Relevant bibliographies by topics / Komet Assay

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Academic literature on the topic 'Komet Assay'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Komet Assay"

1

Ramadhani, Dwi, Devita Tetriana, and Viria Agesti Suvifan. "OPTIMALISASI TES KOMET UNTUK PENENTUAN TINGKAT KERUSAKAN PADA DNA AKIBAT PAPARAN RADIASI." Jurnal Sains dan Teknologi Nuklir Indonesia 17, no. 1 (March 18, 2016): 37. http://dx.doi.org/10.17146/jstni.2016.17.1.2405.

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Tes komet dapat digunakan untuk mengukur tingkat kerusakan asam deoksiribonukleat (DNA) pada sel limfosit darah tepi akibat paparan radiasi. Aspek yang harus diperhatikan saat melakukan tes komet antara lain adalah konsentrasi agarose yang digunakan, waktu inkubasi pada alkali, kondisi elektroforesis (waktu, temperatur serta gradien voltase yang digunakan), serta parameter yang digunakan dalam analisis. Parameter yang sangat disarankan dalam menganalisis citra komet adalah persentase DNA ekor (% DNA ekor). Persentase DNA ekor dapat dikonversi menjadi frekuensi lesion per 106 pasangan basa (bp) DNA dengan menggunakan kurva yang menggambarkan hubungan antara dosis radiasi pengion dengan besarnya % DNA ekor. Untuk mendapatkan hasil analisis tes komet yang akurat perlu dilakukan pembuatan kurva kalibrasi yang menggambarkan hubungan antara dosis radiasi pengion dengan besarnya % DNA ekor. Analisis citra komet sebaiknya dilakukan dengan menggunakan perangkat lunak pengolahan citra sehingga dapat meningkatkan akurasi dan presisi serta mengurangi subjektivitas dalam menganalisis citra komet. OPTIMIZATION ON COMET ASSAY FOR ASSESSMENT OF DNA DAMAGE BECAUSE RADIATION EXPOSURE.Comet assay can be used to measure deoxyribonucleic acid (DNA) damage level caused by natural radiation exposure in peripheral blood lymphocytes. The principle of the comet assay is based on the amount of denatured DNA fragments that migrated out of the cell nucleus during electrophoresis. There are several aspects that must be concerned when doing the comet assay. For example the agarose concentration, duration of alkaline incubation, electrophoresis conditions (time, temperature, and voltage gradient), and the measurement parameters that used in analyze the comet. Percentage of DNA in the comet tail (% tail DNA) is strongly recommended as a parameter when analyze the comet because it can be converted to lesions per 106 base pairs (bp) using calibration curve that show relationship between the dose of ionizing radiation and % tail DNA. To obtain an accurate result, the calibration curve must be made and comet should be analyzing using image processing analysis software since it can be increase the precision and reduce the subjectivity of the measurement process.
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Topalović, Dijana, Lada Živković, Ninoslav Đelić, Vladan Bajić, and Biljana Spremo-Potparević. "Analysis of tiazofurin-induced DNA damage in human whole blood cells using an in vitro comet assay." Medicinski casopis 54, no. 3 (2020): 91–95. http://dx.doi.org/10.5937/mckg54-28798.

