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  • 1
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    Philadelphia, Pa. : Saunders
    Call number: 08-Phys
    Keywords: Nuclear Medicine ; Physics
    Notes: Sorenson's name appears first on the previous edition.
    Pages: xiii, 523 p. : ill., ports.
    Edition: 3rd ed.
    ISBN: 072168341X
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    08-Phys departmental collection or stack – please contact the library
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  • 2
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    Philadelphia : Elsevier/Saunders
    Call number: WN110:11(4)
    Keywords: Medical physics ; Nuclear Medicine ; Health Physics ; Nuclear Medicine
    Description / Table of Contents: What is nuclear medicine -- Basic atomic and nuclear physics -- Modes of radioactive decay -- Decay of radioactivity -- Isotope production & tracer synthesis -- Interaction of radiation with matter -- Radiation detectors -- Electronic instrumentation for radiation detection systems -- Nuclear counting statistics -- Pulse height spectrometry -- Problems in radiation detection and measurement -- Counting systems -- The gamma camera : basic principles -- Gamma camera performance characteristics -- Image quality in nuclear medicine -- Tomographic reconstruction in nuclear medicine -- Single photon emission computed tomography -- Positron emission tomography -- Multimodality imaging : SPECT/CT and PET/CT -- Data acquisition and digital image processing in nuclear medicine -- Tracer kinetic modeling -- Internal radiation dosimetry -- Radiation safety and health physics
    Notes: For online access to this volume please contact the library staff in room D124 (phone 3661, e-mail: http://www.dkfz.de/de/zbib/mitarbeiter/kontakt/fernleihe.php
    Pages: xv, 523 p. : ill.
    Edition: 4th ed.
    ISBN: 9781416051985
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    WN110:11(4) available
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  • 3
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    Boca Raton : Taylor & Francis
    Call number: E040:155 ; WN180:5
    Keywords: Diagnostic Imaging
    Abstract: "This book is the first to offer an authoritative introduction to non-invasive, in vivo imaging technologies as tools for basic, preclinical, and clinical biomedical research. Designed to meet the interdisciplinary needs of the new breed of imaging scientist, the text extends its coverage equally across optical, nuclear, magnetic resonance, ultrasonic, and x-ray computer tomographic imaging modalities, integrating didactic material with animal studies and human molecular imaging applications. Readers gain a solid understanding of how each modality works as well as what information each can obtain"--Provided by publisher
    Notes: For online access to this volume please contact the library staff in room D124 (phone 3661, e-mail: http://www.dkfz.de/de/zbib/mitarbeiter/kontakt/fernleihe.php)
    Pages: xvi, 272 pages : illustrations, portraits
    ISBN: 9781439898741
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    E040:155 available
    WN180:5 available
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  • 4
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  133. Kongress der Deutschen Gesellschaft für Chirurgie; 20160426-20160429; Berlin; DOC16dgch540 /20160421/
    Publication Date: 2016-04-22
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 5
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Deutscher Kongress für Orthopädie und Unfallchirurgie; 72. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie, 94. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie, 49. Tagung des Berufsverbandes der Fachärzte für Orthopädie; 20081022-20081025; Berlin; DOCPO16-334 /20081016/
    Publication Date: 2008-10-17
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 6
    Keywords: ACTIVATION, ANTIGEN, ASSOCIATION, BIOPSY, CANCER, cancer risk, CANCER-RISK, CELLS, DIFFERENTIAL EXPR
    Abstract: Background: Insufficient sensitivity and specificity of prostate biopsies for cancer detection. Objectives: Based on evidence from our microarray analyses, we hypothesized that considerable molecular changes precede morphologically detectable malignant transformation of prostate epithelial tissues. The identification of such changes could lead to novel strategies in the clinical management of prostate cancer. Design, Setting, and Participants: Histologically normal, fresh prostate tissue from prostate cancer patients, healthy donors, and cancer suspect patients with continuous negative biopsies were analyzed. Measurements: To identify molecular changes between 29 tumor-free prostate tissues from healthy donors and 27 patients with proven prostate cancer, we performed a global microarray screening. 'Based on this screening as well as literature data, we selected a subset of 29 genes for validation by arrayed real-time reverse transcription-polymerase chain reaction (RT-PCR) using histologically tumor-free biopsy samples from 114 patients representing three prostate cancer risk groups. Results and Limitations: We identified five genes (FOS, EGR1, MYC, TFRC, and FOLH1), which displayed significant differential expression between morphologically normal prostate tissues from men of each of the three risk groups. These results were independent from age, prostate-specific antigen (PSA), frequency and timing of previous prostate biopsies, tissue composition, tumor stage, and tumor grade. in univariate logistic regression analyses, the transcript levels of these genes were found to be highly indicative for the presence or absence of cancer in the entire prostate. The study was designed as a proof of principle. The clinical relevance of our results has to be evaluated in a larger clinical setting. Conclusions: Our results suggest a measurable molecular cancer phenotype in histologically normal prostate tissue indicating the presence of prostate cancer elsewhere in the organ. (C) 2008 European Association of Urology. Published by Elsevier B.V. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 18501497
