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Search Results: 1 - 10 of 401323 matches for " Roden M "
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Hypertonie und Sekund r-/Terti rpr vention bei Diabetes
Roden M,Pfeiler G
Journal für Hypertonie , 2005,
Abstract: Mindestens 20 60 % aller Diabetiker leiden an Hypertonie. Hypertensive Diabetiker weisen gegenüber normotensiven Diabetikern ein erh htes Risiko auf, kardiovaskul re Ereignisse zu erleiden bzw. an einem solchen zu versterben. Randomisierte kontrollierte Untersuchungen zeigen, da intensive Blutdruck-Einstellung und -Kontrolle dieses erh hte Risiko in diabetischen Kollektiven senken k nnen. Gro angelegte klinische Studien, wie LIFE, ALLHAT, NORDIL, UKPDS or MICRO-HOPE, haben verschiedene Medikamentengruppen in ihrer antihypertensiven als auch risikoreduzierenden Wirksamkeit bezogen auf mikro- und makrovaskul re Folgen bei hypertensiven Diabetikern untersucht. Die vorliegende übersicht vergleicht Studien seit 1985 bezüglich der Bedeutung der Blutdruckkontrolle in der Sekund r- und Terti rpr vention bei hypertensiven Diabetikern.
Mechanisms by which circadian rhythm disruption may lead to cancer
M. Beckett,L. C. Roden
South African Journal of Science , 2010, DOI: 10.4102/sajs.v105i11/12.125
Abstract: Humans have evolved in a rhythmic environment and display daily (circadian) rhythms in physiology, metabolism and behaviour that are in synchrony with the solar day. Modern lifestyles have compromised the exposure to bright light during the day and dark nights, resulting in the desynchronisation of endogenously generated circadian rhythms from the external environment and loss of coordination between rhythms within the body. This has detrimental effects on physical and mental health, due to the misregulation and uncoupling of important cellular and physiological processes. Long-term shift workers who are exposed to bright light at night experience the greatest disruption of their circadian rhythms. Studies have shown an association between exposure to light at night, circadian rhythm disruption and an increased risk of cancer. Previous reviews have explored the relevance of light and melatonin in cancer, but here we explore the correlation of circadian rhythm disruption and cancer in terms of molecular mechanisms affecting circadian gene expression and melatonin secretion.
Molecular cloning and analysis of zebrafish voltage-gated sodium channel beta subunit genes: implications for the evolution of electrical signaling in vertebrates
Sameer S Chopra, Hiroshi Watanabe, Tao P Zhong, Dan M Roden
BMC Evolutionary Biology , 2007, DOI: 10.1186/1471-2148-7-113
Abstract: We identified and cloned single zebrafish gene homologs for beta1-beta3 (zbeta1-zbeta3) and duplicate genes for beta4 (zbeta4.1, zbeta4.2). Sodium channel beta subunit loci are similarly organized in fish and mammalian genomes. Unlike their mammalian counterparts, zbeta1 and zbeta2 subunit genes display extensive alternative splicing. Zebrafish beta subunit genes and their splice variants are differentially-expressed in excitable tissues, indicating tissue-specific regulation of zbeta1-4 expression and splicing. Co-expression of the genes encoding zbeta1 and the zebrafish sodium channel alpha subunit Nav1.5 in Chinese Hamster Ovary cells increased sodium current and altered channel gating, demonstrating functional interactions between zebrafish alpha and beta subunits. Analysis of the synteny and phylogeny of mammalian, teleost, amphibian, and avian beta subunit and related genes indicated that all extant vertebrate beta subunits are orthologous, that beta2/beta4 and beta1/beta3 share common ancestry, and that beta subunits are closely related to other proteins sharing the V-type immunoglobulin domain structure. Vertebrate sodium channel beta subunit genes were not identified in the genomes of invertebrate chordates and are unrelated to known subunits of the para sodium channel in Drosophila.The identification of conserved orthologs to all 4 voltage-gated sodium channel beta subunit genes in zebrafish and the lack of evidence for beta subunit genes in invertebrate chordates together indicate that this gene family emerged early in vertebrate evolution, prior to the divergence of teleosts and tetrapods. The evolutionary history of sodium channel beta subunits suggests that these genes may have played a key role in the diversification and specialization of electrical signaling in early vertebrates.Coordinated electrical signals in the metazoan nervous system, heart, and skeletal muscle depend on the generation of action potentials, rapid changes in membrane potential m
