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ObjectiveTo explore the possible mechanism of Bimin Formula （鼻敏方） in treating lung-spleen qi deficiency syndrome of allergic rhinitis （AR） with high mucin secretion. MethodsThirty-four SD rats were randomly divided into a blank group （8 rats）， a model group （8 rats）， a low-dose Bimin Formula group （8 rats）， and a high-dose Bimin Formula group （10 rats）. Except for the blank group， the other groups were subjected to AR lung-spleen qi deficiency rat models induced by smoking， gavage of Ginkgo biloba leaf extract， and ovalbumin. After modeling， rats in the low- and high-dose Bimin Formula groups were given Bimin Formula concentrate （concentration of 2.16 g/ml） by gavage at doses of 1.08 g/100 g and 2.16 g/100 g， respectively， while rats in the model group were given 0.5 ml/100 g of normal saline by gavage， once daily for 28 days； the blank group was not intervened. Behavioral assessments were performed after intervention. ELISA was used to detect the levels of peripheral blood total immunoglobulin E （IgE）. HE staining was used to observe the pathological changes of nasal mucosa epithelium in rats， while immunohistochemistry was used to detect the expression of transmembrane protein 16A （TMEM16A） and mucin 5AC （MUC5AC） protein in nasal mucosa. Western Blot was used to detect the expression of nuclear factor kappa B （NF-κB） protein， and RT-PCR was used to detect the expression of TMEM16A， MUC5AC， and NF-κB mRNA in nasal mucosa. ResultsHE staining showed that the nasal mucosa epithelial cell structure in the blank group was intact without shedding， swelling， or necrosis； the nasal mucosa epithelial tissue of rats in the model group was thickened and partially shed， with infiltration of eosinophils and lymphocytes visible； the pathological changes in nasal mucosa tissue of rats in the high- and low-dose Bimin Formulagroups were improved， and more improvement was showen in the high-dose group. Compared with those in the blank group， the behavioral scores and peripheral blood total IgE levels of rats in the model group significantly increased， as well as the expression of TMEM16A， MUC5AC， and NF-κB proteins and mRNA in nasal mucosa （P＜0.05 or P＜0.01）. Compared with those in the model group， the behavioral scores and peripheral blood total IgE levels of rats in the high-dose Bimin Formula group decreased， and the expression of TMEM16A， MUC5AC， and NF-κB proteins and mRNA in nasal mucosaalso decreased （P＜0.05 or P＜0.01）； the behavioral scores and peripheral blood total IgE levels of rats in the low-dose Bimin Formula group were reduced， and the expression of TMEM16A and MUC5AC proteins and mRNA in nasal mucosa， as well as the expression of NF-κB protein decreased （P＜0.05 or P＜0.01）， but the difference in NF-κB mRNA expression was not statistically significant （P＞0.05）. Compared with the low-dose Bimin Formula group， the expression of NF-κB protein in the high-dose group decreased （P＜0.01）. ConclusionBimin Formula may improve the symptoms and high mucus secretion of AR lung-spleen qi deficiency by regulating the TMEM16A/NF-κB/MUC5AC signaling pathway in nasalmucosa.
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Objective:To study the risk of malignant tumor in medical X-ray workers in Shanghai and provide scientific data for the study on occupationally exposed population.Methods:A retrospective cohort study was conducted to investigate the risk of cancer. Totally, 715 physicians in radiology departments during 1950-1980 in Shanghai were selected as exposure group, while 738 with non-radiology departments in the same hospital in the same time period as control group. The basic information on the selected physicians and associated cancer incidence were collected. The comulative number of individuals with cancer from 1980 to 2021 was calculated. The relative risk ( RR) of cancer was analyzed using logistic regression model in terms of gender, birth year, and work starting year. As well, stratified analysis based on confounding factors was conducted. Results:A total of 1 369 individuals were followed up, including 668 in exposure group and 701 in control group. The cumulative person-year of observed individuals was 52 980. As of 31 December 2021, a total of 199 patients with various malignant tumors were identified. The results of the logistic regression analysis showed that the risk of malignant tumors in exposure group was significantly higher than that in control group. The adjusted RR of solid cancer and total cancer was 1.49 (95% CI: 1.08-2.05, P=0.015) and 1.40 (95% CI: 1.02-1.92, P=0.036), respectively. In addition, the risk of thyroid cancer in exposure group was significantly higher than that in control group ( RR=10.06, 95% CI: 2.05-49.62, P=0.005). Stratified analysis showed that the exposure group had a higher risk of total cancer both for femals and workers taking their jobs at age of 21-25. Conclusions:The risk of thyroid cancer, solid cancer and total cancer in the medical X-ray workers was significantly higher than that in control group. It is suggested that radiation protection in medical practice should be strengthened for the occupationally exposed workers, especially for femals and workers taking their jobs at low age.
