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Synthetic Protein Circuits for Programmable Control of Mammalian Cell Death

Xia et al., Cell. 2024.

https://pubmed.ncbi.nlm.nih.gov/38657604/

Natural cell-death pathways have been shown to eliminate harmful cells and shape immunity. Researchers used synthetic protein-level cell-death circuits, collectively termed “synpoptosis” circuits, to proteolytically regulate engineered executioner proteins and mammalian cell death. They show that the circuits direct cell death modes, respond to combinations of protease inputs, and selectively eliminate target cells. This work provides a foundation for programmable control of mammalian cell death. Future studies could focus on programmable control of cell death in various contexts, including cancer, senescence, fibrosis, autoimmunity, and infection. Supported by ORIP (F30OD036190) and NIBIB.

Time of Sample Collection Is Critical for the Replicability of Microbiome Analyses

Allaband et al., Nature Metabolism. 2024.

https://pubmed.ncbi.nlm.nih.gov/38951660/

Lack of replicability remains a challenge in microbiome studies. As the microbiome field moves from descriptive and associative research to mechanistic and interventional studies, being able to account for all confounding variables in the experimental design will be critical. Researchers conducted a retrospective analysis of 16S amplicon sequencing studies in male mice. They report that sample collection time affects the conclusions drawn from microbiome studies. The lack of consistency in the time of sample collection could help explain poor cross-study replicability in microbiome research. The effect of diurnal rhythms on the outcomes and study designs of other fields is unknown but is likely significant. Supported by ORIP (T32OD017863), NCATS, NCI, NHLBI, NIAAA, NIAID, NIBIB, NIDDK, and NIGMS.

MRI Characteristics of Japanese Macaque Encephalomyelitis (JME): Comparison to Human Diseases

Tagge et al., Journal of Neuroimaging. 2021.

https://onlinelibrary.wiley.com/doi/10.1111/jon.12868

Magnetic resonance imaging data (MRI) were obtained from 114 Japanese macaques, including 30 animals of both sexes that presented with neurological signs of Japanese macaque encephalomyelitis (JME). Quantitative estimates of blood-brain barrier permeability to gadolinium-based-contrast agent (GBCA) were obtained in acute, GBCA-enhancing lesions, and longitudinal imaging data were acquired for 15 JME animals. Intense, focal neuroinflammation was a key MRI finding in JME. Several features of JME compare directly to human inflammatory demyelinating diseases. The development and validation of noninvasive imaging biomarkers in JME provides the potential to improve diagnostic specificity and contribute to the understanding of human demyelinating diseases. Supported by ORIP (P51OD011092, S10OD018224), NINDS, and NIBIB.