Yasmine Nonose

New York Stem Cell Foundation

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Diogo O. Souza

Universidade Federal do Rio Grande do Sul

Adriano Martimbianco de Assis

Universidade Católica de Pelotas

Iraci Lucena da Silva Torres

EsSALUD

Joanna Ripoll Rozisky

Universidade Federal do Rio Grande do Sul

Gabriela Laste

Hospital de Clínicas de Porto Alegre

Isabel Cristina de Macedo

Hospital de Clínicas de Porto Alegre

Fernanda Urruth Fontella

Universidade Federal do Rio Grande do Sul

Jussemara Souza da Silva

Instituto de Infectologia Emílio Ribas

Vinícius Souza dos Santos

Universidade La Salle

Roberto Farina Almeida

Universidade Federal de Pelotas

Cooperative Institutions

Universidade Federal do Rio Grande do Sul

Hospital de Clínicas de Porto Alegre

Universidade Federal do Rio Grande

Universidade Católica de Pelotas

Universidade Federal de Ciências da Saúde de Porto Alegre

Instituto de Saúde

Universidade Federal da Bahia

University of Rio Grande and Rio Grande Community College

Centro de Aplicaciones Tecnológicas y Desarrollo Nuclear

Centro de Investigación y Desarrollo de medicamentos

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Metabolismo energético cerebral é modulado em ambos os hemisférios de um modelo experimental de isquemia focal permanente

Yasmine Nonose

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UNIVERSIDADE FEDERAL DO RIO GRANDE DO SUL Faculdade de Farmácia Disciplina de Trabalho de Conclusão de Curso de Farmácia

Yasmine Nonose

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Corrigendum to “JM-20 treatment prevents neuronal damage and memory impairment induced by aluminum chloride in rats” [Neurotoxicology 87 (2021) 70–85]

NeuroToxicology (2023)

Maylin Wong-Guerra Yanay Montano-Peguero Jeney Ramírez-Sánchez Javier Jiménez-Martín Luis Arturo Fonseca-Fonseca

Memory Impairment

Neuronal damage

10.1016/j.neuro.2023.09.003

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EB Formation using Aggrewell 400/800 v1

Niraj Sawarkar Regine Tipon Yasmine Nonose Gist F. Croft

Embryoid body formation is the aggregate formation of hPS cells in a three-dimensional format to differentiate into specific lineages. In this,protocol we would discuss some important steps to ensure consistent EB formation using multiple cell lines.

10.17504/protocols.io.14egn64bpl5d/v1

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Neonathal morphine treatment alters glutamate uptake in spinal cord of rats

Vinícius Souza dos Santos Joanna Ripoll Rozisky Yasmine Nonose Fernanda Urruth Fontella Deusa Vendite

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Comportamento hiperalgésico induzido pelo tratamento repetido com morfina no período neonatal é revertido pela melatonina em ratos Wistar

Alícia Deitos Joanna Ripoll Rozisky Gabriela Laste Cleverson Moraes de Oliveira Carla de Oliveira

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Acute Liver Failure Induces Glial Reactivity, Oxidative Stress and Impairs Brain Energy Metabolism in Rats

Frontiers in Molecular Neuroscience (2020)

Pedro Arend Guazzelli Giordano Fabricio Cittolin‐Santos Leo Anderson Meira-Martins Mateus Grings Yasmine Nonose