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Objective. Inosine 5'-monophosphate dehydrogenase (IMPDH) activity in cancer cells is increased. Tiazofurin selectively inhibits the activity of IMPDH, and it has been granted for the treatment of different cancers and new viral diseases. Its widespread use was limited because exposure to tiazofurin under certain circumstances was found to have a higher frequency of severe non-hematologic toxicity. Therefore, the objective of this study was to examine genotoxic action and inducement of DNA damage of tiazofurin using the comet assay. Methods. The ability of tiazofurin to induce DNA damage was evaluated using single-cell gel electrophoresis (SCGE) technique/comet assay. Human whole blood cells were exposed to three final concentrations of tiazofurin (1µM/mL, 2 µM/mL, and 5 µM/mL) for 30 min in vitro. Results. Our results indicate that tiazofurin produced a significant level of DNA damage on whole blood cells after 30 min of exposure vs. control. All tested concentrations were significantly comet-forming, in a concentration-dependent manner. Conclusion. Our investigation on the tiazofurin-treated cells and their relationship to the formation of DNA damage demonstrated that the genotoxic effect was induced after exposure to tiazofurin under described conditions.
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Göbel, A., T. D. Rachner, M. Rauner, and L. C. Hofbauer. "Die Rolle der Wnt-Inhibitoren Sklerostin und Dickkopf-1 bei Erkrankungen des Knochens." Osteologie 25, no. 03 (2016): 198–203. http://dx.doi.org/10.1055/s-0037-1619017.

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ZusammenfassungKnochen wird durch die koordinierte Aktivität von knochenresorbierenden Osteoklasten sowie von Osteoblasten, die neue Knochenmatrix produzieren, kontinuierlich umgebaut. Ein gestörtes Gleichgewicht zwischen beiden Zelltypen stellt ein Leitmotiv vieler metabolischer Knochenerkrankungen dar. Hierbei fällt dem Wnt-Signalweg eine zentrale Bedeutung zu. Dieser fördert die Osteoblastogenese und wird durch die Wnt-Antagonisten Dickkopf-1 (DKK-1) und Sklerostin feinreguliert, da sie eine hemmende Wirkung auf die Osteoblasten-differenzierung entfalten. Beide Proteine sind zellbiologisch gut charakterisiert und lassen sich auch beim Menschen mithilfe sensitiver Assays nachweisen und als Biomarker bestimmen. Sowohl DKK-1 und Sklerostin werden in aktuellen präklinischen und klinischen Studien als therapeutische Ansatzpunkte für Erkrankungen des Knochens diskutiert, bei denen es zu einem Verlust von Knochengewebe und einem erhöhten Frakturrisiko kommt.
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Magbanua, M. J. M., E. Sosa, R. Roy, L. Eisenbud, J. Scott, A. Olshen, D. Pinkel, H. S. Rugo, and J. W. Park. "Genome-wide copy number analysis of circulating tumor cells from patients (pts) with metastatic breast cancer (MBC)." Journal of Clinical Oncology 29, no. 27_suppl (September 20, 2011): 9. http://dx.doi.org/10.1200/jco.2011.29.27_suppl.9.

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9 Background: We developed a novel approach to isolate circulating tumor cells (CTCs) via immunomagnetic enrichment followed by fluorescence activated cell sorting (IE/FACS) and examined copy number alterations in these cells. Methods: Magnetic beads coated with EpCAM mAb were added to blood to enrich for tumor cells. Enriched samples were then subjected to FACS analysis using differentially labeled mAbs to distinguish tumor cells (EpCAM+) from leukocytes (CD45+) during sorting. DNA from isolated tumor cells was subjected to whole genome amplification (WGA) and copy number analysis via array comparative genomic hybridization (aCGH). The assay was evaluated in CTCs from 5 MBC pts with matched archival primary tumors and later extended to an additional 176 MBC pts, 97 of which were successfully profiled. Results: Comparison of CTCs with matched archival primary tumors confirmed shared lineage with notable divergence. In addition, serial testing of CTCs confirmed reproducibility, and indicated genomic change over time. Genomic profiling of CTCs from 102 MBC pts revealed a wide range of copy number alterations including those previously reported in breast cancer. Comparison with a published aCGH dataset of primary breast tumors revealed similar frequencies of recurrent genomic copy number aberrations. Conclusions: It is feasible to isolate CTCs away from hematopoietic cells with high purity via IE/FACS and profile them via aCGH analysis following WGA. Our approach may be utilized to explore genomic events involved in cancer progression and to monitor therapeutic efficacy of targeted therapies in clinical trials in a relatively non-invasive manner. This work was supported by grants from the CALGB, BCRF, TBCRC (Avon, Komen), EDRN and U54.
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Mamounas, Eleftherios P., Gong Tang, Soonmyung Paik, Frederick L. Baehner, Qing Liu, Jong-Hyeon Jeong, Seong-Rim Kim, et al. "Prognostic impact of the 21-gene recurrence score (RS) on disease-free and overall survival of node-positive, ER-positive breast cancer patients (pts) treated with adjuvant chemotherapy: Results from NSABP B-28." Journal of Clinical Oncology 30, no. 27_suppl (September 20, 2012): 1. http://dx.doi.org/10.1200/jco.2012.30.27_suppl.1.

