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    Call number: 01-Finanzw:94
    Pages: 118 p.
    ISBN: 3-8029-1630-1
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    01-Finanzw:94 departmental collection or stack – please contact the library
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  • 3
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    German Medical Science; Düsseldorf, Köln
    In:  122. Kongress der Deutschen Gesellschaft für Chirurgie; 20050405-20050408; München; DOC05dgch3011 /20050615/
    Publication Date: 2005-06-16
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 4
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  GMS German Medical Science; VOL: 15; DOC04 /20170209/
    Publication Date: 2017-02-09
    Description: Aims: The purpose of this study was to analyze the prevalence of depression, anxiety, adjustment disorders, and somatoform disorders in patients diagnosed with age-related macular degeneration (AMD) in Germany.Methods: This study included 7,580 patients between the ages of 40 and 90 diagnosed with AMD between January 2011 and December 2014 in 1,072 primary care practices (index date). The last follow-up was in July 2016. We also included 7,580 controls without AMD, which were matched (1:1) to the AMD cases by age, sex, type of health insurance (private or statutory), physician, and Charlson comorbidity score as a generic marker of comorbidity. The outcome of the study was the prevalence of depression, anxiety, adjustment disorders, and somatoform disorders recorded in the database between the index date and the end of follow-up. Results: The mean age among subjects was 75.7 years (SD=10.1 years), 34.0% were men, and 7.8% had private health insurance coverage. The Charlson comorbidity index was 2.0 (SD=1.8). Depression was the most frequent disease (33.7% in AMD patients versus 27.3% in controls), followed by somatoform disorders (19.6% and 16.7%), adjustment disorders (14.8% and 10.5%), and anxiety disorders (11.7% and 8.2%). Depression (OR=1.37, 95% CI: 1.27-1.47), anxiety (OR=1.50, 95% CI: 1.35-1.67), adjustment disorders (OR=1.50, 95% CI: 1.36-1.65), and somatoform disorders (OR=1.22, 95% CI: 1.12-1.32) were all positively associated with AMD. Conclusion: Overall, a significant association was found between AMD and depression, anxiety, adjustment disorders, and somatoform disorders.
    Description: Ziel: In der vorliegenden Studie wurde die Prävalenz der psychiatrischen Komorbiditäten bei Patienten mit altersbedingten Makuladegeneration (AMD) und Personen ohne MD verglichen.Methoden: Patienten mit einer gesicherten Diagnose der Makuladegeneration (ICD 10: H35.3) im Zeitraum 2011-2014 aus 1.072 allgemeinmedizinischen und internistischen Praxen wurden selektiert. Daten von 7.580 MD-Patienten und 7.580 Personen ohne MD aus allgemeinmedizinischen und internistischen Praxen in Deutschland wurden nach Matching für Alter, Geschlecht, Versicherungsstatus und Indexjahr (der letzte Eintrag in der Datenbank) retrospektiv analysiert. Der Anteil der Patienten mit einer gesicherten Diagnose von Depression, Angststörung, Reaktionen auf schwere Belastungen und Anpassungsstörungen oder somatoformen Störungen wurde ermittelt. Ergebnisse: Patienten waren im Schnitt 75,7 Jahre alt (SD: 10,1), 34,0% waren männlich und 7,8% privat versichert. Charlson Comorbidity Index war im Schnitt 2,0 (SD: 1,8). Depression war die häufigste Diagnose (33,7% bei AMD-Patienten versus 27,3% in der Kontrollgruppe), gefolgt bei somatoformen Störungen (19,6% versus 16,7%), Reaktionen auf schwere Belastungen und Anpassungsstörungen (14,8% versus 10,5%), und Angststörungen (11,7% versus 8,2%). Das Risiko für jede der untersuchten psychiatrischen Kodiagnosen war unter MD-Patienten nach der Adjustierung für Charlson Comorbidity Index insgesamt signifikant höher als bei Patienten ohne MD (Depression (OR: 1,37, 95% CI: 1,27-1,47), Angststörung (OR: 1,50, 95% CI: 1,35-1,67), Reaktionen auf schwere Belastungen und Anpassungsstörungen (OR: 1,50, 95% CI: 1,36-1,65), und somatoforme Störungen (OR: 1,22, 95% CI: 1,12-1,32)).Schlussfolgerung: Makuladegeneration war mit stark erhöhtem Risiko für Depression, Angst-, Belastungs- sowie somatoformer Störung assoziiert.
    Keywords: age-related macular degeneration ; depression ; anxiety ; adjustment disorder ; somatoform disorder ; altersbedingte Makuladegeneration ; Depression ; Angststörung ; Anpassungsstörung ; somatoforme Störung ; ddc: 610
    Language: English
    Type: article
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  • 5
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  68. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 7. Joint Meeting mit der Society of British Neurological Surgeons (SBNS); 20170514-20170517; