Objective To assess the situation and influencing factors of occupational burnout among the staff at the Center for Disease Control and Prevention (CDC) in Sichuan Province. Methods A total of 1 038 CDC staff members in Sichuan Province were selected as the study subjects using the stratified random sampling method. Occupational burnout of the staff was assessed using the Maslach Burnout Inventory General Survey via an online questionnaire. Results The detection rate of occupational burnout was 42.3% (439/1 038). Binary logistic regression analysis result showed that, after controlling for confounding factors such as education level and alcohol consumption, CDC staffs aged at 20-<31, 31-<41, and 41-<51 years were at higher risk of occupational burnout compared with those ≥51 years (all P<0.05). CDC staffs with 5-<10 or ≥10 years of service had higher occupational burnout risk compared with those with <5 years (both P<0.05). CDC staffs with poor or fair health status, irregular diet, and poor sleep quality had higher risk of occupational burnout compared with those healthy, have regular diet, and good sleep quality (all P<0.05). The risk of occupational burnout increased with higher overtime frequency (all P<0.05). Conclusion Occupational burnout among CDC staffs in Sichuan Province is relatively high. Age, years of service, health status, diet, sleep quality, and overtime frequency are key influencing factors.

Objective:To investigate the role and underlying mechanism of parthanatos death in neonatal SD rats with bilirubin encephalopathy(BE).Methods:Eighty 3-day-old neonatal SD rats were selected and randomly divided into control group and BE group.The BE model was established by intraperitoneal injection of bilirubin solution,and the pathological changes in the hippocampus were observed by hematoxylin-eosin(HE)staining and Nissl staining.The protein expressions of the phosphorylation of the core histone protein H2AX(termed gamma H2AX),poly ADP-ribose polymerasw-1(PARP-1)and apoptosis-inducing factor(AIF)in hippocampus were detected by Western blot.Immuno-fluorescence staining was used to detect the expression and distribution of AIF in hippocampus.Results:Compared with the control group,neonatal SD rats developed jaundice 12 hours after bilirubin injection,accompanied by slow weight gain.HE staining and Nissl staining showed that the hippocampus in BE group were damaged and the content of Nissl bodies was decreased.Western blot results showed that the expression of γ-H2AX protein in hippocampus began to increase at 72 h after modeling(P＜0.05),and the levels of PARP-1 and AIF protein in hippocampus increased signif-icantly at 72 h after modeling(P＜0.05).Immunofluorescence staining showed increased AIF expression and nuclear translocation.Conclusion:Intraperitoneal injection of bilirubin can induce DNA damage in hippocampal neurons of neonatal SD rats and activate the PARP-1/AIF pathway to cause parthanatos death of hippocampal neurons.

This study is to explore the antibiofilm activity of tirapazamine(TPZ)against Salmonella and the mechanism of inhibiting biofilm formation.In this study,crystal violet staining was used to determine the effect of TPZ on the minimal biofilm inhibitory concentration(MBIC)of Salmonel-la and on the development stage of Salmonella biofilm.The effects of TPZ on bacteria and biofilm of Salmonella were observed by scanning electron microscope and fluorescence microscope.Phe-nol-sulfuric acid method,spectrophotometer and BCA method were used to detect the effects of the bacteria on the content of main extracellular matrix of Salmonella.The autocoagulation and hydro-phobicity of Salmonella were measured and their effects on the cell wall of Salmonella were meas-ured by AKP method.The result showed that the MBIC value of TPZ on Salmonella ATCC 14028 was 1.563 μmol/L,it had destructive effects on both Salmonella bacteria and mature biofilm structure,it inhibited the formation of early Salmonella biofilm in a concentration-dependent manner,and inhibited the synthesis and secretion of extracellular polymers in Salmonella biofilm.The autoagglutination ability,hydrophobicity and cell wall integrity of Salmonella were affected.To sum up,the TPZ may inhibit the formation of a large number of Salmonella biofilms in the early stage of biofilm development by affecting the extracellular polymer and cell agglutination a-bility,which is expected to be a potential candidate drug against biofilm infection and provide a new idea for finding alternative antibiotics.

