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Objective:To explore the mechanism of lysosomal membrane permeabilization(LMP)inuranyl acetate-induced death of human kidney proximal tubular epithelial HK-2 cells.Methods:HK-2 cells were exposed to uranyl acetate at concentrations of 100, 300 and 600 μmol/L for 24 h, then in tracellular reactive oxygen species (ROS)and mitochondrial superoxide were measured by DCFH-DA and MitoSOX probe, respectively. HK-2 cells were divided into four groups: blank control group, NAC or CA-074 Me group, uranyl acetate exposure group and uranyl acetate exposure plus NAC or CA-074 Me group. Two-color immune of luorescence staining was used to detect the co-localization of galectin-1 and lysosomal associated membrane protein-1 (LAMP-1) to measure the extent of LMP, and to detect the non- co-localization of cathepsin B and LAMP-1 to reflect the release of cathepsin B in lysosomes. Calcein-AM/PI double staining method was used to detect cell death. One-color immune of luorescence staining of cleaved-caspase-3 expression was used to detect apoptosis. Results:Intracellular ROS and mitochondrial superoxide levels were significantly increased in HK-2 cells after exposure with 100, 300 and 600 μmol/L uranyl acetate for 24 h, about 1.1-2.5 times or 4.0-28 times, respectively( tROS=17.98, 11.84, 11.75, P< 0.05; tmitochondrial superoxide=6.14, 16.02, 13.06, P< 0.05), and they also increased with uranyl acetate concentrations ( tROS=10.10, 10.37, 5.59, P< 0.05; tmitochondrial superoxide=21.50, 15.16, 5.93, P< 0.05). The percentage of co-localization of galectin-1 and LAMP-1 and the percentage of non- co-localization of cathepsin B and LAMP-1 were markedly increased in HK-2 cells after exposure with 600 μmol/L uranyl acetate for 24 h, 5.4-6.7 times or 1.5-2.1 times, respectively ( tGalectin-1=15.85, 12.70, P< 0.05; tCathepsin B=5.95, 6.69, P< 0.05), but these increases were inhibited by NAC ( tGalectin-1=4.74, P<0.05; tCathepsin B=4.51, P< 0.05). Moreover, the cell death rate and the cleaved-caspase-3 expression level were also significantly increased in HK-2 cells after exposure with 600 μmol/L uranyl acetate for 24 h, about 28-47 times or 2.4-6.0 times, respectively( tPI=30.40, 10.34, P<0.05; tCleaved-caspase-3=18.49, 9.52, P<0.05), and these increases were obviously diminished by CA-074 Me ( tPI= 6.76, P<0.05; tCleaved-caspase-3=13.47, P<0.05). Conclusions:Exposure to uranyl acetate induces a burst of intracellular ROSthat leads to LMP and consequently causes leakage of cathepsin B from lysosomes to cytoplasm, in turn triggering the lysosomal-dependent cell death and mitochondrial-regulated apoptosis of HK-2 cells.
