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2. Functional complementation of ataxia-telangiectasia group D (AT-D) cells by microcell-mediated chromosome transfer and mapping of the AT-D locus to the region 11q22-23.

Author

Lambert, C, Schultz, RA, Smith, M, Wagner-McPherson, C, McDaniel, LD, Donlon, T, Stanbridge, EJ, and Friedberg, EC

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Neurodegenerative, Ataxia Telangiectasia, Brain Disorders, Rare Diseases, Human Genome, Neurosciences, 2.1 Biological and endogenous factors, Chromosome Mapping, Chromosomes, Human, Pair 11, DNA Damage, DNA Repair, Genetic Complementation Test, Humans, Hybrid Cells, In Vitro Techniques, Karyotyping, Nucleic Acid Hybridization, Phenotype, GENE TRANSFER, HEREDITARY DISEASES, IONIZING RADIATION, CELL CYCLE, DNA SYNTHESIS, Cell cycle, DNA synthesis, Gene transfer, Hereditary diseases, Ionizing radiation, animal cell, article, ataxia telangiectasia, chromosome 11q, chromosome 18, gene mapping, gene transfer, human, human cell, hybrid cell, mouse, nonhuman, priority journal, Human, In Vitro, Support, Non-U.S. Gov't, Support, U.S. Gov't, Non-P.H.S., Support, U.S. Gov't, P.H.S., Animalia, Ataxia, Ataxia telangiectasia
Abstract

The hereditary human disease ataxia-telangiectasia (AT) is characterized by phenotypic complexity at the cellular level. We show that multiple mutant phenotypes of immortalized AT cells from genetic complementation group D (AT-D) are corrected after the introduction of a single human chromosome from a human-mouse hybrid line by microcell-mediated chromosome transfer. This chromosome is cytogenetically abnormal. It consists primarily of human chromosome 18, but it carries translocated material from the region 11q22-23, where one or more AT genes have been previously mapped by linkage analysis. A cytogenetically normal human chromosome 18 does not complement AT-D cells after microcell-mediated transfer, whereas a normal human chromosome 11 does. We conclude that the AT-D gene is located on chromosome 11q22-23.

Published
1991

7. Hybrid deposits and their effect on oriented strandboard press crown and RTO/RCO duct/cold box ignitions

Author

Wantling, Steven, Cotton, Barbara, Zepka, Bonnie, Bacon, Mike, Moberly, Dave, and Donlon, T. Mike

Subjects
Methanol -- Evaluation -- Environmental aspects, Environmental services industry -- Environmental aspects, Pollution control industry -- Environmental aspects, Business, Forest products industry, Evaluation, Environmental aspects
Abstract

Abstract Deposits of hybrid mixtures of airborne contaminants and gases have been known to accumulate on the press, emission control ducting, and in the cold section of emission control units [...]