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Objective:To study the effect of occupational X-ray exposure on non-cancer diseases of radiation workers.Methods:The medical X-ray workers in Chongqing mumicipality were surved in 1980. In 2020, the previous 91 medical institutions distributed across 41 districts and counties of Chongqing continued to be selected as the survyed units, including 53 grade-A top-class hospitals. Using the method of prospective cohort study, the fifth follow-up survey was conducted for Chongqing′s medical X-ray workers and the control groups in 1980 with respect to their personal information, occupational radiation exposure, disease history and others. The incidence rate, relative risk ( RR) and 95% confidence interval of diseases in each system were analyzed. Results:There were 937 individuals in this cohort. So far, 359 cases of non-cancer diseases had been counted. Compared with the control group, the relative risk RR of cardiovascular system, ophthalmology and other unclassified diseases in the exposure group were 1.50, 2.03 and 2.64 ( χ2=5.97, 3.97, 4.25, P <0.05) , respectively. The adjusted confounding factors showed that the RR of the incidence rate of cardiovascular, ophthalmic and digestive diseases in the female exposure group was generally higher than that in the control group ( RR=2.33, 2.59, 7.55; χ2= 7.28, 4.17, 8.64, P < 0.05) , respectively. The RR of the incidence rate of cardiovascular and ophthalmic diseases in exposure group was generally higher than that in the control group among 25-29 year-old workers ( RR=2.26, 5.07; χ2 =8.22, 4.91, P < 0.05) , respectively. For compasion between the the accumulated dose groups, the incidence rate of cardiovascular system, ophthalmology and digestive system diseases in the exposure group was generally higher than that in the control group ( RR=1.86, 2.91, 3.59; χ2= 9.83, 8.21, 5.58, P < 0.05) , respectively. Conclusions:The non-cancer risk of X-ray workers exposed to long-term occupational exposure was increased, among which the risk of cardiovascular system, digestive system, ophthalmic diseases and others might be related to the occupational exposure.
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Objective To provide scientific data for the study of tumor prevalence among medical X-ray workers. Methods In a cohort study, radiation exposure and tumor occurrence were collected from medical X-ray workers and normal persons (control) in Chongqing, China. SPSS 24 software was used to calculate the incidence density of tumor in the follow-up cohort, as well as the relative risk (RR) and 95% confidence interval of various malignant tumors. Results A total of 934 subjects were followed up. By the end of the investigation, 109 cases of malignant tumor were recorded. Compared with the control group, the RRs of liver cancer and colorectal cancer were both 3.4. Dose-specific RR was calculated for the worker groups. Compared with the two groups with < 80 mGy and 80～200 mGy cumulative doses, the group with > 200 mGy cumulative dose showed 2.05 and 2.1 RRs for solid cancer, and 1.89 and 2.17 RRs for whole cancer, respectively. Conclusion The risk of liver cancer and colorectal cancer is higher for medical X-ray workers in Chongqing, and the risk of solid cancer and whole cancer is higher in the high cumulative dose group. Therefore, radiation workers should pay attention to the optimization of protection.
