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139 results on '"Ramos, Alberto Javier"'

1. List of contributors

Author

Acosta, Cristian G., primary, Adam, Cristina, additional, Aggarwal, Nikita, additional, Ahmad, Sarfaraz, additional, Alenina, Natalia, additional, Alexandre-Santos, Beatriz, additional, Alfano, Gaetano, additional, Amin, Ghadir, additional, Arora, Sandeep, additional, Asami, Tomoichiro, additional, Azinheira Nobrega Cruz, Nayara, additional, Bader, Michael, additional, Bagang, Newly, additional, Bedi, Onkar, additional, Bellomo, Rinaldo, additional, Bhat, Anjali, additional, Biancardi, Vinicia Campana, additional, Bitencourt, Letícia, additional, Booz, George W., additional, Brito-Toscano, E.C., additional, Carlo Magliano, D'Angelo, additional, Caroline Gonçalves de Oliveira, Lilian, additional, Chandra Bharti, Alok, additional, Chappell, Mark C., additional, Chaudhary, Apoorva, additional, Chhokar, Arun, additional, Claudia, Bregonzio, additional, Corte Frantz, Eliete Dalla, additional, Cudnoch-Jedrzejewska, Agnieszka, additional, Delforce, Sarah J., additional, de Miranda, A.S., additional, de Oliveira Campos, Juliana Lacerda, additional, de Senanayake, Preenie, additional, De Silva, T. Michael, additional, Diab, Reine, additional, Elena Casarini, Dulce, additional, Ferrario, Carlos M., additional, Fischer, Bruna Luisa, additional, Gallagher, Patricia E., additional, Gupta, Kirti, additional, Gupta, Shabarni, additional, Gustavo, Baiardi, additional, Gwathmey, TanYa M., additional, Habeichi, Nada J., additional, Haznedaroglu, Ibrahim C., additional, Iwasaki, Shin-ichi, additional, Janjua, Divya, additional, Jia, Hongpeng, additional, Kangussu, Lucas M., additional, Kashyap, Manoj Kumar, additional, Kathleen Phillips, Jacqueline, additional, Kowara, Michal, additional, Kumar, Manish, additional, Lankadeva, Yugeesh R., additional, Li, Sheran, additional, Li, Yan Chun, additional, Lin, Qing, additional, Loeffler, Ivonne, additional, Lumbers, Eugenie R., additional, Malkan, Umit Yavuz, additional, Marcu, Dragoş Traian, additional, Massoud, Gaelle, additional, May, Clive N., additional, Melo, Ana Clara, additional, Mericskay, Mathias, additional, Morosin, Saije K., additional, Natalia Andrea, Marchese, additional, Okada, Yasuo, additional, Osvaldo Martín, Basmadjian, additional, Patterson, Sean I., additional, Peliky Fontes, Marco Antônio, additional, Pringle, Kirsty G., additional, Rachid, M.A., additional, Ramchandra, Rohit, additional, Ramos, Alberto Javier, additional, Rao, Rashmi, additional, Rocha, N.P., additional, Sahu, Pratap Kumar, additional, Sascău, Radu Andy, additional, See, Emily J., additional, Seltzer, Alicia M., additional, Senrung, Anna, additional, Sepúlveda-Fragoso, Vinícius, additional, Serio, Rosa, additional, Shaltout, Hossam A., additional, Shanks, Julia, additional, Silveira de Queiroz Campos, Mauro, additional, Simões-e-Silva, Ana Cristina, additional, Singh, Gaaminepreet, additional, Soares de Brito, Stephanie Bruna Camilo, additional, Sobey, Christopher G., additional, Sriramula, Srinivas, additional, Stătescu, Cristian, additional, Subudhi, Bharat Bhusan, additional, Szczepanska-Sadowska, Ewa, additional, Şalaru, Delia Lidia, additional, Tallant, E. Ann, additional, Teixeira, A.L., additional, Thakur, Kulbhushan, additional, Toya, Shuji, additional, Tripathi, Tanya, additional, Valdez, Susana R., additional, Vaz de Castro, Pedro Alves Soares, additional, Victoria Belén, Occhieppo, additional, VonCannon, Jessica L., additional, Wolf, Gunter, additional, Wong Zhang, David E., additional, Wright, Kendra N., additional, Yadav, Joni, additional, Yamaleyeva, Liliya M., additional, Yoshimura, Ken, additional, Zera, Tymoteusz, additional, Zizzo, Maria Grazia, additional, and Zouein, Fouad A., additional

Published
2023
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25. Detrimental Effects of HMGB-1 Require Microglial-Astroglial Interaction: Implications for the Status Epilepticus -Induced Neuroinflammation

Author

Rosciszewski, Gerardo, primary, Cadena, Vanesa, additional, Auzmendi, Jerónimo, additional, Cieri, María Belén, additional, Lukin, Jerónimo, additional, Rossi, Alicia R., additional, Murta, Veronica, additional, Villarreal, Alejandro, additional, Reinés, Analia, additional, Gomes, Flávia C. A., additional, and Ramos, Alberto Javier, additional

Published
2019
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27. Cannabidiol (CBD) Inhibited Rhodamine-123 Efflux in Cultured Vascular Endothelial Cells and Astrocytes Under Hypoxic Conditions.

