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Objective To provide a theoretical basis for radiation health supervision through an analysis of the situation of computed tomography (CT) equipment quality control and CT room radiological protection in Guangdong Province, China in recent years. Methods We collected the data of 392 times of CT quality control and radiological protection testing by a third-party radiological health technical service institution in Guangdong Province from 2019 to 2021. We analyzed the levels of CT-owning hospitals, CT manufacturers, CT quality control test results, and the pass rate of radiation protection tests. Results The examined CT scanners were from different levels of hospitals in Guangdong Province, and were manufactured by nine major CT equipment manufacturers at home and abroad. The pass rate of CT room radiological protection was 99.88%, and the ambient dose equivalent rates of five monitoring points exceeded the limit, with four at the control room door and one at the shield wall of the room. The overall pass rate of CT equipment quality control was 99.49%, and the non-conforming parameters were the accuracy of positioning light and the deviation of reconstructed slice thickness. Conclusion In recent years, CT equipment quality control and room radiation protection in Guangdong Province have been at a high level.
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Objective @#To investigate the protective effects of different types of lead collars on the thyroid during radio- therapy after breast-conserving surgery. @*Methods@#Forty breast cancer patients undergoing radiotherapy after breast-con- serving surgery were randomly divided into four groups to wear different lead collars for thyroid protection: control group (0 mm Pb), common material group (0.5 mm Pb), common material group (2 mm Pb), and new radiation-shielding material group (2 mm Pb). Radiation doses inside and outside lead collars were monitored. A questionnaire survey was conducted to acquire information on patient acceptance of the lead collars.@*Results@#All the groups (except the control group) showed significant differences between scattered radiation doses inside and outside lead collars (P < 0.05). The scattered radiation was attenuated by 33.64% on average in the 2-mm new material group, which was significantly higher than in the other groups (P < 0.05). After radiotherapy, there was no significant change in the color and appearance of skin under lead collars in any group. All the patients were normal at the first thyroid ultrasound re-examination. The 2-mm new material lead collar was the most acceptable.@*Conclusion @#The lead collar made of the new radiation-shielding material has a good protective effect on the thyroid gland, and is easily accepted by patients, which can be promoted for application.
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Objective@#To screen the target genes of long non-coding RNA LOC102606465, which was previously identified to be induced by ionizing radiation, in order to examine its potential biological role.@*Methods@#The downstream differentially expressed genes (DEGs) of LOC102606465 were detected by microarray and partially verified by qRT-PCR. GO and KEGG enrichment analysis was performed, and PPI protein interaction network was constructed to screen significant modules and hub genes.@*Results@#The expression of LOC102606465 targeted by siRNA-447 and siRNA-541 was significantly lower than that of siRNA-NC (t=29.095, 13.751, P<0.01). A total of 374 common DEGs were identified(112 up-regulated/262 down-regulated) in both siRNA-447 and siRNA-541. The qRT-PCR was used to validate the expression of DEGs, which was consistent with the microarray result. In GO enrichment analysis, down-regulated DEGs were significantly enriched in " oxidoreductase activity, acting on the CH-CH group of donors, NAD or NADP as acceptor" (molecular function), " basal lamina" (cellular component), " ammonium ion metabolic process" (biological process). Up-regulated DEGs were mainly enriched in " protein phosphatase inhibitor activity" (molecular function), " SNARE complex" (cellular component), " negative regulation of fibrinolysis" (biological process). In addition, the KEGG enrichment analysis revealed that DEGs were significantly enriched in " metabolism of xenobiotics by cytochrome P450" , " dorso-ventral axis formation" , " lysosome glycerophospholipid metabolism" and " p53 signaling pathway" . Based on the STRING database, the PPI network was constructed (including 194 nodes and 268 edges), and one significant module and five key hub genes ACTRT3, CDKN1A, DPYD, TMP4, and PRKACB were identified.@*Conclusions@#LOC102606465 could be a potential biomarker for the regulation of ionizing radiation sensitivity, and the down-regulation of LOC102606465 plays an important role in the response to radiation, which would be an important target for regulating radiation sensitivity.