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Objective:To investigate the radiosensitizing effect of Ta 4C 3-PVP nanosheets on the tumor of 4T1 murine triple-negative breast cancer cells planted in mice. Methods:4T1 tumor-bearing mice model was established by subcutaneous injection of 4T1 cells into the right flank of the female BALB/c mice. The mice were divided into four groups uniformly according to their tumor size: blank control group, Ta 4C 3-PVP group, ionizing radiation (IR) group and Ta 4C 3-PVP plus IR group. A single dose of 8 Gy X-ray local irradiation was given to xenograft tumor at 24 h after tail intravenous injection of Ta 4C 3-PVP (20 mg/kg). The xenograft tumor volume and weight, the pathological changes of tumor tissue, the expression of tumor proliferative marker Ki-67 protein, and the formation of γ-H2AX foci [a DNA double-strand breaks (DSBs) molecular marker] were detected. Tumor growth curve was established, and enhancement factor (EF) and tumor inhibition rate were calculated. Results:Compared with the blank control group, tumor growth was significantly inhibited ( t=5.41, 9.59, P < 0.05) and tumor weight was markedly decreased ( t=2.67, 4.40, P < 0.05) in both IR group and Ta 4C 3-PVP plus IR group at day 16 after IR. The EF in Ta 4C 3-PVP plus IR group was 1.57, and tumor inhibition rate in Ta 4C 3-PVP plus IR group were about 64%, which was much higher than that of IR group alone(42%). Immunohistochemistry and immunofluorescence histochemistry assays showed that the expression of Ki-67 protein was obviously decreased and the amount of γ-H2AX foci was significantly increased in both IR group and Ta 4C 3-PVP plus IR group in comparison with the blank control group ( t=5.73, 8.02, 2.97, 9.86, P < 0.05). Moreover, the inhibition of Ki-67 protein expression and the increase of γ-H2AX foci were much higher in Ta 4C 3-PVP plus IR group than that in IR group ( t=4.75, 4.42, P < 0.05). Conclusions:Ta 4C 3-PVP nanosheets could enhance radiosensitivity of xenograft tumor in 4T1 tumor-bearing mice through increasing the IR-induced DNA DSBs.
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Objectives Comparative analysis on epidemiological characteristics of measles in Minhang District before and after Large scale supplementary immunization activities of measles containing vaccine(MCV) in 2010. Methods Measles incidence data of MCV-SIA in 2010 and the first five years before 2010 (from January 1, 2005 to December 31, 2009), the next five years (from January 1, 2011 to December 31, 2015) and the second five years (from January 1, 2016 to December 31, 2020) after were collected. Descriptive epidemiological method was used for comparative analysis. Results The incidence rate of measles in Minhang District, Shanghai after MCV-SIA in 2010 showed a significant downward trend, The average annual incidence (per 100 0000) in the first 5 years before 2010 was 155.96, SIA was 30.08,The next five years was 29.52, The second five years was 2.84,There was statistical difference in the annual incidence rate between the four groups.(χ2=3165.821,P2=1.646,P=0.223)The proportion of 8-month-old children under the age of MCV decreased from 15.46% in the first five years of MCV-sia to 5.88%,In the second five years after MCV-sia, the proportion of 10-14 age group increased from 7.81% to 13.83%, The susceptible population of measles before MCV-SIA was less than 8 month old and under the age of MCV initial immunization, no migrant workers with no history of immunization and adults with registered residence. Once there is a source of infection, it is easy to cause the spread of the epidemic. After MCV-SIA, foreign students in international schools and nonworking population became the focus of measles. Of the 95 cases in which measles virus genotypes were available in the next five years, 2 (2.11%) were A genotype, and 93 (97.89%)were the indigenous H1 genotype ; Of the 7 cases in which measles virus genotypes were available in the second five years,7 (100%)were the indigenous H1 genotype . Conclusions After MCV-SIA, the comprehensive measles prevention and control measures can effectively control the incidence and prevalence of measles in Minhang District. But circulation of the indigenous H1 genotype was not interrupted, the work of normalization measures to eliminate measles also needs to cooperate with many departments to strengthen the prevention and control measures of measles in foreign schools and the nonworking population.