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Objective@#To study on the genomic stability of male workers engaged in e-waste dismantling area in Tianjin.@*Methods@#In 2016, an e-waste dismantling area in Tianjin and an area 50 km away from the e-waste dismantling area (no e-waste or other chemical, industrial and agricultural pollution nearby) were selected as the study area and the reference area. Male residents of the study area and male farmers who planted vegetables, fruits, and crops in the reference area were selected as the exposed and reference group by using the convenient sampling method. The exposed group included 146 workers who engaged in e-waste recycling work more than 1 year. The reference group included 121 farmers who never engaged in e-waste recycling work. Questionnaires were used to collect information of all subjects. The semen and peripheral blood were also collected. Trace elements and polychlorinated biphenyl concentration in blood were detected. DNA damage in peripheral blood and sperm was detected, and gene expression was analyzed. DNA damage was assessed using tail DNA% (TDNA%), tail moment (TM) and olive tail moment (OTM) of comet assay.@*Results@#The ages of the exposed group and the reference group were (33.6±12.1) and (33.9±11.9) years old, respectively. The proportions of subjects with exposure time of ≤3, 4-6, ≥7 years were 43% (63 cases), 26% (53 cases) and 21% (30 cases), respectively. The Pb and polychlorinated biphenyl(PCB) concentrations in the exposed group [(90.4±15.3) μg/ml and (101±30) ng/ml, respectively] were higher than those in the reference group [Pb and PCB concentrations were (60.2±8.9) μg/ml, and (2.5±1.4) ng/ml, respectively (both P values <0.05)]. The TDNA%, TM and OTM of peripheral blood and sperm in the exposed group were 5.9%±0.3% and 2.6%±0.90%, 0.93±0.16 and 0.51±0.20, 0.82±0.09 and 0.56±0.07, respectively, which were all higher than those in the reference group [TDNA%, TM and OTM of peripheral blood and sperm were 1.8%±0.2% and 1.9%±0.2%, 0.21±0.04 and 0.32±0.10, 0.19±0.03 and 0.20±0.08, respectively (all P values <0.001)]. The results of gene expression showed that 20 differentially expressed genes, including 13 up-regulated genes and 7 down-regulated genes, were detected in the exposed group compared with the reference group.@*Conclusion@#There are obvious DNA damage and DNA repair gene disorder in male workers of an e-waste dismantling area in Tianjin. The current operation mode brings potential health risks to workers.
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Objective@#To study on the exposure of polychlorinated biphenyl (PCB) contamination and DNA methylation in male employees in an e-waste dismantling area in Tianjin.@*Methods@#In 2016, an e-waste dismantling area in Tianjin and an area 50 km away from the e-waste dismantling area (no e-waste or other chemical, industrial and agricultural pollution nearby) were selected as the study area and the reference area. Male residents of the study area and male farmers who planted vegetables, fruits, and crops in the reference area were selected as the exposed and reference group by using the convenient sampling method. A total of 60 subjects (30 in each of the exposed group and the reference group) were included. The peripheral blood (5 ml) of the study subject was collected, and the PCB concentration was detected. Eight independent subjects in the exposed group and the reference group were randomly selected by random number table method to detect the methylation level of the promoter region of all gene loci, and the mRNA transcript levels.@*Results@#The PCB concentration in peripheral blood of the exposed group was higher than that of the reference group, and the difference was statistically significant (allP values <0.001). The methylation levels of the promoter region of the exposed group and the reference group showed obvious clustering, and 994 gene loci had different degrees of methylation. Compared with the reference group, there were 391 hypomethylation sites and 553 hypermethylation sites in the exposed group. The proportion of methylation sites in the high CpG-rich region was 59.2% and 48.1%, respectively. The mRNA level of the hypomethylated gene in the exposed group was higher (FAM131A, HBM), and the transcription level of the hypermethylated gene was lower (CAPN15, NFIC, SHISA5, FGF13, GRAMD1A, CLEC3B, LILRB2, DCAF7). The mRNA transcription levels of 10 genes above in the exposed group and the reference group were statistically significant (all P values <0.001).@*Conclusion@#The PCB concentration of peripheral blood in the exposed population of e-waste is high. PCB exposure changes the methylation level of specific genes and affects the mRNA transcription level of some genes.
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Objective To investigate the dynamic changes of gene expressions in mouse jejunum after lethal dose abdomen irradiation (ABI).Methods RNA was extracted from mouse jejunum at 0 and 6 h,3.5 and 5 d after 14 Gy 137Cs γ-ray ABI and then subjected to RNA-sequence analysis.Gene with expressions changed more than 2-fold of control were identified as differentially expressed ones.The selected genes were subsequently analyzed using IPA,Funrich,GO and KEGG software.Results Gene analysis of mouse jejunum samples showed that radiation activated p53 pathway at 6 h and 3.5 d after ABI.Interaction network analysis of genes suggested that Lck,Cdkl and Fyn,genes could play an important role in jejunum damage at 3.5 d after ABI.The gene expression profiles demonstrated that ABI up-regulated DNA damage repair pathways and down-regulated cell adhesion molecules,focal adhesion and IgA production pathways.Conclusions The p53 signaling pathway and some key genes such as Lck,Cdkl,and Fyn may contribute to the radiation-induced intestinal injury.
