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Search Results: 1 - 10 of 5144 matches for " Susanne Krüger-Kjaer "
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Association between Common Germline Genetic Variation in 94 Candidate Genes or Regions and Risks of Invasive Epithelial Ovarian Cancer
Lydia Quaye, Jonathan Tyrer, Susan J. Ramus, Honglin Song, Eva Wozniak, Richard A. DiCioccio, Valerie McGuire, Estrid H?gdall, Claus H?gdall, Jan Blaakaer, Ellen L. Goode, Joellen M. Schildkraut, Douglas F. Easton, Susanne Krüger-Kjaer, Alice S. Whittemore, Simon A. Gayther, Paul D. P. Pharoah
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005983
Abstract: Background Recent studies have identified several single nucleotide polymorphisms (SNPs) in the population that are associated with variations in the risks of many different diseases including cancers such as breast, prostate and colorectal. For ovarian cancer, the known highly penetrant susceptibility genes (BRCA1 and BRCA2) are probably responsible for only 40% of the excess familial ovarian cancer risks, suggesting that other susceptibility genes of lower penetrance exist. Methods We have taken a candidate approach to identifying moderate risk susceptibility alleles for ovarian cancer. To date, we have genotyped 340 SNPs from 94 candidate genes or regions, in up to 1,491 invasive epithelial ovarian cancer cases and 3,145 unaffected controls from three different population based studies from the UK, Denmark and USA. Results After adjusting for population stratification by genomic control, 18 SNPs (5.3%) were significant at the 5% level, and 5 SNPs (1.5%) were significant at the 1% level. The most significant association was for the SNP rs2107425, located on chromosome 11p15.5, which has previously been identified as a susceptibility allele for breast cancer from a genome wide association study (P-trend = 0.0012). When SNPs/genes were stratified into 7 different pathways or groups of validation SNPs, the breast cancer associated SNPs were the only group of SNPs that were significantly associated with ovarian cancer risk (P-heterogeneity = 0.0003; P-trend = 0.0028; adjusted (for population stratification) P-trend = 0.006). We did not find statistically significant associations when the combined data for all SNPs were analysed using an admixture maximum likelihood (AML) experiment-wise test for association (P-heterogeneity = 0.051; P-trend = 0.068). Conclusion These data suggest that a proportion of the SNPs we evaluated were associated with ovarian cancer risk, but that the effect sizes were too small to detect associations with individual SNPs.
Predictors of human papillomavirus infection in women undergoing routine cervical cancer screening in Spain: the CLEOPATRE study
Esther Roura, Thomas Iftner, José Antonio Vidart, Susanne Krüger Kjaer, F Xavier Bosch, Nubia Mu?oz, Santiago Palacios, Maria San Martin Rodriguez, Carmen Morillo, Laurence Serradell, Laurence Torcel-Pagnon, Javier Cortes, Xavier Castellsagué, CLEOPATRE Spain Study Group
BMC Infectious Diseases , 2012, DOI: 10.1186/1471-2334-12-145
Abstract: The CLEOPATRE Spain study enrolled 3 261 women aged 18–65?years attending cervical cancer screening across the 17 Autonomous Communities. Liquid-based cervical samples underwent cytological examination and HPV testing. HPV positivity was determined using the Hybrid Capture II assay, and HPV genotyping was conducted using the INNO-LiPA HPV Genotyping Extra assay. Multivariate logistic regression was used to identify putative risk factors for HPV infection.A lifetime number of two or more sexual partners, young age (18–25?years), a history of genital warts, and unmarried status were the strongest independent risk factors for HPV infection of any type. Living in an urban community, country of birth other than Spain, low level of education, and current smoking status were also independent risk factors for HPV infection. A weak inverse association between condom use and HPV infection was observed. Unlike monogamous women, women with two or more lifetime sexual partners showed a lower risk of infection if their current partner was circumcised (P for interaction, 0.005) and a higher risk of infection if they were current smokers (P for interaction, 0.01).This is the first large-scale, country-wide study exploring risk factors for cervical HPV infection in Spain. The data strongly indicate that variables related to sexual behavior are the main risk factors for HPV infection. In addition, in non-monogamous women, circumcision of the partner is associated with a reduced risk and smoking with an increased risk of HPV infection.
The Survival Processing Memory Effect Should Generalise to Source Memory, but It Doesn’t  [PDF]
Arndt Br?der, Nelli Krüger, Susanne Schütte
Psychology (PSYCH) , 2011, DOI: 10.4236/psych.2011.29135
Abstract: Numerous studies have shown that words judged for their relvance to a scenario of survival are remembered better than words from lists processed differently. Survival processing is even more effective than many mnemonic techniques. This has been interpreted as an evolutionary design feature of memory. It is argued that such a survival effect should be even more pronounced in remembering the context or source of the information. Two experiments used a source monitoring paradigm. Both studies did not find any evidence for enhanced context memory, thus questioning the evolutionary account of the survival processing effect. An alternative interpretation is discussed.