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1 Background: RS predicts outcome in node- and node+, ER+ pts treated with adjuvant endocrine therapy as well as benefit from adjuvant chemotherapy, with high RS receiving most of the benefit. We studied the prognostic impact of RS in node+, ER+ pts treated with adjuvant chemotherapy plus endocrine therapy as part of the NSABP B-28 trial. Methods: B-28 compared doxorubicin/cyclophosphamide (ACX4) with ACX4 followed by paclitaxel X4. Pts >50 yrs and those<50 yrs with ER+ and/or PR+ tumors also received 5 yrs of tamoxifen concurrently with chemotherapy. Between 8/95 and 5/98 3060 pts were accrued. The present study includes 1,065 pts ER+ by central tissue microarray IHC assay, tamoxifen treated, assessed by RS. Median follow-up time was 11.2 yrs. Results: Of the 1,065 pts, 386 (36%) had low RS<18; 364 (34%) intermediate RS,18-30; and 315 (30%) high RS≥31. In univariate analyses RS was a significant predictor of DFS, distant recurrence-free interval (DRFI) and OS (Table). In multivariate analyses, RS provided independent prognostic information for all three endpoints beyond clinical and pathologic factors, e.g., treatment, age, tumor size, tumor grade, number of + nodes and type of surgery (p<0.001). Conclusions: The 21-gene RS maintains significant prognostic impact in ER+, node+ pts who have received anthracycline- or anthracycline/taxane-based adjuvant chemotherapy. These findings emphasize the need to target pts with high residual risk for recurrence with additional therapies to overcome unfavorable biology, potential endocrine and/or chemotherapy resistance. Supported by: NCI, HHS, PHS, grants U10-CA-12027, -69651, -37377, -69974, and U24-CA-114732, and grants from Susan G. Komen for the Cure and Bristol-Myers Squibb Pharmaceutical Research Institute. [Table: see text]
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Olawaiye, A. B., H. Sakamoto, T. Serikawa, A. Friel, R. Kiyama, A. Inoue, R. Drapkin, R. Foster, R. R. Gonzalez, and B. R. Rueda. "Defining the mechanisms by which leptin stimulates proliferation of ovarian cancer cells." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 15017. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.15017.