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Objective:To assess the radiosensitivity of polyvinylpyrrolidone (PVP) modified tantalum carbide (Ta 4C 3) nanosheets in human triple-negative breast cancer MDA-MB-231 cells in vitro. Methods:PVP-modified Ta 4C 3 nanosheets were synthesized and characterized. The uptake of fluoresceine isothiocyanate(FITC) labeled Ta 4C 3-PVP nanosheets in MDA-MB-231 cells was examined by fluorescent microscope. The toxicity of Ta 4C 3-PVP in the cells was measured by CCK-8 assay.These cells were divided into 4 groups: control group, Ta 4C 3-PVP group, irradiation group alone and Ta 4C 3-PVP plus irradiation group. The colony formation assay was used to evaluate the radiosensitivity. The levels of intracellular reactive oxygen species (ROS) and lipid oxidation production, malondialdehyde (MDA), were detected with an automatic microplate reader.γH2AX foci and mitotic catastrophe were observed by immunofluorescence staining. Results:Ta 4C 3-PVP nanosheets with a single-layer flaky shape were successfully synthesized. The hydrodynamic diameter and thick of Ta 4C 3-PVP nanosheets were about 143.93 nm and 1.35 nm, respectively. The FITC labeled Ta 4C 3-PVP nanosheets were uptaken by MDA-MB-231 cells, which was mainly distributed in the cytoplasm.Treatment of Ta 4C 3-PVP nanosheets at concentrations up to 400 μg/ml was noncytotoxic to MDA-MB-231 cells. The colony formation assay showed that pretreatment with Ta 4C 3-PVP at 50 and 100 μg/ml moved the survival curve of the irradiated cells downward in a concentration-dependent manner, compared to irradiation group alone. The sensitization enhancement ratio (SER D0 ) of Ta 4C 3-PVP at 50 and 100 μg/ml were 1.21 and 1.45, respectively.The intracellular ROS level in Ta 4C 3-PVP plus irradiation group was significantly higher than that in irradiation group alone at 2 and 12 h after irradiation ( q=20.01, 7.193, P<0.05). The percentage of positive cells with more than five γH2AX foci in Ta 4C 3-PVP plus irradiation group was higher than that of irradiation group alone at 1, 4 and 8 h after irradiation ( q=36.78, 14.87, 8.217, P<0.05). The content of MDA in Ta 4C 3-PVP plus irradiation group was significantly higher than that of irradiation group alone at 24 and 48 h after irradiation ( q=14.02, 7.015, P<0.05). The percentage of cells that succumbed to mitotic catastrophe in Ta 4C 3-PVP plus irradiation group was significantly higher than that in irradiation group alone at 72 h after irradiation ( q=16.33, P<0.05). Conclusions:Ta 4C 3-PVP nanosheets could enhance the radiosensitivity of human triple-negative breast cancer MDA-MB-231 cells through an increase of the intracellular ROS induced by irradiation.
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Objective To investigate the effects of glycogen synthase kinase-3β (GSK-3β) and β-catenin signaling on the human renal proximal tubular epithelial HK-2 cell injury induced by depleted uranium(DU),and provide a new enlightenment for the development of DU antidotes.Methods H K-2 cells were exposed to different concentrations of DU for 3-24 h,then the protein expressions of kidney injury molecule 1 (KIM-1),neutrophil gelatinase-associated lipocalin (NGAL) and nuclear β-catenin were detected by immunofluorescence staining.The protein expressions of p-GSK-3 β(S9),GSK-3β and cmyc were detected by Western blot assay.HK-2 cells were transiently transfected by GSK-3β (KD) plasmid or treated by TDZD-8 to inhibit the activity of GSK-3β specifically.Other HK-2 cells were transiently transfected by β-catenin plasmid to overexpress the β-catenin protein.Results The percentages of KIM-1 and NGAL-positive cells increased with DU exposure time and concentrations from 300 and 600 μmol/L,and they were significantly higher than those of the blank control at 6-24 h of DU exposure (KIM-1-positive cells:t =11.06,18.97,30.49,P <0.05;t =6.79,16.02,85.45,P < 0.05;NGAL-positive cells:t =11.78,11.37,34.29,P <0.05;t =7.34,21.63,36.84,P <0.05).In contrast,the ratio of p-GSK-3β (S9) to GSK-3β and percentage of nuclear β-catenin-positive cells were significantly higher than that of the blank control at 3-24 h of DU exposure (p-GSK-3β(S9)/GSK-3β:t =3.95,4.69,5.40,3.34,P < 0.05;nuclear β-catenin-positive cells:t =4.61,6.52,36.64,14.93,P < 0.05) with a maximum response at 9 h of DU exposure accompanied with corresponding increase of protein level of c-myc,a downstream target gene of β-catenin.Transient transfection of HK-2 cells with GSK-3β (KD) plasmid significantly inhibited the activity of GSK-3β (t =8.07,P < 0.05) and reduced the DU-increased percentage of KIM-1-positive cells (t =24.77,P < 0.05).Treatment cells with TDZD-8 inhibited the activity of GSK-3β and enhanced the percentage of nuclear β-catenin-positive cells,and it also significantly reduced the percentage of KIM-1-positive cells in HK-2 cells exposed to DU (t =6.25,6.73,P < 0.05).Moreover,overexpression of β-catenin significantly reduced DU-induced cell injury (t =7.48,P < 0.05).Conclusions GSK-3β/β-catenin signaling plays a key role in regulating the DU-induced cytotoxicity of HK-2 cells.Inhibition of GSK-3β activity and overexpression of β-catenin can protect the HK-2 cells from DU-induced damage.