Published
2007

10. Abstracts of Selected Posters

Author

Albanese, R., Antoine, J. L., Dutrillaux, B., Ashley, T., Avivi, L., Kariv, I., Barigozzi, C., Baratelli, L., Profeta, S., Bartram, C. R., de Klein, A., Hagemeijer, A., Grosveld, G., Bootsma, D., Bennett, Michael D., Smith, J. B., Ward, J. P., Heslop-Harrison, J. S., Blin, N., Kopun, M., Buys, C. H. C. M., Koerts, T., van der Veen, A. Y., de Leij, L., Civitelli, M. V., Capanna, E., Couturier, J., Arnason, U., Mandahl, N., Créau-Goldberg, N., Turleau, C., Cochet, C., de Grouchy, J., Dietrich, A. J. J., Delhanty, J. D. A., Mazzullo, H. A., Cooke, H. M. G., Dotan, A., Dresser, M. E., Moses, M. J., Evans, E. P., Burgoyne, P. B., Ferraro, M., Lavia, P., Fonatsch, C., Kirchner, H. H., Pajunk, A., Schaadt, M., Burrichter, H., Diehl, V., Ford, J. H., Roberts, C. G., Friebe, B., Vogel, R., Friedländer, M., Gamperl, R., Amtmann, E., Pfister, H., Gebhart, E., Wagner, H., Goetz, P., Chandley, A. C., Speed, R. M., Goyanes, V. J., Schvartzman, J. B., Graeven, U., Weh, H. J., Hossfeld, D. K., Greenblatt, I. M., Gripenberg, U., Söderlund, V., Wahlberg, C., Blomqvist, L., Guichaoua, M. R., Delafontaine, D., Taillemite, J. L., Luciani, J. M., Naaf, T., Grunert, D., Schmid, M., Hameister, H., Sperling, K., Hamers, A., Jongbloet, P., Peeters, G., Geraedts, J., Hartley-Asp, B., Heneen, W. K., Hens, L., Kirsch-Volders, M., Susanne, C., Herbst, E. W., Winking, H., Claussen, C. P., Putz, B., Sellin, D., Kolbus, U., Gropp, A., Bennett, M. D., Heyting, C., Koperdraad, F., Redeker, E. J. W., Holmquist, G., Goldman, M., Jaworska, Halina, Johannisson, R., Kerem, B., Goitein, R., Richier, C., Marcus, M., Cedar, H., Koch, H., Hoehn, H., Kubbies, Manfred, Rabinovitch, Peter S., Kunz, W., Franz, G., Lacadena, J. R., Cermeno, M. C., Orellana, J., Santos, J. L., Lemeunier, F., Derbin, C., Lin, C. C., Hoar, D. I., Hoo, J. J., Macgregor, H. C., Sims, S., Horner, H. A., Pellatt, P., Mackay, J. M., Fox, D. P., Brunt, P. W., Johnston, A. W., Magenis, R. E., Chamberlin, J., Allen, L., Tomar, D., Olson, S., Donlon, T., Marlekaj, P., Balcini, A., Fantoni, A., de Capoa, A., Martinsson, T., Dahllöf, B., Levan, G., Matsukuma, S., Utakoji, T., del Mazo, J., Avila, J., Miller, D. A., Feinstein, S. I., Miller, O. J., Morita, T., Delarbre, C., Gachelin, G., Kourilsky, P., Moritz, K., Moriwaki, K., Miyashita, N., Imai, H. T., Wang, C. H., Bonhomme, F., Murer-Orlando, M., Peterson, A. C., Neitzel, H., Bogenberger, J., Fittler, F., Gaenge, M., Schulze, C., Nietzel, H., Nürnberger, F., Höhn, H., van Ommen, G. J. B., Baas, F., Arnberg, A. C., Pearson, P. L., De Vijilder, J. J. M., Bakker, E., Hofker, M., Wapenaar, M. C., Parrington, J. M., West, L. F., Povey, S., Pasquali, F., Casalone, R., Bernasconi, P., Paul, J., Froster-Iskenius, U., Schwinger, E., Moje, W., Pearson, P. O., Beverstock, G. C., Veenema, H., v.d Kamp, J. J., Petitpierre, E., Philip, J., Lundsteen, C., van der Ploeg, M., van Prooijen-Knegt, A. C., Bauman, J. G. J., van Duijn, P., Puertas, M. J., de la Pena, A., Estades, B., Merino, F., Rao, S. R. V., Vasantha, K., Thelma, B. K., Juyal, R. C., Jhanwar, S. C., Ratomponirina, Ch, Hamilton, A., Rumpler, Y., Moses, M., Raveh, D., Ben-Zeoev, A., Redi, C. A., Garagna, S., Italy, C. N. R., Robert-Nicoud, M., Streichhan, I., Möhr, E., Westermann, R., Grossbach, U., Sandberg, P., Levan, A., Schäfer, Mireille, Schempp, W., Scheres, J. M. J. C., Hustinx, T. W. J., Holdrinet, R. S. G., Tice, R. R., Schwarzacher, T., Finch, R. A., Searle, J. B., Sharma, T., Sen, S., Cheong, N., Siebert, E., Loidl, J., Slater, R. M., de Kraker, J., Voute, P. A., Delemarre, J. F. M., Smeets, D. F. C. M., Smits, A. P. T., Solleder, E., Inglin, B., Geile, B., Somssich, I., Schwarz, E., Speit, G., Mehnert, K., Vogel, W., Stahl, A., Hartung, M., Devictor, M., Guichaoua, M., Stoll, C., Roth, M.-P., Dott, B., Tabor, A., Madsen, M., Tommerup, N., Traut, W., Chavin-Colin, F., Junien, C., Vekemans, M., Esseltine, D., Venegas, W., Lasne, Cl, Chouroulinkov, I., Vidal, F., Navarro, J., Templado, C., Egozcue, J., Viegas-Péquignot, E., Malfoy, B., Taillandier, E., Leng, M., Viinikka, Y., Spielmann, H., Boldin, S., Volobouev, V. T., Webb, G. C., Krumins, E., Wegner, R.-D., Lüdtke, E.-L., Weith, A., Westerman, M., Thomson, R., Sinclair, A., Yacobi, Y. Z., Feldman, M., Yoon, J. S., Bennett, M. D., editor, Gropp, A., editor, and Wolf, U., editor