Role of L2 cysteines in papillomavirus infection and neutralization
Ratish Gambhira, Subhashini Jagu, Balasubramanyam Karanam, Patricia M Day, Richard Roden
Virology Journal , 2009, DOI: 10.1186/1743-422x-6-176
Abstract: Papillomavirus infection requires cleavage of minor capsid protein L2 by furin [1]. Mature virions in solution are resistant to furin cleavage and RG-1 binding [2-4]. The binding of virions to cell surfaces, presumably via heparan sulfate proteoglycans [5], promotes furin cleavage of L2, and this can occur on the cell surface. Furin cleavage triggers a conformational change that improves the accessibility of L2 on the capsid surface and its recognition by RG-1 [4]. RG-1 recognizes L2 residues 17-36 [2], and vaccination with this peptide in the appropriate context triggers high titers of neutralizing antibodies and protection against experimental challenge with homologous as well as heterologous virus types [6]. The cross-protective nature of this L2 epitope is consistent with its high degree of sequence conservation among diverse papillomavirus genotypes, and may reflect evolutionary constraints due to critical biological functions within this region [7]. Therefore, we sought to identify L2 residues critical to papillomavirus biology by deletion and alanine scanning mutagenesis within the epitope defined by RG-1. The role of L2 in infection is conserved in diverse papillomavirus types [8], but here we focus upon HPV16 because it is associated with a half of cervical cancer cases and the majority of HPV+vaginal, vulval, penile, anal, and head and neck cancers [9].Sequences of the codon-modified HPV16 L2 gene within the region encoding the RG-1 epitope were deleted to generate the Δ17-30 and Δ23-36 deletion mutants [10]. As controls, two additional deletion mutants Δ353-362 and Δ393-403 were prepared with similarly sized deletions introduced at the C-terminus of HPV16 L2. The four deletion mutants or wild type HPV16 L2 were co-transfected into 293TT cells with an HPV16 L1 expression vector [10] and the SEAP reporter plasmid [11,12]. Three days later the cells were harvested and detergent lysates were treated with benzonase to remove unencapsidated DNA. HPV16 pseudovir
Comparison of Antigenic Regions Identified on IgG1Fc Using Bioinformatics vs Pepscan Analysis
Paul N. Nelson,Olwyn M.R. Westwood,Graham Freimanis,Denise Roden
Clinical Medicine : Arthritis and Musculoskeletal Disorders , 2008,
Abstract: Epitope mapping allowed the location of antigenic determinants on a protein macromolecule to be identified. In particular, pepscan techniques that utilize a series of overlapping peptides, help detect key amino acid residues that are important in antibody recognition and binding. In a previous study, we employed 15-mer peptides spanning the entire length of IgG1Fc to ascertain successfully the target epitopes of isotypic/allotypic monoclonal reagents. As an extension to this work we have used these peptides to evaluate the location of epitope targets of five IgM rheumatoid factor antibodies (RFAbs). Overall, 2 antibodies, RFAb TS2 and TS1, detected a similar epitope within the CH3 domain (360-KNQVSLTCLVKGFYP-374), whilst 1 (RFAb SJ1) recognised an epitope in the CH2 domain (294- EQYNSTYRVVSVLTV-308). In contrast, 2 RFAbs, PRSJ2 and PRTS1 detected four and five epitopes respectively within the Fc region. RFAb PRSJ2 recognised epitopes detected by RFAB TS2 and TS1 but also further epitopes in the CH2 domain (256-TPEVTCVVVDVSHED-270) and CH3 domain (418-QQGNVFSCSVMHEAL-432). Similarly, RFAb PRTS1 detected all four epitopes plus a fifth in the CH3 domain (382-ESNGQPENNYKTTPP-396). In essence there was a consensus of target epitopes identified by these rheumatoid factor antibodies. Interestingly, two epitopes (256–270, CH2 domain and 360–374, CH3 domain) were novel in that they had not been identified in previous pepscan studies. The other epitopes recognised, either overlapped or were immediately adjacent to previous epitopes detected by poly/monoclonal rheumatoid factor antibodies. Molecular modelling (PCImdad) of IgG1Fc showed that all five epitopes were exposed and surface accessible for antibody interaction. In addition, a bioinformatics analysis of the Fc region using ExPASy was employed to identify key antigenic determinants. This ‘in silico’ approach may provide a means of determining key regions without the need to develop overlapping peptides spanning the entire length of a macromolecule.
