COVID-19 has disrupted science in the way it has disrupted everything else. In the short term, universities have largely closed shop as a way to maximize social distancing, and lots of science – or at least, lots of bench work – is not getting done.

BioWorld looks at translational medicine, including: Microbiome changes precede tumor development in CRC; Converting catch and release to PARP traps; Smart bacterium senses environment; The dose makes the poison – timing, too; Minimal phenotyping gives minimal insights into MDD genetics; Hypoxia linked to common form of muscular dystrophy; Stopping tau in its tracks; Optogenetic plaque model traces neurodegeneration in AD; Once repulsive, always repulsive.

COVID-19 has disrupted science in the way it has disrupted everything else. In the short term, universities have largely closed shop as a way to maximize social distancing, and lots of science – or at least, lots of bench work – is not getting done.

Indian scientists have discovered a previously unknown mechanism underlying life-threatening sepsis and proposed a new treatment strategy centered upon cell-free chromatin (cfCh), they reported in the March 4, 2020, edition of PLOS ONE. Notably, they showed that sepsis could be caused by cfCh released from dying host cells following microbial infection.

Indian scientists have discovered a previously unknown mechanism underlying life-threatening sepsis and proposed a new treatment strategy centered upon cell-free chromatin (cfCh), they reported in the March 4, 2020, edition of PLOS ONE. Notably, they showed that sepsis could be caused by cfCh released from dying host cells following microbial infection.

LONDON – Two papers published online in Nature following accelerated peer review provide fine detail of how the spike protein on the COVID-19 coronavirus binds to the angiotensin converting enzyme 2 (ACE2) through which it infects its human host.