Published
1984
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24. Fine mapping of the Autosomal Dominant Split Hand/Split Foot Locus on Chromosome 7, Band q21.3-q22.1

Author

Scherer, S. W., Poorkaj, P., Allen, T., Kim, J., Geshuri, D., Nunes, M., Soder, S., Stephens, K., Pagon, R. A., Patton, M. A., Berg, M. A., Donlon, T., Rivera, H., Pfeiffer, R. A., Naritomi, K., Hughes, H., Genuardi, M., Fiorella Gurrieri, Neri, G., Lovrein, E., Magenis, E., Tsui, L. -C, and Evans, J. P.

Subjects
Chromosome mapping, Chromosomes, human, pair 7, Chromosome deletion, Chromosome aberrations - genetics, Original Articles, Chromosome disorders
Abstract

Split hand/split foot (SHFD) is a human developmental defect characterized by missing digits, fusion of remaining digits, and a deep median cleft in the hands and feet. Cytogenetic studies of deletions and translocations associated with this disorder have indicated that an autosomal dominant split hand/split foot locus (gene SHFD1) maps to 7q21-q22. To characterize the SHFD1 locus, somatic cell hybrid lines were constructed from cytogenetically abnormal individuals with SHFD. Molecular analysis resulted in the localization of 93 DNA markers to one of 10 intervals surrounding the SHFD1 locus. The translocation breakpoints in four SHFD patients were encompassed by the smallest region of overlap among the SHfD-associated deletions. The order of DNA markers in the SHFD1 critical region has been defined as PON-D7S812-SHFD1-D7S811-ASNS. One DNA marker, D7S811, detected altered restriction enzyme fragments in three patients with translocations when examined by pulsed-field gel electrophoresis (PFGE). These data map SHFD1, a gene that is crucial for human limb differentiation, to a small interval in the q21.3-q22.1 region of human chromosome 7., published_or_final_version

Published
1994

33. Report of the fourth international workshop on human chromosome 15 mapping 1997.

Author

Morton, C. C., Christian, St., Donlon, T. A., Driscoll, D. J., Fink, J. K., Gabriel, J. M., Gotway, G., Greally, J. M., Hitchins, M. P., Howard, H. C., Ji, Y., Leonard, S., Lerner, T., Magenis, E., Malcolm, S., Ohta, T., Rainier, S., Rees, M., Riley, B., and Robinson, W. P.

Subjects
FORUMS, HUMAN gene mapping, HUMAN chromosomes, HUMAN genome
Abstract

The fourth international workshop on human chromosome 15 mapping was held at the Genome Database in Baltimore, Maryland on October 28, 1997, and was attended by 31 participants from five countries. Construction of a new YAC STS-content map of the chromosome is described in the report. The first physical map of this region, developed in 1993, extended from D15S18 to D15S12 and was comprised of 22 YAC and 21 SIS with two gaps present in the contig. The Stanford radiation hybrid map contains 10 SIS of which four were novel.

Published
1999
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36. Treatment of myelodysplastic syndromes with recombinant human granulocyte colony-stimulating factor. A phase I-II trial.