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Objective To evaluate the potential feasibility of γ-H2AX foci as a biodosimetry after exposure to ionizing radiation by comparing DNA double-strand break repair kinetics in rat blood lymphocytes with that in human lymphocytes.Methods Peripheral blood lymphocytes separated from Sprague-Dawley(SD) male rats and healthy adults were exposed to γ-rays,and some rats were also subjected to total body irradiation.The inductions of DNA repair-related foci of γ-H2AX,pATM (S1981) and pDNA-PKcs (T2609) were detected with immunofluorescence staining technique at different time points post-irradiation,and the status of their co-localization was analyzed.Results The induction kinetics of γ-H2AX foci in rat lymphocytes was similar to that observed in human lymphocytes.The frequencies of γ-H2AX foci peaked at 30 min after γ-ray irradiation (trst =62.64,th =28.52,P < 0.05),then decreased rapidly after 6 h post-irradiation (trat =45.96,th =14.80,P <0.05),and the residual foci number remained only about 3%-8% of its maximal value at 24 h post-irradiation.At 30 min after γ-ray irradiation,the frequencies of pATM (S1981) and pDNA-PKcs (T2609) foci in rat and human lymphocytes significantly higher than those of nonirradiated control (trat =21.05,25.80,th =11.07,29.52,P < 0.05),and the frequencies of co-localization of pATM (S1981) or pDNA-PKcs (T2609) foci with γ-H2AX foci also markedly increased by 26%-32% in irradiated lymphocytes of rat and human (trat =5.34,9.14,thuman =18.32,51.28,P <0.05).Moreover,γ-H2AX foci incidence in rat lymphocytes in vitro was consistent with that induced by total body irradiation of rat.The number of γ-H2AX foci in irradiated rat lymphocytes increased with irradiation dose in a linear dose-dependent manner,its slope was similar to that of irradiated human lymphocytes reported by other laboratory.Conclusions Rat is a useful animal model to evaluate radiation biodosimetry with γ-H2AX foci in lymphocytes.The co-activation of ATM and DNA-PK plays an important role in DSB repair in the irradiated lymphocytes of rat and human.
