literature.
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Annabi E, Dupin N, Sohier P, Garel B, Franck N, Aractingi S, Guégan S, and Oulès B
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- Administration, Cutaneous, COVID-19 Vaccines, Humans, SARS-CoV-2, COVID-19, Drug-Related Side Effects and Adverse Reactions
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- 2021
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10. Tebuconazole induced cytotoxic and genotoxic effects in HCT116 cells through ROS generation.
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Othmène YB, Salem IB, Hamdi H, Annabi E, and Abid-Essefi S
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- Animals, Apoptosis, HCT116 Cells, Humans, Oxidative Stress, Reactive Oxygen Species, DNA Damage, Triazoles toxicity
- Abstract
Tebuconazole (TEB) is a common triazole fungicide that has been widely used for the control of plant pathogenic fungi, suggesting that mammal exposure occurs regularly. Several studies demonstrated that TEB exposure has been linked to a variety of toxic effects, including neurotoxicity, immunotoxicity, reprotoxicity and carcinogenicity. However, there is a few available data regarding the molecular mechanism involved in TEB-induced toxicity. The current study was undertaken to investigate the toxic effects of TEB in HCT116 cells. Our results showed that TEB caused cytotoxicity by inhibiting cell viability as assessed by the MTT assay. Furthermore, we have demonstrated that TEB induced a significant increase in the reactive oxygen species (ROS) production leading to the induction of lipid peroxidation and DNA fragmentation and increased superoxide dismutase (SOD) and catalase (CAT) activities. Moreover, TEB exposure induced mitochondrial membrane potential loss and caspase-9/-3 activation. Treatment with general caspases inhibitor (Z-VAD-fmk) significantly prevented the TEB-induced cell death, indicating that TEB induced caspases-dependent cell death. These findings suggest the involvement of oxidative stress and apoptosis in TEB-induced toxicity in HCT116., (Copyright © 2021. Published by Elsevier Inc.)
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- 2021
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11. Effect of di(2-ethylhexyl) phthalate on Nrf2-regulated glutathione homeostasis in mouse kidney.
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Amara I, Salah A, Timoumi R, Annabi E, Scuto M, Trovato A, Neffati F, Calabrese V, and Abid-Essefi S
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- Animals, Antioxidants metabolism, Apoptosis drug effects, Biomarkers blood, Glutamate-Cysteine Ligase metabolism, Heme Oxygenase-1 metabolism, Kidney drug effects, Lipid Peroxidation drug effects, Male, Malondialdehyde metabolism, Mice, Inbred BALB C, Oxidation-Reduction, Protein Carbonylation drug effects, Signal Transduction drug effects, Sulfhydryl Compounds metabolism, Diethylhexyl Phthalate toxicity, Glutathione metabolism, Homeostasis drug effects, Kidney metabolism, NF-E2-Related Factor 2 metabolism
- Abstract
Environmental toxicants such as phthalate have been involved in multiple health disorders including renal diseases. Oxidative damage is implicated in many alterations caused by phthalate especially the di(2-ethylhexyl) phthalate (DEHP), which is the most useful phthalate. However, information regarding its mechanism of renal damage is lacking. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) regulates gene expression implicated in free radical scavenging and cytoprotection including the antioxidant glutathione (GSH) pathway. The aim of this study was to assess whether DEHP affects the Nrf2 pathway and the GSH concentration. Mice were divided into four groups: a control group and three groups treated with DEHP at different concentrations (5, 50, and 200 mg/kg body weight) for 30 days. Our results showed that DEHP altered the normal levels of serum biochemical parameters creatinine (CREA), urea, and lactate dehydrogenase (LDH). This phthalate caused oxidative damage through the induction of lipid peroxidation and protein oxidation as marked by increase of protein carbonyl (PC) and loss of protein-bound sulfhydryls (PSH). Simultaneously, DEHP treatment decreased the protein level of Nrf-2, HO-1, and GCLC (responsible of GSH synthesis) and decreased the GSH level. Inhibition of the Nrf2 pathway is related to the activation of the mitochondrial pathway of apoptosis. This apoptotic process is evidenced by an upregulation of p53 and Bax protein levels in addition to a downregulation of Bcl-2. Collectively, our data demonstrated that depletion of Nrf2 and GSH was associated with the elevation of oxidative stress and the activation of intrinsic apoptosis in mouse kidney treated with DEHP.