Acute liver failure (ALF) implies a severe and rapid liver dysfunction that leads to impaired liver metabolism and hepatic encephalopathy (HE). Recent studies have suggested that several brain alterations such as astrocytic dysfunction and energy metabolism impairment may synergistically interact, playing a role in the development of HE. The purpose of the present study is to investigate early alterations in redox status, energy metabolism and astrocytic reactivity of rats submitted to ALF. Adult male Wistar rats were submitted either to subtotal hepatectomy (92% of liver mass) or sham operation to induce ALF. Twenty-four hours after the surgery, animals with ALF presented higher plasmatic levels of ammonia, lactate, ALT and AST and lower levels of glucose than the animals in the sham group. Animals with ALF presented several astrocytic morphological alterations indicating astrocytic reactivity. The ALF group also presented higher mitochondrial oxygen consumption, higher enzymatic activity and higher ATP levels in the brain (frontoparietal cortex). Moreover, ALF induced an increase in glutamate oxidation concomitant with a decrease in glucose and lactate oxidation. The increase in brain energy metabolism caused by astrocytic reactivity resulted in augmented levels of reactive oxygen species (ROS) and Poly [ADP-ribose] polymerase 1 (PARP1) and a decreased activity of the enzymes superoxide dismutase and glutathione peroxidase (GSH-Px). These findings suggest that in the early stages of ALF the brain presents a hypermetabolic state, oxidative stress and astrocytic reactivity, which could be in part sustained by an increase in mitochondrial oxidation of glutamate.

10.3389/fnmol.2019.00327

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Morphine treatment in early life alters glutamate uptake in the spinal synaptosomes of adult rats

Neuroscience Letters (2012)

Joanna Ripoll Rozisky Deusa Vendite Fernanda Urruth Fontella Yasmine Nonose Gabriela Laste

Morphine exposure during the neonatal period can promote changes in pain signaling pathways that can be expressed as an increased nociceptive response in adult life. Glutamate is the major excitatory neurotransmitter in primary afferent terminals and plays a critical role in normal spinal excitatory synaptic transmission. Considering the importance of a better understanding of the mechanisms that underlie nociceptive changes throughout the life course, the aim of this study was investigate the effects of repeated morphine administration at postnatal days 8 (P8) to 14 (P14) on glutamate uptake in spinal synaptosomes at P30 and P60. The morphine group showed decreased [3H]-glutamate uptake as compared to control groups in both P30 and P60. These findings suggest that morphine exposure in early life leads to changes in glutamatergic signaling at least until the 60th day of age, which may lead to increased levels of glutamate in the spinal synaptic cleft and, consequently, an increased nociceptive response in adult life. Thus, this study highlights the importance of conducting research in this field to provide a comprehensive knowledge of the long-term effects of early-life morphine treatment on nociceptive pathways.

10.1016/j.neulet.2012.09.008

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Alterações nas respostas nociceptiva e bioquímica após intervenção farmacológica com isoflurano, associado ou não à cirurgia

Liciane Fernandes Medeiros Andressa de Souza Joanna Ripoll Rozisky Yasmine Nonose Vinícius Souza dos Santos

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Cerebral Ketone Body Oxidation Is Facilitated by a High Fat Diet Enriched with Advanced Glycation End Products in Normal and Diabetic Rats

Frontiers in Neuroscience (2016)

Adriano Martimbianco de Assis Jussemara Souza da Silva Anderson Rech Aline Longoni Yasmine Nonose

Diabetes mellitus (DM) causes important modifications in the availability and use of different energy substrates in various organs and tissues. Similarly, dietary manipulations such as high fat diets also affect systemic energy metabolism. However, how the brain adapts to these situations remains unclear. To investigate these issues, control and alloxan-induced type I diabetic rats were fed either a standard or a high fat diet enriched with advanced glycation end products (AGEs) (HAGE diet). The HAGE diet increased their levels of blood ketone bodies, and this effect was exacerbated by DM induction. To determine the effects of diet and/or DM induction on key cerebral bioenergetic parameters, both ketone bodies (β-hydroxybutyric acid) and lactate oxidation were measured. In parallel, the expression of Monocarboxylate Transporter 1 (MCT1) and 2 (MCT2) isoforms in hippocampal and cortical slices from rats submitted to these diets was assessed. Ketone body oxidation increased while lactate oxidation decreased in hippocampal and cortical slices in both control and diabetic rats fed a HAGE diet. In parallel, the expression of both MCT1 and MCT2 increased only in the cerebral cortex in diabetic rats fed a HAGE diet. These results suggest a shift in the preferential cerebral energy substrate utilization in favor of ketone bodies in animals fed a HAGE diet, an effect that, in DM animals, is accompanied by the enhanced expression of the related transporters.

10.3389/fnins.2016.00509

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