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Objective To investigate the radiation induced pulmonary fibrosis with a dose-response mouse model, based on the CT image changes of pulmonary fibrosis.Methods Female C57BL6 mice aged 8-10 weeks were randomly divided into 20 Gy or escalated doses of X-ray whole thoracic irradiation ( WTI) groups. CT scan was performed at different time points before and after radiation. The average lung density and lung volume changes were obtained by three-dimensional segmentation algorithm. After gene chip and pathological validation, the parameters of CT scan were subject to the establishment of logistic regression model. Results At the endpoint of 24 weeks post-irradiation, the lung density in the 20 Gy irradiation group was (-289.81± 12.06) HU, significantly increased compared with (-377.97± 6.24) HU in the control group ( P<0.001) . The lung volume was ( 0.66±0.01) cm3 in the control group, significantly larger than ( 0.44±0.03) cm3 in the irradiated mice ( P<0.001) . The results of quantitative imaging analysis were in accordance with the findings of HE and Mason staining, which were positively correlated with the fibrosis-related biomarkers at the transcriptional level ( all R2=0.75, all P<0.001) . The ED50 for increased lung density was found to be ( 13.64± 0.14) Gy ( R2=0.99, P<0.001) and ( 16.17± 4.36) Gy ( R2=0.89, P<0.001) for decreased lung volume according to the logistic regression model. Conclusions Quantitative CT measurement of lung density and volume are reliable imaging parameters to evaluate the degree of radiation-induced pulmonary fibrosis in mouse models. The dose-response mouse models with pulmonary fibrosis changes can provide experimental basis for comparative analysis of high-dose hypofractioned irradiation-and half-lung irradiation-induced pulmonary fibrosis.
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Objective To explore the clinical manifestation, diagnosis and treatment of Budd-Chiari syndrome in neonates. Method The clinical data of Budd-Chiari syndrome in a neonate were retrospectively reviewed and relevant literature was reviewed. Results The 21-day-old girl was born through vaginal delivery with gestational age of 39 weeks and birth weight of 3150 g. Her clinical manifestations included abdominal distention, hepatosplenomegaly, ascites, repeated hypoproteinemia and low platelet count, similar to sepsis. Imaging examination indicated hepatic segment stenosis of the inferior vena cava (the stenosis segment was about 24 mm in length and 1.59 mm in diameter at the narrowest place) . The girl was diagnosed with BuddChiari syndrome and died after abandoning treatment. Conclusion Neonatal Budd-Chiari syndrome is rare, easily misdiagnosed and has a high mortality.
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OBJECTIVE: To investigate the effect of ultraviolet B( UVB) on autophagy and apoptosis in human epidermal melanoma A375 cells. METHODS: i) A375 cells at logarithmic growth phase were exposed to UVB at doses of 10. 0 and15. 0 m J/cm~2. Then cells were collected at time point of 3,6,9 and 12 hours after irradiation. The effect of UVB on cell autophagy was observed by monodansylcadaverine staining and the effect of UVB on cell apoptosis was observed by acridine orange/ethidium bromide staining. ii) A375 cells of 10. 0 m J/cm~2 group and 15. 0 m J/cm~2 group were exposed to corresponding dose of UVB irradiation. Then cells were collected at time point of 18,24,36 and 48 hours after irradiation,and cell survival rate was examined using CCK-8 assay. iii) A375 cells were irradiated with UVB at doses of 10. 0 and15. 0 m J/cm~2 and then cells were collected at time point of 3,6,9 and 12 hours after irradiation. After that,A375 cells were irradiated at doses of 2. 5,5. 0,7. 5,10. 0 and 15. 0 m J/cm~2 of UVB,then cells were collected at time point of 9 hours after irradiation. The expressions of B-lymphoblastoma-2( Bcl-2),Bcl-2 related X protein( Bax),Bcl-2 interacting protein( Beclin-1) and microtubule-associated protein 1 light chain 3( LC3) Ⅱ were detected by Western blotting. A375 cells with no UVB irradiation were set as the control( pseudo-irradiation) in each experiment. RESULTS: i) Both autophagy and apoptosis of A375 cells induced by UVB irradiation at doses of 10. 0 and 15. 0 m J/cm~2 increased with time after irradiation. The effect on autophagy decreased at 12 hours time point with 15. 0 m J/cm~2 UVB irradiation. ii) The cell viability increased with time after irradiation in the 10. 0 and 15. 0 m J/cm~2 groups( P < 0. 05). From 18-48 hours after irradiation,the cell viability of the 10. 0 and 15. 