Conduction system disorders, defective electrogenesis in the heart, lead to slow heart rates that are insufficient to support the circulation, necessitating the implantation of electronic pacemakers. Although effective, current electronic devices have lead or generator malfunction, lack of autonomic responsiveness, undesirable interactions with strong magnetic fields, and device-related infections. Biological pacemakers,...(More)
How does the immune system eradicate SARS-CoV-2-infected cells? Why does the viral clearance rate differ among patients? In a study published in Journal of Clinical Investigation, a team led by Dr. Shih-Yu Chen at the Institute of Biomedical Sciences, Academia Sinica, showed that natural killer (NK) cells are the key immune cells responsible for the rate of SARS-CoV-2 viral clearance. ...(More)
Dr. Tang K. Tang, a distinguished research fellow in the Institute of Biomedical Sciences of Academia Sinica, leads a research group, working on the roles of centriolar proteins in neuron progenitors during cerebellar development and investigating how the defects in this process impacts the pathogenesis of Joubert syndrome. This work was published in Genes & Development,...more...
Polyethylene glycol (PEG) is a polymer that is attached to peptides, proteins, nucleic acids, liposomes and nanoparticles to create effective medicines. However, immune responses to PEG can adversely impact drug efficacy and safety. We provide a framework to understand PEG immunogenicity and how antibodies against PEG affect pegylated medicines. The widespread use of SARS-CoV-2 RNA vaccines that incorporate PEG in lipid nanoparticles make understanding effects of anti-PEG antibodies on pegylated medicines even more critical.
The cytosolic LPS-sensing pathway mediated by caspase-4/5/11 is regarded as the final line of host defense. When this defensive line is triggered, the host immune system may respond in extreme ways, including cytokine storm and inflammatory cell death, leading to sepsis. Galectin-3 recognizes cytosolic LPSs from various bacteria and amplifies LPS-induced caspase-4/11 oligomerization and activation, causing a more intense inflammatory response. By intracellularly recognizing LPS glycan moieties, galectin-3 may act as a critical regulator of LPS-mediated sepsis.