Objective To investigate the diagnosis and prognosis of patients with coronary artery aneurysm in Kawasaki disease.Methods The data of ultrasonic diagnosis and follow-up of 338 children with Kawasaki disease complicated with coronary artery aneurysms were analyzed.Results The incidence of coronary artery aneurysm in the acute stage of Kawasaki disease was 21.2％ (338/1 594).Of all the 338 cases,small aneurysms was 66.6％ (225 cases),medium aneurysms was 25.1％ (85 cases),and giant aneurysms was 8.3％ (28 cases).There were 719 branches involved in 338 cases,32.8％ of them in left main coronary artery and 31.1％ in right coronary artery;25.3％ in left anterior descending branch,and 10.8％ in left circumflex branch.A total of 382 branches were followed up,including 218 branches of small coronary aneurysm group and 82.1％ of them were completely recovered to the normal diameter.The medium aneurysm group was 124 brunches,the proportion of no significant change,retraction,and normal were 23.4％,68.5％ and 8.1％,respectively.There were 40 brunches in the giant anuerysm group,in which the proportion of no significant change,retraction,and normal were 70.0％,27.5％ and 2.5％,respectively.A total of 30 thrombosiswere detected by echocardiography in the acute stage,20 thrombosis were regularly followed up,12 thrombosis gradually subsided,and the other remained persist.Five thrombosis were detected in the sequelae stage,and all located in the giant coronary aneurysm.Seven children were clinically diagnosed with ischemic heart disease,of them,acute myocardial infarction in 1 case,1 died of heart failure.Conclusions Kawasaki disease coronary artery disease are common in small coronary aneurysms,of which the left main artery and right coronary artery lesions are the most common,and the prognosis is better;medium and giant aneurysm need more time to recovery,and are easy to complicated with thrombosis.

Objective To investigate whether norepinephrine (NE) regulates the oxidative stress in human endom-etrial epithelial cells (hEECs) by activating nuclear factor E2-related factor 2(Nrf2)/ heme oxygenase -1(HO-1) signal pathway.Methods Cultured hEECs were used.The expression of α and β adrenergic receptors was detec-ted by reverse transcription-polymerase chain reaction (RT-PCR).Cell counting kit-8(CCK-8) assay was applied to test the effect of NE on cell viability, then the cells were divided into Control group and NE treatment group, and the appropriate concentrations were chosen.The expression of tight junction proteins Occludin and zona occludens-1(ZO-1), apoptosis-related proteins apoptosis-related protein B-cell lymphoma-2 protein(Bcl-2) and Bcl-2 associ-ated X protein(Bax) , antioxidant proteins Nrf2 and HO-1 were examined by Western blot.The apoptosis was de-tected by flow cytometry.The malonaldehyde (MDA) and superoxide dismutase(SOD) in the cell culture medium were detected by enzyme-linked immunosorbent assays kit (ELISA).Results The mRNA expression of α1 a,α1 b,α2 a,α2 b,α2 c,β1, β3 was detected in the hEECs.After the NE treatment, no significant change in cell viability was observed in low concentration (5 μmol/L and 10 μmol/L) groups, while 15 μmol/L and 20μmol/L NE treatments for 6 h or 24 h promoted the cell viability significantly.The expression of ZO-1 and Occlu-din increased significantly in 15 μmol/L group after 24 h treatment, the expression of ZO-1 decreased in 6 h treat-ment group, significant down regulation was observed after 15 μmol/L NE application, the expression of Occludin increased in 6 h group.The cell apoptosis increased compared with the control group after NE stimulation, espe-cially a significantly increase in 6 h 15 μmol/L group was detected,while the fall in increased apoptosis was ob-served after 24 h treatment.The ration of Bcl-2/Bax>1.The expression of Nrf2 and HO-1 was elevated by NE.There was no obvious change in MDA level while significant elevation in SOD was detected in cell culture medium.Conclusion Nrf2/HO-1 signal is activated after application of NE to the hEECs, which may responsible for the upregulation of SOD, antioxidant and anti-apoptotic effect in the hEECs.

Objective : To explore the application of ZnxNi1－xS@ DOX nanostructures in combined photothermal- chemotherapy treatment of tumors，and to provide new ideas for the study of tumor treatment methods． Methods: The morphology and elementary composition of ZnxNi1－xS nanostructures were characterized by scanning emission e- lectron microscopy and other methods．The photothermal properties of ZnxNi1－xS nanostructures were explored by infrared thermal camera．The release of DOX under different temperature and pH was investigated by fluorescence spectrophotometer．The biosafety of ZnxNi1－xS nanostructures and the in vitro antitumor properties of ZnxNi1－xS@ DOX nanostructures were investigated by MTT assay. Results : The as-prepared ZnxNi1－xS nanostructure had good dispersion and uniform size．The ZnxNi1－xS nanostructures had good photothermal effect．The drug release behavior showed temperature and pH responsiveness．The MTT assay showed that ZnxNi1－xS nanostructures were nontoxic to normal cells．ZnxNi1－xS@ DOX nanostructures could significantly inhibit the growth of tumor cells under near-infra- red illumination． Conclusion The as-prepared ZnxNi1－xS nanostructure has good biocompatibility，on the basis of which the ZnxNi1－xS@ DOX nanostructures achieve good antitumor performance，which can be used for combined photothermal-chemotherapy treatment of tumors.

Environmental pollution is closely linked to the occurrence and development of cancer. Chemical carcinogens are the most important environmental factors causing cancer in humans. Among them, persistent organic pollutants (POPs) are characterized by their widespread distribution, persistence, and bioaccumulation. Research on the carcinogenic effects of POPs has received considerable attention in recent years. This article reviewed the internal exposure, association with cancer risk, and potential carcinogenic mechanisms of five typical classes of POPs in the environment, including polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), per- and poly-fluoroalkyl substances (PFAS), brominated flame retardants (BFRs), and short-chain chlorinated paraffins (SCCPs). These five types of POPs have distinct carcinogenic mechanisms, including interfering with cell proliferation cycle, altering epigenetic inheritance, promoting oxidative stress, altering energy metabolism, and affecting immune function. The development of cancer is the result of interaction between intrinsic genetic factors and external environmental factors. In addition to focusing on how environmental POPs affect the genetic material of organisms, it is also important to consider their effects on the tumor microenvironment, including tumor immunity and angiogenesis. Understanding these effects is crucial for guiding future efforts in pollution control and precision medicine in cancer treatment.