Publications by authors named "J S Nickels"

Solvent toxicity limits -butanol fermentation titer, increasing the cost and energy consumption for subsequent separation processes and making biobased production more expensive and energy-intensive than petrochemical approaches. Amphiphilic solvents such as -butanol partition into the cell membrane of fermenting microorganisms, thinning the transverse structure, and eventually causing a loss of membrane potential and cell death. In this work, we demonstrate the deleterious effects of -butanol partitioning upon the lateral dimension of the membrane structure, called membrane domains or lipid rafts.

View Article and Find Full Text PDF

Mice lacking monoacylglycerol acyltransferase 2 (mMGAT2) are resistant to diet-induced fatty liver, suggesting hMOGAT2 inhibition is a viable option for treating metabolic dysfunction-associated steatotic liver disease (MASLD)/metabolic dysfunction-associated steatohepatitis (MASH). We generated humanized hMOGAT2 mice (HuMgat2) for use in pre-clinical studies testing the efficacy of hMOGAT2 inhibitors for treating MASLD/MASH. HuMgat2 mice developed MASH when fed a steatotic diet.

View Article and Find Full Text PDF
Article Synopsis
  • Histone H3.3 is often mutated in tumors, particularly the K36M mutation, which is commonly found in chondroblastomas, affecting the way genes are expressed.
  • The study investigates how the H3.3K36M mutation influences gene silencing and epigenetic memory by using a synthetic reporter system and analyzing changes in histone modifications.
  • Findings suggest that the K36M mutation reduces epigenetic memory and alters methylation patterns, highlighting the importance of the H3K36 methylation pathway in maintaining stable epigenetic memory, which could inform future cancer research and therapeutic approaches.
View Article and Find Full Text PDF

Histone H3.3 is frequently mutated in cancers, with the lysine 36 to methionine mutation (K36M) being a hallmark of chondroblastomas. While it is known that H3.

View Article and Find Full Text PDF

The ongoing epidemic caused by the coronavirus SARS-CoV-2 is characterized by a variety of pathologic processes within the syndrome of COVID-19. Usually beginning as an upper respiratory infection with potential progression to a pneumonitis, many cases of COVID-19 that show minimal signs or symptoms initially may develop adverse systemic sequelae later, such as widespread thrombo-embolic phenomena, systemic inflammatory disorders (especially in children), or vasculitis. Here, we present a patient who suffered a sudden cardiac death following persistent SARS-CoV-2 viral positivity for four-and-one-half months after a mild clinical viral course.

View Article and Find Full Text PDF