Grażyna Nowak
Researcher
Also affiliated: Rzeszów University of Technology (1991–2013); University of Georgia (1995); University of Arkansas Medical Center (2015); Institute for Transfusion Medicine (2015); Instytut Hematologii i Transfuzjologi (2005–2020); University of Applied Management Studies (2020)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Grażyna Nowak's research focuses on the protective effects of γ-tocotrienol against mitochondrial dysfunction and organ damage following renal ischemia. Her work investigates how this compound can mitigate energy deficits, morphological damage, and decreased renal function in preclinical models. Nowak also contributes to health sciences education, having published on the effectiveness of microlearning activities in improving student comprehension and performance in biochemistry courses. She has a distinguished publication record with 76 total publications and 1,183 citations, reflected in her h-index of 20. Her recent work also includes studies on kidney tubule cells, mitochondria, and oxygen consumption, utilizing animal models including rabbits. Nowak collaborates with researchers at the University of Arkansas for Medical Sciences, including Olivia Speed, Jasna Vuk, and Judit Megyesi.
Metrics
- h-index: 20
- Publications: 76
- Citations: 1,192
Selected Publications
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Microlearning activities improve student comprehension of difficult concepts and performance in a biochemistry course (2023)
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γ-Tocotrienol Protects against Mitochondrial Dysfunction, Energy Deficits, Morphological Damage, and Decreases in Renal Functions after Renal Ischemia (2021)
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Deletion of VDAC1 Hinders Recovery of Mitochondrial and Renal Functions After Acute Kidney Injury (2020)
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Protein kinase Cα mediates recovery of renal and mitochondrial functions following acute injury (2019)
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Protein kinase Cε targets respiratory chain and mitochondrial membrane potential but not F<sub>0</sub>F<sub>1</sub>‐ATPase in renal cells injured by oxidant (2018)
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Deletion of protein kinase C-ε attenuates mitochondrial dysfunction and ameliorates ischemic renal injury (2016)
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Protein Kinase C-α Interaction with F0F1-ATPase Promotes F0F1-ATPase Activity and Reduces Energy Deficits in Injured Renal Cells (2015)
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Radiation-Induced Alterations in Mitochondria of the Rat Heart (2014)
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes (2013)
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Protein kinase C-α interaction with iHSP70 in mitochondria promotes recovery of mitochondrial function after injury in renal proximal tubular cells (2013)
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes (2013)
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Protein kinase C-α activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cells (2012)
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Protein kinase C-ε activation induces mitochondrial dysfunction and fragmentation in renal proximal tubules (2011)
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γ-Tocotrienol Protects against Mitochondrial Dysfunction and Renal Cell Death (2011)
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The repair of Na <sup>+</sup> ‐dependent glucose uptake following injury is regulated by PKC‐α and PKC‐ε . (2007)
Collaboration Network
Top Collaborators
- γ-Tocotrienol Protects against Mitochondrial Dysfunction, Energy Deficits, Morphological Damage, and Decreases in Renal Functions after Renal Ischemia
- Microlearning activities improve student comprehension of difficult concepts and performance in a biochemistry course
- Microlearning activities improve student comprehension of difficult concepts and performance in a biochemistry course
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