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1169 records – page 1 of 117.

A 9.6 kilobase deletion in the low density lipoprotein receptor gene in Norwegian familial hypercholesterolemia subjects.

https://arctichealth.org/en/permalink/ahliterature36531
Source
Clin Genet. 1992 Dec;42(6):288-95
Publication Type
Article
Date
Dec-1992
Author
O K Rødningen
O. Røsby
S. Tonstad
L. Ose
K. Berg
T P Leren
Author Affiliation
Department of Medical Genetics, Ullevål Hospital, Oslo, Norway.
Source
Clin Genet. 1992 Dec;42(6):288-95
Date
Dec-1992
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Base Sequence
Blotting, Southern
Child
Cholesterol - blood
DNA - analysis
Exons - genetics
Female
Haplotypes
Humans
Hypercholesterolemia, Familial - genetics
Male
Middle Aged
Molecular Sequence Data
Norway
Pedigree
Polymerase Chain Reaction
Polymorphism, Restriction Fragment Length
Receptors, LDL - genetics
Research Support, Non-U.S. Gov't
Sequence Analysis, DNA
Sequence Deletion
Xanthomatosis - etiology
Abstract
Haplotype analysis of the low density lipoprotein receptor (LDLR) gene was performed in Norwegian subjects heterozygous for familial hypercholesterolemia (FH). Southern blot analysis of genomic DNA, using an exon 18 specific probe and the restriction enzyme NcoI, showed that two out of 57 unrelated FH subjects had an abnormal 3.6 kb band. Further analyses revealed that this abnormal band was due to a 9.6 kb deletion that included exons 16 and 17. The 5' deletion breakpoint was after 245 bp of intron 15, and the 3' deletion breakpoint was in exon 18 after nucleotide 3390 of cDNA. Thus, both the membrane-spanning and cytoplasmatic domains of the receptor had been deleted. A polymerase chain reaction (PCR) method was developed to identify this deletion among other Norwegian FH subjects. As a result of this screening one additional subject was found out of 124 subjects screened. Thus, three out of 181 (1.7%) unrelated Norwegian FH subject possessed this deletion. The deletion was found on the same haplotype in the three unrelated subjects, suggesting a common mutagenic event. The deletion is identical to a deletion (FH-Helsinki) that is very common among Finnish FH subjects. However, it is not yet known whether the mutations evolved separately in the two countries.
PubMed ID
1362925 View in PubMed
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50bp deletion in the promoter for superoxide dismutase 1 (SOD1) reduces SOD1 expression in vitro and may correlate with increased age of onset of sporadic amyotrophic lateral sclerosis.

