Publications by authors named "Anthony Schulte"
Proliferation and differentiation of the mammary gland during pregnancy is regulated by a wide variety of factors. Using gene expression data, we have predicted that the E2F5 transcription factor has a role in the mammary gland during pregnancy. Using CUT&RUN for E2F5 in combination with gene expression data revealed that there were a number of E2F5 target genes associated with gene expression in early pregnancy, suggesting a critical role.
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- Acetaminophen (APAP) overdose is a major cause of acute liver failure (ALF), and neutrophil activation may worsen outcomes by enhancing coagulation, but their exact role in liver injury is unclear.
- A study used a strategy to deplete neutrophils in mice to investigate their involvement in liver damage after APAP exposure at different doses (300 or 600 mg/kg).
- Results showed that neutrophil depletion reduced liver necrosis in mice exposed to higher APAP doses and suggested that neutrophils contribute to liver injury through interactions with platelets, particularly in cases of severe overdose.
Background: Hepatic deposition of cross-linked fibrin(ogen) occurs alongside platelet accumulation as a hallmark of acetaminophen (APAP)-induced liver injury.
Objectives: We sought to define the precise role of the fibrinogen γ-chain C-terminal integrin αβ binding domain in APAP-induced liver injury.
Methods: Mice expressing mutant fibrinogen incapable of engaging integrin αβ due to a C-terminal fibrinogen γ-chain truncation (mutant fibrinogen-γ [Fibγ] mice) and wild-type mice were challenged with APAP (300 mg/kg, intraperitoneally).
Background: Patients with acetaminophen (APAP)-induced acute liver failure (ALF) display both hyper- and hypocoagulable changes not necessarily recapitulated by standard hepatotoxic doses of APAP used in mice (eg, 300 mg/kg).
Objectives: We sought to examine coagulation activation in vivo and plasma coagulation potential ex vivo in experimental settings of APAP-induced hepatotoxicity and repair (300-450 mg/kg) and APAP-induced ALF (600 mg/kg) in mice.
Results: APAP-induced ALF was associated with increased plasma thrombin-antithrombin complexes, decreased plasma prothrombin, and a dramatic reduction in plasma fibrinogen compared with lower APAP doses.