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6. Contributors

Author

Aggarwal, Manoj, primary, Akingbasote, James, additional, Anadón, Arturo, additional, Anger, Gregory J., additional, Archibong, Anthony E., additional, Ares, Irma, additional, Aschner, Michael, additional, Avila, Daiana S., additional, Bailey, Denise C., additional, Barlow, Norman J., additional, Beedanagari, Sudheer, additional, Beltyukov, P.P., additional, Bischoff, Karyn, additional, Boeck, Carina Rodrigues, additional, Bracken, William M., additional, Brehm, Emily, additional, Breyer, Richard M., additional, Bright-Ponte, Susan, additional, Brockett, Mirjana Milosevic, additional, Campagnolo, Luisa, additional, Carney, Edward W., additional, Charrette, Andrew, additional, Chebekoue, Sandrine Fleur, additional, Chiang, Catheryne, additional, Chou, Wei-Chun, additional, Cleal, Jane K., additional, Cole, Toby B., additional, Cook, Daniel, additional, Coppock, Robert W., additional, Costa, Lucio G., additional, Curras-Collazo, Margarita, additional, Dai, Wanying, additional, Dao, Khoi, additional, Da Silva, Rosane Souza, additional, Davis, T. Zane, additional, Dominguez, Francisco, additional, Doss, Robin B., additional, Dziwenka, Margitta M., additional, Enright, Brian, additional, Estevan, Carmen, additional, Evans, Timothy J., additional, Fan, Anna M., additional, Farina, Marcelo, additional, Fenton, Suzanne E., additional, Filazi, Ayhan, additional, Fitsanakis, Vanessa A., additional, FitzGerald, Rex, additional, Flaskos, John, additional, Flaws, Jodi A., additional, Flora, S.J.S., additional, Ganjam, Vekataseshu K., additional, Gardner, Dale R., additional, Garg, Ramesh C., additional, Garrick, Jacqueline M., additional, Garry, Vincent F., additional, Gelineau-van Waes, Janee, additional, Godfrey, Keith M., additional, Golubentseva, Yu V., additional, González-Martín, Roberto, additional, Green, Benedict T., additional, Guerri, Consuelo, additional, Gulati, Kavita, additional, Gupta, P.K., additional, Gupta, Ramesh C., additional, Gupta, Rekha K., additional, Guthrie, Najla, additional, Hall, Jeffery O., additional, Hargreaves, Alan J., additional, Harris, Kenneth J., additional, Hill, Bridgett N., additional, Hilmas, Corey J., additional, Hoberman, Alan M., additional, Hougaard, Karin S., additional, Ince, Sinan, additional, Iyer, Poorni R., additional, Jacobsen, Nicklas R., additional, Kalpana, Starling, additional, Kandimalla, Ramesh, additional, Kanthasamy, Arthi, additional, Kanthasamy, Anumantha, additional, Khlebnikova, N.S., additional, Klüver, Nils, additional, Kodavanti, Prasada Rao S., additional, Krishnan, Kannan, additional, Kulkarni, Shaila, additional, Kuzukiran, Ozgur, additional, Lall, Rajiv, additional, Legradi, Jessica, additional, Lewis, Rohan M., additional, Lewis, Elise M., additional, Li, Xin, additional, Lin, Pinpin, additional, Loganathan, Bommanna G., additional, Machado, Ivo F., additional, Mahadevan, Brinda, additional, Makris, Susan L., additional, Malik, Jitendra K., additional, Marreilha dos Santos, Ana Paula, additional, Marsillach, Judit, additional, Martínez-Larrañaga, María Rosa, additional, Martínez, María Aránzazu, additional, Matouskova, Klara, additional, McClellan, Roger O., additional, Milatovic, Dejan, additional, Mohammed, Ali Mustafa, additional, Montine, Thomas J., additional, Møller, Peter, additional, Multani, Pushpinder Kaur, additional, Ni, Mingwei, additional, Nikolaidis, Efstathios, additional, Novilla, Meliton N., additional, Padilla, Stephanie, additional, Palmeira, Carlos M., additional, Pamies, David, additional, Panner Selvam, Manesh Kumar, additional, Pascual, María, additional, Patwa, Jayant, additional, Phillips, Ashley, additional, Piquette-Miller, Micheline, additional, Popov, V.B., additional, Pratt, M. Margaret, additional, Protasova, G.A., additional, Rai, Nishant, additional, Ramalho-Santos, João, additional, Ramesh, Aramandla, additional, Ray, Kausik, additional, Ray, Arunabha, additional, Ren, Aiguo, additional, Renaud, Stephen J., additional, Roberts, Drucilla J., additional, Rongzhu, Lu, additional, Sachana, Magdalini, additional, Sahlman, Heidi, additional, Saini, Nitin, additional, Saini, Vandna, additional, Shabasheva, L.V., additional, Sharma, Abha, additional, Sikka, Suresh C., additional, Silva, Marilyn Helen, additional, Simsek, Ilker, additional, Singh Kalra, Rajkumar, additional, Sinha, Anita, additional, Sogorb, Miguel A., additional, Soldin, Offie P., additional, Song, Chunjuan, additional, Srivastava, Ajay, additional, Stice, Szabina A., additional, Stoker, Tammy E., additional, Stonecipher, Clinton A., additional, Szlapinski, Sandra, additional, Tanabe, Shihori, additional, Tatiparthi, Arun, additional, Teixeira da Rocha, João Batista, additional, Thokchom, Suresh Kumar, additional, Tornesi, Belen, additional, Torous, Vanda, additional, Truran, Peter, additional, Valdez, Matthew C., additional, Vandenberg, Laura N., additional, Vargesson, Neil, additional, Vilanova, Eugenio, additional, Vähäkangas, Kirsi H., additional, Vulimiri, Suryanarayana V., additional, Warner, Genoa R., additional, Welch, Kevin D., additional, Williams, Daniel C., additional, Woldemeskel, Moges, additional, Yang, Jae-Ho, additional, Yin, Zhaobao, additional, Ying, Xiaoyou, additional, Yurdakok-Dikmen, Begum, additional, Zaja-Milatovic, Snjezana, additional, and Zhou, Changqing, additional

Published
2022
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7. Cobinamide is effective for treatment of hydrogen sulfide–induced neurological sequelae in a mouse model