The Pathology of Lung Allograft Rejection: A Concise Review
Anja Roden,Henry Tazelaar
Turk Toraks Dergisi , 2012,
Abstract: Lung transplantations in humans have been performed for almost 50 years. However, allograft rejection, non-rejection diseases such as harvest/reperfusion injury, infection, drug toxicity, post-transplant lymphoproliferative diseases, and recurrent disease are still significant complications. Although the clinical impression might suggest the possibility of any of these conditions, tissue diagnosis is usually necessary to establish a definitive diagnosis. This article mainly focuses on reviewing the morphological features of lung allograft rejection and its grading according to the revised 2007 ISHLT consensus classification of allograft rejection. Acute and chronic alloreactive injuries affect both the vasculature and the airways. Currently, the guidelines of the 2007 ISHLT consensus conference are used for the histolopathologic assessment of rejection. Although antibody mediated rejection is recognized in heart and kidney transplants, at present, there is no consensus about its diagnosis in transplanted lungs. Mimickers of rejection and post-transplant diseases will also be discussed. The collaboration between the transplant clinician and pathologist cannot be overemphasized to establish an optimal treatment for the individual patient following lung transplantation.
Comparison of Antigenic Regions Identified on IgG1Fc Using Bioinformatics vs Pepscan Analysis
Paul N. Nelson, Olwyn M.R. Westwood, Graham Freimanis, Denise Roden, Samir Sissaoui, Paul Rylance and Frank C. Hay
Clinical Medicine Insights: Arthritis and Musculoskeletal Disorders , 2012,
Abstract: Epitope mapping allowed the location of antigenic determinants on a protein macromolecule to be identified. In particular, pepscan techniques that utilize a series of overlapping peptides, help detect key amino acid residues that are important in antibody recognition and binding. In a previous study, we employed 15-mer peptides spanning the entire length of IgG1Fc to ascertain successfully the target epitopes of isotypic/allotypic monoclonal reagents. As an extension to this work we have used these peptides to evaluate the location of epitope targets of five IgM rheumatoid factor antibodies (RFAbs). Overall, 2 antibodies, RFAb TS2 and TS1, detected a similar epitope within the CH3 domain (360-KNQVSLTCLVKGFYP-374), whilst 1 (RFAb SJ1) recognised an epitope in the CH2 domain (294- EQYNSTYRVVSVLTV-308). In contrast, 2 RFAbs, PRSJ2 and PRTS1 detected four and five epitopes respectively within the Fc region. RFAb PRSJ2 recognised epitopes detected by RFAB TS2 and TS1 but also further epitopes in the CH2 domain (256-TPEVTCVVVDVSHED-270) and CH3 domain (418-QQGNVFSCSVMHEAL-432). Similarly, RFAb PRTS1 detected all four epitopes plus a fifth in the CH3 domain (382-ESNGQPENNYKTTPP-396). In essence there was a consensus of target epitopes identified by these rheumatoid factor antibodies. Interestingly, two epitopes (256–270, CH2 domain and 360–374, CH3 domain) were novel in that they had not been identified in previous pepscan studies. The other epitopes recognised, either overlapped or were immediately adjacent to previous epitopes detected by poly/monoclonal rheumatoid factor antibodies. Molecular modelling (PCImdad) of IgG1Fc showed that all five epitopes were exposed and surface accessible for antibody interaction. In addition, a bioinformatics analysis of the Fc region using ExPASy was employed to identify key antigenic determinants. This ‘in silico’ approach may provide a means of determining key regions without the need to develop overlapping peptides spanning the entire length of a macromolecule.