Author

Negrin, Robert S., Haeuber, Douglas H., Nagler, Arnon, Olds, Lynne C., Donlon, Timothy, Souza, Lawrence M., Greenberg, Peter L., Negrin, R S, Haeuber, D H, Nagler, A, Olds, L C, Donlon, T, Souza, L M, and Greenberg, P L

Subjects
MYELODYSPLASTIC syndromes, HEMATOPOIESIS, GRANULOCYTE-colony stimulating factor, ANEMIA treatment, MYELODYSPLASTIC syndromes treatment, ERYTHROCYTES, BONE marrow, CELL physiology, CLINICAL trials, COLONY-stimulating factors (Physiology), COMPARATIVE studies, CLINICAL drug trials, RESEARCH methodology, MEDICAL cooperation, NEUTROPHILS, PHAGOCYTOSIS, RECOMBINANT proteins, RESEARCH, RESEARCH funding, RETICULOCYTES, EVALUATION research, LEUKOCYTE count
Abstract

Study Objective: To determine the hematopoietic effects and toxicity of recombinant human granulocyte colony-stimulating factor (G-CSF) in patients with myelodysplastic syndromes.Design: The G-CSF was administered by daily subcutaneous injection to outpatients in a phase I-II trial. Dose was escalated every 2 weeks between 0.1 to 3.0 micrograms/kg body weight.d over an 8-week treatment period.Setting: Outpatient clinical research center at a university hospital.Patients: Twelve consecutive patients with myelodysplastic syndromes: two refractory anemia, seven refractory anemia with excess of blasts, three refractory anemia with excess of blasts in transformation.Measurements and Main Results: In 10 of 12 patients, elevations in blood leukocyte counts (2- to 10-fold) and absolute neutrophil counts (5- to 40-fold) were seen over the 8-week treatment period. Five of seven severely neutropenic patients (absolute neutrophil count, less than 0.5 x 10(9)/L) had a rise in count to 1.2 to 16.3 x 10(9)/L. Increased reticulocyte counts occurred in 5 patients, and were associated with decreased transfusion requirements in 2 of 9 erythrocyte transfusion-dependent patients. Treatment with G-CSF enhanced marrow myeloid cell maturation in 9 of 11 evaluable patients. Neutrophil chemotaxis and phagocytosis in vitro were improved or unchanged after treatment in 6 of 8 patients tested. In 11 of 12 patients, there were no substantial changes in platelet, lymphocyte, eosinophil, or monocyte counts. Three responding patients initially had abnormal cytogenetics that persisted after G-CSF therapy, suggesting induced differentiation of the abnormal clone. The therapy was associated with minimal toxicity. None of the patients' conditions converted to acute leukemia during treatment or in short-term follow-up.Conclusions: Treatment with G-CSF administered by subcutaneous injection is well tolerated and effective for improving the neutropenia, and less commonly the transfusion-dependent anemia, over 6 to 8 weeks in patients with myelodysplastic syndromes. [ABSTRACT FROM AUTHOR]

Published
1989
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37. Correlation between growth control, neoplastic potential and endogenous connexin43 expression in HeLa cell lines: implications for tumor progression.

Author

King, T J, Fukushima, L H, Donlon, T A, Hieber, A D, Shimabukuro, K A, and Bertram, J S

Abstract

A HeLa cell line, obtained from the ATCC, was cloned and found to exhibit a spectrum of in vitro and in vivo growth characteristics as well as variable expression of endogenous connexin43 (Cx43), a widely expressed gap junction protein implicated in growth control. The majority of clones expressed functional Cx43, which contrasted with previous studies reporting that HeLa cells are completely negative for Cx43 mRNA/protein expression. This endogenous Cx43 expression correlated with increased growth control: Cx43-positive clones exhibited a decreased saturation density and a diminished growth capacity when in co-culture with growth-controlled normal cells in constrast to Cx43-negative clones. Endogenous Cx43 expression was negatively correlated with neoplastic potential as evidenced by attenuated anchorage-independent growth and decreased tumorigenicity in immunodeficient mice. Treatment of Cx43-negative cells with 5-aza-2'-deoxycytidine resulted in expression of Cx43, suggesting gene silencing via DNA methylation. These results support the concept of growth control via junctionally transmitted signals and suggest an epigenetic mechanism for tumor cells to circumvent this control during carcinogenesis. Moreover, the heterogeneous nature of this cell line and the ease of connexin43 gene induction suggest caution in the interpretation of results involving gene transfection using noninducible gene expression systems.