Author

Anantharam, Poojya, Whitley, Elizabeth M, Mahama, Belinda, Kim, Dong‐Suk, Sarkar, Souvarish, Santana, Cristina, Chan, Adriano, Kanthasamy, Anumantha G, Kanthasamy, Arthi, Boss, Gerry R, and Rumbeiha, Wilson K

Subjects
Pharmacology and Pharmaceutical Sciences, Biomedical and Clinical Sciences, Prevention, Neurosciences, Animals, Cobamides, Dose-Response Relationship, Drug, Hydrogen Sulfide, Male, Mental Disorders, Mice, Inbred C57BL, Models, Neurological, Seizures, Survival Analysis, Time Factors, Treatment Outcome, Vitamin B Complex, Weight Loss, cobinamide, hydrogen sulfide, neurological sequelae, neuroprotection, General Science & Technology
Abstract

Hydrogen sulfide (H2 S) is a highly neurotoxic gas. Acute exposure can lead to neurological sequelae among survivors. A drug for treating neurological sequelae in survivors of acute H2 S intoxication is needed. Using a novel mouse model we evaluated the efficacy of cobinamide (Cob) for increasing survival of, and reducing neurological sequalae in, mice exposed to sublethal doses of H2 S. There were two objectives: (1) to determine the dose-response efficacy of Cob and (2) to determine the effective therapeutic time window of Cob. To explore objective 1, mice were injected intramuscularly with Cob at 0, 50, or 100 mg/kg at 2 min after H2 S exposure. For objective 2, mice were injected intramuscularly with 100 mg/kg Cob at 2, 15, and 30 min after H2 S exposure. For both objectives, mice were exposed to 765 ppm of H2 S gas. Cob significantly reduced H2 S-induced lethality in a dose-dependent manner (P

Published
2017

8. Characterizing a mouse model for evaluation of countermeasures against hydrogen sulfide–induced neurotoxicity and neurological sequelae

Author

Anantharam, Poojya, Whitley, Elizabeth M, Mahama, Belinda, Kim, Dong‐Suk, Imerman, Paula M, Shao, Dahai, Langley, Monica R, Kanthasamy, Arthi, and Rumbeiha, Wilson K

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Psychology, Prevention, Behavioral and Social Science, Vaccine Related, Neurosciences, Brain Disorders, Foodborne Illness, Neurological, Mental health, Animals, Body Weight, Brain, Disease Models, Animal, Dyspnea, Female, Humans, Hydrogen Sulfide, Inhalation Exposure, Male, Mice, Respiratory Insufficiency, Seizures, inhalation exposure, hydrogen sulfide, neurotoxicity, neurodegeneration, acute toxicity, translational model, General Science & Technology
Abstract

Hydrogen sulfide (H2 S) is a highly neurotoxic gas. It is the second most common cause of gas-induced deaths. Beyond mortality, surviving victims of acute exposure may suffer long-term neurological sequelae. There is a need to develop countermeasures against H2 S poisoning. However, no translational animal model of H2 S-induced neurological sequelae exists. Here, we describe a novel mouse model of H2 S-induced neurotoxicity for translational research. In paradigm I, C57/BL6 mice were exposed to 765 ppm H2 S for 40 min on day 1, followed by 15-min daily exposures for periods ranging from 1 to 6 days. In paradigm II, mice were exposed once to 1000 ppm H2 S for 60 minutes. Mice were assessed for behavioral, neurochemical, biochemical, and histopathological changes. H2 S intoxication caused seizures, dyspnea, respiratory depression, knockdowns, and death. H2 S-exposed mice showed significant impairment in locomotor and coordinated motor movement activity compared with controls. Histopathology revealed neurodegenerative lesions in the collicular, thalamic, and cortical brain regions. H2 S significantly increased dopamine and serotonin concentration in several brain regions and caused time-dependent decreases in GABA and glutamate concentrations. Furthermore, H2 S significantly suppressed cytochrome c oxidase activity and caused significant loss in body weight. Overall, male mice were more sensitive than females. This novel translational mouse model of H2 S-induced neurotoxicity is reliable, reproducible, and recapitulates acute H2 S poisoning in humans.

Published
2017

9. Mitochondrial stress-induced H4K12 hyperacetylation dysregulates transcription in Parkinson’s disease.

Author

Minhong Huang, Huajun Jin, Anantharam, Vellareddy, Kanthasamy, Arthi, and Kanthasamy, Anumantha G.

Subjects
HISTONE acetyltransferase, HISTONE acetylation, HISTONE deacetylase, GENETIC transcription, EPIGENOMICS, PHARMACOGENOMICS
Abstract

Aberrant epigenetic modification has been implicated in the pathogenesis of Parkinson’s disease (PD), which is characterized by the irreversible loss of dopaminergic (DAergic) neurons. However, the mechanistic landscape of histone acetylation (ac) in PD has yet to be fully explored. Herein, we mapped the proteomic acetylation profiling changes at core histones H4 and thus identified H4K12ac as a key epigenomic mark in dopaminergic neuronal cells as well as in MitoPark animal model of PD. Notably, the significantly elevated H4K12ac deposition in post-mortem PD brains highlights its clinical relevance to human PD. Increased histone acetyltransferase (HAT) activity and decreased histone deacetylase 2 (HDAC2) and HDAC4 were found in experimental PD cell models, suggesting the HAT/HDAC imbalance associated with mitochondrial stress. Following our delineation of the proteasome dysfunction that possibly contributes to H4K12ac deposition, we characterized the altered transcriptional profile and diseaseassociated pathways in the MitoPark mouse model of PD. Our study uncovers the axis of mitochondrial impairment-H4K12ac deposition-altered transcription/ disease pathways as a neuroepigenetic mechanism underlying PD pathogenesis. These findings provide mechanistic information for the development of potential pharmacoepigenomic translational strategies for PD. [ABSTRACT FROM AUTHOR]

Published
2024
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10. High-Yield α-Synuclein Purification and Ionic Strength Modification Pivotal to Seed Amplification Assay Performance and Reproducibility.

Author

Janarthanam, Chelva, Clabaugh, Griffin, Wang, Zerui, Melvin, Bradley R., Scheibe, Ileia, Jin, Huajun, Anantharam, Vellareddy, Urbauer, Ramona J. B., Urbauer, Jeffrey L., Ma, Jiyan, Kanthasamy, Arthi, Huang, Xuemei, Donadio, Vincenzo, Zou, Wenquan, and Kanthasamy, Anumantha G.

