16 results on '"N. T. Bech-Hansen"'
Search Results
2. Cone dystrophy and ectopic synaptogenesis in a Cacna1f loss of function model of congenital stationary night blindness (CSNB2A)
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L Nguyen, William K. Stell, N. T. Bech-Hansen, Stephan Bonfield, Ioannis S. Dimopoulos, Derek Waldner, Yves Sauve, and N C Giraldo Sierra
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0301 basic medicine ,Retinal degeneration ,retina ,Retinal Disorder ,genetic structures ,Calcium Channels, L-Type ,Cacna1f ,Biophysics ,Biology ,Biochemistry ,03 medical and health sciences ,Mice ,0302 clinical medicine ,channelopathy ,Cone dystrophy ,Night Blindness ,medicine ,Myopia ,Animals ,Rod cell ,Cone Dystrophy ,Outer nuclear layer ,CSNB ,Mice, Knockout ,Retina ,medicine.diagnostic_test ,Eye Diseases, Hereditary ,Genetic Diseases, X-Linked ,medicine.disease ,photoreceptor ,Cav1.4 ,Disease Models, Animal ,030104 developmental biology ,medicine.anatomical_structure ,Mutation ,Synapses ,Female ,sense organs ,Calcium Channels ,Neuroscience ,030217 neurology & neurosurgery ,Electroretinography ,Photopic vision ,Research Paper - Abstract
Congenital stationary night blindness 2A (CSNB2A) is an X-linked retinal disorder, characterized by phenotypically variable signs and symptoms of impaired vision. CSNB2A is due to mutations in CACNA1F, which codes for the pore-forming α1F subunit of a L-type voltage-gated calcium channel, Cav1.4. Mouse models of CSNB2A, used for characterizing the effects of various Cacna1f mutations, have revealed greater severity of defects than in human CSNB2A. Specifically, Cacna1f-knockout mice show an apparent lack of visual function, gradual retinal degeneration, and disruption of photoreceptor synaptic terminals. Several reports have also noted cone-specific disruptions, including axonal abnormalities, dystrophy, and cell death. We have explored further the involvement of cones in our ‘G305X’ mouse model of CSNB2A, which has a premature truncation, loss-of-function mutation in Cacna1f. We show that the expression of genes for several phototransduction-related cone markers is down-regulated, while that of several cellular stress- and damage-related markers is up-regulated; and that cone photoreceptor structure and photopic visual function – measured by immunohistochemistry, optokinetic response and electroretinography – deteriorate progressively with age. We also find that dystrophic cone axons establish synapse-like contacts with rod bipolar cell dendrites, which they normally do not contact in wild-type retinas – ectopically, among rod cell bodies in the outer nuclear layer. These data support a role for Cav1.4 in cone synaptic development, cell viability, and synaptic transmission of cone-dependent visual signals. Although our novel finding of cone-to-rod-bipolar cell contacts in this mouse model of a retinal channelopathy may challenge current views of the role of Cav1.4 in photopic vision, it also suggests a potential new target for restorative therapy.
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- 2018
3. Channeling Vision: CaV1.4—A Critical Link in Retinal Signal Transmission
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N. T. Bech-Hansen, William K. Stell, and Derek Waldner
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0301 basic medicine ,genetic structures ,Calcium Channels, L-Type ,lcsh:Medicine ,Review Article ,Neurotransmission ,Biology ,Synaptic Transmission ,Synaptic vesicle ,Retinal ganglion ,Retina ,General Biochemistry, Genetics and Molecular Biology ,Exocytosis ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Retinal Rod Photoreceptor Cells ,medicine ,Animals ,Humans ,Secretion ,Vision, Ocular ,General Immunology and Microbiology ,Voltage-dependent calcium channel ,lcsh:R ,Retinal ,General Medicine ,030104 developmental biology ,medicine.anatomical_structure ,chemistry ,Retinal Cone Photoreceptor Cells ,sense organs ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Voltage-gated calcium channels (VGCC) are key to many biological functions. Entry of Ca2+into cells is essential for initiating or modulating important processes such as secretion, cell motility, and gene transcription. In the retina and other neural tissues, one of the major roles of Ca2+-entry is to stimulate or regulate exocytosis of synaptic vesicles, without which synaptic transmission is impaired. This review will address the special properties of one L-type VGCC,CaV1.4, with particular emphasis on its role in transmission of visual signals from rod and cone photoreceptors (hereafter called “photoreceptors,” to the exclusion of intrinsically photoreceptive retinal ganglion cells) to the second-order retinal neurons, and the pathological effects of mutations in theCACNA1Fgene which codes for the pore-formingα1Fsubunit ofCaV1.4.