Published
2000
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38. Differential amplification, assembly, and relocation of multiple DNA sequences in human neuroblastomas and neuroblastoma cell lines.

Author

Shiloh, Y, Shipley, J, Brodeur, G M, Bruns, G, Korf, B, Donlon, T, Schreck, R R, Seeger, R, Sakai, K, and Latt, S A

Abstract

DNA amplification, manifested by homogeneously staining regions in chromosomes and by extrachromosomal, double minute bodies, is characteristic of many neuroblastoma cell lines. Sequences recruited from a specific domain on the short arm of chromosome 2 (2p) are amplified in advanced-stage primary neuroblastomas, whereas sequences from distinctly different regions of 2p are amplified in the neuroblastoma cell line IMR-32. Five different DNA segments, which include the oncogene N-myc, three other fragments derived from the homogeneously staining region of the neuroblastoma cell line IMR-32, and a fifth fragment, derived from the neuroblastoma cell line NB-9, showed differential and variable amplification in 24 advanced-stage neuroblastoma tumors out of 112 tested specimens. All five fragments were mapped within the chromosomal region 2p23-2p25 by three different approaches. However, eight other fragments cloned from the homogeneously staining region of IMR-32 cells, which were not amplified in the tumor tissues examined, were mapped to two more proximal domains of 2p, thousands of kilobases apart from each other and from the chromosomal domain that is amplified in the tumors. These results establish the amplification, to different degrees, of a variable-sized segment of one domain near the terminus of 2p in advanced neuroblastomas. These tumors might ultimately be distinguished according to the pattern of amplification of DNA segments within this domain. The data presented also indicate the existence of a new and complex amplification mechanism in at least one neuroblastoma cell line (IMR-32), which involves not only relocation of DNA from specific genomic domains but also the formation of novel units by splicing together very distant DNA segments.

Published
1985
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39. Localization of the restriction fragment length polymorphism D14S1 (pAW-101) to chromosome 14q32.1 leads to 32.2 by in situ hybridization

Author

Donlon, T A, Litt, M, Newcom, S R, and Magenis, R E

Subjects
Polymorphism, Genetic, Humans, Nucleic Acid Hybridization, DNA, DNA, Neoplasm, Burkitt Lymphoma, Chromosomes, Human, 13-15, Research Article, Cell Line, Chromosome Banding
Abstract

The restriction fragment length polymorphism D14S1 is delineated by the cloned, single-copy DNA fragment pAW-101. This cloned fragment can therefore serve as a useful marker for gene linkage studies, and the exact location on the gene map is of great interest. pAW-101 was 3H-labeled and hybridized in situ to normal, prometaphase chromosome preparations. Analysis of the grain distribution shows this fragment to be localized to the long arm of chromosome 14 at band q32. Using lymphoid cell lines with 8;14 reciprocal translocations (q24.1;q32.3) from patients with Burkitt lymphoma, we found that the DNA fragment hybridizes to the rearranged chromosome 14 proximal to the breakpoint. These results localize D14S1 to the region 14q32.1 leads to 32.2 This is consistent with localization of this fragment utilizing somatic cell hybrids and family studies.

Published
1983

41. A non-centromeric C band variant on chromosome 11q23.2.

Author

Spak, D K, Johnston, K, and Donlon, T A

Abstract

An extra G band was found inserted into chromosome 11q23.2 in a boy who had severe developmental delay and anal stenosis. Cytogenetic characterisation of this extra band showed that it was composed of Q band brilliant, C band heterochromatin. It was also present in clinically normal subjects in two other generations and was therefore presumed to be unrelated to the clinical abnormalities in the proband. Although rare, this cytogenetic anomaly may be useful as a genetic marker for 11q23.2. [ABSTRACT FROM PUBLISHER]

Published
1989

42. Fourth International Workshop on Human Chromosome 15 Mapping, Genome Database, Baltimore, MD, October 28 1997

Author

Morton, C. C., Christian, S. L., Donlon, T. A., Driscoll, D. J., Fink, J. K., Gabriel, J. M., Gotway, G., Greally, J. M., Hitchins, M. P., Howard, H. C., Ji, Y., Leonard, S., Lerner, T., Magenis, E., Malcolm, S., Ohta, T., Rainier, S., Rees, M., Riley, B., Robinson, W. P., Shinji Saitoh, Schultz, R., Sell, S., Sharp, J. D., Talbot, C., Trent, R., Wevrick, R., and Nicholls, R. D.