https://arctichealth.org/en/permalink/ahliterature156293
Source
Amyotroph Lateral Scler. 2008 Aug;9(4):229-37
Publication Type
Article
Date
Aug-2008
Author
Wendy J Broom
Matthew Greenway
Ghazaleh Sadri-Vakili
Carsten Russ
Kristen E Auwarter
Kelly E Glajch
Nicolas Dupre
Robert J Swingler
Shaun Purcell
Caroline Hayward
Peter C Sapp
Diane McKenna-Yasek
Paul N Valdmanis
Jean-Pierre Bouchard
Vincent Meininger
Betsy A Hosler
Jonathan D Glass
Meraida Polack
Guy A Rouleau
Jang-Ho J Cha
Orla Hardiman
Robert H Brown
Author Affiliation
Day Neuromuscular Research Laboratory, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA. wendy.broom@gmail.com
Source
Amyotroph Lateral Scler. 2008 Aug;9(4):229-37
Date
Aug-2008
Language
English
Publication Type
Article
Keywords
Age of Onset
Amyotrophic Lateral Sclerosis - enzymology - epidemiology - genetics
Base Sequence
DNA Mutational Analysis
Female
Gene Expression
Genetic Predisposition to Disease
Genotype
Homozygote
Humans
Ireland - epidemiology
Male
Middle Aged
Phenotype
Polymorphism, Genetic
Promoter Regions, Genetic
Quebec - epidemiology
Risk factors
Scotland - epidemiology
Sequence Deletion
Sp1 Transcription Factor - metabolism
Superoxide Dismutase - genetics - metabolism
United States - epidemiology
Abstract
The objective was to test the hypothesis that a described association between homozygosity for a 50bp deletion in the SOD1 promoter 1684bp upstream of the SOD1 ATG and an increased age of onset in SALS can be replicated in additional SALS and control sample sets from other populations. Our second objective was to examine whether this deletion attenuates expression of the SOD1 gene. Genomic DNA from more than 1200 SALS cases from Ireland, Scotland, Quebec and the USA was genotyped for the 50bp SOD1 promoter deletion. Reporter gene expression analysis, electrophoretic mobility shift assays and chromatin immunoprecipitation studies were utilized to examine the functional effects of the deletion. The genetic association for homozygosity for the promoter deletion with an increased age of symptom onset was confirmed overall in this further study (p=0.032), although it was only statistically significant in the Irish subset, and remained highly significant in the combined set of all cohorts (p=0.001). Functional studies demonstrated that this polymorphism reduces the activity of the SOD1 promoter by approximately 50%. In addition we revealed that the transcription factor SP1 binds within the 50bp deletion region in vitro and in vivo. Our findings suggest the hypothesis that this deletion reduces expression of the SOD1 gene and that levels of the SOD1 protein may modify the phenotype of SALS within selected populations.
PubMed ID
18608091 View in PubMed
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70 K type IV collagenase (gelatinase).

https://arctichealth.org/en/permalink/ahliterature24598
Source
Matrix Suppl. 1992;1:45-50
Publication Type
Article
Date
1992
Author
K. Tryggvason
P. Huhtala
M. Höyhtya
E. Hujanen
T. Hurskainen
Author Affiliation
Biocenter, University of Oulu, Finland.
Source
Matrix Suppl. 1992;1:45-50
Date
1992
Language
English
Publication Type
Article
Keywords
Amino Acid Sequence
Animals
Base Sequence
Basement Membrane - metabolism
Collagenases - chemistry - genetics - immunology - physiology
Gelatinase B
Genes
Humans
Molecular Sequence Data
Molecular Weight
Neoplasm Invasiveness
Neoplasm Proteins - physiology
Rabbits
Rats
Research Support, Non-U.S. Gov't
Sequence Alignment
Substrate Specificity
Abstract
Type IV collagenase (gelatinase) is a 70,000 dalton neutral metalloproteinase that specifically cleaves type IV collagen in addition to degrading denatured collagen (gelatin). It is secreted in a latent proenzyme form that is converted proteolytically in the extracellular space to a 62,000 dalton active enzyme. The primary structure, enzymatic properties as well as gene structure, demonstrate that type IV collagenase is closely related with the other well characterized metalloproteinases, interstitial collagenase and stromelysin. However, the structure of type IV collagenase differs from the others in that it is larger and contains three internal repeats that resemble the type II domains of fibronectin. Also, initial characterization of the promoter region of the gene indicates that its regulation differs from the other proteinase genes. Type IV collagenase is presumably required for the normal turnover of basement membranes. Augmented activity is linked with the invasive potential of tumor cells and the enzyme is believed to play a major role in the penetration of basement membranes by metastatic cells. Measurements of enzyme activity and mRNA levels as well as immunostaining of a variety of tumor cells and tissues suggest that assays for the enzyme may have value in the follow-up of malignant growth.
PubMed ID
1480085 View in PubMed
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657del5 mutation in the gene for Nijmegen breakage syndrome (NBS1) in a cohort of Russian children with lymphoid tissue malignancies and controls.