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- 2020
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12. Oxidative stress, DNA damage and apoptosis induced by tebuconazole in the kidney of male Wistar rat.
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Othmène YB, Hamdi H, Salem IB, Annabi E, Amara I, Neffati F, Najjar MF, and Abid-Essefi S
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- Animals, Dose-Response Relationship, Drug, Fungicides, Industrial toxicity, Gene Expression Regulation, Glutathione metabolism, Glutathione Disulfide metabolism, Glutathione Reductase metabolism, Kidney drug effects, Kidney metabolism, Male, Oxidation-Reduction, Rats, Rats, Wistar, Apoptosis drug effects, DNA Damage drug effects, Kidney pathology, Oxidative Stress drug effects, Triazoles toxicity
- Abstract
Tebuconazole (TEB) is a broad-spectrum conazole fungicide that has been used in agriculture in the control of foliar and soil-borne diseases of many crops. The present study has investigated the adverse effects of subchronic exposure to TEB on the kidney of male rats. Animals were divided into four equal groups and treated with TEB at increasing doses 0.9, 9 and 27 mg/kg body weight for 28 consecutive days. The results showed that TEB induced oxidative stress in the kidney demonstrated by an increase in malondialdehyde (MDA), protein carbonyl (PC), advanced oxidation protein product (AOPP) levels and DNA damage, as compared to the controls. Furthermore, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities were increased in the renal tissue of treated rats. Moreover, significant decrease in reduced glutathione (GSH) content in TEB-treated rats was observed, while oxidized glutathione (GSSG) levels were increased, thus a marked fall in GSH/GSSG ratio was registered in the kidney. Glutathione reductase (GR) activity showed a significant increase after TEB exposure. Moreover, TEB down-regulated the expression of Bcl2 and up-regulated the expression of Bax and caspase 3, which triggered apoptosis via the Bax/Bcl2 and caspase pathway. Also, TEB administration resulted in altered biochemical indicators of renal function and varying lesions in the overall histo-architecture of renal tissues. Taken together, our findings brought into light the renal toxicity induced by TEB, which was found to be significant at low doses., (Copyright © 2020 Elsevier B.V. All rights reserved.)
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- 2020
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13. Tebuconazole induced cardiotoxicity in male adult rat.
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Ben Othmène Y, Hamdi H, Annabi E, Amara I, Ben Salem I, Neffati F, Najjar MF, and Abid-Essefi S
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- Animals, Apoptosis drug effects, Cardiotoxicity genetics, Cardiotoxicity metabolism, Cardiotoxicity physiopathology, Cholesterol, LDL metabolism, Cytochromes c metabolism, DNA Fragmentation drug effects, Humans, Male, Rats, Rats, Wistar, Triglycerides metabolism, Cardiotoxicity etiology, Fungicides, Industrial toxicity, Triazoles toxicity
- Abstract
Tebuconazole is an effective systemic fungicide that belongs to the triazoles family. It has been widely used in both agricultural and medical sectors for the control of fungal diseases. Although TEB poses serious threats to mammals health, studies regarding its cardiotoxicity are very limited. Thus, we aimed to evaluate the effects of TEB on some biochemical parameters, the induction of apoptosis and DNA damage in the heart tissue. Male Wistar rats were treated with TEB at varied oral doses for 28 consecutive days. This study demonstrates that TEB decreased cardiac acetylcholinesterase, increased serum marker enzymes such as creatinine phosphokinase (CPK) and lactate dehydrogenase (LDH), and altered the lipid profile by increasing serum levels of total cholesterol (T-CHOL), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and reduced high-density lipoprotein cholesterol (HDL-C) levels. Furthermore, TEB increased levels of p53 and Bax/Bcl2 ratio, released the cytochrome c into the cytosol and activated caspase-9 and caspase-3. Besides, our results showed that TEB induced genotoxic effects. TEB induced DNA fragmentation and increased the frequency of micronucleated bone marrow cells. Moreover, TEB treatment developed fibrosis in the myocardium. Our results suggest that TEB exposure may affect myocardial cells normal functioning and triggers apoptosis., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)
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- 2020
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14. Protective effects of fennel essential oil against oxidative stress and genotoxicity induced by the insecticide triflumuron in human colon carcinoma cells.