Subjects
ALPHA-synuclein, PARKINSON'S disease, SUBMANDIBULAR gland, SEEDS, LIQUID chromatography, IONIC strength
Abstract

Alpha-synuclein seed amplification assays (αSyn-SAAs) have emerged as promising diagnostic tools for Parkinson's disease (PD) by detecting misfolded αSyn and amplifying the signal through cyclic shaking and resting in vitro. Recently, our group and others have shown that multiple biospecimens, including CSF, skin, and submandibular glands (SMGs), can be used to seed the aggregation reaction and robustly distinguish between patients with PD and non-disease controls. The ultrasensitivity of the assay affords the ability to detect minute quantities of αSyn in peripheral tissues, but it also produces various technical challenges of variability. To address the problem of variability, we present a high-yield αSyn protein purification protocol for the efficient production of monomers with a low propensity for self-aggregation. We expressed wild-type αSyn in BL21 Escherichia coli, lysed the cells using osmotic shock, and isolated αSyn using acid precipitation and fast protein liquid chromatography (FPLC). Following purification, we optimized the ionic strength of the reaction buffer to distinguish the fluorescence maximum (Fmax) separation between disease and healthy control tissues for enhanced assay performance. Our protein purification protocol yielded high quantities of αSyn (average: 68.7 mg/mL per 1 L of culture) and showed highly precise and robust αSyn-SAA results using brain, skin, and SMGs with inter-lab validation. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Mito-metformin protects against mitochondrial dysfunction and dopaminergic neuronal degeneration by activating upstream PKD1 signaling in cell culture and MitoPark animal models of Parkinson’s disease

Author

Ay, Muhammet, primary, Charli, Adhithiya, additional, Langley, Monica, additional, Jang, Ahyoung, additional, Padhi, Piyush, additional, Jin, Huajun, additional, Anantharam, Vellareddy, additional, Kalyanaraman, Balaraman, additional, Kanthasamy, Arthi, additional, and Kanthasamy, Anumantha G., additional

Published
2024
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13. Epitranscriptomic Reader YTHDF2 Regulates SEK1(MAP2K4)-JNK-cJUN Inflammatory Signaling in Astrocytes during Neurotoxic Stress

Author

Malovic, Emir, primary, Ealy, Alyssa, additional, Hsu, Phillip J., additional, Sarkar, Souvarish, additional, Miller, Cameron, additional, Rokad, Dharmin, additional, Goeser, Cody, additional, Hartman, Aleah Kristen, additional, Zhu, Allen, additional, Palanisamy, Bharathi, additional, Zenitsky, Gary, additional, Jin, Huajun, additional, Anantharam, Vellareddy, additional, Kanthasamy, Arthi, additional, He, Chuan, additional, and Kanthasamy, Anumantha, additional

Published
2024
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14. Prokineticin-2 upregulation during neuronal injury mediates a compensatory protective response against dopaminergic neuronal degeneration.

Author

Gordon, Richard, Neal, Matthew L, Luo, Jie, Langley, Monica R, Harischandra, Dilshan S, Panicker, Nikhil, Charli, Adhithiya, Jin, Huajun, Anantharam, Vellareddy, Woodruff, Trent M, Zhou, Qun-Yong, Kanthasamy, Anumantha G, and Kanthasamy, Arthi

Subjects
Central Nervous System, Substantia Nigra, Animals, Mice, Inbred C57BL, Mice, Transgenic, Humans, Mice, Parkinson Disease, Gastrointestinal Hormones, Extracellular Signal-Regulated MAP Kinases, Neuropeptides, Recombinant Proteins, Gene Expression Profiling, Polymerase Chain Reaction, Behavior, Animal, Signal Transduction, Cell Death, Dopaminergic Neurons, Neurodegenerative, Genetics, Parkinson's Disease, Aging, Neurosciences, Brain Disorders, 2.1 Biological and endogenous factors, Neurological, Inbred C57BL, Transgenic, Behavior, Animal
Abstract

Prokineticin-2 (PK2), a recently discovered secreted protein, regulates important physiological functions including olfactory biogenesis and circadian rhythms in the CNS. Interestingly, although PK2 expression is low in the nigral system, its receptors are constitutively expressed on nigrostriatal neurons. Herein, we demonstrate that PK2 expression is highly induced in nigral dopaminergic neurons during early stages of degeneration in multiple models of Parkinson's disease (PD), including PK2 reporter mice and MitoPark mice. Functional studies demonstrate that PK2 promotes mitochondrial biogenesis and activates ERK and Akt survival signalling pathways, thereby driving neuroprotection. Importantly, PK2 overexpression is protective whereas PK2 receptor antagonism exacerbates dopaminergic degeneration in experimental PD. Furthermore, PK2 expression increased in surviving nigral dopaminergic neurons from PD brains, indicating that PK2 upregulation is clinically relevant to human PD. Collectively, our results identify a paradigm for compensatory neuroprotective PK2 signalling in nigral dopaminergic neurons that could have important therapeutic implications for PD.

Published
2016

15. Acute hydrogen sulfide–induced neuropathology and neurological sequelae: challenges for translational neuroprotective research

Author

Rumbeiha, Wilson, Whitley, Elizabeth, Anantharam, Poojya, Kim, Dong‐Suk, and Kanthasamy, Arthi

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Psychology, Neurodegenerative, Prevention, Neurosciences, Brain Disorders, Neurological, Animals, Humans, Hydrogen Sulfide, Nervous System Diseases, Neuroprotective Agents, Translational Research, Biomedical, brain, hydrogen sulfide, neuropathology, neurodegeneration, neuroprotection, General Science & Technology
Abstract

Hydrogen sulfide (H2 S), the gas with the odor of rotten eggs, was formally discovered in 1777, over 239 years ago. For many years, it was considered an environmental pollutant and a health concern only in occupational settings. Recently, however, it was discovered that H2 S is produced endogenously and plays critical physiological roles as a gasotransmitter. Although at low physiological concentrations it is physiologically beneficial, exposure to high concentrations of H2 S is known to cause brain damage, leading to neurodegeneration and long-term neurological sequelae or death. Neurological sequelae include motor, behavioral, and cognitive deficits, which are incapacitating. Currently, there are concerns about accidental or malicious acute mass civilian exposure to H2 S. There is a major unmet need for an ideal neuroprotective treatment, for use in the field, in the event of mass civilian exposure to high H2 S concentrations. This review focuses on the neuropathology of high acute H2 S exposure, knowledge gaps, and the challenges associated with development of effective neuroprotective therapy to counteract H2 S-induced neurodegeneration.