- Published
- 2018
4. A summary of 20 CACNA1F mutations identified in 36 families with incomplete X-linked congenital stationary night blindness, and characterization of splice variants
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Tracy A. Maybaum, Kym M. Boycott, Richard G. Weleber, Johane M Robitaille, Margaret J. Naylor, Arthur A.B. Bergen, N. T. Bech-Hansen, Mary Ella M Pierpont, William G. Pearce, Yozo Miyake, and Other departments
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DNA, Complementary ,X Chromosome ,Calcium Channels, L-Type ,genetic structures ,Genetic Linkage ,RNA Splicing ,Molecular Sequence Data ,Mutation, Missense ,Biology ,Mice ,Night Blindness ,Genetics ,medicine ,Animals ,Humans ,splice ,Amino Acid Sequence ,Gene ,Genetics (clinical) ,X chromosome ,Congenital stationary night blindness ,Base Sequence ,Sequence Homology, Amino Acid ,medicine.disease ,Human genetics ,eye diseases ,Eye disorder ,Calcium Channels ,X-linked congenital stationary night blindness ,Founder effect - Abstract
Incomplete X-linked congenital stationary night blindness (CSNB) is a recessive, non-progressive eye disorder characterized by abnormal electroretinogram and psychophysical testing and can include impaired night vision, decreased visual acuity, myopia, nystagmus, and strabismus. Including the 20 families previously reported (Bech-Hansen et al. 1998b), we have now analyzed patients from a total of 36 families with incomplete CSNB and identified 20 different mutations in the calcium channel gene CACNA1F. Three of the mutations account for incomplete CSNB in two or more families, and a founder effect is clearly demonstrable for one of these mutations. Of the 20 mutations identified, 14 (70%) are predicted to cause premature protein truncation and six (30%) to cause amino acid substitutions or deletions at conserved positions in the alpha1F protein. In characterizing transcripts of CACNA1F we have identified several splice variants and defined a prototypical sequence based on the location of mutations in splice variants and comparison with the mouse orthologue, Cacnalf.
- Published
- 2001
5. Localization of a gene for incomplete X-linked congenital stationary night blindness to the interval between DXS6849 and DXS8023 in Xp11.23
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Kym M. Boycott, Daniel Ross, William G. Pearce, L. Leigh Field, Kathy Gratton, and N. T. Bech-Hansen
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Male ,Visual acuity ,Retinal Disorder ,X Chromosome ,genetic structures ,Genetic Linkage ,Locus (genetics) ,Nystagmus ,Biology ,Gene mapping ,Night Blindness ,Genetics ,medicine ,Electroretinography ,Humans ,Genetics (clinical) ,Congenital stationary night blindness ,medicine.diagnostic_test ,Chromosome Mapping ,Darkness ,medicine.disease ,Adaptation, Physiological ,eye diseases ,Pedigree ,Female ,medicine.symptom ,X-linked congenital stationary night blindness - Abstract
Congenital stationary night blindness (CSNB) is a nonprogressive retinal disorder characterized by night blindness, nystagmus, myopia, a variable decrease in visual acuity, an abnormal electroretinographic response, and a disturbance in dark adaptation. Two forms of X-linked CSNB have been defined, complete CSNB in which rod function is extinguished, and incomplete CSNB in which rod function is reduced but not extinguished, as seen by electroretinography and dark adaptometry. In studying a large family of Mennonite ancestry, we have confirmed linkage between the locus (CSNB2) for incomplete CSNB and genetic markers in the Xp11 region. In particular, lod scores of 12.25 and 15.26 at zero recombination were observed between CSNB2 and the markers DXS573 and DXS255. Detailed analysis of critical recombinant chromosomes in this extended family have refined the minimal region for the CSNB2 locus to the interval between DXS6849 and DXS8023 in Xp11.23.
