ObjectiveTo explore the impacts of material type and loading volume of rigid containers on the hydrogen peroxide low temperature plasma sterilization of thoracoscopic instruments, to identify the best rigid containers and loading volume of thoracoscopic instruments. MethodsThoracoscopic instruments sterilized by STERRAD^® 100NX hydrogen peroxide low temperature plasma in Shanghai Pulmonary Hospital affiliated to Tongji University from August to September 2024 were selected as the research items. According to the material of rigid containers, the instruments were divided into polyethylene case group (A), stainless steel case group (B) and silicone resin case group (C). In terms of the loading volume, the rigid containers were divided into (loading capacity <80%) groups of 8, 10 and 12 instruments. The results of physical monitoring, the first type of chemical indicator card monitoring, and the five types of card luminal chemical process challenge device (PCD) monitoring of the 9 groups of A8, A10, A12, B8, B10, B12, C8, C10 and C12 were compared and evaluated. ResultsCompared to A8, A10 A12, C8, C10 or C12 groups, the thoracoscope instruments in the stainless steel containers in B8, B10 or B12 group had higher hydrogen peroxide concentrations and shorter elapsed time in the pressure check phases 1 and phases 2, with the differences statistically significant (P<0.05), followed by the silicone resin case group and the polyethylene case group. The nine groups of physical parameter monitoring, the first type of chemical indicator monitoring, and the five types of chemical PCD monitoring for lumen sterilization achieved 100% qualification rates, and there were no significant differences in the qualified rates of sterilization among the 9 groups (P>0.05). ConclusionWhen using hydrogen peroxide low temperature plasma to sterilize thoracoscopic instruments, it is recommended to use stainless steel or silicone resin rigid containers with a controlled loading capacity (≤12) to ensure optimal sterilization quality.

Acetaminophen (APAP) is the primary cause of drug-induced acute liver failure. Ovarian tumor deubiquitinase 6A (OTUD6A), a recently discovered deubiquitinase of the OTU family, has been primarily studied in tumor contexts. However, its role in APAP-induced liver injury (AILI) remains unclear. Therefore, this study aimed to investigate the involvement of OTUD6A in the pathogenesis of AILI. Our findings demonstrated a substantial upregulation of OTUD6A in both the liver tissue and isolated hepatocytes of mice following APAP stimulation. OTUD6A knockout exacerbated APAP-induced inflammation, hepatocyte necrosis, and liver injury, whereas OTUD6A overexpression alleviated these pathologies. Mechanistically, OTUD6A directly interacted with the enhancer of zeste homolog 2 (EZH2) and selectively removed K48-linked polyubiquitin chains from EZH2, enhancing its stability. This resulted in increased protein levels of EZH2 and H3K27me3, as well as reduced endoplasmic reticulum (ER) stress and cell death in hepatocytes. Collectively, our research uncovers a novel role for OTUD6A in mitigating APAP-induced liver injury by promoting EZH2 stabilization.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.

ABSRACT The development of hepatocellular car-cinoma(HCC)is closely related to the formation of tumour blood vessels.VEGF-mediated angiogenesis is a major driver of the immune escape response in tumours.VEGF binds to vascular endothelial growth factor receptor2(VEGFR2)on endothelial cells,promoting endothelial cell proliferation and migration,inducing vascular changes in HCC,and thus promote the growth of hepatocellular carcino-ma cells.Anti-VEGF and its receptor-targeted mo-lecular drugs are currently effective new treat-ments for HCC.Monoclonal antibodies against VEGF and small-molecule tyrosine kinase inhibitors targeting VEGF have been shown to block its angio-genic activity,alleviate the inhibitory effect of the tumour microenvironment,and ultimately achieve tumour regression.This article provides a review of the research progress of VEGF/VEGFR inhibitors in HCC treatment.