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15017 Background: Ovarian cancer (OvCa) ranks fourth as the cause of death related to cancer in women in the U.S. The vast majority (>90%) of OvCa originates from the ovarian surface epithelium. There is sufficient evidence to suggest that hormones, especially estrogen, may be involved in the etiopathogenesis of epithelial OvCa. Recent studies indicate that leptin participates either directly or indirectly to promote carcinogenesis in both breast and endometrial cancers. Furthermore it has been proposed that leptin may elicit its action via an estrogen related pathway. Leptin can stimulate proliferation of some OvCa cell lines and has been implicated as a potential biomarker for OvCa. However the mechanism(s) by which leptin contributes to the growth of OvCa has yet to be defined. We hypothesize that leptin’s effect will be mediated in part by estrogen receptor (ER) pathways. Methods: Three epithelial OvCa cell lines (IGROV1, OVCAR5 and TOV21G) and one benign human ovarian surface epithelial cell line (HOSE) were evaluated. Enzyme linked immunosorbent assay (ELISA) and Western blotting were used to assess leptin and leptin receptor (ObR), respectively. Leptin (0.06 nM–6.25 nM) induced effects on cell proliferation were assessed in the presence or absence of an aromatase enzyme inhibitor (Anastrozole) or the ER antagonist (ICI182780). Further, we explored leptin-induced effects on ERα promoter activity as evidenced by change in fluorescence via a dual luciferase promoter reporter. All experiments were conducted in triplicate. All data were subjected to ANOVA followed by Tukey’s post hoc test (p < 0.05). Results: All ovarian cell lines expressed ObR; whereas, no measurable amounts of leptin were detected in conditioned media. Leptin stimulated cell proliferation in both the benign and malignant lines. Leptin-induced cell proliferation was inhibited by Anastrozole and ICI182780. Furthermore, leptin stimulated luciferase activity of the ERα promoter/reporter. Conclusions: Leptin promotes proliferation of benign and malignant ovarian epithelial cells and appears to be mediated, at least in part, via aromatase and ER which may have therapeutic implications. This work was supported by the Vincent Memorial Hospital, SG Komen Foundation and the Advanced Medical Research Foundation. No significant financial relationships to disclose.
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Leitzel, K., H. Y. Hou, V. Shrivastava, U. Anyanwu, S. M. Ali, W. Koestler, E. Fuchs, S. Brown-Shimer, W. Carney, and A. Lipton. "Use of pretreatment serum CA9 (carbonic anhydrase 9) to predict PFS and survival in trastuzumab-treated metastatic breast cancer." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 11092. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.11092.

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11092 Background: Approximately half of HER2-positive breast cancer patients will respond to first-line trastuzumab-containing therapy. However, in those patients with an initial trastuzumab response, most will progress within a year with acquired resistance. Since trastuzumab treatment is also now used in the HER2-positive adjuvant breast cancer setting, trastuzumab resistance will continue to be a vexing clinical problem, and better predictive and prognostic biomarkers are urgently needed. Methods: Serum HER2, tissue inhibitor of metalloproteinase-1 (TIMP-1), urokinase-type plasminogen activator (uPA), CA9, VEGF-165, and endoglin were measured using ELISA assays in 66 metastatic breast cancer patients before starting first-line trastuzumab-containing therapy. The HER2, TIMP-1, uPA, CA9, and VEGF-165 ELISAs were from Oncogene Science/Siemens Healthcare Diagnostics, Cambridge, MA; and the endoglin ELISA was from R&D Systems, Minneapolis, MN. Progression-free (PFS) and overall survival (OS) were analyzed using the Kaplan-Meier method and Cox modeling with continuous pretreatment serum biomarker variables. Results: Pretreatment serum HER2 (p= 0.005), TIMP-1 (p< 0.0001), uPA (p= 0.006), endoglin (p= 0.008), and CA9 (p <0.0001) were all significant as univariate continuous biomarkers for predicting PFS to first-line trastuzumab-containing therapy, but VEGF was not. In multivariate analysis for PFS with all six biomarkers, only serum CA9 (p= 0.002) was a significant independent covariate. For OS, pretreatment serum HER2 (p= 0.018), TIMP-1 (p< 0.0001), uPA (p< 0.0001), endoglin (p= 0.002), and CA9 (p< 0.0001) were all significant as univariate continuous biomarkers for prognosis, but serum VEGF was not. In multivariate analysis for OS with all six biomarkers, only serum CA9 was a significant independent prognostic covariate (p= 0.001). Conclusions: Elevated pretreatment serum CA9 (a marker of hypoxia) predicts reduced progression-free survival and overall survival in metastatic breast cancer patients treated with first-line trastuzumab-containing therapy. These serum biomarkers deserve further study in larger trials of HER2-targeted breast cancer treatment. Supported by a grant from Komen for the Cure. [Table: see text]
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Ali, Suhail M., Kim Leitzel, Uchechi Anyanwu, Hui Ying Hou, Matthew Stephen Evans, Vikas Shrivastava, Wolfgang Köstler, et al. "Elevated pretreatment serum biomarkers and correlation with progression-free (PFS) and overall survival (OS) in first-line trastuzumab-treated metastatic breast cancer." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 622. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.622.

