Establishment of a workflow for high-throughput identification of anti-inflammatory peptides from sea cucumbers DOI
Bingxue Jiang,

Jinqiu Liu,

Zihao Zhu

et al.

Food Research International, Journal Year: 2024, Volume and Issue: 197, P. 115171 - 115171

Published: Sept. 30, 2024

Language: Английский

A novel label-free biosensor for myocardial ischemia biomarker detection via CRISPR/12a DOI

Chunping Liu,

Qiaojing Liu,

Xiaoling Chen

et al.

Biosensors and Bioelectronics, Journal Year: 2024, Volume and Issue: 270, P. 116954 - 116954

Published: Nov. 17, 2024

Language: Английский

Citations

1

Autophagy deficiency exacerbated hypoxia-reoxygenation induced inflammation and cell death via a mitochondrial DNA/STING/IRF3 pathway DOI Creative Commons
Eddie Tam, Erfei Song,

Nina Noskovičová

et al.

Life Sciences, Journal Year: 2024, Volume and Issue: 358, P. 123173 - 123173

Published: Oct. 24, 2024

Language: Английский

Citations

1

Transcriptomic analysis reveals the lipid metabolism-related gene regulatory characteristics and potential therapeutic agents for myocardial ischemia-reperfusion injury DOI Creative Commons
Jiahe Wu, Huanhuan Cai, Xiaorong Hu

et al.

Frontiers in Cardiovascular Medicine, Journal Year: 2024, Volume and Issue: 11

Published: Jan. 29, 2024

Background Impaired energy balance caused by lipid metabolism dysregulation is an essential mechanism of myocardial ischemia-reperfusion injury (MI/RI). This study aims to explore the metabolism-related gene (LMRG) expression patterns in MI/RI and find potential therapeutic agents. Methods Differential analysis was performed screen differentially expressed genes (DEGs) LMRGs MI/RI-related dataset GSE61592. Enrichment protein-protein interaction (PPI) analyses were identify key signaling pathways genes. The trends validated external datasets GSE160516 GSE4105. corresponding online databases predicted miRNAs, transcription factors (TFs), agents targeting LMRGs. Finally, identified confirmed H9C2 cell hypoxia-reoxygenation (H/R) model mouse model. Results suggested that “lipid metabolic process” one critical MI/RI. Further differential PPI 120 15 126 55 TFs, 51 these Lastly, Acadm, Acadvl, Suclg1 datasets, H/R Conclusion may be involved dysregulation; acting upon serve as a strategy.

Language: Английский

Citations

0

Cardiac Magnetic Resonance Studies in a Large Animal Model that Simulates the Cardiac Abnormalities of Human Septic Shock DOI Open Access
Verity J. Ford, Willard N. Applefeld, Jeffrey Wang

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Feb. 8, 2024

Abstract Background Septic shock, in humans and our well-established animal model, is associated with increases biventricular end diastolic volume (EDV) decreases ejection fraction (EF). These abnormalities occur over 2 days reverse within 10 days. non-survivors do not develop an increase EDV. The mechanism for this cardiac dysfunction EDV differences unknown. Methods Purpose-bred beagles randomized to receive intrabronchial Staphylococcus aureus (n=27) or saline (n=6) were provided standard ICU care including sedation, mechanical ventilation, fluid resuscitation a pulmonary arterial occlusion pressure of 10mmHg. No catecholamines administered. Over 96h, magnetic resonance imaging, echocardiograms, invasive hemodynamics serially performed, laboratory data was collected. Tissue obtained at 66h from six septic animals. Results From 0-96h after bacterial challenge, animals vs. controls had significantly increased left ventricular wall edema (6%) thinning loss mass (15%) which more pronounced 48h than survivors. On histology, located predominantly myocytes, the interstitium, endothelial cells. Edema worse function (lower EFs), ventricular-arterial coupling, circumferential strain. In animals, 0-24h, decreased baseline and, despite filling pressures being similar, non-survivors. 24-48h, all chamber sizes. Survivors EDVs greater non-survivors, where different baseline. Preload, afterload, HR did explain these differential serial changes size. Conclusion Systolic during sepsis edema. Rather preload, heart rate, structural alterations best account outcome sepsis. induces severe dysfunction, further decreasing survivors may, part explain, 24-48h. However, continued even accelerated into recovery phase consistent reparative process rather ongoing injury. Clinical Perspective What new? Utilizing multimodal imaging hemodynamics, we demonstrate have injury phases. (0-24h) has profound compliance, myocardial edema, dysfunction. that explains (24-96h). progressed EF removing damaged tissue. This first controlled CMR study supporting fundamental aspect pathophysiology dry mechanism. are clinical implications? Despite optimizing pressures, structure survival non-survival still occurred, thereby discounting as major factor therapeutic importance survival. reported here potential implications treatment especially field resuscitation. findings yield new understanding allow novel phenotyping prognosticating syndrome compliance EDVs. also offers potentially high yielding targets research approaches failure.

Language: Английский

Citations

0

Cardiac Magnetic Resonance Studies in a Large Animal Model That Simulates the Cardiac Abnormalities of Human Septic Shock DOI Creative Commons
Verity J. Ford, Willard N. Applefeld, Jeffrey Wang

et al.

Journal of the American Heart Association, Journal Year: 2024, Volume and Issue: 13(15)

Published: Aug. 5, 2024

Septic shock is associated with increases in end-diastolic volume (EDV) and decreases ejection fraction that reverse within 10 days. Nonsurvivors do not develop EDV increases. The mechanism unknown.

Language: Английский

Citations

0

Establishment of a workflow for high-throughput identification of anti-inflammatory peptides from sea cucumbers DOI
Bingxue Jiang,

Jinqiu Liu,

Zihao Zhu

et al.

Food Research International, Journal Year: 2024, Volume and Issue: 197, P. 115171 - 115171

Published: Sept. 30, 2024

Language: Английский

Citations

0