排序方式: 共有40条查询结果,搜索用时 156 毫秒
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Christopher W. Schmidt Ashley Remy Rebecca Van Sessen John Willman Kristin Krueger Rachel Scott Patrick Mahoney Jeremy Beach Jaqueline McKinley Ruggero D'Anastasio Laura Chiu Michele Buzon J. Rocco De Gregory Susan Sheridan Jacqueline Eng James Watson Haagen Klaus Pedro Da-Gloria Jeremy Wilson Abigail Stone Paul Sereno Jessica Droke Rose Perash Christopher Stojanowski Nicholas Herrmann 《American journal of physical anthropology》2019,169(2):207-226
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Csillag C Nielsen OH Borup R Nielsen FC Olsen J 《American journal of physiology. Gastrointestinal and liver physiology》2007,292(1):G298-G304
The clinical course varies significantly among patients with Crohn's disease (CD). This study investigated whether gene expression profiles generated by DNA microarray technology might predict disease progression. Biopsies from the descending colon were obtained colonoscopically from 40 CD patients. Gene profiling analyses were performed using a Human Genome U133 Plus 2.0 GeneChip Array, and summarization into a single expression measure for each probe set was performed using the robust multiple array procedure. Principal component analysis demonstrated that three components explain two-thirds of the total variation. The most important parameters for the determination of the colonic gene expression patterns were the presence of disease (CD) and presence of inflammation. Superimposition of clinical phenotype data revealed a grouping of the samples from patients with stenosis toward negative values on the axis of the second principal component. The functional annotation analysis suggested that the expression of genes involved in intracellular transport and cytoskeletal organization might influence the development of stenosis. In conclusion, even though most variation in the colonic gene expression patterns is due to presence or absence of CD and inflammation status, the development of stenosis is a parameter that affects colonic gene expression to some extent. 相似文献
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Barjaktarovic Z Schmaltz D Shyla A Azimzadeh O Schulz S Haagen J Dörr W Sarioglu H Schäfer A Atkinson MJ Zischka H Tapio S 《PloS one》2011,6(12):e27811
BACKROUND: Radiation therapy treatment of breast cancer, Hodgkin's disease or childhood cancers expose the heart to high local radiation doses, causing an increased risk of cardiovascular disease in the survivors decades after the treatment. The mechanisms that underlie the radiation damage remain poorly understood so far. Previous data show that impairment of mitochondrial oxidative metabolism is directly linked to the development of cardiovascular disease. METHODOLOGY/PRINCIPAL FINDINGS: In this study, the radiation-induced in vivo effects on cardiac mitochondrial proteome and function were investigated. C57BL/6N mice were exposed to local irradiation of the heart with doses of 0.2 Gy or 2 Gy (X-ray, 200 kV) at the age of eight weeks, the control mice were sham-irradiated. After four weeks the cardiac mitochondria were isolated and tested for proteomic and functional alterations. Two complementary proteomics approaches using both peptide and protein quantification strategies showed radiation-induced deregulation of 25 proteins in total. Three main biological categories were affected: the oxidative phophorylation, the pyruvate metabolism, and the cytoskeletal structure. The mitochondria exposed to high-dose irradiation showed functional impairment reflected as partial deactivation of Complex I (32%) and Complex III (11%), decreased succinate-driven respiratory capacity (13%), increased level of reactive oxygen species and enhanced oxidation of mitochondrial proteins. The changes in the pyruvate metabolism and structural proteins were seen with both low and high radiation doses. CONCLUSION/SIGNIFICANCE: This is the first study showing the biological alterations in the murine heart mitochondria several weeks after the exposure to low- and high-dose of ionizing radiation. Our results show that doses, equivalent to a single dose in radiotherapy, cause long-lasting changes in mitochondrial oxidative metabolism and mitochondria-associated cytoskeleton. This prompts us to propose that these first pathological changes lead to an increased risk of cardiovascular disease after radiation exposure. 相似文献
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de Morrée A Hensbergen PJ van Haagen HH Dragan I Deelder AM 't Hoen PA Frants RR van der Maarel SM 《PloS one》2010,5(11):e13854