Objective:To investigate the role and underlying mechanism of parthanatos death in neonatal SD rats with bilirubin encephalopathy(BE).Methods:Eighty 3-day-old neonatal SD rats were selected and randomly divided into control group and BE group.The BE model was established by intraperitoneal injection of bilirubin solution,and the pathological changes in the hippocampus were observed by hematoxylin-eosin(HE)staining and Nissl staining.The protein expressions of the phosphorylation of the core histone protein H2AX(termed gamma H2AX),poly ADP-ribose polymerasw-1(PARP-1)and apoptosis-inducing factor(AIF)in hippocampus were detected by Western blot.Immuno-fluorescence staining was used to detect the expression and distribution of AIF in hippocampus.Results:Compared with the control group,neonatal SD rats developed jaundice 12 hours after bilirubin injection,accompanied by slow weight gain.HE staining and Nissl staining showed that the hippocampus in BE group were damaged and the content of Nissl bodies was decreased.Western blot results showed that the expression of γ-H2AX protein in hippocampus began to increase at 72 h after modeling(P＜0.05),and the levels of PARP-1 and AIF protein in hippocampus increased signif-icantly at 72 h after modeling(P＜0.05).Immunofluorescence staining showed increased AIF expression and nuclear translocation.Conclusion:Intraperitoneal injection of bilirubin can induce DNA damage in hippocampal neurons of neonatal SD rats and activate the PARP-1/AIF pathway to cause parthanatos death of hippocampal neurons.

This study is to explore the antibiofilm activity of tirapazamine(TPZ)against Salmonella and the mechanism of inhibiting biofilm formation.In this study,crystal violet staining was used to determine the effect of TPZ on the minimal biofilm inhibitory concentration(MBIC)of Salmonel-la and on the development stage of Salmonella biofilm.The effects of TPZ on bacteria and biofilm of Salmonella were observed by scanning electron microscope and fluorescence microscope.Phe-nol-sulfuric acid method,spectrophotometer and BCA method were used to detect the effects of the bacteria on the content of main extracellular matrix of Salmonella.The autocoagulation and hydro-phobicity of Salmonella were measured and their effects on the cell wall of Salmonella were meas-ured by AKP method.The result showed that the MBIC value of TPZ on Salmonella ATCC 14028 was 1.563 μmol/L,it had destructive effects on both Salmonella bacteria and mature biofilm structure,it inhibited the formation of early Salmonella biofilm in a concentration-dependent manner,and inhibited the synthesis and secretion of extracellular polymers in Salmonella biofilm.The autoagglutination ability,hydrophobicity and cell wall integrity of Salmonella were affected.To sum up,the TPZ may inhibit the formation of a large number of Salmonella biofilms in the early stage of biofilm development by affecting the extracellular polymer and cell agglutination a-bility,which is expected to be a potential candidate drug against biofilm infection and provide a new idea for finding alternative antibiotics.

Mesangial cell proliferation is an early pathological indicator of diabetic nephropathy (DN). Growing evidence highlights the pivotal role of paired-related homeobox 1 (Prrx1), a key regulator of cellular proliferation and tissue differentiation, in various disease pathogenesis. Notably, Prrx1 is highly expressed in mesangial cells under DN conditions. Both in vitro and in vivo studies have demonstrated that Prrx1 overexpression promotes mesangial cell proliferation and contributes to renal fibrosis in db/m mice. Conversely, Prrx1 knockdown markedly suppresses hyperglycemia-induced mesangial cell proliferation and mitigates renal fibrosis in db/db mice. Mechanistically, Prrx1 directly interacts with the Yes-associated protein 1 (YAP) promoter, leading to the upregulation of YAP expression. This upregulation promotes mesangial cell proliferation and exacerbates renal fibrosis. These findings emphasize the crucial role of Prrx1 upregulation in high glucose-induced mesangial cell proliferation, ultimately leading to renal fibrosis in DN. Therefore, targeting Prrx1 to downregulate its expression presents a promising therapeutic strategy for treating renal fibrosis associated with DN.