0 m J/cm~2 groups was lower than that of the control group( P < 0. 05).From 24-48 hours after irradiation,the cell viability of the 15. 0 m J/cm~2 group was lower than that of the 10. 0 m J/cm~2 group( P < 0. 05). iii) The relative expression of Beclin-1 and LC3 Ⅱ protein at the 10. 0 m J/cm~2 group increased with time after 0-12 hours irradiation( P < 0. 05). The above changes of the 15. 0 m J/cm~2 group were observed within 0 to 9 hours,and the above two autophagy-related proteins were significantly decreased at the 12 hours time point( P < 0. 05).The relative expression of Bcl-2 protein at the 10. 0 and 15. 0 m J/cm~2 groups decreased with increasing time from 3 to 12 hours after irradiation( P < 0. 05). The relative expression of Bax protein increased with time from 0 to 12 hours after irradiation( P < 0. 05). The relative expression of Beclin-1 and LC3 protein in cells at 0. 0-10. 0 m J/cm~2,and the relative expression of Bax protein in cells at 0. 0-15. 0 m J/cm~2 increased with increase of irradiation dose( P < 0. 05). The relative expression of Bcl-2 protein decreased with increase of irradiation dose at 5. 0-15. 0 m J/cm~2( P < 0. 05). CONCLUSION: Autophagy and apoptosis of A375 cells can be induced by UVB irradiation at doses of 10. 0 and 15. 0 m J/cm~2. Autophagy induced by UVB irradiation at 10. 0 m J/cm~2 partially resisted the induction of apoptosis by UVB and enhanced cell viability. 15. 0 m J/cm~2 UVB-induced autophagy was insufficient to exert the above-mentioned effects,and the induction of apoptosis was the dominant effect.
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Objective To study the effect of PM2.5 combined with UVB treatment on human keratinocytes HaCaT. Methods The PM2.5 in the air was collected in Guangzhou and the metal ingredients were analyzed. The cells were divided into four groups:negative control group(NC group),simple PM2.5 treatment group with the concentration of IC50(PM2.5 group),simple UVB irradiation group with the dose of 30 mJ/cm2(UVB group)and PM2.5 combined with UVB treatment group(combined treatment group). The effects of different treatments on cell viability were measured by MTT assay and those of different treatments on apoptosis were detected by flow cytometry. The expressions of PARP and LC3 protein were detected by Western blot. Results The metal components in PM2.5 samples included Ca ,Zn ,Ba ,Al ,Cu ,Pb ,etc. After the treatment of PM2.5 on HaCaT cells ,we concluded that the IC50 was about 300 μg/mL. The inhibitory effect on cell viability after 24 h in different groups showed significant difference (P < 0.001) and the viability of the combined treatment group was the lowest (P < 0.001). Flow cytometry analysis showed that compared with that of NC group,the apoptosis rate of PM2.5 group(P < 0.01),UVB group(P < 0.01)and the combined treatment group(P < 0.01)increased,but the apoptosis rate in the combined treatment group was higher than that of PM2.5 group(P < 0.05),but lower than that in UVB group(P < 0.01). Western blot showed that the level of LC3-Ⅱ and PARP in another three groups was higher than that of NC group;PARP in the combined treatment group was lower than that in UVB group and LC3-Ⅱ increased compared with that in PM2.5 and UVB group. Conclusion PM2.5 can increase the harm of UVB on HaCaT cells and the main mechanism may be through increasing autophagy rather than apop-tosis.
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Objective To investigate the autophagy effect and the crosstalk with apoptosis by UV in A375 cells.Methods GFP-RFP-LC3 lentivirus were used to evaluate the effect of autophagy after being irradiated with UV of different doses (0、10、30、50 mJ/cm2).After being treated with 30 mJ/cm2 irradiation,the apoptosis rate of A375 with or without autophagy inducer was evaluated by annexin V-FITC/PI with flow cytometry.Western blot was used to distinguish the biomarker of autophagy (BECN,LC3) and apoptosis (Caspase 3,9).Results After being irradiated with 10 mJ/cm2 or 30 rnJ/cm2 UV,the autophagosome was observed at 6 h and rich at 9 h.However,the dots of autophagy had been abundant continually from 3 h with 50 mJ/cm2.The ability of inducing autophagy of UVB is stronger than UVA.UVA and UVB showed synergistic effect in autophagy with the dose of 30 mJ/cm2.The Caspase 3 and Caspase 9 proteins were downregulated after 30 mJ/cm2 UV irradiation with autophagy biomarkers increasing,whereas the apoptosis biomarkers were enriched with the inhibition of autophagy.Conclusions UV can induce autophagy with more significant effect of UVB.Autophagy paly protective role by delaying apoptosis after 30 mJ/cm2 UV irradiation in A375.