- Published
- 1998
6. Manifestations of X-linked congenital stationary night blindness in three daughters of an affected male: demonstration of homozygosity
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N T, Bech-Hansen and W G, Pearce
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Adult ,Male ,X Chromosome ,Adolescent ,Genetic Linkage ,Homozygote ,Visual Acuity ,Pedigree ,Haplotypes ,Night Blindness ,Child, Preschool ,Humans ,Female ,Child ,Research Article - Abstract
X-linked congenital stationary night blindness (CSNB1) is a hereditary retinal disorder in which clinical features in affected males usually include myopia, nystagmus, and impaired visual acuity. Electroretinography demonstrates a marked reduction in b-wave amplitude. In the study of a large Mennonite family with CSNB1, three of five sisters in one sibship were found to have manifestations of CSNB1. All the sons of these three sisters were affected. Each of the two nonmanifesting sisters had at least one unaffected son. Analysis of Xp markers in the region Xp21.1-Xp11.22 showed that the two sisters who were unaffected had inherited the same maternal X chromosome (i.e., M2). Two of the daughters who manifested with CSNB had inherited the other maternal X chromosome (M1). The third manifesting sister inherited a recombinant X chromosome with a crossover between TIMP and DXS255, which suggests that the CSNB1 locus lies proximal to TIMP. One of the affected daughters' sons had inherited the maternal M1 X chromosome, a finding consistent with that chromosome carrying a mutant CSNB gene; the other affected sons inherited the grandfather's X chromosome (i.e., P). Molecular analysis of DNA from three sisters with manifestations of CSNB is consistent with their being homozygous at the CSNB1 locus and with their mother being a carrier of CSNB1.
- Published
- 1993
7. A locus for X-linked congenital stationary night blindness is located on the proximal portion of the short arm of the X chromosome
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L. Leigh Field, M. Reedyk, W. G. Pearce, N. T. Bech-Hansen, N. J. Fraser, A. M. Schramm, and Ian W. Craig
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Genetic Markers ,Male ,Recombination, Genetic ,Congenital stationary night blindness ,Genetics ,X Chromosome ,Genetic Linkage ,Restriction Mapping ,Locus (genetics) ,Biology ,medicine.disease ,Pedigree ,Night Blindness ,Genetic linkage ,Genetic marker ,medicine ,Humans ,Female ,X-linked congenital stationary night blindness ,Polymorphism, Restriction Fragment Length ,Genetics (clinical) ,X chromosome ,Lod score ,Recombination Fraction - Abstract
Linkage between X-linked congenital stationary night blindness (CSNB1) and seven markers on the X chromosome was investigated in a large four-generation Albertan kindred. We detected significant linkage between the CSNB1 locus and the locus DXS255 (maximum lod score = 6.73 at a recombination fraction of 6%; confidence interval of 1% to 18%), which anchors the CSNB1 locus to the proximal region near p11.22 on the short arm of the X chromosome.
- Published
- 1990
8. Recent Progress in the Identification of the X-Linked Infantile Spinal Muscular Atrophy (Xl-SMA) Gene: Implications for Neuronal Apoptosis
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Mary Ellen Ahearn, Lisa Baumbach, R. D. Clark, N. T. Bech-Hansen, Eric P. Hoffman, Devin Dressman, H. Basterrechea, and A. Meind
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Gynecology ,medicine.medical_specialty ,lcsh:T ,business.industry ,lcsh:R ,Short Report ,lcsh:Medicine ,General Medicine ,lcsh:Technology ,General Biochemistry, Genetics and Molecular Biology ,Infantile spinal muscular atrophy ,Medicine ,lcsh:Q ,lcsh:Science ,business ,Neuronal apoptosis ,General Environmental Science - Abstract
L.L. Baumbach*, D. Dressman, H. Basterrechea, M.E. Ahearn, N.T. Bech-Hansen, R.D. Clark, A. Meindl, E. Hoffman Dept of Pediatrics, Univ Miami Sch Medicine, PO Box 016820, Miami, FL., 33136; Children's National Medical Center, Washington, D.C; Univ. of Pittsburgh, Pittsburgh, PA; University of Calgary, Calgary, Alberta; USC Cancer Center, Los Angeles, CA; Ludwig Maximilians Universtat, Munich, Germany * lbaumbac@med.miami.edu
- Published
- 2001