https://arctichealth.org/en/permalink/ahliterature184730
Source
Am J Med Genet A. 2003 Jul 15;120A(2):174-9
Publication Type
Article
Date
Jul-15-2003
Author
Igor B Resnick
Irina Kondratenko
Eugeni Pashanov
Alexey A Maschan
Alexander Karachunsky
Oleg Togoev
Andrey Timakov
Alexander Polyakov
Svetlana Tverskaya
Oleg Evgrafov
Alexander G Roumiantsev
Author Affiliation
Department of Immunology, Research Institute for Paediatric Hematology, Moscow, Russia. gashka@hadassah.org.il
Source
Am J Med Genet A. 2003 Jul 15;120A(2):174-9
Date
Jul-15-2003
Language
English
Publication Type
Article
Keywords
Base Sequence
Child
Child, Preschool
Chromosome Breakage - genetics
Chromosomes, Human, Pair 8
Cohort Studies
Genetic Predisposition to Disease
Genetic Testing
Heterozygote
Humans
Loss of Heterozygosity
Lymphoma, Non-Hodgkin - genetics - pathology
Lymphoproliferative Disorders - genetics - pathology
Male
Mutation
Pedigree
Pilot Projects
Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics - pathology
Russia
Sequence Deletion
Syndrome
Abstract
Nijmegen breakage syndrome (NBS, OMIM 251260) is a rare hereditary disease, characterized by immune deficiency, microcephaly, and an extremely high incidence of lymphoid tissue malignancies. The gene mutated in NBS, NBS1, was recently cloned from its location on chromosome 8q21. The encoded protein, nibrin (p95), together with hMre11 and hRad50, is involved in the double-strand DNA break repair system. We screened two Russian cohorts for the 657del5 NBS1 mutation and found no carriers in 548 controls and two carriers in 68 patients with lymphoid malignancies: one with acute lymphoblastic leukemia (ALL) and one with non-Hodgkin lymphoma (NHL). Several relatives of the second patient, who were carriers of the same mutation, had cancer (ALL, breast cancer, GI cancers). These preliminary data suggest that NBS1 mutation carriers can be predisposed to malignant disorders.
PubMed ID
12833396 View in PubMed
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The ABCA4 2588G>C Stargardt mutation: single origin and increasing frequency from South-West to North-East Europe.

https://arctichealth.org/en/permalink/ahliterature50771
Source
Eur J Hum Genet. 2002 Mar;10(3):197-203
Publication Type
Article
Date
Mar-2002
Author
Alessandra Maugeri
Kris Flothmann
Nadine Hemmrich
Sofie Ingvast
Paula Jorge
Eva Paloma
Reshma Patel
Jean-Michel Rozet
Jaana Tammur
Francesco Testa
Susana Balcells
Alan C Bird
Han G Brunner
Carel B Hoyng
Andres Metspalu
Francesca Simonelli
Rando Allikmets
Shomi S Bhattacharya
Michele D'Urso
Roser Gonzàlez-Duarte
Josseline Kaplan
Gerard J te Meerman
Rosário Santos
Marianne Schwartz
Guy Van Camp
Claes Wadelius
Bernhard H F Weber
Frans P M Cremers
Author Affiliation
Department of Human Genetics, University Medical Center Nijmegen, Nijmegen, The Netherlands. a.maugeri@antrg.azn.nl
Source
Eur J Hum Genet. 2002 Mar;10(3):197-203
Date
Mar-2002
Language
English
Publication Type
Article
Keywords
ATP-Binding Cassette Transporters - genetics
Alleles
Base Sequence
Europe
Gene Frequency
Heterozygote
Humans
Molecular Sequence Data
Mutation
Point Mutation
Research Support, Non-U.S. Gov't
United States
Abstract
Inherited retinal dystrophies represent the most important cause of vision impairment in adolescence, affecting approximately 1 out of 3000 individuals. Mutations of the photoreceptor-specific gene ABCA4 (ABCR) are a common cause of retinal dystrophy. A number of mutations have been repeatedly reported for this gene, notably the 2588G>C mutation which is frequent in both patients and controls. Here we ascertained the frequency of the 2588G>C mutation in a total of 2343 unrelated random control individuals from 11 European countries and 241 control individuals from the US, as well as in 614 patients with STGD both from Europe and the US. We found an overall carrier frequency of 1 out of 54 in Europe, compared with 1 out of 121 in the US, confirming that the 2588G>C ABCA4 mutation is one of the most frequent autosomal recessive mutations in the European population. Carrier frequencies show an increasing gradient in Europe from South-West to North-East. The lowest carrier frequency, 0 out of 199 (0%), was found in Portugal; the highest, 11 out of 197 (5.5%), was found in Sweden. Haplotype analysis in 16 families segregating the 2588G>C mutation showed four intragenic polymorphisms invariably present in all 16 disease chromosomes and sharing of the same allele for several markers flanking the ABCA4 locus in most of the disease chromosomes. These results indicate a single origin of the 2588G>C mutation which, to our best estimate, occurred between 2400 and 3000 years ago.
PubMed ID
11973624 View in PubMed
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Absence of RAS and p53 mutations in thyroid carcinomas of children after Chernobyl in contrast to adult thyroid tumours.