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Objective To explore the role of 14-3-3σ in cell cycle arrest,proliferation inhibition of HaCaT cells after UVB exposure.Methods Crystal violet assay was used to determine the viable density of HaCaT,HaCaTKD cells after being irradiated with UVB of different doses (10,20,30,40,50,60 and 80 mJ/cm2) for 48 h.After HaCaT and HaCaTKD being treated with 30 mJ/cm2irradiation,cell growth and cell cycle distribution were detected by CCK-8 assay and PI staining combined with flow cytometry,respectively.Western blot was used to evaluate the protein expression of 14-3-3σ,Cdc2,Cdc25c and Cyclin B1.Results After 48 h,the survival rate of both HaCaT and HaCaTKD decreased in a dosedependent manner.Especially,HaCaTKD cells had drastically low proliferation rate compared with normal HaCaT at 10 mJ/cm2 (t =8.83-49.63,P ＜ 0.05).The proliferation rate of HaCaTKD cells was significantly lower than that of HaCaT cells (F =32.89,P ＜ 0.05).After treatment with 30 mJ/cm2 UV irradiation,the ability of proliferation in normal HaCaT cells was recovered after 24 h while there was no proliferation in HaCaTKD cells within 72 h after the same treatment.The distribution of cell cycle has little change in HaCaTKD (P ＞ 0.05).UVB treatment led to cell cycle arrest from 6 to 18 h in HaCaT cells(t =7.41,9.22,9.16,P ＜0.05)while no cell cycle arrest could be observed in the HaCaTKID cell.Western blot detection indicated that the expression of 14-3-3σ in HaCaT cells was upregulated(t =5.42-9.57,P ＜0.05)while the Cdc25c and Cyclin B1 proteins were downregulated in both HaCaT and HaCaTKD cells (t =3.95-11.21,P ＜0.05).Specifically,Cdc2 protein decreased in HaCaT cells(t =4.93-5.37,P ＜ 0.05)but there was no change in HaCaT~ cells.Conclusions 14-3-3σ protein affects the proliferation and cell cycle of HaCaT cells after UVB irradiation.14-3-3oσ co-activates the expression of Cdc2,Cdc25cand Cyclin B1 to mediate UVB-induced G2/M arrest in HaCaT cells.
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<p><b>OBJECTIVE</b>To investigate the effect of ginseng-derived compound K (C-K) on apoptosis, immunosuppressive activity, and pro-inflammatory cytokine production of myeloid-derived suppressor cells (MDSCs) from mice bearing colorectal cancer xenograft.</p><p><b>METHODS</b>Flow-sorted bone marrow MDSCs from Balb/c mice bearing CT26 tumor xenograft were treated with either C-K or PBS for 96 h and examined for apoptosis with Annexin V/7-AAD, Cox-2 and Arg-1 expressions using qRT-PCR, and supernatant IL-1β, IL-6, and IL-17 levels with ELISA. C-K- or PBS-treated MDSCs were subcutaneously implanted along with CT26 tumor cells in WT Balb/c mice, and the tumor size and morphology were evaluated 21 days later.</p><p><b>RESULTS</b>C-K treatment significantly increased the percentages of early and late apoptotic MDSCs in vitro (P<0.01 and P<0.05, respectively), decreased the expressions of immunosuppression-related genes Cox-2 (P<0.05) and Arg-1 (P<0.01), and suppressed the production of IL-1β (P<0.05), IL-6 (P<0.01), and IL-17 (P<0.05) by the MDSCs . Compared with PBS-pre-treated cells, C-K-pretreated MDSCs showed significantly attenuated activity in promoting CT26 tumor growth in mice (P<0.01).</p><p><b>CONCLUSION</b>C-K can suppress the immunosuppresive effect of MDSCs to inhibit tumor cell proliferation in mice, which suggests a new strategy of tumor therapy by targeting MDSCs.</p>
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Animales , Humanos , Ratones , Apoptosis , Proliferación Celular , Neoplasias Colorrectales , Patología , Modelos Animales de Enfermedad , Ginsenósidos , Farmacología , Terapia de Inmunosupresión , Interleucina-17 , Metabolismo , Interleucina-1beta , Metabolismo , Interleucina-6 , Metabolismo , Ratones Endogámicos BALB C , Células Mieloides , Trasplante de NeoplasiasRESUMEN