Published
2016

17. List of contributors

Author

Ahmad, Abul H., primary, Akingbasote, James, additional, Anadón, Arturo, additional, Anand, Rashmi, additional, Anantharam, Vellareddy, additional, András, Csaba, additional, Ares, Irma, additional, Avdonin, Pavel V., additional, Ay, Muhammet, additional, Banerjee, Aryamitra, additional, Barnett, Reid E., additional, Belinskaia, Daria A., additional, Bertero, Alessia, additional, Bharti, Vijay K., additional, Bian, Wan-Ping, additional, Bischoff, Karyn L., additional, Caloni, Francesca, additional, Castela, Ana Catarina, additional, Chand, Naresh, additional, Chanderbhan, Ronald F., additional, Charli, Adhithiya, additional, Charrette, Andrew, additional, Chen, Si, additional, Chen, Tao, additional, Choudhuri, Supratim, additional, Choudhury, Soumen, additional, Coccini, Teresa, additional, Cope, Rhian B., additional, Coppock, Robert W., additional, Costa, Lucio G., additional, Damodaran, Tirupapuliyur, additional, Darvesh, Altaf S., additional, Dhruw, Leena, additional, Dormán, György, additional, Doss, Robin B., additional, DuBourdieu, Dan, additional, Dziwenka, Margitta, additional, Eades, Joshua, additional, Esch, Harald L., additional, Filazi, Ayhan, additional, Fitsanakis, Vanessa A., additional, Flachner, Beáta, additional, Fossati, Paola, additional, Gambaryan, Stepan P., additional, Garg, Ramesh C., additional, Garg, Satish K., additional, Gil, Fernando, additional, Goncharov, Nikolay V., additional, Gulati, Kavita, additional, Guo, Lei, additional, Guo, Xiaoqing, additional, Gupta, Bhanushree, additional, Gupta, Ramesh C., additional, Guthrie, Najla, additional, Gwaltney-Brant, Sharon M., additional, Hajdú, István, additional, Hartsel, Joshua A., additional, Hazzah, Trina, additional, Hernández, Antonio F., additional, Hickory, Brian, additional, Hilmas, Corey J., additional, Hoeng, Julia, additional, Jain, Amul, additional, Jenkins, Richard O., additional, Jin, Huajun, additional, Joshi, Jagdish Chandra, additional, Kalinovsky, Tatiana, additional, Kalpana, Starling, additional, Kalidindi, Sanyasi R., additional, Kanthasamy, Anumantha G., additional, Kanthasamy, Arthi, additional, Kaore, Navinchandra M., additional, Kaore, Shilpa N., additional, Kapoor, Vijay Kumar, additional, Kaur, Gurjot, additional, Kolanos, Renata, additional, Korf, Ekaterina A., additional, Krishna, Gopala, additional, Krishna, Mayur, additional, Kuča, Kamil, additional, Kudryavtsev, Igor V., additional, Kumar, Amit, additional, Kumar, Dinesh, additional, Kumar, Prafull, additional, Lall, Rajiv, additional, La Mesa, Camillo, additional, Latino, Diogo A.R.S., additional, Lehmann, Leane, additional, Li, Xilin, additional, Machado, Ivo F., additional, Makriyannis, Alexandros, additional, Malik, Jitendra K., additional, Martín-Domingo, M. Concepción, additional, Martínez, María-Aránzazu, additional, Martínez-Larrañaga, María-Rosa, additional, Mei, Nan, additional, Messinis, Dimitris E., additional, Mindukshev, Igor V., additional, Negi, Poonam, additional, Niedzwiecki, Aleksandra, additional, Ning, Baitang, additional, Novozhilov, Artem V., additional, Palmeira, Carlos Marques, additional, Papas, Andreas M., additional, Pei, De-Sheng, additional, Peitsch, Manuel C., additional, Peterson, Jeffrey D., additional, Pistollato, Francesca, additional, Pitt, Jason, additional, Pitt, Yiuka, additional, Pospisil, Pavel, additional, Poussin, Carine, additional, Pradhan, Aanchal, additional, Prakash, Atul, additional, Prasad, Sahdeo, additional, Rahal, Anu, additional, Rai, Nishant, additional, Raina, Rajinder, additional, Rath, Matthias, additional, Ray, Arunabha, additional, Rehman, Sana, additional, Richter, Gary, additional, Risuleo, Gianfranco, additional, Roberts, Ashley, additional, Rolo, Anabela Pinto, additional, Roomi, M. Waheed, additional, Sachana, Magdalini, additional, Satoh, Tetsuo, additional, Serebriakova, Maria K., additional, Sharma, Rahul, additional, Shukla, Amit, additional, Sinha, Anita, additional, Sinha, Priynak, additional, Spicer, Leon J, additional, Srivastava, Ajay, additional, Stice, Szabina A., additional, Sudnitsyna, Julia S., additional, Taku, Ila, additional, Talukder, Jamil, additional, Teodoro, João Soeiro, additional, Thokchom, Suresh Kumar, additional, Trulioff, Andrey S., additional, Ukolov, Anton I., additional, Umegaki, Keizo, additional, Verma, Pankaj, additional, Verma, Pawan K., additional, Wan, Dan, additional, Wilson-Frank, Christina, additional, Woldemeskel, Moges, additional, Wu, Qinghua, additional, Yang, Mildred S., additional, Yurdakok-Dikmen, Begum, additional, Zaja-Milatovic, Snjezana, additional, and Zoltani, Csaba K., additional

Published
2021
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18. Quercetin

Author

Ay, Muhammet, primary, Charli, Adhithiya, additional, Jin, Huajun, additional, Anantharam, Vellareddy, additional, Kanthasamy, Arthi, additional, and Kanthasamy, Anumantha G., additional

Published
2021
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19. Neurotoxicity of Vanadium

Author

Ngwa, Hilary Afeseh, Ay, Muhammet, Jin, Huajun, Anantharam, Vellareddy, Kanthasamy, Arthi, Kanthasamy, Anumantha G., Schousboe, Arne, Series editor, Aschner, Michael, editor, and Costa, Lucio G., editor

Published
2017
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20. Chronic Traumatic Encephalopathy

Author

Kanthasamy, Anumantha, Anantharam, Vellareddy, Jin, Huajun, Ghaisas, Shivani, Zenitsky, Gary, Kanthasamy, Arthi, Ikezu, Tsuneya, editor, and Gendelman, Howard E., editor

Published
2017
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27. Environmental neurotoxin dieldrin induces apoptosis via caspase-3-dependent proteolytic activation of protein kinase C delta (PKCdelta): Implications for neurodegeneration in Parkinson's disease.