- Author
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Timoumi R, Salem IB, Amara I, Annabi E, and Abid-Essefi S
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- Benzamides toxicity, Catalase metabolism, Colonic Neoplasms chemistry, DNA Damage, Humans, Oxidative Stress, Antioxidants chemistry, Benzamides chemistry, Catalase chemistry, Colonic Neoplasms physiopathology, Foeniculum, Insecticides, Oils, Volatile, Superoxide Dismutase chemistry
- Abstract
The increased use of pesticides is the origin of multiple damages to the environment and to humans; thus, the search for new strategies to reduce or even protect the toxic effects caused by these synthetic products became a necessity. In this context, our study attempted to evaluate the protective effects of fennel essential oil (FEO), the main essential oil extracted from Faeniculum vulgare Mill., a plant with aromatic, flavorful, and medicinal uses, against toxicity induced by an insecticide-triflumuron (TFM)-in human carcinoma cells (HCT116). Our methodological approach consists of the cytotoxicity assay starting with the cell viability test, the ROS generation, the malondialdehyde (MDA) production, the DNA fragmentation, and the measurement of some antioxidant enzymes activities such as catalase (CAT) and superoxide dismutase (SOD). Also, we measured the mitochondrial transmembrane potential. The outcome of the current study showed clearly that after 2 h of HCT 116 cell pretreatment with FEO, there were increase in cell viability, reduction in ROS generation, and modulation in CAT and SOD activities induced by TFM. In the same manner, significant decreases in MDA levels were found. Mainly, the results indicated a perceptible decrease in DNA damages and a significant reduction in the mitochondrial membrane potential loss. Our work demonstrates that FEO can be an important protector against toxic effects induced by TFM in HCT 116 cells.
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- 2020
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15. Di (2-ethylhexyl) phthalate targets the thioredoxin system and the oxidative branch of the pentose phosphate pathway in liver of Balb/c mice.
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Amara I, Timoumi R, Annabi E, Di Rosa G, Scuto M, Najjar MF, Calabrese V, and Abid-Essefi S
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- Animals, DNA Damage, Dose-Response Relationship, Drug, Glucosephosphate Dehydrogenase metabolism, Injections, Intraperitoneal, Liver metabolism, Male, Mice, Mice, Inbred BALB C, Reactive Oxygen Species metabolism, Superoxide Dismutase metabolism, Diethylhexyl Phthalate toxicity, Environmental Pollutants toxicity, Liver drug effects, Oxidative Stress drug effects, Pentose Phosphate Pathway drug effects, Plasticizers toxicity, Thioredoxins metabolism
- Abstract
Di (2-ethylhexyl) phthalate (DEHP) is a plasticizer that gives flexibility to various polyvinyl chloride products. It is a pollutant easily released into the environment and can cause many adverse effects to living organisms including hepatotoxicity. The thioredoxin system is a determining factor in the redox balance maintaining in the liver, which is a vulnerable tissue of reactive oxygen species overproduction because of its high energy needs. In order to determine if the thioredoxin system is a target in the development of DEHP hepatotoxicity, Balb/c mice were administered with DEHP intraperitoneally daily for 30 days. Results demonstrated that after DEHP exposure, biochemical profile changes were observed. This phthalate causes oxidative damage through the induction of lipid peroxydation as well as the increase of superoxide dismutase and catalase activities. As new evidence provided in this study, we demonstrated that the DEHP affected the thioredoxin system by altering the expression and the activity of thioredoxin (Trx) and thioredoxin Reductase (TrxR1). The two enzyme activities of the oxidative phase of the pentose phosphate pathway: Glucose-6-phosphate dehydrogenase and 6-Phosphogluconate dehydrogenase were also affected by this phthalate. This leads to a decrease in the level of nicotinamide adenine dinucleotide phosphate used by the TrxR1 to maintain the regeneration of the reduced Trx. We also demonstrated that such effects can be responsible of DEHP-induced DNA damage., (© 2019 Wiley Periodicals, Inc.)
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- 2020
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16. Di(2-ethylhexyl) phthalate inhibits glutathione regeneration and dehydrogenases of the pentose phosphate pathway on human colon carcinoma cells.