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622 Background: Approximately one-half of HER2-positive breast cancer patients will respond tofirst-line trastuzumab-containing therapy. However, in those patients with an initial trastuzumab response, most will progress within a year with acquired resistance. Since trastuzumab treatment is also now used in the HER2-positive adjuvant breast cancer setting, trastuzumab resistance will continue to be a recurring clinical problem, and better predictive and prognostic biomarkers are urgently needed. Methods: Seven serum biomarkers (carbonic anhydrase 9 (CA9), endoglin, HER2, IGF-1R, tissue inhibitor of metalloproteinase-1 (TIMP-1), urokinase-type plasminogen activator (uPA), and VEGF-A (isoform 165) were measured using ELISA assays in 81 metastatic breast cancer patients before starting first-line trastuzumab-containing therapy. The endoglin and IGF-IR ELISAs were from R&D Systems; others were from WILEX/Oncogene Science, Cambridge, MA. PFS and OS were analyzed using the Kaplan-Meier method and Cox modeling with continuous pretreatment serum biomarker variables. Results: For univariate PFS analysis, higher pretreatment serum biomarkers (except IGF-1R and VEGF-A) predicted reduced PFS (p<0.05) to first-line trastuzumab-containing therapy. In multivariate PFS analysis, only serum CA9 (p= 0.038) remained a significant independent covariate. In univariate OS analysis, higher pretreatment serum biomarkers (except IGF-1R and VEGF-A) were prognostic for reduced OS (p<0.05). In multivariate analysis for OS, TIMP-1 (p=0.001) and CA9 (p=0.04) remained significant independent prognostic factors, as well as line of chemotherapy (3 vs. 2 or 1 line)(p=0.005), and hormone receptor status (ER and/or PR positive vs. negative)(p=0.013). Conclusions: Higher pretreatment serum CA9 (a marker of hypoxia) predicted reduced PFS, and higher serum CA9 and TIMP-1 predicted reduced OS in metastatic breast cancer patients treated with first-line trastuzumab-containing therapy. These serum biomarkers deserve further study in larger trials of HER2-targeted breast cancer treatment. Supported by a grant from Komen for the Cure.
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Sparano, Joseph A., Robert James Gray, William C. Wood, Della F. Makower, Tracy G. Lively, Thomas James Saphner, Maccon M. Keane, et al. "TAILORx: Phase III trial of chemoendocrine therapy versus endocrine therapy alone in hormone receptor-positive, HER2-negative, node-negative breast cancer and an intermediate prognosis 21-gene recurrence score." Journal of Clinical Oncology 36, no. 18_suppl (June 20, 2018): LBA1. http://dx.doi.org/10.1200/jco.2018.36.18_suppl.lba1.