Author

Kanthasamy, Anumantha G, Kitazawa, Masashi, Yang, Yongjie, Anantharam, Vellareddy, and Kanthasamy, Arthi

Subjects
Brain, Cell Nucleus, Mitochondria, Animals, Rats, Rats, Sprague-Dawley, Parkinson Disease, Nerve Degeneration, Reactive Oxygen Species, Dieldrin, Cytochromes c, Neurotoxins, Environmental Pollutants, Apoptosis, DNA Fragmentation, Protein Processing, Post-Translational, Enzyme Activation, Male, Mutant Proteins, Protein Kinase C-delta, Caspase 3, Biocatalysis, Caspase Inhibitors, Sprague-Dawley, Protein Processing, Post-Translational, Neurology & Neurosurgery, Medical and Health Sciences
Abstract

BackgroundIn previous work, we investigated dieldrin cytotoxicity and signaling cell death mechanisms in dopaminergic PC12 cells. Dieldrin has been reported to be one of the environmental factors correlated with Parkinson's disease and may selectively destroy dopaminergic neurons.MethodsHere we further investigated dieldrin toxicity in a dopaminergic neuronal cell model of Parkinson's disease, namely N27 cells, using biochemical, immunochemical, and flow cytometric analyses.ResultsIn this study, dieldrin-treated N27 cells underwent a rapid and significant increase in reactive oxygen species followed by cytochrome c release into cytosol. The cytosolic cytochrome c activated caspase-dependent apoptotic pathway and the increased caspase-3 activity was observed following a 3 hr dieldrin exposure in a dose-dependent manner. Furthermore, dieldrin caused the caspase-dependent proteolytic cleavage of protein kinase C delta (PKCδ) into 41 kDa catalytic and 38 kDa regulatory subunits in N27 cells as well as in brain slices. PKCδ plays a critical role in executing the apoptotic process in dieldrin-treated dopaminergic neuronal cells because pretreatment with the PKCδ inhibitor rottlerin, or transfection and over-expression of catalytically inactive PKCδ(K)³⁷⁶(R), significantly attenuates dieldrin-induced DNA fragmentation and chromatin condensation.ConclusionTogether, we conclude that caspase-3-dependent proteolytic activation of PKCδ is a critical event in dieldrin-induced apoptotic cell death in dopaminergic neuronal cells.

Published
2008

31. Contributors

Author

Anadón, Arturo, primary, Anantharam, Vellareddy, additional, Archibong, Anthony E., additional, Ares, Irma, additional, Aulbach, Adam D., additional, Awasthee, Nikee, additional, Banerjee, Aryamitra, additional, Banks, Leah D., additional, Barile, Frank A., additional, Beedanagari, Sudheer R., additional, Belantis, Charalampos, additional, Bergamaschi, Enrico, additional, Bhandari, Sadikshya, additional, Bhatia, Sneha P., additional, Bischoff, Karyn, additional, Borts, David J., additional, Brehm, Emily, additional, Chandra Gupta, Subash, additional, Chatterjee, Saurabh, additional, Chiang, Catheryne, additional, Chintalapati, Anirudh J., additional, Cohn, P., additional, Coppock, Robert W., additional, Costa, Lucio G., additional, Damodaran, Tirupapuliyur V., additional, D'Souza, Clinton, additional, Dettbarn, Wolf-D., additional, Devlin, Amy A., additional, Doss, Robin B., additional, Dwivedi, Shiwangi, additional, Dziwenka, Margitta M., additional, Estévez, Jorge, additional, Fabricant, Daniel S., additional, Fan, A.M., additional, Fitsanakis, Vanessa A., additional, Flaskos, John, additional, Flaws, Jodi A., additional, Flora, Swaran J.S., additional, Ford, Sue M., additional, Fortin, Jessica S., additional, Fragou, Domniki, additional, Gad, Shayne C., additional, Galateanu, Bianca, additional, Gardner, Dale R., additional, Georgiadis, George, additional, Gil, Fernando, additional, Goel, Saryu, additional, Gulumian, Mary, additional, Gupta, P.K., additional, Gupta, Ramesh C., additional, Gupta, Rekha K., additional, Gwaltney-Brant, Sharon, additional, Hargreaves, Alan J., additional, Harris, Kelly L., additional, Harris, Kenneth J., additional, Hatfield, Holly E., additional, Hayes, Wallace A., additional, Heretis, Ioannis, additional, Hernández, Antonio F., additional, Hilmas, Corey J., additional, Hood, Darryl B., additional, Huuskonen, Pasi, additional, Jacobson, Stewart B., additional, James-Yi, Sandra A., additional, Jin, Huajun, additional, Kanno, Jun, additional, Kanthasamy, Arthi, additional, Kanthasamy, Anumantha G., additional, Kaore, Shilpa N., additional, Kaore, Navinchandra M., additional, Kaphalia, Bhupendra S., additional, Karttunen, Vesa, additional, Kaur, Gurjot, additional, Kaur, Ravneet, additional, Kodavanti, Prasada Rao S., additional, Kodavanti, Urmila P., additional, Kontadakis, George A., additional, Krishna, Gopala, additional, Krishna, Priya A., additional, Krishna, Kavya A., additional, Kummu, Maria, additional, Kymionis, George D., additional, Lall, Rajiv, additional, Lin, P., additional, Loganathan, Bommanna G., additional, Loikkanen, Jarkko, additional, Lotti, Marcello, additional, Lynes, Michael A., additional, Mahadevan, Brinda, additional, Malik, Jitendra K., additional, Mamoulakis, Charalampos, additional, Mantey, Jane A., additional, Martínez-Larrañaga, María Rosa, additional, Martínez, María Aránzazu, additional, Mavridis, Charalampos, additional, McClellan, Roger O., additional, Meador, Vincent P., additional, Mikkelsen, Lars Friis, additional, Milatovic, Dejan, additional, Miller Mukherjee, Ida R., additional, Mukherjee, Anupama, additional, Multani, Pushpinder Kaur, additional, Myllynen, Päivi, additional, Myöhänen, Kirsi, additional, Negga, Rekek, additional, Negrei, Carolina, additional, Novilla, Meliton N., additional, Padilla, Stephanie, additional, Palmeira, Carlos M., additional, Panter, Kip E., additional, Pasanen, Markku, additional, Patrick, Daniel J., additional, Pavanello, Sofia, additional, Pedersen, Henrik Duelund, additional, Pelkonen, Olavi, additional, Pellizzon, Michael A., additional, Pitt, Jason, additional, Plaka, Argyro, additional, Ramesh, Aramandla, additional, Rattan, Saniya, additional, Repo, Jenni, additional, Ricci, Matthew R., additional, Rolo, Anabela P., additional, Sachana, Magdalini, additional, Sahlman, Heidi, additional, Saini, Nitin, additional, Saini, Vandana, additional, Savolainen, Kai, additional, Seth, Ratanesh Kumar, additional, Sharma, Abha, additional, Sharma, Anurag, additional, Sieppi, Elina, additional, Silva, Rui, additional, Sinha, Anita, additional, Skamagkas, Iordanis, additional, Snow, Samantha J., additional, Sogorb, Miguel A., additional, Srivastava, Ajay, additional, Stice, Szabina A., additional, Storvik, Markus, additional, Szabo, David T., additional, Teodoro, João S., additional, Tsatsakis, Aristidis M., additional, Tsiaoussis, John, additional, Vähäkangas, Kirsi, additional, Verma, Sumit Singh, additional, Vilanova, Eugenio, additional, Vulimiri, Suryanarayana V., additional, Warner, Genoa R., additional, Welch, Kevin D., additional, Wilson-Frank, Christina, additional, You, S.H., additional, Zaja-Milatovic, Snjezana, additional, Zisis, Ioannis E., additional, and Zoltani, Csaba K., additional

