Aim: This study aimed to explore the relationship between nurses' occupational exposure to antineoplastic agents and adverse pregnancy outcomes.Design: Meta‐analysis.Methods: Data were retrieved from studies published before April 2022 in PubMed, the Cochrane Library, the Web of Science, Embase databases, the China National Knowledge Infrastructure (CNKI), China Biology Medicine disc (CBM), China Science and Technology Journal databases (VIP) and Wan Fang databases (WF). Stata MP (Version 17.0) was used to conduct this meta‐analysis.Results: The current evidence shows that occupational exposure to antineoplastic agents increases nurses' risk of spontaneous abortions, stillbirths, and congenital abnormalities. It is necessary to pay attention to occupational exposures caused by antineoplastic agents, especially for female nurses of reproductive age. Managers should take timely and effective countermeasures to ensure their occupational safety and reduce the risk of adverse pregnancy outcomes.

Background Although the therapeutic effect of antineoplastic drugs is incontestable, these agents can also potentially act as carcinogens, mutagens and/or teratogens in people. The aim of this study was to assess the effect of occupational exposure to antineoplastic drugs on DNA damage, assessed by the comet assay and cytokinesis-block micronucleus (CBMN) assay, in nurses. Methods The cross-sectional study enrolled 305 nursing staff members from 7 public hospitals in Shenzhen who handled antineoplastic drugs, and 150 healthy nursing staff members who were not exposed to antineoplastic drugs as the control group. DNA damage was assessed by the comet and CBMN assay. Multiple linear regressions and logistic regressions models were used to analyse the effect of occupational exposure to antineoplastic drugs on DNA damage. Results After adjustment for confounding factors, compared with non-exposure to antineoplastic drugs, exposure to antineoplastic drugs was positively related to tail moment, olive moment, tail length and tail DNA per cent, and adjusted β or OR (95% CI) was 0.17 (0.08 to 0.26), 0.18 (0.10 to 0.27), 1.03 (0.47 to 1.60) and 1.16 (1.04 to 1.29) (all p<0.05). Moreover, similar significant relationships were observed for the biomarkers of the CBMN assay. Additionally, other than age, there was no interaction between antineoplastic drug exposure and other variables for the levels of biomarkers of the CBMN assay and the comet assay. Conclusions The present results showed that exposure to antineoplastic drugs was positively related to the risk of DNA damage in nurses. The results imply that occupational exposure to antineoplastic agents is an important global public health problem that requires urgent attention.

Phosphatidylinositol 4-phosphate 5-kinase type I c (PIP5K1c) catalyses the synthesis of phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2) by phosphorylating phosphatidylinositol 4 phosphate, which plays multiple roles in regulating focal adhesion formation, invasion, and cell migration signal transduction cascades. Here, a new physiological mechanism of PIP5K1c in adipocytes and systemic metabolism is reported. Adipose-specific conditional knockout mice were generated to delete the PIP5K1c gene in adipocytes. In addition, in vitro research investigated the effect of PIP5K1c deletion on adipogenesis. Deletion of PIP5K1c in adipocytes significantly alleviated high fat diet (HFD)-induced obesity, hyperlipidaemia, hepatic steatosis, and insulin resistance. PIP5K1c deficiency in adipocytes also decreased adipocyte volume in HFD-induced obese mice, whereas no significant differences were observed in body weight and adipose tissue weight under normal chow diet conditions. PIP5K1c knockout in adipocytes significantly enhanced energy expenditure, which protected mice from HFD-induced weight gain. In addition, adipogenesis was markedly impaired in mouse stromal vascular fraction (SVF) from PIP5K1c-deleted mice. Under HFD conditions, PIP5K1c regulates adipogenesis and adipose tissue homeostasis. Together, these data indicate that PIP5K1c could be a novel potential target for regulating fat accumulation, which could provide novel insight into the treatment of obesity.

Liver T-cells respond to the inflammatory insult generated during organ procurement and contribute to the injury following reperfusion. The mode of liver donation alters various metabolic and inflammatory pathways but the way it affects intrahepatic T-cells is still unclear. We investigated the modifications occurring in the proportion and function of T-cells during liver procurement for transplantation. We isolated hepatic mononuclear cells (HMC) from liver perfusate of living donors (LD) and donors after brain death (DBD) or cardiac death (DCD) and assessed the frequency of T-cell subsets, their cytokine secretion profile and CD8 T-cell cytotoxicity function, responsiveness to a danger associated molecular pattern (High Mobility Group Box1, HMGB1) and association with donor and recipient clinical parameters and immediate graft outcome. We found that T-cells in healthy human livers were enriched in memory CD8 T-cells exhibiting a phenotype of non-circulating tissue-associated lymphocytes, functionally dominated by more cytotoxicity and IFN-γ-production in DBD donors, including upon activation by HMGB1 and correlating with peak of post-transplant AST. This liver-specific pattern of CD8 T-cell was prominent in DBD livers compared to DCD and LD livers suggesting that it was influenced by events surrounding brain death, prior to retrieval. Mode of liver donation can affect liver T-cells with increased liver damage in DBD donors. These findings may be relevant in designing therapeutic strategies aimed at organ optimization prior to transplantation.

Background: Sister chromatid exchange (SCE) can be used to identify early occupational health status in health care workers. Our aim is to comprehensively assess the relationship between long-term exposure to antineoplastic drugs (ADs) and SCE in health care workers via meta-analysis. Methods: Five databases were systematically searched for relevant articles published from inception to November 30, 2022. Literature data are expressed as mean difference and 95% confidence intervals (CI) or relative risk and 95% CI. For I ² > 50% trials, random effect model is used for statistical analysis, otherwise fixed effect model is used. This review was registered in the International Prospective Register of Systematic Reviews (identifier CRD42023399914). Results: Fourteen studies were included in this study. Results showed the level of SCE in healthcare workers exposed to ADs was significantly higher than in controls. The mean difference of the SCE trial was 0.53 (95% CI: 0.10–0.95, P = .01) under a random-effects model. Conclusions: The findings suggested a significant correlation between occupational exposure to ADs in health care workers and SCE, requiring the attention of health care workers in general.