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Amara I, Timoumi R, Annabi E, Salem IB, and Abid-Essefi S
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- Antioxidants metabolism, Glutathione metabolism, Humans, Lipid Peroxidation drug effects, Oxidative Stress drug effects, Oxidative Stress physiology, Phthalic Acids pharmacology, Plasticizers pharmacology, Superoxide Dismutase metabolism, Carcinoma drug therapy, Diethylhexyl Phthalate pharmacology, Glutathione drug effects, Pentose Phosphate Pathway drug effects, Regeneration drug effects
- Abstract
Phthalates, particularly di(2-ethylhexyl) phthalate (DEHP), are compounds widely used as plasticizers and have become serious global contaminants. Because of the bioaccumulation of such substances, the food chain is at risk. The food contamination by some phthalates has been linked to different side effects in experimental animals. That is why we have chosen the intestinal system's cells which represent the primary targets of these compounds to test their toxic effects. Human colon carcinoma cells (HCT 116) were chosen to elucidate whether DEHP triggers oxidative stress and apoptosis. Our results indicated that DEHP is cytotoxic; it induces the overexpression of Hsp70 protein and causes oxidative damage through the generation of free radicals leading to lipid peroxidation induction and the increase of superoxide dismutase (SOD) and catalase (CAT) activities. In addition, cell treatment with DEHP resulted in a glutathione (GSH) content decrease and a decrease in the glutathione reductase (GR) activity. As new evidence provided in this study, we demonstrated that the DEHP affected the two enzymes' activities of the oxidative phase of the pentose phosphate pathway: Glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD). This leads to a decrease in the level of NADPH used by the GR to maintain the regeneration of the reduced GSH. We also demonstrated that such effects can be responsible for DEHP-induced apoptosis.
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- 2020
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17. Acetamiprid, a neonicotinoid insecticide, induced cytotoxicity and genotoxicity in PC12 cells.
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Annabi E, Ben Salem I, and Abid-Essefi S
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- Animals, Cell Survival drug effects, Comet Assay, Dose-Response Relationship, Drug, Lipid Peroxidation drug effects, Membrane Potential, Mitochondrial drug effects, PC12 Cells, Rats, Reactive Oxygen Species metabolism, DNA Damage, Environmental Pollutants toxicity, Insecticides toxicity, Neonicotinoids toxicity
- Abstract
Neonicotinoids are a group of pesticides widely used in agriculture and at home. Among those pesticides, acetamiprid (ACM) is a broad-spectrum insecticide used for the protection of vegetables and fruits from pest. The extensive use of this pesticide had led to contamination of environment including soil, water, as well as food products. However, there are few informations regarding the molecular mechanism by which ACM exerts its cytotoxic and genotoxic effects. The aim of the present study was to investigate the toxic effects of ACM in PC12 cells. We demonstrated that ACM significantly decreased cell viability as assessed by the MTT assay. We also shown that ACM-induced reactive oxygen species (ROS) generation followed by lipid peroxidation as evidenced by an increase in the MDA levels. The increase in cell death was accompanied by a reduction in the mitochondrial membrane potential. Besides, pretreatment with Z-VAD-FMK, a general caspases inhibitor, significantly decreased the ACM-induced cell death. Our results also indicate that ACM induced a concentration-dependent increase in DNA damage as evident by the Comet assay. These data indicate that ACM produces cytotoxicity and DNA damage in mammalian cells. Highlights ACM is cytotoxic toward rat pheochromocytoma adrenal medulla cells (PC12). ACM induces ROS generation, lipid peroxidation, and DNA fragmentation. ACM induces caspase-dependent apoptosis in PC12 cells.
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- 2019
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18. Di (2-ethylhexyl) phthalate induces cardiac disorders in BALB/c mice.