Dysferlin is critical for repair of muscle membranes after damage. Mutations in dysferlin lead to a progressive muscular dystrophy. Recent studies suggest additional roles for dysferlin. We set out to study dysferlin's protein-protein interactions to obtain comprehensive knowledge of dysferlin functionalities in a myogenic context. We developed a robust and reproducible method to isolate dysferlin protein complexes from cells and tissue. We analyzed the composition of these complexes in cultured myoblasts, myotubes and skeletal muscle tissue by mass spectrometry and subsequently inferred potential protein functions through bioinformatics analyses. Our data confirm previously reported interactions and support a function for dysferlin as a vesicle trafficking protein. In addition novel potential functionalities were uncovered, including phagocytosis and focal adhesion. Our data reveal that the dysferlin protein complex has a dynamic composition as a function of myogenic differentiation. We provide additional experimental evidence and show dysferlin localization to, and interaction with the focal adhesion protein vinculin at the sarcolemma. Finally, our studies reveal evidence for cross-talk between dysferlin and its protein family member myoferlin. Together our analyses show that dysferlin is not only a membrane repair protein but also important for muscle membrane maintenance and integrity. 相似文献
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Gijsbert C. de Gast Inez-Anne Haagen Anja A. van Houten Sigrid C. Klein Ashley J. Duits Roel A. de Weger Thea M. Vroom Mike R. Clark Jenny Phillips Anette J. G. van Dijk Wim B. M. de Lau Bert J. E. G. Bast 《Cancer immunology, immunotherapy : CII》1995,40(6):390-396
A bispecific antibody directed to T and B cells (CD3×CD19 bsAb) was daily infused intravenously in escalating doses from 10 g up to 5 mg in three patients with chemotherapy-resistant non-Hodgkin lymphoma; in this way we aimed to activate T cells to kill the malignant B cells. Only limited toxicity was observed, consisting of moderate fever preceded by chills or shivers and mild thrombocytopenia. No human anti-(mouse Ig) antibodies were found. Pharmacokinetics showed at
1/2 of 10.5 h with peak levels of 200–300 ng/ml after infusion of 2.5 mg bsAb. bsAb in serum was functionally active in vitro. After bsAb infusion a rise in serum tumour necrosis factor was observed, accompanied by an increase in soluble CD8 and to some extent in soluble interleukin-2 receptor (IL-2R), but not in interferon , IL-4 or soluble CD4. No evidence was found for monocyte activation (no increases in IL-6, IL-8 or IL-1ß in serum). No gross changess in histology or number of IL-2R+, CD4+ or CD8+ cells were found in the lymph nodes after therapy, but one patient showed activated CD8+ T cells within the tumour nodules. In conclusion, after intravenously administered CD3×CD19 bsAb only moderate toxicity was found, probably due to CD8+ T cell activation and cytokine release, without CD4+ T cell activation. 相似文献
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Kristina M. Hettne Mark Thompson Herman H. H. B. M. van Haagen Eelke van der Horst Rajaram Kaliyaperumal Eleni Mina Zuotian Tatum Jeroen F. J. Laros Erik M. van Mulligen Martijn Schuemie Emmelien Aten Tong Shu Li Richard Bruskiewich Benjamin M. Good Andrew I. Su Jan A. Kors Johan den Dunnen Gert-Jan B. van Ommen Marco Roos Peter A.C. ‘t Hoen Barend Mons Erik A. Schultes 《PloS one》2016,11(2)
High-throughput experimental methods such as medical sequencing and genome-wide association studies (GWAS) identify increasingly large numbers of potential relations between genetic variants and diseases. Both biological complexity (millions of potential gene-disease associations) and the accelerating rate of data production necessitate computational approaches to prioritize and rationalize potential gene-disease relations. Here, we use concept profile technology to expose from the biomedical literature both explicitly stated gene-disease relations (the explicitome) and a much larger set of implied gene-disease associations (the implicitome). Implicit relations are largely unknown to, or are even unintended by the original authors, but they vastly extend the reach of existing biomedical knowledge for identification and interpretation of gene-disease associations. The implicitome can be used in conjunction with experimental data resources to rationalize both known and novel associations. We demonstrate the usefulness of the implicitome by rationalizing known and novel gene-disease associations, including those from GWAS. To facilitate the re-use of implicit gene-disease associations, we publish our data in compliance with FAIR Data Publishing recommendations [https://www.force11.org/group/fairgroup] using nanopublications. An online tool (http://knowledge.bio) is available to explore established and potential gene-disease associations in the context of other biomedical relations. 相似文献
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There are two types of indeterminacy problems in factor analysis: the indeterminacy of the parameters, which is also known as the problem of identification, and the indeterminacy of the factor scores. The second problem, which will be treated here, is of great importance to the social sciences, given that the factor analysis model was historically developed with the theory of measuring intelligence, where the main interest was to determine one person's intelligence numerically. As a consequence of the indeterminacy of factor scores we will show, by means of a numerical example, that any criterion, including the dates of easter sunday, can be perfectly predicted by the intelligence factors. 相似文献
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