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Biology subjects

Hammond, N.

Publications and source records attributed to Hammond, N..

2 recordsLinked to original sources

Chronic High Intensity Interval Training (HIIT) exercise in adolescent rat's result in cocaine place aversion and ΔFosB induction

High-Intensity Interval Training (HIIT) is a form of exercise that has been greatly popularized over the past few years for its many health benefits. Similar to other forms of exercise, HIIT may be beneficial in the prevention of substance use behaviors; however, the extent to which HIIT can impact the reinforcing effects of drugs of abuse during adolescence has not been fully evaluated. Here, we assess the effects of HIIT during adolescence on subsequent cocaine conditioned place preference (CPP) in male Lewis rats. The HIIT exercise exposed rats ran on a treadmill for 30 minutes daily (ten three-minute cycles) for six weeks with progressive speed-increased up to 0.8 mph (21.5m/min), while the sedentary rats remained in their home cage. Following the six weeks of exercise, rats were tested for cocaine (25 mg/kg) CPP. Following completion of the behavior test {Delta}FosB levels were measured in the brain. Results showed that the HIIT rats showed significantly attenuated place preference (-19%) in their time spent in the cocaine-paired chamber compared to the sedentary environment rats. In addition, HIIT rats had significantly higher (65%) striatum {Delta}FosB levels compared to the sedentary rats. Our findings show that HIIT exercise during adolescence could be protective against cocaine abuse which may be mediated by an increase in {Delta}FosB. This finding has important clinical implications with respect to exercise mediated protection against substance misuse and abuse. Future studies will examine this effect in females as well as the potential underlying mechanisms.

neuroscience↗

A spatial map of human liver cirrhosis reveals the patho-architecture and gene signatures associated with cell state transitions during liver disease

Liver fibrosis is a major cause of death worldwide. As a progressive step in chronic liver disease, fibrosis is almost always diagnosed too late with limited treatment options. Here, we uncover the spatial transcriptional landscape driving human liver fibrosis using single nuclei RNA and Assay for Transposase-Accessible Chromatin (ATAC) sequencing to deconvolute multi-cell spatial transcriptomic profiling in human liver cirrhosis. Through multi-modal data integration, we define molecular signatures driving cell state transitions in liver disease and define an impaired cellular response and directional trajectory from hepatocytes to cholangiocytes associated with disease remodelling. We identify pro-fibrogenic signatures in non-parenchymal cell subpopulations co-localised within the fibrotic niche and localise transitional cell states at the scar interface. This combined approach provides a spatial atlas of gene regulation and defines molecular signatures associated liver disease for targeted therapeutics or as early diagnostic markers of progressive liver disease.

genomics↗