Carlos A Dias-Junior

Prof. Carlos A Dias-Junior

orcid

Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 July 2016 in Nitric Oxide
Verified
Journal Article
Closed access
VGVictor Hugo Gonçalves-Rizzi
Victor Hugo Gonçalves-Rizzi
JPJose Sergio Possomato-Vieira
Jose Sergio Possomato-Vieira
TGTamiris Uracs Sales Graça
Tamiris Uracs Sales Graça
RNRegina Aparecida Nascimento
Regina Aparecida Nascimento
CDCarlos A Dias-Junior
Carlos A Dias-Junior

8 November 2014 in Basic & Clinical Pharmacology & Toxicology
Verified
Journal Article
Closed access
PDF file
RNRegina A. Nascimento
Regina A. Nascimento
GMGabryella Mendes
Gabryella Mendes
JPJose S. Possomato‐Vieira
Jose S. Possomato‐Vieira
VGVictor Hugo Gonçalves‐Rizzi
Victor Hugo Gonçalves‐Rizzi
HKHélio Kushima
Hélio Kushima
CDCarlos A Dias-Junior
Carlos A Dias-Junior

14 October 2018 in Basic & Clinical Pharmacology & Toxicology
Verified
Journal Article
Closed access
PDF file
JCJessica Sabbatine Chimini
Jessica Sabbatine Chimini
JPJose Sergio Possomato‐Vieira
Jose Sergio Possomato‐Vieira
MSMaria Luiza Santos da Silva
Maria Luiza Santos da Silva
CDCarlos A Dias-Junior
Carlos A Dias-Junior

1 June 2008 in Jornal Brasileiro de Pneumologia
Verified
Journal Article
Open access
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CDCarlos A Dias-Junior
Carlos A Dias-Junior
SCStefany Bruno de Assis Cau
Stefany Bruno de Assis Cau
Jose Tanus-SantosJose Tanus-Santos
Jose Tanus-Santos
O nitric oxide (NO, óxido nítrico) é um mediador endógeno vasoativo que contribui para a homeostase vascular pulmonar. O NO é produzido por três isoformas das nitric oxide synthases (NOS, óxido nítrico sintases)-NOS neuronial (nNOS); NOS induzida (iNOS); e NOS endotelial (eNOS)-estando as três presentes no pulmão. Estudos que utilizaram inibidores farmacológicos ou camundongos knockout têm demonstrado que o NO derivado da eNOS desempenha importantes papéis ao modular o tônus vascular pulmonar e atenuar a hipertensão pulmonar. Por outro lado, estudos focados no papel da iNOS têm mostrado que essa isoforma contribui para a fisiopatologia da lesão pulmonar aguda e da síndrome do desconforto respiratório agudo. Esta revisão objetivou delinear o papel desempenhado pelo NO no controle da circulação pulmonar, tanto em condições fisiológicas como fisiopatológicas. Além disso, revisamos as evidências de que a via L-arginina-NO-guanosina monofosfato cíclico seja um importante alvo farmacológico para a terapia de doenças vasculares pulmonares.

1 January 2015 in BioMed Research International
Verified
Journal Article
Open access
PDF file
TRThalita L. A. Rocha
Thalita L. A. Rocha
CDCarlos A Dias-Junior
Carlos A Dias-Junior
JPJose S. Possomato-Vieira
Jose S. Possomato-Vieira
VGVictor H. Gonçalves-Rizzi
Victor H. Gonçalves-Rizzi
FNFlávia R. Nogueira
Flávia R. Nogueira
MBMariana G. Braz
Mariana G. Braz
Taking into account that there are controversial antioxidative effects of inhalational anesthetics isoflurane and sevoflurane and absence of comparison of genotoxicity of both anesthetics in animal model, the aim of this study was to compare DNA damage and antioxidant status in Wistar rats exposed to a single time to isoflurane or sevoflurane. The alkaline single-cell gel electrophoresis assay (comet assay) was performed in order to evaluate DNA damage in whole blood cells of control animals (unexposed;n= 6) and those exposed to 2% isoflurane (n= 6) or 4% sevoflurane (n= 6) for 120 min. Plasma antioxidant status was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. There was no statistically significant difference between isoflurane and sevoflurane groups regarding hemodynamic and temperature variables (P> 0.05). Sevoflurane significantly increased DNA damage compared to unexposed animals (P= 0.02). In addition, Wistar rats anesthetized with isoflurane showed higher antioxidative status (MTT) than control group (P= 0.019). There were no significant differences in DNA damage or antioxidant status between isoflurane and sevoflurane groups (P> 0.05). In conclusion, our findings suggest that, in contrast to sevoflurane exposure, isoflurane increases systemic antioxidative status, protecting cells from DNA damage in rats.

1 March 2016 in Environmental Toxicology and Pharmacology
Verified
Journal Article
Closed access
JCJoao Leandro Chaguri
Joao Leandro Chaguri
AGAntonio Francisco Godinho
Antonio Francisco Godinho
DHDaniel França Horta
Daniel França Horta
VGVictor Hugo Gonçalves-Rizzi
Victor Hugo Gonçalves-Rizzi
JPJose Sergio Possomato-Vieira
Jose Sergio Possomato-Vieira
CDCarlos A Dias-Junior
Carlos A Dias-Junior