Excellent and detailed review on #LongCOVID#cell#LongCOVIDwww.cell.com/cell/fulltex...

Mechanisms of long COVID and the path toward therapeutics

Known under competing terms and definitions such as post-COVID-19 condition, post-COVID-19 conditions, post-acute sequelae of SARS-CoV-2 (PASC), post-COVID-19 syndrome, post-COVID-19, or long COVID, t...

(BioRxiv All) Plasma amyloid beta ratios in autosomal dominant Alzheimers disease: the influence of genotype: In-vitro studies of autosomal dominant Alzheimers disease (ADAD) implicate longer A{beta} peptides in pathogenesis, however less is known about… http://dlvr.it/TFS3CT#MassSpecRSS

📃Scientific paper: Impact of iodine intake on the pathogenesis of autoimmune thyroid disease in children and adults ➡️ Continued on ES/IODE

Vibrio cholerae: a fundamental model system for bacterial genetics and pathogenesis research #JBacteriologyjournals.asm.org/doi/10.1128/...

We're a fun, collaborative, and highly international group. Other group members work on comparative genomics, pan-transcriptomics, antifungal resistance, lncRNAs in fungal pathogenesis and drug resistance, and environmental mycobiomes.

Granulocyte colony-stimulating factor protects against arthritogenic alphavirus pathogenesis in a type I IFN-dependent manner www.biorxiv.org/content/10.1101/2024.10.09.617470v1

Granulocyte colony-stimulating factor protects against arthritogenic alphavirus pathogenesis in a type I IFN-dependent manner https://www.biorxiv.org/content/10.1101/2024.10.09.617470v1

Arthritogenic alphaviruses cause disease characterized by fever, rash, and incapacitating joint pain

Granulocyte colony-stimulating factor protects against arthritogenic alphavirus pathogenesis in a type I IFN-dependent manner www.biorxiv.org/content/10.1101/2024.10.09.617470v1

Granulocyte colony-stimulating factor protects against arthritogenic alphavirus pathogenesis in a type I IFN-dependent manner https://www.biorxiv.org/content/10.1101/2024.10.09.617470v1

Arthritogenic alphaviruses cause disease characterized by fever, rash, and incapacitating joint pain

2/ Used a small sample to study blood cells. "The results support a disease model of immune dysfunction ranging from autoimmunity to immunodeficiency and point to amyloidotic neurodegenerative signaling pathways in the pathogenesis of ME/CFS” #MECFS#CFS#PwME

TOMM40-APOE chimera linking Alzheimer's highest risk genes: a new pathway for mitochondria regulation and APOE4 pathogenesis www.biorxiv.org/content/10.1101/2024.10.09.617477v1

TOMM40-APOE chimera linking Alzheimer's highest risk genes: a new pathway for mitochondria regulation and APOE4 pathogenesis https://www.biorxiv.org/content/10.1101/2024.10.09.617477v1

The patho-mechanism of apolipoprotein variant, APOE4, the strongest genetic risk for late-onset Alzh

TOMM40-APOE chimera linking Alzheimer's highest risk genes: a new pathway for mitochondria regulation and APOE4 pathogenesis www.biorxiv.org/content/10.1101/2024.10.09.617477v1

TOMM40-APOE chimera linking Alzheimer's highest risk genes: a new pathway for mitochondria regulation and APOE4 pathogenesis https://www.biorxiv.org/content/10.1101/2024.10.09.617477v1

The patho-mechanism of apolipoprotein variant, APOE4, the strongest genetic risk for late-onset Alzh