https://arctichealth.org/en/permalink/ahliterature21720
Source
Br J Cancer. 1998 Mar;77(6):952-5
Publication Type
Article
Date
Mar-1998
Author
B. Suchy
V. Waldmann
S. Klugbauer
H M Rabes
Author Affiliation
Institute of Pathology, University of Munich, Germany.
Source
Br J Cancer. 1998 Mar;77(6):952-5
Date
Mar-1998
Language
English
Publication Type
Article
Keywords
Accidents, Radiation
Adult
Age Factors
Base Sequence
Byelarus
Child
Exons
Gene Rearrangement
Genes, Regulator
Genes, p53
Genes, ras
Humans
Mutagenesis
Neoplasms, Radiation-Induced - etiology - genetics
Polymerase Chain Reaction
Polymorphism, Single-Stranded Conformational
Radioactive fallout
Research Support, Non-U.S. Gov't
Thyroid Neoplasms - etiology - genetics
Ukraine
Abstract
Thyroid carcinomas of an additional series of 34 children exposed to radioactive fall-out after the Chernobyl reactor accident were analysed for mutations in the H-, K- and N-RAS and the p53 gene. Allele-specific oligonucleotide hybridization, single-strand conformation polymorphism (SSCP) and direct sequencing did not disclose mutations in codons 12, 13 and 61 of RAS genes nor mutations in exons 5, 7 and 8 of p53. Considering the recently reported high prevalence of RET rearrangements of the PTC3 type in childhood tumours after Chernobyl (Klugbauer et al, 1995, Oncogene 11: 2459-2467), it follows that RET rearrangements are the most relevant molecular aberration in these radiation-induced tumours. RAS or p53 mutations do not play a role in childhood thyroid carcinogenesis after Chernobyl.
PubMed ID
9528840 View in PubMed
Less detail

Absence of the Asian-specific region V mitochondrial marker in Native Beringians.

