Browse research papers in Clinical Biochemistry - Biochemistry, Genetics and Molecular Biology Discover 4 academic papers with AI-powered analysis

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Biochemistry, Genetics and Molecular Biology

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Clinical Biochemistry

The analysis of body fluids and tissues for diagnostic and therapeutic monitoring, including development of biomarkers, clinical assays, point-of-care testing, and the biochemical basis of disease

4 papers in this specialization

Papers

Altered high-density lipoprotein composition and functions during severe COVID-19

This study found that severe COVID-19 is associated with significant changes in the protein composition and function of high-density lipoproteins (HDLs). HDLs from COVID-19 patients had reduced levels of protective proteins like ApoA-I and paraoxonase 1, and increased levels of inflammatory proteins like serum amyloid A. These altered HDLs were less effective at protecting endothelial cells from inflammation and apoptosis.

Predicting antimicrobial resistance in Pseudomonas aeruginosa with machine learning-enabled molecular diagnostics

By combining genomic and transcriptomic data with machine learning, researchers achieved high accuracy in predicting antibiotic resistance in Pseudomonas aeruginosa for several antibiotics. Gene expression data significantly improved prediction, especially for ceftazidime, meropenem, and tobramycin, and classifiers performed better when MIC values were further from breakpoints.

Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury

The study found that inhibiting the HMGB1-RAGE axis decreased the number of pro-inflammatory cells while increasing anti-inflammatory cells in rats with spinal cord injuries. This led to reduced neuronal and myelin loss, and improved functional recovery. It suggests that targeting HMGB1-RAGE may be a promising therapeutic strategy for SCI.

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s12974-020-01973-4.pdf

Jul 14, 07:01 AM

Indirect regulation of HMGB1 release by gasdermin D

This study found that HMGB1 release from macrophages following inflammasome activation isn't through GSDMD pores as previously thought, but rather due to cell lysis. In an endotoxemia mouse model, HMGB1 release was independent of GSDMD, suggesting different pathways for these molecules in vivo.

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s41467-020-18443-3.pdf

Jul 14, 07:01 AM