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Objective To investigate the radiosensitization effect of antihelminthic niclosamide on human triple-negative breast cancer MDA-MB-231 cells and the potential mechanism related to Wnt/β-catenin signaling pathway.Methods Four methyl thiazolyl tetrazolium(MTT) assay was used to measure the effect of niclosamide on cell viability at different concentrations and 50% inhibitory concentration(IC50)value was calculated.MDA-MB-231 cells were divided into 4 groups:untreated control,niclosamide treatment alone group,radiation alone group and niclosamide plus radiation treatment group.The cells with or without 1.0 and 1.5 μmol/L niclosamide pre-treatment were irradiated with 137Cs γ-rays at doses of 0,2,4 and 6 Gy.Cell survival was assayed with the colony formation method,radiation-induced γH2AX foci was analyzed with immunofluorescence,cell cycle progression was assayed with flow cytometry,and the changes of phospho-and non-phospho-β-catenin and Cyclin D1 protein expressions were measured with Western blot.Results Niclosamde obviously inhibited the viability of MDA-MB-231 cells in a dosedependent manner with a IC50 value of 13.63 μmol/L.Pretreatment of cells with 1.0 and 1.5 μmol/L niclosamide evidently enhanced the radiosensitivity of MDA-MB-231 cells to γ-rays,and the values of SER were 1.37 and 1.62,respectively.Niclosamide pretreatment significantly increased radiation-induced γH2AX foci formation(t =3.91,P <0.05),diminished the radiation-induced G2/M arrest(t =8.05,P <0.01),and inhibited radiation-induced expressions of phospho-β-catenin (S675),non-phospho-β-catenin and Cyclin D1 proteins in MDA-MB-231 cells.Conclusions Niclosamide significantly can enhance the sensitivity of MDA-MB-231 cells to γ-ray irradiation through inhibiting Wnt/β-catenin signaling pathway,which results in the inhibition of DNA DSBs repair and the reduction of radiation-induced G2/M arrest.Wnt/β-catenin signaling pathway may serve as an ideal molecular target for radiosensitization of triplenegative breast cancer.
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Objective To investigate the characteristics of repair of DNA double strand breaks (DSB) induced by high-LET α-particle irradiation and their relationship with chromatin structure in the G0 lymphocytes of human peripheral blood,in order to provide the experimental basis for the judgement and dose evaluation of internal α-particle radiation.Methods Peripheral whole blood were collected from four healthy adults and lymphocytes were separated.A monocellular layer of human lymphocytes attached in Mylar film were irradiated with 0 and 0.5 Gy of α-particles and the lymphocytes suspensions were irradiated with 0 and 0.5 Gy of γ-rays.The formations of γH2AX foci as a surrogate marker of DSB and Rad51 foci as a marker of homologous recombination (HR) repair and their spatial localization in chromatin structure were measured by immunofluorescence staining technique at 10 min-48 h post-irradiation.Results Linear-γH2AX foci tracks were observe at 10 min-2 h post-irradiation in lymphocytes exposed to α-particle irradiation(t =11.12,14.40,16.56,P < 0.05),and almost completely disppeared at 6 h postirradiation.The frequencies of γH2AX foci peaked at 30 min after α-particle irradiation (t =51.72,P <0.05) and then decreased rapidly during 6 h post-irradiation (t =29.83,P < 0.05).The average number of foci remained only about 16% at 24-48 h post-irradiation.Moreover,27% of γH2AX foci located at DAPI-bright heterochromatin region at 10 min after α-particle radiation,suggesting that the efficacy of DSB repair may be decreased.In contrast,at 10 min-48 h after γ-ray irradiation,no linear γH2AX foci track was observed and the γH2AX foci diffused randomly in nucleus and predominantly located in DAPI-weak euchromatin region.The numbers of formative and residual γH2AX foci after γ-ray irradiation were significantly less than those after α-particle radiation.During 30 min-2 h after α-particle and γ-ray irradiation,the frequencies of Rad51 foci slightly but not significantly increased in comparison with background level,and the frequencies of co-localization of Rad51 foci and γH2AX foci were only 3%-8%.Conclusions The formation of linear γH2AX foci tracks induced by high-LET α-particle irradiation in Go human lymphocyte could be used as biological indicator to estimate whether a person has been exposed to internal α-particle radiation.Prolonged persistence of residual γH2AX foci may be applicable for biological dosimetry.