https://arctichealth.org/en/permalink/ahliterature224068
Source
Am J Hum Genet. 1992 Apr;50(4):758-65
Publication Type
Article
Date
Apr-1992
Author
G F Shields
K. Hecker
M I Voevoda
J K Reed
Author Affiliation
Institute of Arctic Biology, University of Alaska, Fairbanks.
Source
Am J Hum Genet. 1992 Apr;50(4):758-65
Date
Apr-1992
Language
English
Publication Type
Article
Keywords
Alaska - ethnology
Asia, Central - ethnology
Base Sequence
Chromosome Deletion
DNA Probes - diagnostic use
DNA, Mitochondrial - analysis - genetics
Far East - ethnology
Genetic Markers - genetics
Humans
Molecular Sequence Data
Polymerase Chain Reaction
USSR - ethnology
Abstract
The Asian-specific 9-bp deletion between the genes for mitochondrial cytochrome oxidase II and lysine transfer RNA has been used to trace aboriginal human movements out of Southeast Asia and into portions of the South Pacific. Although it has been used to estimate the number of independent lineages that occur in the New World, it has not been studied in native peoples of the Beringian region. Thus, we have used PCR to amplify and compare the lengths of DNA segments surrounding this deletion in native peoples of Beringia and the adjacent regions, as well as natives of the Altai Mountains of Southwestern Siberia. Of the 176 individuals analyzed here, the deletion was found in only 3 of 25 individuals from the Ust-Kan region of the Altai Mountains. We comment on the distribution of this marker and on potential relationships between Beringians and other Native American groups in which this marker has been surveyed. One Chukchi possessed three copies of the 9-bp sequence, which suggests (1) that the number of copies of this sequence in humans may be more variable than had been believed and (2) that a mechanism of replication based on tandem duplication may be a potential explanation for the origin of this length mutation in humans.
Notes
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PubMed ID
1550120 View in PubMed
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Acceptable protective efficacy of influenza vaccination in young military conscripts under circumstances of incomplete antigenic and genetic match.

https://arctichealth.org/en/permalink/ahliterature194986
Source
Vaccine. 2001 Apr 30;19(23-24):3253-60
Publication Type
Article
Date
Apr-30-2001
Author
R. Pyhälä
M. Haanpää
M. Kleemola
R. Tervahauta
R. Visakorpi
L. Kinnunen
Author Affiliation
National Public Health Institute, Helsinki, Finland. reijo.pyhala@ktl.fi
Source
Vaccine. 2001 Apr 30;19(23-24):3253-60
Date
Apr-30-2001
Language
English
Publication Type
Article
Keywords
Adult
Amino Acid Sequence
Antibodies, Viral - blood
Antigens, Viral - genetics
Base Sequence
DNA Primers - genetics
Disease Outbreaks
Finland - epidemiology
Genes, Viral
Humans
Influenza A virus - genetics - immunology - isolation & purification
Influenza Vaccines - genetics - immunology - pharmacology
Influenza, Human - epidemiology - immunology - prevention & control - virology
Male
Military Personnel
Molecular Sequence Data
Phylogeny
Abstract
Commercial inactivated parenteral influenza vaccines reduced febrile (> or = 38 degrees C) respiratory illness by 53% (95% CL: 41-63%) during a 3 week outbreak in 1998 when A/Sydney/5/97(H3N2)-like influenza viruses were shown to be the predominant etiological agents and an older antigenic variant, A/Nanchang/933/95, served as the vaccine virus. The calculatory efficacy for preventing virologically diagnosed influenza infections was 57% (95% CL: 40-68%). The study population consisted of 1374 young male military conscripts. Vaccination coverage on a voluntary basis was 67%. Vaccination was ineffective in preventing febrile illness during a second epidemic wave lasting 2 weeks when mainly adenoviruses were shown to have been circulating in the garrison. Out of the 36 nasopharyngeal aspirates positive for influenza A by antigen detection, 18 A/Sydney/5/97-like strains (10 from non-vaccinated and eight from vaccinated subjects) and two A/Nanchang/933/95-like strains (both from non-vaccinated subjects) were isolated in MDCK cell cultures. Intraepidemic variation was detected among the A/Sydney/5/97-like field strains in their HA1 sequences and reactivity in HI tests, but no evidence was obtained that this variation would have been of significance to the virus in breaking through the vaccination-induced immunity.
PubMed ID
11312022 View in PubMed
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Activated protein C resistance caused by a common factor V mutation has a single origin.