Published
2019
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34. Chronic Manganese Exposure and the Enteric Nervous System: An in Vitro and Mouse in Vivo Study

Author

Ghaisas, Shivani, Harischandra, Dilshan S., Palanisamy, Bharathi, Proctor, Alexandra, Jin, Huajun, Dutta, Somak, Sarkar, Souvarish, Langley, Monica, Zenitsky, Gary, Anantharam, Vellareddy, Kanthasamy, Arthi, Phillips, Gregory J., and Kanthasamy, Anumantha

Subjects
Manganese -- Environmental aspects -- Health aspects, Nerves, Peripheral -- Health aspects -- Models, Mitochondria -- Physiological aspects -- Health aspects, Digestive system diseases -- Risk factors -- Models, Environmental issues, Health
Abstract

Background: Chronic environmental exposure to manganese (Mn) can cause debilitating damage to the central nervous system. However, its potential toxic effects on the enteric nervous system (ENS) have yet to be assessed. Objective: We examined the effect of Mn on the ENS using both cell and animal models. Method: Rat enteric glial cells (EGCs) and mouse primary enteric cultures were exposed to increasing concentrations of Mn and cell viability and mitochondrial health were assessed using various morphological and functional assays. C57BL/6 mice were exposed daily to a sublethal dose of Mn (15 mg/kg/d) for 30 d. Gut peristalsis, enteric inflammation, gut microbiome profile, and fecal metabolite composition were assessed at the end of exposure. Results: EGC mitochondria were highly susceptible to Mn neurotoxicity, as evidenced by lower mitochondrial mass, adenosine triphosphate-linked respiration, and aconitase activity as well as higher mitochondrial superoxide, upon Mn exposure. Minor differences were seen in the mouse model: specifically, longer intestinal transit times and higher levels of colonic inflammation. Conclusion: Based on our findings from this study, Mn preferentially induced mitochondrial dysfunction in a rat EGC line and in vivo resulted in inflammation in the ENS. https://doi.org/10.1289/EHP7877, Introduction Manganese (Mn) is an essential trace metal for many enzymatic reactions, taking part in several metabolic as well as biological functions in the body (Bowman et al. 2011; Harischandra [...]

Published
2021
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38. Impact of Environmental Risk Factors on Mitochondrial Dysfunction, Neuroinflammation, Protein Misfolding, and Oxidative Stress in the Etiopathogenesis of Parkinson’s Disease

Author

Huang, Minhong, primary, Bargues-Carot, Alejandra, additional, Riaz, Zainab, additional, Wickham, Hannah, additional, Zenitsky, Gary, additional, Jin, Huajun, additional, Anantharam, Vellareddy, additional, Kanthasamy, Arthi, additional, and Kanthasamy, Anumantha G., additional

Published
2022
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41. List of Contributors