Author

Auzmendi, Jerónimo, Palestro, Pablo, Blachman, Agustín, Gavernet, Luciana, Merelli, Amalia, Talevi, Alan, Calabrese, Graciela Cristina, Ramos, Alberto Javier, and Lazarowski, Alberto

Subjects
VASCULAR endothelial cells, CANNABIDIOL, ASTROCYTES, VIMPAT, ATP-binding cassette transporters, DRUG development
Abstract

Despite the constant development of new antiepileptic drugs (AEDs), more than 30% of patients develop refractory epilepsy (RE) characterized by a multidrug-resistant (MDR) phenotype. The "transporters hypothesis" indicates that the mechanism of this MDR phenotype is the overexpression of ABC transporters such as P-glycoprotein (P-gp) in the neurovascular unit cells, limiting access of the AEDs to the brain. Recent clinical trials and basic studies have shown encouraging results for the use of cannabinoids in RE, although its mechanisms of action are still not fully understood. Here, we have employed astrocytes and vascular endothelial cell cultures subjected to hypoxia, to test the effect of cannabidiol (CBD) on the P-gp-dependent Rhodamine-123 (Rho-123) efflux. Results show that during hypoxia, intracellular Rho-123 accumulation after CBD treatment is similar to that induced by the P-gp inhibitor Tariquidar (Tq). Noteworthy, this inhibition is like that registered in non-hypoxia conditions. Additionally, docking studies predicted that CBD could behave as a P-gp substrate by the interaction with several residues in the α-helix of the P-gp transmembrane domain. Overall, these findings suggest a direct effect of CBD on the Rho-123 P-gp-dependent efflux activity, which might explain why the CBD add-on treatment regimen in RE patients results in a significant reduction in seizure frequency. [ABSTRACT FROM AUTHOR]

Published
2020
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35. The Proinflammatory RAGE/NF-κB Pathway Is Involved in Neuronal Damage and Reactive Gliosis in a Model of Sleep Apnea by Intermittent Hypoxia

Author

Angelo, Maria Florencia, primary, Aguirre, Alejandra, additional, Avilés Reyes, Rolando X., additional, Villarreal, Alejandro, additional, Lukin, Jerónimo, additional, Melendez, Matías, additional, Vanasco, Virginia, additional, Barker, Phil, additional, Alvarez, Silvia, additional, Epstein, Alberto, additional, Jerusalinsky, Diana, additional, and Ramos, Alberto Javier, additional

Published
2014
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50. The 5HT1A receptor agonist, 8-OH-DPAT, protects neurons and reduces astroglial reaction after ischemic damage caused by cortical devascularization

Author

Ramos, Alberto Javier, Rubio, María Dolores, Defagot, Cristina, Hischberg, Lotta, Villar, Marcelo J., and Brusco, Alicia

Subjects
*SEROTONIN, *CENTRAL nervous system, *NERVOUS system, *SERUM
Abstract

Abstract: Serotonin 1A (5HT1A) receptor agonists have shown neuroprotective properties in different models of central nervous system injury. Activation of neuronal 5HT1A receptors appears to be involved in the neuroprotective effects. It remains to be elucidated if astroglial cells are responsive to the 5HT1A neuroprotective effects. The participation of astroglial S100B trophic factor has been proposed since 5HT1A activation leads to S100B release and nanomolar concentration level of this molecule showed pro-survival activity in neuronal cultures. Using the cortical devascularization model (CD; unilateral pial disruption), a procedure that results in localized ischemia without producing direct physical damage to brain tissue, we tested the effects of a full 5HT1A agonist, 8-OH-DPAT, or the antagonist WAY-100635 on cortical neuronal survival, astroglial cell response and S100B expression. Wistar rats were subjected to CD lesion which consisted of a craniotomy followed by physical damage to the underlying pial blood vessels. Two and twenty-four hours after the CD lesion, animals received intraperitoneally 8-OH-DPAT (1 mg/kg), WAY-100635 (1 mg/kg) or vehicle (sterile saline). At 3, 7 or 14 days post-lesion, animals were sacrificed and their brains processed for immunohistochemistry to detect GFAP, vimentin, MAP-2, S100B and nuclear Hoechst staining. S100B level in the brain cortex and serum was quantified by an ELISA assay. Serum S100B was considered an index of S100B release. 8-OH-DPAT treatment reduced neuronal death, dendrite loss, astroglial hypertrophy and hyperplasia. In contrast, WAY-100635 treatment increased these parameters of damage. S100B intracellular immunoreactivity in astrocytes and total S100B level showed long-lasting changes after the CD lesion and subsequent treatments depending on the 5HT1A activity. The level of serum S100B was increased in 8-OH-DPAT-treated animals. Increased damage observed in WAY-100635-treated animals supports the hypothesis that the protective 8-OH-DPAT action may be mediated by specific 5HT1A receptors. The reduction in astroglial hypertrophy and hyperplasia as well as long-term changes in S100B immunoreactivity and increased S100B release that we observed allows us to hypothesize that astroglial cells may play an important role in 5HT1A-mediated neuroprotection. [Copyright &y& Elsevier]

Published
2004
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