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LBA1 Background: In hormone receptor (HR)-positive, HER2-negative, axillary node (AN)-negative breast cancer, the 21-gene expression assay (Oncotype DX Recurrence Score [RS]) is prognostic for distant recurrence, prognostic for low recurrence with endocrine therapy alone if low (0-10), and predictive of chemotherapy benefit if high (26 or higher). We performed a prospective, randomized trial of endocrine therapy (ET) versus chemoendocrine therapy (CET) in women with a mid-range RS of 11-25. Methods: Eligibility criteria included women 18-75 years of age with HR-positive, HER2-negative, axillary node (AN)-negative breast cancer and tumors 1.1-5.0 cm in size (or 0.6-1.0 cm and int/high grade) and agreed to have chemotherapy assigned or randomized based on the RS. Women with a mid-range RS (11-25) were randomized to receive ET or CET. The primary endpoint was invasive disease-free survival (iDFS), and the trial was designed to show non-inferiority for ET alone by not rejecting equality (hazard ratio [HR] margin up to 1.322 for omission of chemotherapy, 1-sided type I error rate 10%, type II error rate 5%). The target sample size was adjusted to compensate for non-adherence to randomized treatment, and the protocol-specified final analysis was triggered after 835 iDFS events. Results: Of the 10,253 eligible women enrolled between 4/7/06-10/6/10, 6711 (65.5%) had a RS of 11-25 and adequate information. There were 836 iDFS events at final analysis with a median followup of 90 months. ET was non-inferior to CET for iDFS (HR 1.08, 95% confidence intervals [CI] 0.94, 1.24, p=0.26) in the intention-to-treat (ITT) population. ET was also non-inferior for distant recurrence-free interval (DRFI; HR 1.03, p=0.80), recurrence-free interval (RFI; HR 1.12, p=0.28), and overall survival (OS; HR 0.97, p=0.80). Nine year rates were similar for iDFS (83.3% vs. 84.3%), DRFI (94.5% vs. 95.0%), RFI (92.2% vs. 92.9%), and OS (93.9% vs. 93.8%). Recurrence accounted for 338 (41.6%) the first iDFS event, of which 199 (23.8%) were distant recurrences. Treatment interaction tests were significant for age (iDFS p=0.03; RFI p= 0.02), but not menopause, tumor size, grade, or RS (continuous or RS 11-15, 16-20, 21-25). Conclusions: In women with HR-positive, HER2-negative, AN-negative breast cancer and a RS of 11-25, adjuvant ET was not inferior to CET in the ITT analysis. (Funded by NCI, BCRF, and Komen Foundation.) Clinical trial information: NCT00310180.
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Dissertations / Theses on the topic "Komet Assay"

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Kahmann, Cindy. "Quantifizierung von DNA-Schäden an adhaerenten Zelllinien nach Bestrahlung mit 188 Re- bzw. Röntgenstrahlung unter Zugabe von Methimazol, Nicotinamid und Perchlorat durch den Comet Assay." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2008. http://nbn-resolving.de/urn:nbn:de:bsz:14-ds-1219154119996-02487.

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Bergqvist, Michael. "Radiosensitivity in lung cancer with focus on p53." Doctoral thesis, Uppsala University, Oncology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2673.

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In Sweden approximately 2800 new lung cancer patients are diagnosed every year. Radiotherapy is used with curative intention in certain groups of patients. The aim of this thesis is to study the basis of differences in radioresistance and the possibility to predict response to radiotherapy.

In the first study we investigated, using the comet assay, four lung cancer cell lines with different sensitivity towards radiation. A clear dose-response relationship for radiation-induced DNA single strand and double strand breaks were found. All cell lines showed a remarkably efficient repair of both the DNA single strand and double strand breaks one hour after irradiation. However, further studies in one radioresistant and one radiosensitive cell line demonstrated that repair during the first 15 min had the best accordance with radiosensitivity measured as surviving fraction.

In the second and third study, sequencing studies of the p53 gene were performed on cell lines as well as on tumour material. Cell lines that were expressing a mutation in exon 7 were associated with increased radiosensitivity compared with tumor cell lines with mutations in other exons. In the clinical study, 10 patients were found to be mutated in the p53 gene whereas the other 10 patients were not. No correlation to clinical parameters could be drawn.

In the fourth study, serum from 67 patients with a confirmed diagnosis of non-small cell lung cancer was investigated for the presence of p53 antibodies. P53 antibodies in sera, taken prior to radiation treatment, were associated with increased survival.