44. DNA-based Detection of Chromosome Deletion and Amplification: Diagnostic and Mechanistic Significance

Author

Latt, S.A., primary, Lalande, M., additional, Donlon, T., additional, Wyman, A., additional, Rose, E., additional, Shiloh, Y., additional, Korf, B., additional, Muller, U., additional, Sakai, K., additional, Kanda, N., additional, Kang, J., additional, Stroh, H., additional, Harris, P., additional, Bruns, G., additional, Wharton, R., additional, and Kaplan, L., additional

Published
1986
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50. Association of methylenetetrahydrofolate reductase polymorphism C677T and dietary folate with the risk of cervical dysplasia.

Author

Goodman MT, McDuffie K, Hernandez B, Wilkens LR, Bertram CC, Killeen J, Le Marchand L, Selhub J, Murphy S, and Donlon TA

Subjects
Adult, Case-Control Studies, DNA, Viral analysis, Diet, Epidemiologic Studies, Ethnicity, Female, Genotype, Humans, Methylenetetrahydrofolate Reductase (NADPH2), Odds Ratio, Papanicolaou Test, Papillomaviridae pathogenicity, Papillomavirus Infections complications, Polymorphism, Genetic, Precancerous Conditions etiology, Risk Factors, Tumor Virus Infections complications, Uterine Cervical Neoplasms pathology, Vaginal Smears, Folic Acid Deficiency complications, Oxidoreductases Acting on CH-NH Group Donors genetics, Precancerous Conditions genetics, Uterine Cervical Neoplasms etiology, Uterine Cervical Neoplasms genetics
Abstract

Epidemiological studies have been inconsistent regarding a role for folate in the etiology of cervical dysplasia. Methylenetetrahydrofolate reductase (MTHFR) catalyzes the synthesis of 5-methyltetrahydrofolate, which is involved in the methylation of homocysteine to methionine. A common variant of this enzyme, resulting from a 677C-->T (Ala-->Val) substitution in the gene, has been shown to have reduced activity and is associated with mild hyperhomocysteinemia. A multiethnic case-control study was used to examine the association of dietary folate and MTHFR genotype with the odds ratios (ORs) for cervical dysplasia among women identified from several clinics on Oahu, Hawaii, between 1992 and 1996. We collected blood samples for DNA extraction, cervical smears for cytological diagnosis, exfoliated cervical cells for human papillomavirus (HPV) DNA testing, and personal interviews from 150 women with squamous intraepithelial lesions (SILs) and from 179 women with cytologically normal (Pap) smears. We found a positive, monotonic trend (P = 0.02) in the ORs for cervical SILs associated with the number of variant MTHFR T alleles, after multivariate adjustment. Women with the heterozygous CT genotype had twice the risk of cervical SILs [OR, 2.0; 95% confidence interval (CI), 1.1-3.7], and women with the homozygous TT genotype had almost three times the risk of SILs (OR, 2.9; 95% CI, 1.0-8.8) compared to women with the homozygous MTHFR CC genotype. The dietary intakes of folate, vitamin B(6), and vitamin B(12) were inversely related to the ORs for cervical SILs, after adjustment for HPV DNA and other confounders. The OR among women in the highest quartile compared with women in the lowest quartile of folate intake was 0.3 (95% CI, 0.1-0.7; P for trend = 0.002). Women with the variant T allele and folate intakes below the median were at significantly elevated risk of cervical SILs (OR, 5.0; 95% CI, 2.0-12.2) compared to women with CC alleles and folate intakes above the median. HPV infection was a strong risk factor for cervical dysplasia, particularly among women with the variant T allele (OR, 46.6; 95% CI, 15.9-136.2). All associations of MTHFR genotype with the ORs for cervical SILs were independent of other risk factors under study. These findings suggest that the MTHFR T allele and reduced dietary folate may increase the risk for cervical SILs.

Published
2001

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