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Objective To investigate the influence of collective motion excitation on the anxiety/depression and the quality of life of COPD patients at stable stage? Methods Ninety-six patients with chronic obstructive pulmonary disease(COPD)at stable stage were divided into the intervention group and the control group,both treated with regular medical treatment and general nursing?Collective motion excitation was implemented in the intervention group twice per week in 12 weeks? The Hamilton Anxiety Scale (HAMA),the Hamilton Depression Scale(HAMD)and the Short Form-36 Health Survey(SF-36)were used to assess all patients before and after the 12-week nursing? Result Compared to the control group,the intervention group demonstrated significant improvements in HAMA ,HAMD and SF-36 scores at the endpoint of 12 weeks(P 0?05)? Conclusion The anxiety/depression and the quality of life can be improved with COPD patients at stable stage through collective motion excitation?
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Objective To explore the dose- and time-responses of BPCBG on the decorporation of uranium and its protective effects for uranium-induced kidney injury in rats. Methods Sprague-Dawley (SD) male rats were randomly divided into 4 -7 groups:normal control group,uranium poisoning group,different doses of BPCBG groups and DTPA-CaNa3 group. Rats in chelating agents-treated groups were either injected intramuscularly with 60,120 and 600 μmol/kg of BPCBG or 120 and 600 μmol/kg of DTPA-CaNa3 immediately after intraperitoneal injection of uranyl acetate dihydrate,or injected with 120 μmol/kg of BPCBG 0.5,2 h before or 0,0.5,1 and 2 h after injection of uranium. Uranium poisoning group rats were injected with normal saline after intraperitoneal injection of uranyl acetate dihydrate,and the normal control group rats were merely injected with normal saline. The uranium content in urine,kidney and femurs were detected 24 h after chelator injections by ICP-MS method.After injecting a dose of 500 μg uranyl acetate dihydrate,rats were injected with 600 μmol/kg of BPCBG or 1200 μmol/kg of DTPA-CaNa3. Histopathological changes in the kidney and serum creatinine and urea nitrogen were examined 48 h after chelator administration.Results Prompt injections of BPCBG resulted in 37% -61% ( t =2.22,4.43,5.80,P < 0.05 ) increase in 24 h-urinary uranium excretion,and significantly decreased the levels of uranium in kidney and bone by 59% -69% (t=3.33,5-59,4-53,P<0.01) and 14% -58% (t =2.15,8.70,9.10,P < 0.05 ) respectively in a dose-dependent manner. BPCRG injection obviously reduced the severity of the uranium-induced histological alterations in the kidney,which was in parallel with the amelioration noted in serum indicators,serum creatinine and urea nitrogen,of uranium nephrotoxicity.Advanced 0.5 h or delayed 0.5 and 1 h administrations of BPCBG were effective in 24 h-urinary uranium excretion ( advanced 0.5 h:t =4.34,delayed 0.5 h:t =3.35,P < 0.05 ),decreasing accumulation of kidney uranium ( t =5.75,7.74,5.87,P < 0.05 ) and accumulation of hone uranium (t =6.43,5.222,2.60,P <0.05),but the efficacy decreased with the interval time between uranium and BPCBG injection. Although DTPA-CaNa3 markedly reduced uranium retention in kidney (120,600 μmol/kg,t =2.28,3.35,P < 0.05 ),its efficacy in uranium removal was significantly lower than that of BPCBG,and it had no protective effects against uranium-induced nephrotoxicity.Conclusions BPCBG can effectively decorporate uranium from rats and protect against uranium-induced kidney injury of rats.