ZODET: Software for the Identification, Analysis and Visualisation of Outlier Genes in Microarray Expression Data
Daniel L. Roden, Gavin W. Sewell, Anna Lobley, Adam P. Levine, Andrew M. Smith, Anthony W. Segal
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0081123
Abstract: Summary Complex human diseases can show significant heterogeneity between patients with the same phenotypic disorder. An outlier detection strategy was developed to identify variants at the level of gene transcription that are of potential biological and phenotypic importance. Here we describe a graphical software package (z-score outlier detection (ZODET)) that enables identification and visualisation of gross abnormalities in gene expression (outliers) in individuals, using whole genome microarray data. Mean and standard deviation of expression in a healthy control cohort is used to detect both over and under-expressed probes in individual test subjects. We compared the potential of ZODET to detect outlier genes in gene expression datasets with a previously described statistical method, gene tissue index (GTI), using a simulated expression dataset and a publicly available monocyte-derived macrophage microarray dataset. Taken together, these results support ZODET as a novel approach to identify outlier genes of potential pathogenic relevance in complex human diseases. The algorithm is implemented using R packages and Java. Availability The software is freely available from http://www.ucl.ac.uk/medicine/molecular-?medicine/publications/microarray-outlier?-analysis.
Enabling Genomic-Phenomic Association Discovery without Sacrificing Anonymity
Raymond D. Heatherly, Grigorios Loukides, Joshua C. Denny, Jonathan L. Haines, Dan M. Roden, Bradley A. Malin
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0053875
Abstract: Health information technologies facilitate the collection of massive quantities of patient-level data. A growing body of research demonstrates that such information can support novel, large-scale biomedical investigations at a fraction of the cost of traditional prospective studies. While healthcare organizations are being encouraged to share these data in a de-identified form, there is hesitation over concerns that it will allow corresponding patients to be re-identified. Currently proposed technologies to anonymize clinical data may make unrealistic assumptions with respect to the capabilities of a recipient to ascertain a patients identity. We show that more pragmatic assumptions enable the design of anonymization algorithms that permit the dissemination of detailed clinical profiles with provable guarantees of protection. We demonstrate this strategy with a dataset of over one million medical records and show that 192 genotype-phenotype associations can be discovered with fidelity equivalent to non-anonymized clinical data.
Characterization of Genome-Wide Association-Identified Variants for Atrial Fibrillation in African Americans
Jessica T. Delaney, Janina M. Jeff, Nancy J. Brown, Mias Pretorius, Henry E. Okafor, Dawood Darbar, Dan M. Roden, Dana C. Crawford
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0032338
Abstract: Background Despite a greater burden of risk factors, atrial fibrillation (AF) is less common among African Americans than European-descent populations. Genome-wide association studies (GWAS) for AF in European-descent populations have identified three predominant genomic regions associated with increased risk (1q21, 4q25, and 16q22). The contribution of these loci to AF risk in African American is unknown. Methodology/Principal Findings We studied 73 African Americans with AF from the Vanderbilt-Meharry AF registry and 71 African American controls, with no history of AF including after cardiac surgery. Tests of association were performed for 148 SNPs across the three regions associated with AF, and 22 SNPs were significantly associated with AF (P<0.05). The SNPs with the strongest associations in African Americans were both different from the index SNPs identified in European-descent populations and independent from the index European-descent population SNPs (r2<0.40 in HapMap CEU): 1q21 rs4845396 (odds ratio [OR] 0.30, 95% confidence interval [CI] 0.13–0.67, P = 0.003), 4q25 rs4631108 (OR 3.43, 95% CI 1.59–7.42, P = 0.002), and 16q22 rs16971547 (OR 8.1, 95% CI 1.46–45.4, P = 0.016). Estimates of European ancestry were similar among cases (23.6%) and controls (23.8%). Accordingly, the probability of having two copies of the European derived chromosomes at each region did not differ between cases and controls. Conclusions/Significance Variable European admixture at known AF loci does not explain decreased AF susceptibility in African Americans. These data support the role of 1q21, 4q25, and 16q22 variants in AF risk for African Americans, although the index SNPs differ from those identified in European-descent populations.
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