9. Incomplete X-linked congenital stationary night blindness: Characterization of mutations in the CACNAIF gene and an assessment of clinical variability
- Author
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N T Bech-Hansen, W G Pearcel, and Kym M. Boycott
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Congenital stationary night blindness ,medicine.medical_specialty ,Visual acuity ,genetic structures ,Genetic heterogeneity ,business.industry ,Nystagmus ,Audiology ,medicine.disease ,eye diseases ,Ophthalmology ,Decreased Visual Acuity ,medicine ,Scotopic vision ,medicine.symptom ,Strabismus ,X-linked congenital stationary night blindness ,business ,Genetics (clinical) - Abstract
X-linked congenital stationary night blindness (CSNB) is a clinically and genetically heterogeneous non-progressive retinal disorder characterized by impaired night vision, decreased visual acuity, myopia, nystagmus, and strabismus. Two loci for CSNB exist on the X chromosome. The locus for complete CSNB (nonrecordable scotopic b-wave and lack of rod dark adaptation) has been mapped to Xp11.4 (Boycott et al. AJHG 62:865-875, 1998), while the gene responsible for incomplete CSNB (subnormal scotopic b-wave and mildly elevated rod adaptation), CACNA1F, has been identified in Xp11.23 (Bech-Hansen et al. Nature Genet. 19:264-267). Our analysis of this retina-specific L-type calcium channel α1-subunit gene has identified a total of 17 different mutations (two-thirds of which are predicted to cause a loss-of-function) in 36 families with incomplete CSNB. One of these mutations, L1045insC, is seen in 15 families of Mennonite ancestry from Western Canada. Clinical variability was examined in 66 patients from these families in terms of night blindness, myopia, visual acuity, congenital nystagmus and strabismus. In 80% of the patients at least one of the main features of CSNB (night blindness, myopia, and nystagmus) was absent. The only clinical feature present in all 66 patients tested was impaired visual acutiy. Among these Patients who shared the common CACNA1F mutation, considerable variability in clinical expression is evident and suggests the presence of genetic modifiers. This research was supported in part by the RP Research Foundation (Canada), the Alberta Heritage Foundation for Medical Research and the Roy Allen Endowment.
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- 1999
10. SOMATIC SEGREGATION, RECOMBINATION, ASYMMETRICAL DISTRIBUTION AND COMPLEMENTATION TESTS OF CYTOPLASMICALLY-INHERITED ANTIBIOTIC-RESISTANCE MITOCHONDRIAL MARKERS IN S. CEREVISIAE
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N. T. Bech-Hansen and G. H. Rank
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Heterozygote ,Mitochondrial DNA ,Mating type ,Genotype ,Somatic cell ,Extrachromosomal Inheritance ,Mitosis ,Saccharomyces cerevisiae ,Investigations ,Biology ,law.invention ,law ,Genetics ,Crosses, Genetic ,Recombination, Genetic ,Genetic Complementation Test ,Homozygote ,Drug Resistance, Microbial ,Spores, Fungal ,Molecular biology ,Heteroplasmy ,Culture Media ,Erythromycin ,Mitochondria ,Complementation ,Chloramphenicol ,Recombinant DNA ,Ploidy - Abstract
Genetic analyses of 48-hr-old zygote-daughter-colony cells from crosses between chloramphenicol and erythromycin resistance markers located in mitochondrial DNA demonstrated homoplasmons of parental and recombinant genotypes, and heteroplasmons with recombinant and/or parental genotypes. Although the heteroplasmons were unstable and the homoplasmic components could be segregated by plating on selective media, the heteroplasmic state was often maintained beyond 19 cell divisions when grown on non-selective medium. Homoplasmons of recombinant genotype from repulsion crosses were observed with a frequency of 7.2, 9.0, 11.2 and 11.4 percent; two crosses with the resistance markers in coupling had 5.4 and 11.5 percent recombinants. Under non-selective conditions, the mitochondrial marker derived from the haploid parent of a mating type predominated in zygote-daughter-cells; this asymmetrical distribution could be reversed by selective pressure for the marker transmitted with low frequency. The challenge with chloramphenicol and erythromycin of zygotes from crosses of resistance-markers in repulsion revealed that inter-mitochondrial complementation was not occurring.