https://arctichealth.org/en/permalink/ahliterature209414
Source
Thromb Res. 1997 Feb 1;85(3):237-43
Publication Type
Article
Date
Feb-1-1997
Author
B. Zöller
A. Hillarp
B. Dahlbäck
Author Affiliation
Department of Clinical Chemistry, Lund University, University Hospital, Malmö, Sweden.
Source
Thromb Res. 1997 Feb 1;85(3):237-43
Date
Feb-1-1997
Language
English
Publication Type
Article
Keywords
Adult
Aged
Base Sequence
Exons
Factor V - genetics
Female
Genotype
Humans
Male
Middle Aged
Molecular Sequence Data
Point Mutation
Protein C - genetics - metabolism
Restriction Mapping
Sweden
Abstract
A point mutation (FV:R506Q) in the human coagulation factor V gene is associated with resistance to activated protein C and life-long increased risk of venous thrombosis. The mutation is common in populations of Caucasian origin but virtually absent among other populations. In this study of 140 healthy Swedish volunteers and 110 homozygotes for the FV:R506Q mutation, we determined the allele frequencies of the FV:R506Q mutation and four other dimorphisms, C/T at nucleotide positions 2298 and 2325, and A/G at nucleotide positions 2379 and 2391. Manifest linkage disequilibrium was found between the FV:R506Q mutation and the four different dimorphisms. The finding of a single FV:R506Q haplotype in all homozygotes constitutes strong evidence of a common ancestor of Swedish individuals with the FV:R506Q mutation.
PubMed ID
9058498 View in PubMed
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Active Microbial Communities Inhabit Sulphate-Methane Interphase in Deep Bedrock Fracture Fluids in Olkiluoto, Finland.

https://arctichealth.org/en/permalink/ahliterature274433
Source
Biomed Res Int. 2015;2015:979530
Publication Type
Article
Date
2015
Author
Malin Bomberg
Mari Nyyssönen
Petteri Pitkänen
Anne Lehtinen
Merja Itävaara
Source
Biomed Res Int. 2015;2015:979530
Date
2015
Language
English
Publication Type
Article
Keywords
Bacteria - genetics - metabolism
Base Sequence
Ecosystem
Finland
Geologic Sediments - microbiology
Groundwater - microbiology
High-Throughput Nucleotide Sequencing
Methane - metabolism
Phylogeny
RNA, Messenger - genetics - metabolism
RNA, Ribosomal, 16S - genetics
Sulfates - metabolism
Abstract
Active microbial communities of deep crystalline bedrock fracture water were investigated from seven different boreholes in Olkiluoto (Western Finland) using bacterial and archaeal 16S rRNA, dsrB, and mcrA gene transcript targeted 454 pyrosequencing. Over a depth range of 296-798?m below ground surface the microbial communities changed according to depth, salinity gradient, and sulphate and methane concentrations. The highest bacterial diversity was observed in the sulphate-methane mixing zone (SMMZ) at 250-350?m depth, whereas archaeal diversity was highest in the lowest boundaries of the SMMZ. Sulphide-oxidizing e-proteobacteria (Sulfurimonas sp.) dominated in the SMMZ and ?-proteobacteria (Pseudomonas spp.) below the SMMZ. The active archaeal communities consisted mostly of ANME-2D and Thermoplasmatales groups, although Methermicoccaceae, Methanobacteriaceae, and Thermoplasmatales (SAGMEG, TMG) were more common at 415-559?m depth. Typical indicator microorganisms for sulphate-methane transition zones in marine sediments, such as ANME-1 archaea, a-, ß- and d-proteobacteria, JS1, Actinomycetes, Planctomycetes, Chloroflexi, and MBGB Crenarchaeota were detected at specific depths. DsrB genes were most numerous and most actively transcribed in the SMMZ while the mcrA gene concentration was highest in the deep methane rich groundwater. Our results demonstrate that active and highly diverse but sparse and stratified microbial communities inhabit the Fennoscandian deep bedrock ecosystems.
Notes
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PubMed ID
26425566 View in PubMed
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1169 records – page 1 of 117.