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  • 7
    Keywords: MODEL ; DISEASE ; POPULATION ; FAMILY ; treatment ; HEALTH ; statistics ; CENTRAL-NERVOUS-SYSTEM ; POPULATION-BASED SAMPLE ; EUROPE ; INJURY ; OBSTRUCTIVE SLEEP-APNEA ; QUALITY-OF-LIFE ; GUILLAIN-BARRE-SYNDROME ; 3 SICILIAN MUNICIPALITIES ; COMMON MENTAL-DISORDERS ; IDIOPATHIC PARKINSONS-DISEASE ; SCHOOL-AGE-CHILDREN ; TREATMENT OUTCOME RESEARCH
    Abstract: Background: The spectrum of disorders of the brain is large, covering hundreds of disorders that are listed in either the mental or neurological disorder chapters of the established international diagnostic classification systems. These disorders have a high prevalence as well as short- and long-term impairments and disabilities. Therefore they are an emotional, financial and social burden to the patients, their families and their social network. In a 2005 landmark study, we estimated for the first time the annual cost of 12 major groups of disorders of the brain in Europe and gave a conservative estimate of 386 billion for the year 2004. This estimate was limited in scope and conservative due to the lack of sufficiently comprehensive epidemiological and/or economic data on several important diagnostic groups. We are now in a position to substantially improve and revise the 2004 estimates. In the present report we cover 19 major groups of disorders, 7 more than previously, of an increased range of age groups and more cost items. We therefore present much improved cost estimates. Our revised estimates also now include the new EU member states, and hence a population of 514 million people. Aims: To estimate the number of persons with defined disorders of the brain in Europe in 2010, the total cost per person related to each disease in terms of direct and indirect costs, and an estimate of the total cost per disorder and country. Methods: The best available estimates of the prevalence and cost per person for 19 groups of disorders of the brain (covering well over 100 specific disorders) were identified via a systematic review of the published literature. Together with the twelve disorders included in 2004, the following range of mental and neurologic groups of disorders is covered: addictive disorders, affective disorders, anxiety disorders, brain tumor, childhood and adolescent disorders (developmental disorders), dementia, eating disorders, epilepsy, mental retardation, migraine, multiple sclerosis, neuromuscular disorders, Parkinson's disease, personality disorders, psychotic disorders, sleep disorders, somatoform disorders, stroke, and traumatic brain injury. Epidemiologic panels were charged to complete the literature review for each disorder in order to estimate the 12-month prevalence, and health economic panels were charged to estimate best cost-estimates. A cost model was developed to combine the epidemiologic and economic data and estimate the total cost of each disorder in each of 30 European countries (EU27 + Iceland, Norway and Switzerland). The cost model was populated with national statistics from Eurostat to adjust all costs to 2010 values, converting all local currencies to Euro, imputing costs for countries where no data were available, and aggregating country estimates to purchasing power parity adjusted estimates for the total cost of disorders of the brain in Europe 2010. Results: The total cost of disorders of the brain was estimated at (sic)798 billion in 2010. Direct costs constitute the majority of costs (37% direct healthcare costs and 23% direct non-medical costs) whereas the remaining 40% were indirect costs associated with patients production losses. On average, the estimated cost per person with a disorder of the brain in Europe ranged between (sic)285 for headache and (sic)30,000 for neuromuscular disorders. The European per capita cost of disorders of the brain was (sic)1550 on average but varied by country. The cost (in billion (sic)PPP 2010) of the disorders of the brain included in this study was as folows: addiction: (sic)65.7; anxiety disorders: (sic)74.4; brain tumor: (sic)5.2; child/adolescent disorders: (sic)21.3; dementia: (sic)105.2; eating disorders: (sic)0.8; epilepsy: (sic)13.8; headache: (sic)43.5; mental retardation: (sic)43.3; mood disorders: (sic)113.4; multiple sclerosis: (sic)14.6; neuromuscular disorders: (sic)7.7; Parkinson's disease: (sic)13.9; personality disorders: (sic)27.3
    Type of Publication: Journal article published
    PubMed ID: 21924589
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  • 8
    Keywords: THERAPY ; DENSITY ; chemotherapy ; MUTATIONS ; REVEALS ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; ANDROGEN RECEPTOR ; GLIOBLASTOMA ; TUMOR EVOLUTION
    Abstract: Despite much evidence on epigenetic abnormalities in cancer, it is currently unclear to what extent epigenetic alterations can be associated with tumors' clonal genetic origins. Here, we show that the prostate intratumor heterogeneity in DNA methylation and copy-number patterns can be explained by a unified evolutionary process. By assaying multiple topographically distinct tumor sites, premalignant lesions, and lymph node metastases within five cases of prostate cancer, we demonstrate that both DNA methylation and copy-number heterogeneity consistently reflect the life history of the tumors. Furthermore, we show cases of genetic or epigenetic convergent evolution and highlight the diversity in the evolutionary origins and aberration spectrum between tumor and metastatic subclones. Importantly, DNA methylation can complement genetic data by serving as a proxy for activity at regulatory domains, as we show through identification of high epigenetic heterogeneity at androgen-receptor-bound enhancers. Epigenome variation thereby expands on the current genome-centric view on tumor heterogeneity.