Tagging Single Nucleotide Polymorphisms in the BRIP1 Gene and Susceptibility to Breast and Ovarian Cancer
Honglin Song, Susan J. Ramus, Susanne Krüger Kjaer, Estrid Hogdall, Richard A. DiCioccio, Alice S. Whittemore, Valerie McGuire, Claus Hogdall, Ian J. Jacobs, Douglas F. Easton, Bruce A.J. Ponder, Alison M. Dunning, Simon A. Gayther, Paul D.P. Pharoah
PLOS ONE , 2007, DOI: 10.1371/journal.pone.0000268
Abstract: Background BRIP1 interacts with BRCA1 and functions in regulating DNA double strand break repair pathways. Germline BRIP1 mutations are associated with breast cancer and Fanconi anemia. Thus, common variants in the BRIP1 are candidates for breast and ovarian cancer susceptibility. Methods We used a SNP tagging approach to evaluate the association between common variants (minor allele frequency≥0.05) in BRIP1 and the risks of breast cancer and invasive ovarian cancer. 12 tagging SNPs (tSNPs) in the gene were identified and genotyped in up to 2,270 breast cancer cases and 2,280 controls from the UK and up to 1,513 invasive ovarian cancer cases and 2,515 controls from the UK, Denmark and USA. Genotype frequencies in cases and controls were compared using logistic regression. Results Two tSNPs showed a marginal significant association with ovarian cancer: Carriers of the minor allele of rs2191249 were at reduced risk compared with the common homozygotes (Odds Ratio (OR) = 0.90 (95% CI, 0.82–1.0), P-trend = 0.045) and the minor allele of rs4988344 was associated with increased risk (OR = 1.15 (95%CI, 1.02–1.30), P-trend = 0.02). When the analyses were restricted to serous ovarian cancers, these effects became slightly stronger. These results were not significant at the 5% level after adjusting for multiple testing. None of the tSNPs was associated with breast cancer. Conclusions It is unlikely that common variants in BRIP1 contribute significantly to breast cancer susceptibility. The possible association of rs2191249 and rs4988344 with ovarian cancer risks warrant confirmation in independent case-control studies.
Molecular Diagnostics, Targeted Therapy, and the Indication for Allogeneic Stem Cell Transplantation in Acute Lymphoblastic Leukemia
Anthony Oyekunle,Torsten Haferlach,Nicolaus Krger,Evgeny Klyuchnikov,Axel Rolf Zander,Susanne Schnittger,Ulrike Bacher
Advances in Hematology , 2011, DOI: 10.1155/2011/154745
Abstract: In recent years, the panel of known molecular mutations in acute lymphoblastic leukemia (ALL) has been continuously increased. In Philadelphia-positive ALL, deletions of the IKZF1 gene were identified as prognostically adverse factors. These improved insights in the molecular background and the clinical heterogeneity of distinct cytogenetic subgroups may allow most differentiated therapeutic decisions, for example, with respect to the indication to allogeneic HSCT within genetically defined ALL subtypes. Quantitative real-time PCR allows highly sensitive monitoring of the minimal residual disease (MRD) load, either based on reciprocal gene fusions or immune gene rearrangements. Molecular diagnostics provided the basis for targeted therapy concepts, for example, combining the tyrosine kinase inhibitor imatinib with chemotherapy in patients with Philadelphia-positive ALL. Screening for BCR-ABL1 mutations in Philadelphia-positive ALL allows to identify patients who may benefit from second-generation tyrosine kinase inhibitors or from novel compounds targeting the T315I mutation. Considering the central role of the molecular techniques for the management of patients with ALL, efforts should be made to facilitate and harmonize immunophenotyping, cytogenetics, and molecular mutation screening. Furthermore, the potential of high-throughput sequencing should be evaluated for diagnosis and follow-up of patients with B-lineage ALL. 1. Introduction Acute lymphoblastic leukemia (ALL) is a heterogeneous disorder, which consists of various clinical, morphological, and immunological phenotypes, underpinned by extreme genetic diversity [2–4]. Adaptation of treatment intensity to the probability of relapse in the individual patient requires a thorough understanding of the risks represented by the various stratified leukemia subtypes. This has been achieved, to a large extent, using a broad spectrum of diagnostic techniques including cytomorphology, immunophenotyping, cytogenetics, fluorescence in situ hybridization (FISH), and molecular techniques. The panel of known prognostically important molecular alterations is constantly increasing, as demonstrated by the recent detection of alterations of TGF-beta and PI3K-AKT pathway genes and prognostically adverse deletions at 6q15-16 in T-ALL [5]. In Philadelphia-positive (B-lineage) ALL, deletions of the IKZF1 gene confer a more adverse prognosis [6, 7]. Genetic alterations are now detectable in most ALL patients, when cytogenetic and molecular techniques are combined. These genetic alterations are linked to distinct
Constraining Forces Causing the Meissner Effect  [PDF]
Ekkehard Krüger
Journal of Modern Physics (JMP) , 2017, DOI: 10.4236/jmp.2017.88074
Abstract: As shown in former papers, the nonadiabatic Heisenberg model presents a novel mechanism of Cooper pair formation which is not the result of an attractive electron-electron interaction but can be described in terms of quantum mechanical constraining forces. This mechanism operates in narrow, roughly half-filled superconducting bands of special symmetry and is evidently responsible for the formation of Cooper pairs in all superconductors. Here we consider this new mechanism within an outer magnetic field. We show that in the magnetic field the constraining forces produce Cooper pairs of non-vanishing total momentum with the consequence that an electric current flows within the superconductor. This current satisfies the London equations and, consequently, leads to the Meissner effect. This theoretical result is confirmed by the experimental observation that all superconductors, whether conventional or unconventional, exhibit the Meissner effect.
