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In atherosclerosis, chronic inflammatory processes in local diseased areas may lead to the accumulation of reactive oxygen species (ROS). In this study, we devised a highly sensitive H2O2-scavenging nano-bionic system loaded with probucol (RPP-PU), to treat atherosclerosis more effectively. The RPP material had high sensitivity to H2O2, and the response sensitivity could be reduced from 40 to 10 μmol/L which was close to the lowest concentration of H2O2 levels of the pathological environment. RPP-PU delayed the release and prolonged the duration of PU in vivo. In Apolipoprotein E deficient (ApoE‒/‒) mice, RPP-PU effectively eliminated pathological ROS, reduced the level of lipids and related metabolic enzymes, and significantly decreased the area of vascular plaques and fibers. Our study demonstrated that the H2O2-scavenging nano-bionic system could scavenge the abundant ROS in the atherosclerosis lesion, thereby reducing the oxidative stress for treating atherosclerosis and thus achieve the therapeutic goals with atherosclerosis more desirably.
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Acute radiation syndrome (ARS) is a systemic disease caused by radiation exposure, which mainly includes damage to the hematopoietic system and intestinal tract. At present, the application of cytokines to repair hematopoiesis and restore the integrity of the intestinal mucosa is one of the clinical treatment. Cytokines related to hematopoietic system repair include granulocyte colony stimulating factor (G-CSF), granulocyte-macrophage colony stimulating factor (GM-CSF), thrombopoietin and interleukin-12 (IL-12). Meanwhile, the cytokines related to intestinal mucosal repair mainly are epidermal growth factor (EGF) and fibroblast growth factor 2 (FGF2). The application of cytokines can improve the survival of ARS, however, there are still some obstacles such as easily degraded and inactivated by enzymes, short half-life and high toxicity in vivo. In order to overcome these issues, there are numerous developing effective delivery systems were carried out, including nanoparticles, hydrogels and microspheres. All of the delivery systems implied obvious advantages in protecting cytokines from degradation, prolonging half-life and reducing system toxicity. In this paper, the research progress of the functions, mechanism and delivery systems of cytokines in ARS treatment in recent years was reviewed.
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Objective To analyze peripheral blood hemogram, lymphocyte micronucleus and chromosomal aberrations of radiologists, so as to provide basis for occupational protection and health monitoring of radiologists. Methods Lymphocyte micronucleus, chromosome and blood hemogram analysis were performed on 127 radiologists who received health examinations in 2015, 2017 and 2019, and they were assigned to the radiation group. In addition, 133 medical staff with no history of radiation exposure were selected as the control group. Results The micronucleus rate and chromosome aberration rate of the radiation group were higher than those of the control group, and the white blood cell and platelet counts were lower than those of the control group, both of which were statistically significant (P < 0.05). The total number of white blood cells in peripheral blood of 127 radiologists decreased gradually with the increase of exposure time to ionizing radiation, and the chromosome aberration rate increased gradually, all of which had statistical significance (P < 0.05). The rate of chromosomal aberration was higher in radiologists with damage work age of more than 20 years than in the low-work age group, and there was no statistical significance between different damage work age (P > 0.05). The chromosome aberration rate of nuclear medicine and interventional therapy was higher than that of other types, with statistical significance (P < 0.05). Conclusion Long-term exposure to low-dose ionizing radiation can reduce the total number of white blood cells and increase the chromosome aberration rate of radiologists. It is necessary to strengthen the protective measures for radiologists to reduce the degree of ionizing radiation damage, especially to strengthen the occupational protection for radiologists in nuclear medicine and interventional therapy.
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Objective To investigate the clinical significance and biological role of G-protein coupled receptor 49(GPR49) expression in pancreatic carcinoma.Methods GPR49 expression in tumor and adjacent normal tissues of 77 patients with pancreatic cancer was compared by tissue microarray and immunohistochemistry.And then, the GPR49 expression levels in the tumor tissues of patients with different pathological grades and clinical stages were analyzed.GPR49 positive pancreatic cancer cell line CFPAC-1 was taken as cellular model.CFPAC-1 cells were stimulated with roof plate-specific spondin(RSPO)1, the ligand of GPR49, in vitro.The effect of RSPO1 on CFPAC-1 cells proliferation was evaluated with cell counting.The effect of RSPO1 on the expression of membrane molecular CD44 in CFPAC-1 cells was detected by flow cytometry.CFPAC-1 cells incubated with RSPO1 were subcutaneously implanted into nude mice.And then, the time of tumor formation and tumor size were observed.T test and single factor analysis of variance were performed for statistical analysis.Results GPR49 was widely expressed in all 77 pancreatic cancer tissues.By immunohistochemistry, the score of GPR49 expression in pancreatic cancer tissues was 9.0±2.4, which was higher than that of adjacent normal tissues (5.7±2.4), and the difference was statistically significant (t=8.995, P0.05).The results of experiments in vitro indicated that RSPO1 could promote CFPAC-1 cells proliferation and up-regulate CD44 expression in CFPAC-1 cells.Experiments in vivo demonstrated that after 30 days the tumor volume of mice implanted with RSPO1-pretreated CFPAC-1 cells was (606.0±188.0) mm3, which was larger than that of PBS-pretreated group ((364.2±83.7) mm3), and the difference was statistically significant (t=2.616, P=0.031).Conclusion GPR49 is widely expressed in pancreatic cancer cells and RSPO1/GPR49 pathway has play a role in promoting the proliferation of pancreatic cancer cells, which might be a potential target for interfering pancreatic cancer.