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Objective To investigate the effects of Olaparib on cell proliferation and radiosensitization of human non-small cell lung cancer cells.Methods Non-small cell lung H460 and H1299 cell lines were cultured in vitro and the cells in logarithmic growth phase were selected for experiments.MTT and colony formation assays were used to determine cell proliferation and radiosensitization,respectively.Single cell gel electrophoresis assay (comet assay) was used to detect irradiation-induced DNA damage.Results The results of MTT assay showed that Olaparib inhibited the proliferation of H460 and H1299 cells in a dose-dependent pattern (all P＜0.05).H1299 cell line was more sensitive to Olaparib than H460 cells.The results of colony formation assay showed that Olaparib enhanced the radiosensitizition of H460 and H1299 cells (all P＜0.05).The results of comet assay showed that Olaparib increased γ ray-induced DNA damage.Conclusions Olapani can enhance the radiosensitization of human non-small cell lung cancer cells,and the radiosensitization effect of Olaparib may be associated with the inhibition of cell proliferation and induction of irradiation-induced DNA damage.
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Objective To investigate the correlation between the level of apoptosis protein 1 (c-IAP1) and the radiosensitivity of lung cancer cells.Method The survival rate and proliferation of the lung cancer cells lines (A549,H460,H1299,H358,HCC827,H1650) from six human were detected by thiazolyl blue tetrazolium bromide (MTT) and cell colony formation assay.The DNA damage effects of radiation on lung cancer cells were detected by comet assay.The expressions of c-IAP1 protein and its mRNA were determined by Western blot and real-time quantitative PCR.Results The results of MTT and colony formation showed that the radiosensitivity of different lung cancer cells was also different,among which H358 and H460 cells had the highest radiosensitivity than that of H1650 and HCC827 cells,and H1299 and A549 cells had the weakest radiosensitivity.The results of comet assay showed that six kinds of lung cancer cells were suffered by DNA damage after radiation,and the DNA damage of H358 cells was most serious.The results of Western blot and real-time quantitative PCR showed that the c-IAP1 protein level was negatively correlated with the radiosensitivity of lung cancer cells.The higher the c-IAP1 protein level,the weaker the radiosensitivity of cells.The radiosensitivity was also affected by Smac protein levels.Conclusions c-IAP1 may be a selective target gene in mediating the radiosensitivity of lung cancer cells and this paper may contribute to the study of radioresistance and radiosensitization of cancer cell.
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Objective To investigate the correlation between the level of apoptosis protein 1 (c-IAP1) and the radiosensitivity of lung cancer cells.Method The survival rate and proliferation of the lung cancer cells lines (A549,H460,H1299,H358,HCC827,H1650) from six human were detected by thiazolyl blue tetrazolium bromide (MTT) and cell colony formation assay.The DNA damage effects of radiation on lung cancer cells were detected by comet assay.The expressions of c-IAP1 protein and its mRNA were determined by Western blot and real-time quantitative PCR.Results The results of MTT and colony formation showed that the radiosensitivity of different lung cancer cells was also different,among which H358 and H460 cells had the highest radiosensitivity than that of H1650 and HCC827 cells,and H1299 and A549 cells had the weakest radiosensitivity.The results of comet assay showed that six kinds of lung cancer cells were suffered by DNA damage after radiation,and the DNA damage of H358 cells was most serious.The results of Western blot and real-time quantitative PCR showed that the c-IAP1 protein level was negatively correlated with the radiosensitivity of lung cancer cells.The higher the c-IAP1 protein level,the weaker the radiosensitivity of cells.The radiosensitivity was also affected by Smac protein levels.Conclusions c-IAP1 may be a selective target gene in mediating the radiosensitivity of lung cancer cells and this paper may contribute to the study of radioresistance and radiosensitization of cancer cell.