Mast Cells: The Key to Multiple Sclerosis?  [PDF]
Per G?ran Krüger
World Journal of Neuroscience (WJNS) , 2014, DOI: 10.4236/wjns.2014.42014
Abstract:

Mast cells are present in high numbers in the border-zones of the multiple sclerosis-plaques. They are located in small clusters along capillaries and venules, and they are more abundant in females than in men. Mast cells can be stimulated to release specific mediators such as histamine, resulting in oedema formation, as well as proteases that may cause demyelination, by several different activation mechanisms. We hypothesize that a putative mast cell activation may be induced by diet factor(s) as well as long lasting mental stress that may lead to the release of catestatin, as well as ACTH released from the pituitary gland. Given a natural flux of mast cell recovery and activation, a putative phenomenon of massive release of mediators and “silent” reload periods may explain the relapsing-remitting phases of multiple sclerosis.

Investigation of the Hyperfine Structure of Atomic Niobium (Nb I) Spectral Lines Based on the Lower Energy Levels at 22936, 23010, and 23048 cm-1  [PDF]
L. Windholz, S. Krger
Spectral Analysis Review (SAR) , 2018, DOI: 10.4236/sar.2018.62004
Abstract: The hyperfine (hf) structure constants of three atomic niobium energy levels in the energy range around 23000 cm-1 (at 22936.90, 23010.58, and 23048.58 cm-1) are known with only limited accuracy, and the constants of combining levels are sometimes even unknown. Thus we performed laser spectroscopic investigations in the wavelength range between 5600 and 6500 Å, and we excited altogether 16 transitions in which these lower levels are involved. Beside a more precise determination of the hf structure constants of the three lower levels (which were determined on several lines sharing a common upper level), these experiments led to the knowledge of the hf constants of nine levels with previously unknown constants. Beside these results, also the hf constants of 13 further energy levels are reported. For six of these levels, the constants were previously unknown.
Multiple Sclerosis: A Mast Cell Mediated Psycho-Somatic Disease?  [PDF]
Per G?ran Krüger
World Journal of Neuroscience (WJNS) , 2018, DOI: 10.4236/wjns.2018.84035
Abstract: This paper reviews evidence that the presence of mast cells in specific sites of central nervous system, suggesting inflammatory processes, may explain all the symptoms observed in multiple sclerosis. This hypothesis would be relatively easy to test.
LRRK2 in Parkinson's disease – drawing the curtain of penetrance: a commentary
Rejko Krüger
BMC Medicine , 2008, DOI: 10.1186/1741-7015-6-33
Abstract: Parkinson's disease (PD) is the most common neurodegenerative movement disorder, and has been regarded as a prototypic non-genetic disorder for a long time. First insight into the genetic contribution to the typical Parkinsonian phenotype came from large families with classical Mendelian inheritance of the disease trait. The discovery of disease-causing mutations in the alpha-synuclein gene for autosomal dominant forms and in the Parkin, PINK1 and DJ-1 gene for autosomal recessive forms of PD allowed a first insight into the molecular mechanisms that mediate neurodegeneration in PD. Heterozygous mutations in the alpha-synuclein gene and homozygous mutations in the Parkin, PINK1 and DJ-1 gene show, in general, full penetrance and account for less than 1% of all PD cases [1]. Thus, due to the small proportion of PD patients that carried mutations in the respective genes, genetic testing and counselling of presymptomatic mutation carriers was not relevant and common recommendations limited molecular testing to symptomatic individuals. These premises have now changed due to the identification and characterization of mutations in the LRRK2 gene in PD [2,3].Mutations in the LRRK2 gene encoding the leucine-rich, repeat kinase 2 protein are the most frequent genetic cause of PD known to date. Clinicogenetic studies clearly showed that the majority of all LRRK2 mutation carriers present with symptoms indistinguishable from idiopathic PD [4-7]. To date, more than 50 variants are known, but only about 10% have been proven pathogenic and account for approximately 2% of sporadic and 10% of familial PD cases [4,8,9]. Initially identified in large families with autosomal dominant inheritance of PD, it turned out that mutations in the LRRK2 gene were also found in patients with the sporadic form of the disease (without positive family history). Among these mutations, a glycine to serine exchange in position 2019 of the peptide sequence (G2019S) is the most frequent worldwide with f
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