The production of healthy agricultural products has increased the demand for innovative and sustainable plant protection technologies, and the rapid advancement of nanotechnology has brought revolutionary breakthroughs to traditional agriculture. Nanocarrier-based drug delivery systems can not only significantly improve the utilization efficiency of pesticides, achieving enhanced efficacy and reduced application, but also decrease the pesticide residues and environmental pollution. Additionally, they have made breakthrough progress in the stability and persistence of RNA pesticides. This review summarized the research progress on nanopesticides and RNA pesticides, focusing on the mechanisms of nanocarriers in improving pesticide bioactivity and RNA interference (RNAi) efficiency. It also systematically summarized the types of nanomaterials and their applications in pest and disease management and provided an in-depth outlook for the future development of nanopesticides and RNA pesticides, which provided technical support for the high-quality development of agriculture in the future.
Pesticides/chemistry* ; Nanotechnology ; Nanostructures ; RNA ; Agriculture/methods* ; RNA Interference ; Drug Delivery Systems

Objective : Based on glycolysis of hypoxia inducible factor-1α(HIF-1α)/Bcl2/adenovirus E1B interacting protein 3(BNIP3) pathway, to study the mechanism of oxygen-induced retinal angiogenesis in neonatal mice. Methods : Human umbilical vein endothelial cells(HUVECs) were divided into normoxic group, hypoxia+si-NC group, hypoxia +si-HIF-1α group and hypoxia+si-HIF-1α+BNIP group. In normoxic group, HUVECs were exposed to normoxic(21% O2) and cultured. Hypoxia +si-NC group, hypoxia +si-HIF-1α group and hypoxia +si-HIF-1α+BNIP3 group were treated with si-NC, si-HIF-1α or si-HIF-1α combined with BNIP3 plasmid for 36 h, and then exposed to hypoxia(1% O2) for culture. The autophagy, glycolysis, proliferation, migration and tube formation of mitochondria were investigated by immunofluorescence, metabolic measurement, cell viability, scratch experiment and tube formation experiment. On the 7th day after birth, C57BL/6J mice were randomly assigned to different treatment groups: control group, oxygen-induced retinopathy(OIR) group, OIR+si-HIF-1α group and OIR+si-BNIP group. The neovascularization and vascular occlusion were measured. Results: Compared with normoxic group, the rate of LC3+MitoTracker+ spots, glucose uptake and lactic acid release in HUVECs in hypoxia +si-NC group increased significantly(P<0.001). Compared with hypoxia +si-NC group, the rate of LC3+MitoTracker+ spots, glucose uptake and lactic acid release in HUVECs in hypoxia +si-HIF-1α group decreased significantly(P<0.01). Compared with normoxic group, the proliferation activity of HUVECs in hypoxia +si-NC group decreased significantly(P<0.05), and the wound healing area and the number of tubes formed increased significantly(P<0.01). Compared with hypoxia+si-NC group, the proliferation activity of HUVECs in hypoxia +si-HIF-1α group decreased significantly at the 24th, 48th and 72th hours of culture(P<0.05), and the wound healing area and the number of tubes formed decreased significantly(P<0.001). Overexpression of BNIP3 reversed the effects of HIF-1α knock-down on mitochondrial autophagy, glycolysis and biological function. Compared with OIR group, the neovascularization and vascular occlusion areas in retina of mice in OIR+si-HIF-1α group and OIR+si-BNIP3 group reduced significantly(P<0.05). Conclusion HIF-1α/BNIP3 signaling pathway promotes mitochondrial autophagy activation in HUVECs under hypoxia, which plays an important role in controlling endothelial function and angiogenesis.

Alzheimer′s disease (AD) is a major public health challenge with no curative treatment at present and has become the fifth leading cause of death for urban and rural residents in China. Although diagnostic technology has made significant progress in recent years, precise identification of AD still faces certain limitations and challenges due to its heterogeneity and complex pathogenesis. It is possible to shift the paradigm and focus on the key "window" of the early stage of AD dementia to achieve breakthroughs. This article is based on MIND-CHINA (randomized controlled Multimodal INterventions to delay Dementia and disability in rural China) to discuss the etiology, prediction, risk-factors assessment, diagnosis, and intervention research of AD, in order to develop AD prediction and prevention strategies that are in line with China′s national conditions, and make a multi-perspective analysis of the current limitations and challenges on AD diagnosis and prevention to promote the future of precision medicine for AD.