- Published
- 1972
11. A multigene deletion within the immunoglobulin heavy-chain region
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H, Chaabani, N T, Bech-Hansen, and D W, Cox
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Base Sequence ,Genes ,Sequence Homology, Nucleic Acid ,Humans ,Nucleic Acid Hybridization ,DNA Restriction Enzymes ,Chromosome Deletion ,Immunoglobulin Allotypes ,Immunoglobulin Heavy Chains ,Research Article - Abstract
The immunoglobulin heavy-chain genes are located in a cluster on chromosome 14. The simultaneous absence of the human IgG1, IgG2, IgG4, and IgA1 subclasses was previously reported in a healthy Tunisian Berber and was later shown to be due to a multigene deletion. We now describe a serological and molecular study of a different deletion observed in a healthy Tunisian. Blot hybridization analysis of the proband's DNA using gamma, epsilon, alpha, and mu switch probes showed that the deletion involves a large region of the immunoglobulin heavy-chain gene cluster: C psi epsilon, C alpha 1, C psi gamma, C gamma 2, and C gamma 4. Incidentally, we showed that the restriction enzyme EcoRI alone can be used with the alpha probe to differentiate A2m types. The deletion described, present in a person homozygous for GM-Am haplotypes (Gm1,17;..;5,14,11,13,10 A2m2), is consistent with previous location, by association analysis, of C psi gamma between C alpha 1 and C gamma 2. There is evidence to suggest that deletions may be more common in the Mediterranean region than in North American Caucasians.
- Published
- 1985
12. Restriction fragment length polymorphisms associated with immunoglobulin C gamma genes reveal linkage disequilibrium and genomic organization
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N T Bech-Hansen, Diane W. Cox, and P S Linsley
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Genetics ,Linkage disequilibrium ,Multidisciplinary ,Polymorphism, Genetic ,Genetic Linkage ,Immunoglobulin gamma-Chains ,Haplotype ,Immunoglobulins ,Nucleic Acid Hybridization ,DNA Restriction Enzymes ,Biology ,Molecular biology ,Genes ,Genetic linkage ,Humans ,BamHI ,Restriction fragment length polymorphism ,Immunoglobulin Constant Regions ,Immunoglobulin Heavy Chains ,Alleles ,Genetic association ,Genomic organization ,Research Article - Abstract
We have demonstrated that restriction fragment length polymorphisms (RFLPs) produced by BamHI can be used as markers for constant (C) region heavy chain genes C psi gamma (C gamma pseudogene), C gamma 2, and C gamma 4. These RFLPs were found nonrandomly associated in the population sample studied. Of the eight combinations (haplotypes) of RFLPs theoretically possible, only two accounted for a total of 88% of the 116 chromosomes examined, a value greater than the total of 25% expected from random segregation of alleles. This indicates considerable linkage disequilibrium between C psi gamma, C gamma 2, and C gamma 4. Quantitative assessment of the degree of association between C gamma gene RFLPs, Gm markers, and switch region RFLPs adjacent to C mu and C alpha 1 revealed that C psi gamma is most tightly associated with C gamma 2 (r = 0.81 and 0.95 for the two common haplotypes), suggesting that C psi gamma maps to a position lying between C alpha 1 and C gamma 2. The association analysis used here should have general applicability for studying the genomic organization of other multigene families.