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Amara I, Timoumi R, Annabi E, Neffati F, Najjar MF, Bouaziz C, and Abid-Essefi S
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- Animals, Antioxidants, Catalase, Lipid Peroxidation, Male, Malondialdehyde, Mice, Mice, Inbred BALB C, Oxidation-Reduction, Oxidative Stress, Phthalic Acids, Toxicity Tests, Diethylhexyl Phthalate toxicity, Hazardous Substances toxicity, Heart drug effects, Heart Diseases chemically induced
- Abstract
Because of the extensive use of phthalates for domestic, medical, and industrial applications, the evaluation of their toxic effects is of major concern to public health. The aim of the present study was to assess the propensity of di (2-ethylhexyl) phthalate (DEHP), one of the most used phthalates, to cause oxidative cardiac damage in mice. DEHP was administered intraperitoneally at doses of 5, 50, and 200 mg/kg body weight for 30 consecutive days in BALB/c mice. We assessed the effect of DEHP on cardiac injury using biochemical profile (such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatinine phosphokinase (CPK), total cholesterol (T-CHOL), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C)), parameters related to myocardiac oxidative stress, such as malondialdehyde (MDA) level, protein carbonyl (PC) concentration, and DNA fragmentation. In addition, we evaluated antioxidant status; enzymatic (catalase (CAT) and superoxide dismutase (SOD) activities) and non-enzymatic (protein-bound sulfhydryl concentration (PSH)) antioxidants. Acetylcholinesterase (AChE) activity and histopathological changes were also assessed in heart mice treated with DEHP. Our results showed that DEHP induced an elevation of serum marker enzymes and perturbated the lipid profile. In addition, this phthalate increased lipid peroxidation, protein carbonyl levels, and DNA fragmentation in the heart in a dose-dependent manner. Antioxidant status was also perturbated by the increase of the CAT and SOD activities and the decrease of the protein-bound sulfhydryl concentration. AChE activity was also inhibited in the heart following the treatment with DEHP. These biochemical alterations were also confirmed by histopathological changes. Increased free radical production at various doses of DEHP would result in impairment of the redox status leading to an enhanced dose-dependent cardiotoxicity.
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- 2019
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19. The involvement of ROS generation on Epoxiconazole-induced toxicity in HCT116 cells.
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Hamdi H, Ben Salem I, Ben Othmène Y, Annabi E, and Abid-Essefi S
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- Acetylcysteine pharmacology, Comet Assay, DNA Damage, HCT116 Cells, Humans, Lipid Peroxidation, Membrane Potential, Mitochondrial drug effects, Mitochondria drug effects, Oxidative Stress, Epoxy Compounds toxicity, Fungicides, Industrial toxicity, Reactive Oxygen Species metabolism, Triazoles toxicity
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- 2018
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20. The use of metformin is associated with decreased lumbar radiculopathy pain.
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Taylor A, Westveld AH, Szkudlinska M, Guruguri P, Annabi E, Patwardhan A, Price TJ, and Yassine HN
- Abstract
Lumbar radiculopathy pain represents a major public health problem, with few effective long-term treatments. Preclinical neuropathic and postsurgical pain studies implicate the kinase adenosine monophosphate activated kinase (AMPK) as a potential pharmacological target for the treatment of chronic pain conditions. Metformin, which acts via AMPK, is a safe and clinically available drug used in the treatment of diabetes. Despite the strong preclinical rationale, the utility of metformin as a potential pain therapeutic has not yet been studied in humans. Our objective was to assess whether metformin is associated with decreased lumbar radiculopathy pain, in a retrospective chart review. We completed a retrospective chart review of patients who sought care from a university pain specialist for lumbar radiculopathy between 2008 and 2011. Patients on metformin at the time of visit to a university pain specialist were compared with patients who were not on metformin. We compared the pain outcomes in 46 patients on metformin and 94 patients not taking metformin therapy. The major finding was that metformin use was associated with a decrease in the mean of "pain now," by -1.85 (confidence interval: -3.6 to -0.08) on a 0-10 visual analog scale, using a matched propensity scoring analysis and confirmed using a Bayesian analysis, with a significant mean decrease of -1.36 (credible interval: -2.6 to -0.03). Additionally, patients on metformin showed a non-statistically significant trend toward decreased pain on a variety of other pain descriptors. Our proof-of-concept findings suggest that metformin use is associated with a decrease in lumbar radiculopathy pain, providing a rational for larger retrospective trials in different pain populations and for prospective trials, to test the effectiveness of metformin in reducing neuropathic pain.
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- 2013
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21. Transcranial ultrasound (TUS) effects on mental states: a pilot study.