Author

Aggarwal, Manoj, primary, Agrawal, Shruti, additional, Anadón, Arturo, additional, Anger, Gregory J., additional, Archibong, Anthony E., additional, Ares, Irma, additional, Aschner, Michael, additional, Avila, Daiana S., additional, Bailey, Denise C., additional, Baker, Nancy C., additional, Barlow, Norman J., additional, Beedanagari, Sudheer, additional, Bischoff, Karyn, additional, Bracken, William M., additional, Brehm, Emily, additional, Breyer, Richard M., additional, Bright-Ponte, Susan, additional, Campagnolo, Luisa, additional, Carney, Edward W., additional, Castellano, Victor, additional, Chebekoue, Sandrine Fleur, additional, Chiang, Catheryne, additional, Chou, Wei-Chun, additional, Choudhuri, Supratim, additional, Cleal, Jane K., additional, Coppock, Robert W., additional, Costa, Lucio G., additional, Curras-Collazo, Margarita, additional, da Rocha, João Batista Teixeira, additional, Da Silva, Rosane S., additional, Davis, T. Zane, additional, Doss, Robin B., additional, Dziwenka, Margitta M., additional, Enright, Brian, additional, Eriksson, Per, additional, Estevan, Carmen, additional, Evans, Timothy J., additional, Fadeel, Bengt, additional, Fan, Anna M., additional, Faqi, Ali S., additional, Farina, Marcelo, additional, Fenton, Suzanne E., additional, Feuston, Maureen H., additional, Filazi, Ayhan, additional, Fitsanakis, Vanessa A., additional, Flaskos, John, additional, Flaws, Jodi A., additional, Flora, Swaran J.S., additional, Ganjam, Vekataseshu K., additional, Gardner, Dale R., additional, Gardner, Nicole M., additional, Garg, Ramesh C., additional, Garry, Vincent F., additional, Gelineau-van Waes, Janee, additional, Godfrey, Keith M., additional, Guerri, Consuelo, additional, Guizzetti, Marina, additional, Gulati, Kavita, additional, Gulumian, Mary, additional, Gupta, Pawan K., additional, Gupta, Ramesh C., additional, Gupta, Rekha K., additional, Gwaltney-Brant, Sharon M., additional, Hall, Jeffrey O., additional, Hansen, Deborah K., additional, Hargreaves, Alan J., additional, Harris, Kenneth J., additional, Hoberman, Alan M., additional, Hougaard, Karin S., additional, Ince, Sinan, additional, Inselman, Amy L., additional, Iyer, Poorni, additional, Jacobsen, Nicklas R., additional, Kagan, Valerian E., additional, Kalpana, Starling, additional, Kaneko, Kotaro, additional, Kanthasamy, Anumantha, additional, Kanthasamy, Arthi, additional, Karttunen, Vesa, additional, Kim, Hyung Sik, additional, Knudsen, Thomas B., additional, Kodavanti, Prasada Rao S., additional, Krishnan, Kannan, additional, Kulkarni, Shaila, additional, Lall, Rajiv, additional, Lasher, Michelle A., additional, Laudert, Scott B., additional, Lee, Byung-Mu, additional, Legradi, Jessica, additional, Leung, Maxwell C.K., additional, Lewis, Elise M., additional, Lewis, Rohan M., additional, Li, Xin, additional, Lin, Pinpin, additional, Loganathan, Bommanna G., additional, Lyche, Jan Ludvig, additional, MacPhail, Robert C., additional, Mahadevan, Brinda, additional, Malik, Jitendra K., additional, Marreilha dos Santos, Ana Paula, additional, Martínez, Maria Aranzazu, additional, Martínez-Larrañaga, Maria Rosa, additional, McClary, David, additional, Menezes, Fabiano P., additional, Meyer, Jerrold S., additional, Milatovic, Dejan, additional, Miller Mukherjee, Ida R., additional, Mohammed, Ali Mustafa, additional, Møller, Peter, additional, Montine, Thomas J., additional, Ni, Mingwei, additional, Nikolaidis, Efstathios, additional, Novilla, Meliton N., additional, Padilla, Stephanie, additional, Palmeira, Carlos M., additional, Pamies, David, additional, Panter, Kip E., additional, Pascual, María, additional, Pellacani, Claudia, additional, Piper, Brian J., additional, Piquette-Miller, Micheline, additional, Popov, Vadim B., additional, Pratt, M. Margaret, additional, Protasova, Galina A., additional, Rai, Nishant, additional, Ramalho-Santos, João, additional, Ramesh, Aramandla, additional, Ray, Arunabha, additional, Ray, Kausik, additional, Ren, Aiguo, additional, Renaud, Stephen J., additional, Riley, Ronald T., additional, Roberts, Drucilla J., additional, Rongzhu, Lu, additional, Sachana, Magdalini, additional, Savolainen, Kai M., additional, Shabasheva, Lilia V., additional, Shiverick, Kathleen T., additional, Sikka, Suresh C., additional, Sogorb, Miguel A., additional, Soldin, Offie P., additional, Song, Chunjuan, additional, Srivastava, Ajay, additional, Stice, Szabina A., additional, Stoker, Tammy E., additional, Toor, Jaideep S., additional, Tornesi, Belen, additional, Truran, Peter, additional, Vähäkangas, Kirsi, additional, Valdez, Joseph, additional, Vargesson, Neil, additional, Viberg, Henrik, additional, Vilanova, Eugenio, additional, Voss, Kenneth A., additional, Vulimiri, Suryanarayana V., additional, Welch, Kevin D., additional, Williams, Daniel C., additional, Woldemeskel, Moges, additional, Yang, Jae-Ho, additional, Yin, Zhaobao, additional, Ying, Xiaoyou, additional, Yurdakok-Dikmen, Begum, additional, Zaja-Milatovic, Snjezana, additional, and Zhou, Changqing, additional

Published
2017
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42. Chronic Traumatic Encephalopathy

Author

Kanthasamy, Anumantha, primary, Anantharam, Vellareddy, additional, Jin, Huajun, additional, Ghaisas, Shivani, additional, Zenitsky, Gary, additional, and Kanthasamy, Arthi, additional

Published
2016
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44. Environmental neurotoxic pesticide exposure induces gut inflammation and enteric neuronal degeneration by impairing enteric glial mitochondrial function in pesticide models of Parkinson’s disease: Potential relevance to gut-brain axis inflammation in Parkinson’s disease pathogenesis

Author

Palanisamy, Bharathi N., primary, Sarkar, Souvarish, additional, Malovic, Emir, additional, Samidurai, Manikandan, additional, Charli, Adhithiya, additional, Zenitsky, Gary, additional, Jin, Huajun, additional, Anantharam, Vellareddy, additional, Kanthasamy, Arthi, additional, and Kanthasamy, Anumantha G., additional

Published
2022
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45. Microglial immune regulation by epigenetic reprogramming through histone H3K27 acetylation in neuroinflammation.

Author

Minhong Huang, Malovic, Emir, Ealy, Alyssa, Huajun Jin, Anantharam, Vellareddy, Kanthasamy, Arthi, and Kanthasamy, Anumantha G.

Subjects
HISTONE acetylation, IMMUNOLOGIC memory, MICROGLIA, EPIGENETICS, NEUROINFLAMMATION, POSTMORTEM changes
Abstract

Epigenetic reprogramming is the ability of innate immune cells to form memories of environmental stimuli (priming), allowing for heightened responses to secondary stressors. Herein, we explored microglial epigenetic marks using the known inflammagen LPS as a memory priming trigger and Parkinsonian-linked environmental neurotoxic stressor manganese (Mn) as the secondary environmental trigger. To mimic physiological responses, the memory priming trigger LPS treatment was removed by triple-washing to allow the cells' acute inflammatory response to reset back before applying the secondary insult. Our results show that after the secondary Mn insult, levels of key proinflammatory markers, including nitrite release, iNOS mRNA and protein expression, Il-6, Il-a and cytokines were exaggerated in LPS-primed microglia. Our paradigm implies primed microglia retain immune memory that can be reprogrammed to augment inflammatory response by secondary environmental stress. To ascertain the molecular underpinning of this neuroimmune memory, we further hypothesize that epigenetic reprogramming contributes to the retention of a heightened immune response. Interestingly, Mn-exposed, LPSprimed microglia showed enhanced deposition of H3K27ac and H3K4me3 along with H3K4me1. We further confirmed the results using a PD mouse model (MitoPark) and postmortem human PD brains, thereby adding clinical relevance to our findings. Co-treatment with the p300/H3K27ac inhibitor GNE-049 reduced p300 expression and H3K27ac deposition, decreased iNOS, and increased ARG1 and IRF4 levels. Lastly, since mitochondrial stress is a driver of environmentally linked Parkinson's disease (PD) progression, we examined the effects of GNE-049 on primary trigger-induced mitochondrial stress. GNE-049 reduced mitochondrial superoxide, mitochondrial circularity and stress, and mitochondrial membrane depolarization, suggesting beneficial consequences of GNE-049 on mitochondrial function. Collectively, our findings demonstrate that proinflammatory primary triggers can shape microglial memory via the epigenetic mark H3K27ac and that inhibiting H3K27ac deposition can prevent primary trigger immune memory formation and attenuate subsequent secondary inflammatory responses. [ABSTRACT FROM AUTHOR]