Objectives To discuss the clinical characteristic, cause and measures to prevention and control of nosocomial infection in a neonatal intensive care unit (NICU). Methods Retrospectively analyzed an nosocomial infection outbreak of Klebsiella pneumoniae in NICU. Results From Sept. 3, 2010 to Oct. 3, 2010, there were 7 cases of hospital infection in 12 cases of sputum cultured Klebsiella Pneumoniae. The gestational age (GA) of 7 hospital infection cases was 28.5±2.6 week. The birth weight of infection cases was 941.4±309.8 g. The onset of infection was at 31.7±12.8 d of hospitalization. The nosocomial incidence was 2.41%in the hospital, which was 5.79%in preterm infants, 50.00%in GA<28w infants, and 42.86%in extremely low birth weight infant (ELBW). All sputum culture results were displayed as multi-drug resistant of Klebsiella pneumoniae, penicillin and third-generation cephalosporin antibiotic resistance rate of 75%to 100%. The resistance rates to penicillin and cephem antibiotics were 75% -100%, carbapenems was 58.3%, piperacillin/tazobactam was 25.0%. All nosocomial patients were cured. Conclusions GA<28w and ELBW infants are at increased risk of nosocomial infection in NICU. The emergence of carbapenems resistant Klebsiella Pneumoniae has been increasing with the widespread use of carbapenems. Hospital infection can be controlled by standardized medical behavior, which can decline the nosocomial infection incidence and mortality of preterm infants in NICU.
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Objective To investigate the carcinogeic role of miR-365 in cuntanerous squamous cell carcinoma (cSCC).Methods Normal HaCaT cells were divided into control and irradiation groups,the later was exposed by UVB irradiation (50 J/m2).MicroRNA expression profiles of the two groups were analyzed by microRNA array.The expression variations of miR-365 in HaCaT,A431,Tca8113 and HSC-1 cells were validated by qRT-PCR analysis.The colony-forming and invasion capacities were dectected by colony forming assay and Transwell migration assay in vitro,respectively.HaCaTpre-miR365-2 highly expressing miR-365 was constructed by retroviral vector infection.Tumorigenicity evaluation was carried out by subcutaneously inject of the cells at the right back flank of nude mice.Results There were 30 microRNAs differentially expressed in HaCaT cells after UVB irradiation and miR-365 was one of the most sensitive miRNAs(as high 6.7 times as control).Expression of miR-365 in all the cSCC cell lines A431,Tca8113 and HSC-1 were significantly higher than that in HaCaT cell,in which the maximum was A431 (15.67 ±1.12 times,P ＜ 0.01),and the minimum was TcaS113 (4.72 ± 0.85 times,P ＜ 0.05).Knockdown of miR-365 in cSCC cell lines significantly inhibited the colony forming ability (t =13.68,P ＜ 0.05) and cell migration (t =19.98,P ＜ 0.05) in vitro.HaCaT cells overexpressing miR-365 by transient transfection significantly increased the ability of colony formation (t =7.11,P ＜ 0.05) and cell migration (t =22.03,P ＜0.05) in vitro.In addition,HaCaTpre-miR-365-2 cell line stably expressing miR-365 could successfully establish tumors in nude mice.Conclusions MiR-365 is an oncogene for cutaneous squamous cell carcinoma.
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Objective To investigate the methylation status of E-cadherin(E-cad), p16, RASSF1A, DAPK and MGMT in histologically normal salivary gland tissues and provide reference for determination of the methylation status of salivary gland tumors.Methods Methylation of E-cad, p16, RASSF1A,DAPK and MGMT was analyzed using methylation-specific polymerase chain reaction ( MSP) .The results were compared with the methylation status of these genes in salivary adenoid cystic carcinoma ( ACC) tumor tissues in our previous studies and the association between promoter methylation of E-cad, p16, RASSF1A, DAPK, and MGMT on one hand and the patients′gender, age, smoking and types of gland on the other hand was also analyzed .Results Promoter methylation was detected in 8 of the 60 (13%) salivary glands, E-cad in 4(7%), p16 in 2(4%), RASSF1A in 2(4%), DAPK in 2 (4%), and MGMT in 1(2%).Compared with our previous results, there was a significantly lower methylation ratio in promoter methylation of E-cad(P<0.01), p16 (P<0.01), RASSF1A (P<0.01),and DAPK (P<0.01) in salivary gland tissues than in ACC tumor tissues.Conclusion Promoter methylation of E-cad, p16 and RASSF1A is a rare event in histologically normal salivary gland tissues .