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Hameroff S, Trakas M, Duffield C, Annabi E, Gerace MB, Boyle P, Lucas A, Amos Q, Buadu A, and Badal JJ
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- Adult, Aged, Aged, 80 and over, Cross-Over Studies, Double-Blind Method, Female, Functional Laterality physiology, Humans, Male, Middle Aged, Pain Measurement, Pilot Projects, Time Factors, Affect physiology, Brain physiology, Chronic Pain therapy, Mental Processes physiology, Ultrasonography, Doppler, Transcranial
- Abstract
Background/objective: Transcranial ultrasound (TUS) can modulate brain function. To assess possible TUS modulation of mental states, we investigated effects on subjective reports of pain and mood of sub-thermal TUS versus placebo applied to frontal scalp and brain of chronic pain patient volunteers., Methods: With IRB approval and informed consent, subjects with chronic pain completed two visual analog scales for pain (NRS) and mood (VAMS/Global Affect), and their vital signs were recorded 10 min prior to, and 10 min and 40 min following exposure to either subthermal TUS (8 MHz) or placebo (in a double blind crossover study) using the 12L-RS probe of a LOGIQe ultrasound imaging machine (General Electric, USA). A physician, also blinded for TUS versus placebo, applied the probe (with gel) to scalp over posterior frontal cortex, contralateral to maximal pain, for 15 seconds. A second investigator operated the ultrasound machine, randomizing TUS versus placebo. The process was then repeated, applying the opposite modality (TUS or placebo)., Results: Subjective reports of Mood/Global Affect were improved 10 min (P = 0.03) and 40 min (P = 0.04) following TUS compared with placebo. NRS pain reports slightly improved following TUS (P = 0.07) at 40 min., Conclusion: We found improvement in subjective mood 10 min and 40 min after TUS compared to placebo. TUS can have safe neurophysiological effects on brain function, and is a promising noninvasive therapy for modulating conscious and unconscious mental states and disorders. We suggest TUS acts via intra-neuronal microtubules, which apparently resonate in TUS megahertz range., (Copyright © 2013 Elsevier Inc. All rights reserved.)
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- 2013
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22. Receptor specificity defines algogenic properties of propofol and fospropofol.
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Patwardhan A, Edelmayer R, Annabi E, Price T, Malan P, and Dussor G
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- Animals, Cells, Cultured, Hypnotics and Sedatives adverse effects, Injections, Intravenous, Male, Pain chemically induced, Prodrugs administration & dosage, Prodrugs adverse effects, Propofol adverse effects, Rats, Rats, Sprague-Dawley, TRPA1 Cation Channel, TRPC Cation Channels agonists, Hypnotics and Sedatives administration & dosage, Pain metabolism, Propofol administration & dosage, Propofol analogs & derivatives, TRPC Cation Channels biosynthesis
- Abstract
Background: Propofol-evoked injection site pain is not observed with fospropofol. We hypothesized that unlike propofol, fospropofol does not activate the irritant receptor, transient receptor potential 1 (TRPA1)., Methods: We tested the hypothesis using electrophysiology and behavioral studies., Results: Our data demonstrate that propofol (100 μM) evokes an inward current only in TRPA1-expressing neurons. However, fospropofol (100 μM and 1 mM) is unable to evoke depolarizing currents in either TRPA1-positive or TRPA1-negative neurons. Both propofol and fospropofol produced general anesthesia., Conclusions: The lack of algogenic activity in fospropofol is most likely the result of its inability to activate TRPA1 on nociceptors.
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- 2012
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23. Peripheral nerve stimulation for trigeminal neuropathic pain.
