Day 1 :
Keynote Forum
Thomas R McCune
EVMS, USA
Keynote: High dose vitamin C associated with acute kidney injury and mortality
Time : 09:30-10:30
Biography:
Thomas McCune is the Chair of the Division of Nephrology Department of Internal Medicine at Eastern Virginia Medical School. His current areas of research include SARS-CoV-2 vaccination in transplant patients, APOL-1and other congenital kidney diseases, and technics to decrease AKI in healthcare settings.
Abstract:
Background: The effects of vitamin C on clinical outcomes in critically ill patients remain controversial due to inconclusive studies .Oxalic acid and oxalate toxicity have been shown to occur in myocardial tissue of patients with hereditary and possibly secondary hyperoxaluria . This retrospective observational cohort study evaluated the effects of vitamin C therapy on acute kidney injury (AKI) and mortality among septic patients.
Methods: Electronic medical records of 1390 patients from an academic hospital who were categorized
Results: Data revealed that vitamin C therapy was associated with increases in AKI (OR=2.07 95% CI [1.46-2.93]) and in-hospital mortality (OR= 1.67 95% CI [1.003-2.78]) after adjusting for demographic and clinical covariates. When stratified to examine ICU patients, vitamin C therapy remained a significant risk factor of AKI (OR=1.61 95% CI [1.09-2.39]) and provided no protective benefit against mortality (OR= 0.79 95% CI [0.48-1.31]). The authors recommend ongoing use of high dose vitamin C in sepsis should be appraised due to observed associations with AKI and death
Keynote Forum
Guoli Dai
Indiana University-Purdue University Indianapolis, USA
Keynote: Activin B promotes the initiation and progression of liver fibrosis
Biography:
Dr. Guoli Dai is an associate professor in the Department of Biology, School of Science, Center for Developmental and Regenerative Biology, in Indiana University-Purdue University Indianapolis (IUPUI). His research interest focuses on molecular and cellular mechanisms controlling liver growth and regeneration.
Abstract:
Background & Aims: Liver fibrosis is a pivotal pathology in multiple hepatic disease indications, profoundly characterizing disease severity and outcomes. The role of activin B, a TGFβ superfamily cytokine, in liver health and disease is largely unknown. We aimed to investigate whether activin B modulates liver fibrogenesis.
Methods: Liver and serum activin B, along with its analog activin A, were analyzed in patients with liver fibrosis from different etiologies and in mouse acute and chronic liver injury models. Activin B, activin A, or both was immunologically neutralized in mice with progressive or established carbon tetrachloride (CCl4)-induced liver fibrosis. The direct effects of activin B and A on hepatocytes and hepatic stellate cells (HSCs) were evaluated in vitro.
Results: As a result, hepatic and circulating activin B was increased in human patients with liver fibrosis caused by several liver diseases. In mice, hepatic and circulating activin B exhibited persistent elevation following the onset of several types of liver injury, whereas activin A displayed transient increases. The results revealed a close correlation of activin B with liver injury regardless of etiology and species. We found that neutralizing activin B largely prevented, as well as remarkably regressed, CCl4-induced liver fibrosis, which was augmented by co-neutralizing activin A. Mechanistically, activin B directly promotes hepatocyte death, induces a profibrotic expression profile in HSCs, and stimulates HSCs to form a septa structure. In addition, activin B and A interdependently upregulated the transcription of profibrotic factors including connective tissue growth factor and TGFβ1 in injured livers.
Keynote Forum
Anca Irina Galaction
University of Medicine and Pharmacy of Iasi, Romania