    Type of Publication: Journal article published
    PubMed ID: 25066126
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  • 9
    Keywords: EARLY PSA RECURRENCE ; GENOMIC DELETION
    Abstract: Based on next-generation sequencing of early-onset prostate cancer (PCa), we earlier demonstrated that PCa in young patients is prone to rearrangements involving androgen-regulated genes-such as transmembrane protease, serine 2 (TMPRSS2)-v-ets avian erythroblastosis virus E26 oncogene homolog (ERG) fusion-and provided data suggesting that this situation might be caused by increased androgen signaling in younger men. In the same study, an accumulation of chromosomal deletions was found in cancers of elderly patients. To determine how age-dependent molecular features relate to cancer phenotype, an existing data set of 11 152 PCas was expanded by additional fluorescence in situ hybridization analyses of phosphatase and tensin homolog (PTEN), 6q15 and 5q21. The results demonstrate that the decrease in TMPRSS2-ERG fusions with increasing patient age is limited to low-grade cancers (Gleason 〈= 3 + 4) and that the significant increase in the deletion frequency with age was strictly limited to ERG-negative cancers for 6q15 and 5q21 but to ERG-positive cancers for PTEN. These data suggest that the accumulation of non-androgen-linked genomic alterations with advanced patient age may require an appropriate microenvironment, such as a positive or negative ERG status. The strong link of ERG activation to young patient age and low-grade cancers may help to explain a slight predominance of low-grade cancers in young patients.
    Type of Publication: Journal article published
    PubMed ID: 25015038
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  • 10
    Keywords: CELLS ; EXPRESSION ; GROWTH ; PATHWAY ; BIOMARKERS ; IDENTIFICATION ; LIGAND-BINDING DOMAIN ; ESTROGEN-RELATED-RECEPTOR ; TRANSCRIPTIONAL ACTIVITIES ; ENDOCRINE RESISTANCE
    Abstract: Endocrine treatment regimens for breast cancer that target the estrogen receptor-alpha (ER alpha) are effective, but acquired resistance remains a limiting drawback. One mechanism of acquired resistance that has been hypothesized is functional substitution of the orphan receptor estrogen-related receptor-alpha (ERR alpha) for ER alpha. To examine this hypothesis, we analyzed ERR alpha and ER alpha in recurrent tamoxifen-resistant breast tumors and conducted a genome-wide target gene profiling analysis of MCF-7 breast cancer cell populations that were sensitive or resistant to tamoxifen treatment. This analysis uncovered a global redirection in the target genes controlled by ER alpha, ERR alpha, and their coactivator AIB1, defining a novel set of target genes in tamoxifen-resistant cells. Beyond differences in the ER alpha and ERR alpha target gene repertoires, both factors were engaged in similar pathobiologic processes relevant to acquired resistance. Functional analyses confirmed a requirement for ERR alpha in tamoxifen-and fulvestrant-resistant MCF-7 cells, with pharmacologic inhibition of ERR alpha sufficient to partly restore sensitivity to antiestrogens. In clinical specimens (n - 1041), increased expression of ERR alpha was associated with enhanced proliferation and aggressive disease parameters, including increased levels of p53 in ER alpha-positive cases. In addition, increased ERR alpha expression was linked to reduced overall survival in independent tamoxifen-treated patient cohorts. Taken together, our results suggest that ER alpha and ERR alpha cooperate to promote endocrine resistance, and they provide a rationale for the exploration of ERR alpha as a candidate drug target to treat endocrine-resistant breast cancer.
    Type of Publication: Journal article published
    PubMed ID: 25643697
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