Is this you? As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
Claim your profile
Articles by Sergey A. Sosunov
Mitochondrial calcium buffering depends upon temperature and is associated with hypothermic neuroprotection against hypoxia-ischemia injury
Hypothermia prevented secondary drop in mCBC and attenuated HI brain injury Immediately after HI and prior to the reperfusion, mitochondrial Ca2+ retention capacity at 25°C was significantly decreased compared to controls (Fig 2A and 2B). At 30 minutes of normothermic or hypothermic reperfusion, in NT and HT mice, their mCBCs have significantly recovered and did not differ from that in controls (Fig 2A and 2C).
Cyclophilin D-dependent oligodendrocyte mitochondrial ion leak contributes to neonatal white matter injury
The model of diffuse WMI and study groups As we described (16), C57BL/6J newborn mice were exposed to 30 IH events a day from P1 until P14. Each event consisted of 3 minutes of hypoxia followed by 5 minutes of reoxygenation in room air. Hypoxemia was induced by the exposure to 8% O2/92% N2 at the ambient temperature of 34°C.
Hyperglycemic Conditions Prime Cells for RIP1-dependent Necroptosis
Necroptosis is a RIP1-dependent programmed cell death (PCD) pathway that is distinct from apoptosis. Downstream effector pathways of necroptosis include formation of advanced glycation end products (AGEs) and reactive oxygen species (ROS), both of which depend on glycolysis. This suggests that increased cellular glucose may prime necroptosis. Here we show that exposure to hyperglycemic levels of glucose enhances necroptosis in primary red blood cells (RBCs), Jurkat T cells, and U937 monocytes.
Hyperglycemic conditions prime cells for RIP1-dependent necroptosis
Necroptosis is a RIP1-dependent programmed cell death (PCD) pathway that is distinct from apoptosis. Downstream effector pathways of necroptosis include formation of advanced glycation end products (AGEs) and reactive oxygen species (ROS), both of which depend on glycolysis. This suggests that increased cellular glucose may prime necroptosis. Here we show that exposure to hyperglycemic levels of glucose enhances necroptosis in primary red blood cells (RBCs), Jurkat T cells, and U937 monocytes.
Show More
loading
Actions
Is this you?
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.Get in touch with Sergey A.
Contact Sergey A., search articles and posts on X, monitor coverage, and track replies from one place.
Learn more about Muck Rack