The summary of this thesis indicates that the p53 gene has an impact on the effect of radiotherapy in lung cancer. The presence of p53 antibodies might be of clinical interest for predicting survival after radiotherapy. Further studies on the importance of the p53 gene on early repair are of interest.

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Wendisch, Maria. "Nachweis der adaptiven Antwort nach Bestrahlung von Schilddrüsenzellen mit offenen Radionukliden." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-62681.

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Biologische Systeme sind in der Lage sich an eine Niedrig-Dosis-Bestrahlung anzupassen und eine geringere Sensitivität gegenüber einer nachfolgenden Hoch-Dosis-Bestrahlung zu entwickeln. Dieses Phänomen wird als adaptive Antwort bezeichnet und wurde nach der Bestrahlung mit externen Strahlungsquellen wiederholt in vivo und in vitro untersucht. Im Gegensatz dazu gibt es für die Bestrahlung mit offenen Radionukliden keine systematischen und vergleichenden Untersuchungen. Im Mittelpunkt dieser Arbeit standen der Nachweis sowie die Analyse der adaptiven Antwort an PC Cl3-Zellen nach Bestrahlung mit den offenen Radionukliden Re-188 und Tc-99m. Die Zellschädigung wurde mit dem alkalischen Komet-Assay, zur Bestimmung des initialen DNA-Schadens und dem Koloniebildungstest, zur Ermittlung des klonogenen Überlebens, untersucht. Zur Aufklärung von möglichen Regulationsmechanismen der adaptiven Antwort wurde die Induktion und Reparatur von DSB mit dem gamma-H2AX-Immunfluoreszenz-Assay und die intrazelluläre Radionuklidaufnahme betrachtet. In dieser Arbeit erfolgte erstmals eine systematische Untersuchung der adaptiven Antwort nach Bestrahlung mit offenen Radionukliden in vitro. Insgesamt zeigen diese Ergebnisse, dass nach Bestrahlung mit offenen Radionukliden eine adaptive Antwort ausgebildet wird. Diese ist von der Strahlenqualität während Vor- und Folgebestrahlung sowie der Art der DNA-Schädigung und den initiierten Reparaturprozessen abhängig. Weiter Einflussfaktoren sind die Erholungszeit, die Vorbestrahlung (Dosis, Strahlenqualität) und die Art des Schadensnachweises. Neben den bekannten Regulationsmechanismen wurde erstmals die Reduktion der intrazellulären Radionuklidaufnahme als weitere mögliche adaptive Antwort beschrieben.
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Runge, Roswitha. "Untersuchungen zum Einfluss von 211At, 188Re und Doxorubicin auf die DNA-Schädigung humaner Lymphozyten." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-62472.

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Ionisierende Strahlung verursacht in Abhängigkeit von den strahlenphysikalischen Eigenschaften der Radionuklide Zellschäden unterschiedlicher Komplexität. An humanen Lymphozyten wurde untersucht, ob die biologische Wirksamkeit von Alpha- und Betastrahlung sowie der Einfluss von Doxorubicin der Qualität des Strahlenschadens zugewiesen werden kann. Die DNA-Schäden und deren Reparatur wurden mit zellbiologischen Methoden quantifiziert.
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Runge, Roswitha. "Untersuchungen zum Einfluss von 211At, 188Re und Doxorubicin auf die DNA-Schädigung humaner Lymphozyten." Doctoral thesis, 2009. https://tud.qucosa.de/id/qucosa%3A25426.

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Ionisierende Strahlung verursacht in Abhängigkeit von den strahlenphysikalischen Eigenschaften der Radionuklide Zellschäden unterschiedlicher Komplexität. An humanen Lymphozyten wurde untersucht, ob die biologische Wirksamkeit von Alpha- und Betastrahlung sowie der Einfluss von Doxorubicin der Qualität des Strahlenschadens zugewiesen werden kann. Die DNA-Schäden und deren Reparatur wurden mit zellbiologischen Methoden quantifiziert.
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