Publications by authors named "J C S Pollock"

Disrupted feeding and fasting cycles as well as chronic high fat diet (HFD)-induced obesity are associated with cardiovascular disease risk factors. We designed studies that determined whether two weeks of time-restricted feeding (TRF) intervention in mice fed a chronic HFD would reduce cardiovascular disease risk factors. Mice were fed a normal diet (ND; 10% fat) ad libitum or HFD (45% fat) for 18 weeks ad libitum to establish diet-induced obesity.

View Article and Find Full Text PDF

Introduction: The management of malignant melanomas often involves performing a sentinel lymph node biopsy (SLNB) aided by imaging with lymphoscintigraphy. Whether lymphoscintigraphy should be performed on the same day as the SLNB operation (SD) or the day before (DB) surgery remains debated. This study aims to summarise existing evidence regarding the impact of the relative timings of lymphoscintigraphy and SLNB on clinical outcomes in melanoma.

View Article and Find Full Text PDF

: The main aim of this study is to analyze the outcomes of NSTEMI admissions and test the relevance of TIMI as a risk score in a real-world setting. We also examine any potential social or health care disparities involved with outcomes of NSTEMI admissions. This study also investigates factors associated with mortality in NSTEMI admissions and its correlation with heart catheterization during admission.

View Article and Find Full Text PDF

Excess dietary salt and salt-sensitivity contribute to cardiovascular disease. Distinct T cell phenotypic responses to high salt and hypertension as well as influences from environmental cues are not well understood. The aryl hydrocarbon receptor (AhR) is activated by dietary ligands, promoting T cell and systemic homeostasis.

View Article and Find Full Text PDF

Genetic disruption of the RAS binding domain (RBD) of PI 3-kinase (PI3K) prevents the growth of mutant RAS driven tumors in mice and does not impact PI3K's role in insulin mediated control of glucose homeostasis. Selectively blocking the RAS-PI3K interaction may represent an attractive strategy for treating RAS-dependent cancers as it would avoid the toxicity associated with inhibitors of PI3K lipid kinase activity such as alpelisib. Here we report compounds that bind covalently to cysteine 242 in the RBD of PI3K p110α and block the ability of RAS to activate PI3K activity.

View Article and Find Full Text PDF