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Stidd DA, Wuollet AL, Bowden K, Price T, Patwardhan A, Barker S, Weinand ME, Annabi J, and Annabi E
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- Adult, Aged, Humans, Male, Middle Aged, Electric Stimulation Therapy methods, Eye Enucleation adverse effects, Herpes Zoster complications, Postoperative Complications, Trigeminal Nerve Injuries complications, Trigeminal Neuralgia therapy
- Abstract
Facial pain is a complex disease with a number of possible etiologies. Trigeminal neuropathic pain (TNP) is defined as pain caused by a lesion or disease of the trigeminal branch of the peripheral nervous system resulting in chronic facial pain over the distribution of the injured nerve. First line treatment of TNP includes management with anticonvulsant medication (carbamazepine, phenytoin, gabapentin, etc.), baclofen, and analgesics. TNP, however, can be a condition difficult to adequately treat with medical management alone. Patients with TNP can suffer from significant morbidity as a result of inadequate treatment or the side effects of pharmacologic therapy. TNP refractory to medical management can be considered for treatment with a growing number of invasive procedures. Peripheral nerve stimulation (PNS) is a minimally invasive option that has been shown to effectively treat medically intractable TNP. We present a case series of common causes of TNP successfully treated with PNS with up to a 2 year follow-up. Only one patient required implantation of new electrode leads secondary to electrode migration. The patients in this case series continue to have significant symptomatic relief, demonstrating PNS as an effective treatment option for intractable TNP. Though there are no randomized trials, peripheral neuromodulation has been shown to be an effective means of treating TNP refractory to medical management in a growing number of case series. PNS is a safe procedure that can be performed even on patients that are not optimal surgical candidates and should be considered for patients suffering from TNP that have failed medical management.
- Published
- 2012
24. Transforaminal blood patch for the treatment of chronic headache from intracranial hypotension: a case report and review.
- Author
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Bowden K, Wuollet A, Patwardhan A, Price TJ, Lawall J, Annabi J, Barker S, and Annabi E
- Abstract
This case report describes the successful treatment of chronic headache from intracranial hypotension with bilateral transforaminal (TF) lumbar epidural blood patches (EBPs). The patient is a 65-year-old male with chronic postural headaches. He had not had a headache-free day in more than 13 years. Conservative treatment and several interlaminar epidural blood patches were previously unsuccessful. A transforaminal EBP was performed under fluoroscopic guidance. Resolution of the headache occurred within 5 minutes of the procedure. After three months without a headache the patient had a return of the postural headache. A second transforaminal EBP was performed again with almost immediate resolution. The patient remains headache-free almost six months from the time of first TF blood patch. This is the first published report of the use of transforaminal epidural blood patches for the successful treatment of a headache lasting longer than 3 months.
- Published
- 2012
- Full Text
- View/download PDF
25. Subdural intrathecal catheter placement: experience with two cases.
- Author
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Sorokin A, Annabi E, Yang WC, and Kaplan R
- Subjects
- Baclofen administration & dosage, Catheterization adverse effects, Catheterization instrumentation, Equipment Failure, Humans, Male, Middle Aged, Multiple Sclerosis drug therapy, Muscle Relaxants, Central administration & dosage, Pain drug therapy, Catheterization methods, Injections, Spinal methods, Subdural Space pathology
- Abstract
Background: Subdural migration of epidural catheters is well known and documented. Subdural placement of intrathecal catheters has not been recognized. Two cases of sudural placement of intrathecal catheters are presented., Objective: The possibility of subdural migration of epidural catheters and its manifestations has been well documented. The following 2 cases demonstrate that intrathecal catheters can enter the subdural space upon placement., Case Reports: The first case is a 52-year-old male with multiple sclerosis receiving a pump for intrathecal baclofen. It worked well for 10 years, but after 2 months of inadequate relief despite a 2-fold increase in baclofen, the catheter was imaged. The catheter pierced the arachnoid in the lower thoracic spine and tunneled subdural. It then pierced the arachnoid again, re-entering the cerebrospinal fluid (CSF) in the cephalad portion of the thoracic spine. Over time, the tip became covered with tissue, preventing direct CSF communication and causing subdural drug sequestration. The second case is a 54-year-old male with chronic bilateral lower extremity pain having a pump placed for pain control. Because of inadequate relief after implantation, the catheter was imaged. It pierced the arachnoid at L4-L5 but became subdural at T12-L1. At the time of surgical revision, the catheter was pulled back to L2. Repeat imaging showed it to be entirely subarachnoid, and analgesia was restored., Conclusions: These cases differ from others in the literature because the catheter was apparently subdural at the time of initial implantation. As these 2 cases demonstrate, this placement may manifest immediately, but it may remain undetected for a prolonged period. Initial subdural placement should be considered along with catheter migration into the subdural space in the differential of a malfunctioning pump.
- Published
- 2008
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