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Articles by A Baumgartner
Total Records ( 3 ) for A Baumgartner
  C. M Lu , J Kwan , A Baumgartner , J. F Weier , M Wang , T Escudero , S Munne , H. F Zitzelsberger and H. U. G. Weier

Structural chromosome aberrations are hallmarks of many human genetic diseases. The precise mapping of translocation breakpoints in tumors is important for identification of genes with altered levels of expression, prediction of tumor progression, therapy response, or length of disease-free survival, as well as the preparation of probes for detection of tumor cells in peripheral blood. Similarly, in vitro fertilization (IVF) and preimplantation genetic diagnosis (PGD) for carriers of balanced, reciprocal translocations benefit from accurate breakpoint maps in the preparation of patient-specific DNA probes followed by a selection of normal or balanced oocytes or embryos. We expedited the process of breakpoint mapping and preparation of case-specific probes by utilizing physically mapped bacterial artificial chromosome clones. Historically, breakpoint mapping is based on the definition of the smallest interval between proximal and distal probes. Thus, many of the DNA probes prepared for multiclone and multicolor mapping experiments do not generate additional information. Our pooling protocol, described here with examples from thyroid cancer research and PGD, accelerates the delineation of translocation breakpoints without sacrificing resolution. The turnaround time from clone selection to mapping results using tumor or IVF patient samples can be as short as 3 to 4 days. (J Histochem Cytochem 57:587–597, 2009)

  M Najafzadeh , P. D Reynolds , A Baumgartner and D. Anderson

Inflammatory bowel disease (IBD) including Crohn's disease (CD) and ulcerative colitis (UC) is a chronic inflammatory gastrointestinal autoimmune condition with an inappropriate immune response. We investigated DNA damage induced in vitro in lymphocytes from IBD patients caused by oxidative stress through H2O2 and 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and whether the plant flavonoids, quercetin and epicatechin, found in fruits, tea and soybeans could effectively reduce such stress. Lymphocytes from IBD patients and healthy volunteers were treated with 50 µg/ml H2O2 or IQ in the presence of quercetin (0–250 µg/ml) or epicatechin (0–100 µg/ml). Flavonoid supplementation (250 µM quercetin or 100 µM epicatechin) caused an overall significant decrease of induced DNA damage resulting in a 48.6% (P < 0.001) reduction of H2O2-induced and a 43% (P < 0.001) reduction of IQ-induced DNA damage within the patient groups; for the control groups, reductions in DNA damage were 35.2 and 57.1%, respectively (both, P < 0.001). There was less induced DNA damage within lymphocytes from UC patients compared to CD patients for both series of experiments (H2O2 and quercetin, IQ and epicatechin). In conclusion, flavonoids dramatically reduced oxidative stress in vitro in lymphocytes from IBD patients and healthy individuals. Thus, flavonoids could be very effective in the treatment of oxidative stress and encouraged in the diet of IBD patients.

  V Sipinen , J Laubenthal , A Baumgartner , E Cemeli , J. O Linschooten , R. W. L Godschalk , F. J Van Schooten , D Anderson and G. Brunborg

Exposure to genotoxins may compromise DNA integrity in male reproductive cells, putting future progeny at risk for developmental defects and diseases. To study the usefulness of sperm DNA damage as a biomarker for genotoxic exposure, we have investigated cellular and molecular changes induced by benzo[a]pyrene (B[a]P) in human sperm in vitro, and results have been compared for smokers and non-smokers. Sperm DNA obtained from five smokers was indeed more fragmented than sperm of six non-smokers (mean % Tail DNA 26.5 and 48.8, respectively), as assessed by the alkaline comet assay (P < 0.05). B[a]P-related DNA adducts were detected at increased levels in smokers as determined by immunostaining. Direct exposure of mature sperm cells to B[a]P (10 or 25 µM) caused moderate increases in DNA fragmentation which was independent of addition of human liver S9 mix for enzymatic activation of B[a]P, suggesting some unknown metabolism of B[a]P in ejaculates. In vitro exposure of samples to various doses of B[a]P (with or without S9) did not reveal any significant differences in sensitivity to DNA fragmentation between smokers and non-smokers. Incubations with the proximate metabolite benzo[a]pyrene-r-7,t-8-dihydrodiol-t9,10-epoxide (BPDE) produced DNA fragmentation in a dose-dependent manner (20 or 50 µM), but only when formamidopyrimidine DNA glycosylase treatment was included in the comet assay. These levels of DNA fragmentation were, however, low in relation to very high amounts of BPDE–DNA adducts as measured with 32P postlabelling. We conclude that sperm DNA damage may be useful as a biomarker of direct exposure of sperm using the comet assay adapted to sperm, and as such the method may be applicable to cohort studies. Although the sensitivity is relatively low, DNA damage induced in earlier stages of spermatogenesis may be detected with higher efficiencies.

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