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This study is to assess the efficacy of BPCBG on the decorporation of uranium (VI) and protecting human renal proximal tubular epithelial cells (HK-2) against uranium-induced damage. BPCBG at different doses was injected intramuscularly to male SD rats immediately after a single intraperitoneal injection of UO2(CH3COO)2. Twenty-four hours later uranium contents in urine, kidneys and femurs were measured by ICP-MS. After HK-2 cells were exposed to UO2(CH3COO)2 immediately or for 24 h followed by BPCBG treatment at different doses for another 24 or 48 h, the uranium contents in HK-2 cells were measured by ICP-MS, the cell survival was assayed by cell counting kit-8 assay, formation of micronuclei was determined by the cytokinesis-block (CB) micronucleus assay and the production of intracellular reactive oxygen species (ROS) was detected by 2',7'-dichlorofluorescin diacetate (DCFH-DA) oxidation. DTPA-CaNa3 was used as control. It was found that BPCBG at dosages of 60, 120, and 600 micromol kg(-1) resulted in 37%-61% increase in 24 h-urinary uranium excretion, and significantly decreased the amount of uranium retention in kidney and bone to 41%-31% and 86%-42% of uranium-treated group, respectively. After HK-2 cells that had been pre-treated with UO2(CH3COO)2 for 24 h were treated with the chelators for another 24 h, 55%-60% of the intracellular uranium was removed by 10-250 micromol L(-1) of BPCBG. Treatment of uranium-treated HK-2 cells with BPCBG significantly enhanced the cell survival, decreased the formation of micronuclei and inhibited the production of intracellular ROS. Although DTPA-CaNa3 markedly reduced the uranium retention in kidney of rats and HK-2 cells, its efficacy of uranium removal from body was significantly lower than that of BPCBG and it could not protect uranium-induced cell damage. It can be concluded that BPCBG effectively decorporated the uranium from UO2(CH3COO)2-treated rats and HK-2 cells, which was better than DTPA-CaNa3. It could also scavenge the uranium-induced intracellular ROS and protect against the uranium-induced cell damage. BPCBG is worth further investigation.
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Objective To study the dose rate distribution on cultured cell plane and establish a reference dose rate table of in vitro cell line ~(125)I seed irradiator.Methods Thermoluminescence dosimetry(TLD) was used to measure the irradiation dose rate of a single 6711 model(~(125) I) seed with apparent activity of 10.323 MBq in water at point P.Meanwhile,the theoretic value of the irradiation dose rate at point P was calculated with theoretic formula.The difference between the calculated and observed values within 10% was set as standard to analyze the accuracy of the measurement.The irradiation dose rate of a single 6711 model(~(125) I) seed was measured in 1mm-thick polystyrene + water medium at point P.The value was applied to differential or non-differential proof along with the value from water medium to study the effect of 1 mm thick polystyrene on distribution of irradiation dose in water.Finally,by simulating the(~(125) I) seed plane irradiator with nine(~(125) I) seeds,the distribution table of irradiation dose rate on the cultured cell plane was calculated with theoretical formula.Results The observed value(n= 10) of irradiation dose rate with one(~(125) I) seed in water at point P was(0.359?0.023)cGy/h and the calculated value was 0.347cGy/h,the difference was within 10%.The observed value(n=10) of irradiation dose of one(~(125) I) seed in 1mm-thick polystyrene + water medium at point P was (0.350?0.027)cGy/h,which showed no statistical difference from the observed value in water under differential and non-differential proof.The reference table on dose rate distribution for cells exposed to(~(125) I) seed irradiation in vitro was developed.Conclusions 1mm-thick polystyrene gives no significant effect on irradiation dose rate distribution from(~(125) I) seeds in water.A reference table on the dose rate distribution for cells exposed to(~(125) I) seed irradiation in vitro has been developed,which can be used to determine an optimal irradiating strategy for future work.
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Objective To analyze the kinds of organic compounds in source water and finished water. Methods The organic pollutants in water samples collected from source water and finiched water and enriched by GDX resin, were analyzed by GC/ MS. Results 48 organic compounds including phthalates, phenols, terpanes and aromatic compounds were detected in water samples. Similar kinds of organic compounds were found in source water samples and finished water samples. The main pollutants were phthalates, phenols and cyclic compound which had a high percentages (85%-94% ). Conclusion Many kinds of organic compounds in source water still existed in the finished water.