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- 1983
13. Analysis of a break in chromosome 14 mapping to the region of the immunoglobulin heavy chain locus
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P S Linsley, N T Bech-Hansen, Diane W. Cox, and L Siminovitch
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Genetics ,Chromosome Aberrations ,Multidisciplinary ,Polymorphism, Genetic ,Pseudogene ,Immunoglobulin gamma-Chains ,Chromosome ,Chromosome Mapping ,Nucleic Acid Hybridization ,Locus (genetics) ,Biology ,Molecular biology ,Genes ,Gene cluster ,Gene family ,Humans ,Restriction fragment length polymorphism ,Immunoglobulin Heavy Chains ,Gene ,Chromosomes, Human, 13-15 ,Research Article - Abstract
We have detected restriction fragment length polymorphisms associated with the immunoglobulin heavy chain C gamma genes. DNA from both parents of an individual having an unbalanced rearrangement of the long arm of chromosome 14, region q32 [Cox, D. W., Markovic, V. D. & Teshima, I. E. (1982) Nature (London) 297, 428-430], revealed distinctive patterns of BamHI fragments which hybridized with cloned probes from the C gamma 2-C gamma 4 gene cluster. The number of hybridizing fragments in both cases (five) equaled the number of known C gamma genes. Pedigree and densitometric analyses indicated that the proband did not have any maternal complement of C gamma gene-hybridizing fragments. Included on the deleted chromosomal segment was a C gamma gene having properties of the previously reported C gamma pseudogene. We also examined DNA from this family with a probe for the highly polymorphic locus D14S1, which recently was demonstrated to be tightly linked to the C gamma 1 gene locus [Balazs, I., Purrello, M., Rubinstein, P., Alhadeff, B. & Siniscalco, M. (1982) Proc. Natl. Acad. Sci. USA 79, 7395-7399]. EcoRI and EcoRI-BamHI fragments from both parents hybridized with a probe for this locus in DNA from the proband, indicating that, unlike the C gamma gene family, D14S1 was not deleted from the abnormal chromosome. Thus, the chromosomal breakpoint in the proband lies within region 14q32 between the two tightly linked markers, D14S1 and the C gamma 1 heavy chain gene locus. The D14S1 locus must lie proximal to the centromere relative to the C gamma gene family. The genetic variability detected with C gamma gene probes may prove useful for genetic analysis of structural rearrangements involving this region of chromosome 14.
- Published
- 1983
14. Association of in vitro radiosensitivity and cancer in a family with acute myelogenous leukemia
- Author
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N T, Bech-Hansen, B M, Sell, J J, Mulvihill, and M C, Paterson
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Adult ,Male ,DNA Repair ,Cell Survival ,Dose-Response Relationship, Radiation ,Middle Aged ,Radiation Tolerance ,Cell Line ,Pedigree ,Leukemia, Myeloid, Acute ,Sex Factors ,Child, Preschool ,Humans ,Female ,Child ,Skin - Abstract
The gamma-ray sensitivity of skin fibroblasts from six members of a cancer family was investigated using a colony-forming assay. Fibroblasts from the three members with cancer (two sisters with acute myelogenous leukemia and the mother with cervical carcinoma) showed a significant (p less than 0.05) increase in radiosensitivity, while three members without cancer (the father and two sons) showed a normal radioresponse. The possibility that the increased gamma-ray sensitivity was due to defective DNA repair was investigated using assays for DNA repair replication, single-strand break rejoining, and removal of enzyme-sensitive sites in gamma-irradiated DNA. Results of these assays indicate that the kinetics of enzymatic repair of radiogenic DNA damage in general, and the rejoining of single-strand scissions and excision repair of base and sugar radioproducts in particular, were the same in the cell lines from the sensitive and clinically normal family members.
- Published
- 1981
15. Impaired colony-forming ability following gamma irradiation of skin fibroblasts from tuberous sclerosis patients
- Author
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M C, Paterson, B M, Sell, B P, Smith, and N T, Bech-Hansen
- Subjects
Male ,Cell Survival ,Dose-Response Relationship, Radiation ,Fibroblasts ,In Vitro Techniques ,Radiation Tolerance ,Colony-Forming Units Assay ,Oxygen ,Gamma Rays ,Tuberous Sclerosis ,Humans ,Female ,Cobalt Radioisotopes ,Skin - Published
- 1982
16. TaqI RFLP in human adenylate kinase-1 (AK1) gene region on chromosome 9
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K.J. Marshall, S.L. Kraus, and N T Bech-Hansen
- Subjects
Adenylate kinase 1 ,Genetics ,Polymorphism, Genetic ,TaqI ,Adenylate Kinase ,Phosphotransferases ,Adenylate kinase ,Chromosome 9 ,Biology ,Molecular biology ,chemistry.chemical_compound ,Gene mapping ,chemistry ,Genes ,Humans ,Restriction fragment length polymorphism ,Chromosomes, Human, Pair 9 ,Deoxyribonucleases, Type II Site-Specific ,Gene ,Allele frequency ,Polymorphism, Restriction Fragment Length - Published
- 1989
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