Published
2023
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49. List of Contributors

Author

Ahmad, Abul H., primary, Anadón, Arturo, additional, Anand, Rashmi, additional, Anantharam, Vellareddy, additional, András, Csaba D., additional, Ares, Irma, additional, Avdonin, Pavel, additional, Ay, Muhammet, additional, Bailey, Denise C., additional, Banerjee, Aryamitra, additional, Barnett, Reid E., additional, Bharti, Vijay K., additional, Bhavsar, Shailesh K., additional, Bian, Wan-Ping, additional, Bischoff, Karyn L., additional, Bondy, Stephen C., additional, Burton-Freeman, Britt, additional, Chan, Noel, additional, Chand, Naresh, additional, Chanderbhan, Ronald F., additional, Charli, Adhithiya, additional, Chaudhary, Sulekha, additional, Chen, Si, additional, Chen, Tao, additional, Chen, Youjun, additional, Choudhuri, Supratim, additional, Coppock, Robert W., additional, Costa, Lucio G., additional, Dormán, György, additional, Duarte, Filipe V., additional, Dziwenka, Margitta, additional, Eades, Joshua, additional, Edirisinghe, Indika, additional, Esch, Harald L., additional, Filazi, Ayhan, additional, Fitsanakis, Vanessa A., additional, Flachner, Beáta, additional, Gambaryan, Stepan, additional, Garg, Ramesh C., additional, Garg, Satish K., additional, Garrick, Jacqueline, additional, Ghosh, Dilip, additional, Ghosh, Kallol K., additional, Gil, Fernando, additional, Giri, Rajan, additional, Goncharov, Nikolay, additional, Gonzalez-Suarez, Ignacio, additional, Gopalakrishnan, Gopa, additional, Gulati, Kavita, additional, Guo, Lei, additional, Guo, Xiaoqing, additional, Gupta, Bhanushree, additional, Gupta, Ramesh C., additional, Gwaltney-Brant, Sharon M., additional, Hajdú, István, additional, Hartsel, Joshua A., additional, Hatfield, Holly E., additional, Hernández, Antonio F., additional, Hickory, Brian, additional, Hoeng, Julia, additional, Ivanova, Ekaterina A., additional, Javeri, Indu, additional, Jenkins, Richard, additional, Jin, Huajun, additional, Joshi, Jagdish, additional, Kadakkuzha, Beena M., additional, Kalinovsky, Tatiana, additional, Kalpana, Starling, additional, Kanthasamy, Anumantha G., additional, Kanthasamy, Arthi, additional, Kaore, Navinchandra M., additional, Kaore, S.N., additional, Khmelevskoy, Denis, additional, Kleider, Carolin, additional, Krishna, Gopala, additional, Kubasov, Igor, additional, Kuča, Kamil, additional, Kudryavtsev, Igor, additional, Kumar, Dinesh, additional, Kunes, Martin, additional, Kutyshenko, Anatoliy V., additional, Kvetina, Jaroslav, additional, Lehmann, Leane, additional, Leung, Yiuka, additional, Li, Sandy, additional, Liu, Xin-an, additional, Makriyannis, Alexandros, additional, Malik, Jitendra K., additional, Martin, Florian, additional, Martín-Domingo, M. Concepción, additional, Martínez, María Aránzazu, additional, Martínez-Larrañaga, María Rosa, additional, Maevsky, Eugene, additional, Mei, Nan, additional, Milatovic, Dejan, additional, Mindukshev, Igor, additional, Mondhe, Dilip M., additional, Niedzwiecki, Aleksandra, additional, Ning, Baitang, additional, Novozhilov, Artem, additional, Orekhov, Alexander N., additional, Palmeira, Carlos M., additional, Pei, De-Sheng, additional, Peitsch, Manuel C., additional, Pellacani, Claudia, additional, Perez, Evette, additional, Peterson, Jeffrey D., additional, Petrenko, Alexey S., additional, Pistollato, Francesca, additional, Pitt, Jason, additional, Prakash, Atul, additional, Rahal, Anu, additional, Rai, Nishant, additional, Raina, Rajinder, additional, Rath, Matthias, additional, Ray, Arunabha, additional, Risuleo, Gianfranco, additional, Roberts, Ashley, additional, Rolo, Anabela P., additional, Roomi, M.Waheed, additional, Roque, Pamela J., additional, Sachana, Magdalini, additional, Sandhu, Amandeep, additional, Satoh, Tetsuo, additional, Scheffler, Anne, additional, Serebriakova, Maria, additional, Sharman, Edward H., additional, Singh, Rajendra K., additional, Smirnova, Elena A., additional, Sudnitsyna, Julia, additional, Sukhanov, Boris P., additional, Swarnkar, Supriya, additional, Teodoro, João S., additional, Thaker, Aswin M., additional, Trulioff, Andrey, additional, Tutelyan, Victor A., additional, Ukolov, Anton, additional, Umegaki, Keizo, additional, Voitenko, Natalia, additional, Wan, Dan, additional, Wang, Kejian, additional, Wu, Mei Yi, additional, Wu, Qinghua, additional, Xuan, Jiekun, additional, Yang, Mildred S., additional, Dikmen, Begum Yurdakok, additional, Zaja-Milatovic, Snjezana, additional, Zhang, Zhuhong, additional, and Zoltani, Csaba K., additional

Published
2016
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50. Quercetin

Author

Ay, Muhammet, primary, Charli, Adhithiya, additional, Jin, Huajun, additional, Anantharam, Vellareddy, additional, Kanthasamy, Arthi, additional, and Kanthasamy, Anumantha G., additional

Published
2016
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