Publications by authors named "P E Adams"

Between October 2021 and February 2022, there was an outbreak of Yellow fever that spread within several districts in the northern part of Ghana. Febrile illnesses such as Yellow fever are often misdiagnosed as malaria and vice versa, which delays appropriate management and treatment. Hence, the true burden of Yellow fever and malaria are mostly underestimated.

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The metabolic landscape of cancer greatly influences antitumor immunity, yet it remains unclear how organ-specific metabolites in the tumor microenvironment influence immunosurveillance. We found that accumulation of primary conjugated and secondary bile acids (BAs) are metabolic features of human hepatocellular carcinoma and experimental liver cancer models. Inhibiting conjugated BA synthesis in hepatocytes through deletion of the BA-conjugating enzyme bile acid-CoA:amino acid -acyltransferase (BAAT) enhanced tumor-specific T cell responses, reduced tumor growth, and sensitized tumors to anti-programmed cell death protein 1 (anti-PD-1) immunotherapy.

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The light-harvesting pigment-protein complex II (LHCII) from plants can be used as a component for biohybrid photovoltaic devices, acting as a photosensitizer to increase the photocurrent generated when devices are illuminated with sunlight. LHCII is effective at photon absorption in the red and blue regions of the visible spectrum, however, it has low absorption in the green region (550-650 nm). Previous studies have shown that synthetic chromophores can be used to fill this spectral gap and transfer additional energy to LHCII, but it was uncertain whether this would translate into an improved performance for photovoltaics.

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Objective: To describe intraoperative cardiac arrest in patients undergoing congenital heart surgery.

Methods: The Society of Thoracic Surgeons Congenital Heart Surgery Database was queried. Predictors of intraoperative cardiac arrest were assessed using univariate and multivariable analyses.

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Article Synopsis
  • Hepatocellular carcinoma (HCC) arises from liver cells (hepatocytes) that are damaged and undergoing compensatory growth, particularly due to metabolic disorders like MASH.
  • The tumor-suppressive effects of p53 and the anti-cancer role of the enzyme FBP1 are undermined in HCC, as FBP1 is commonly degraded and suppressed in tumors.
  • Key metabolic pathways involving AKT and NRF2 play a role in reversing the effects of cellular senescence, boosting the growth of HCC cells and leading to the accumulation of genetic mutations that contribute to cancer progression.
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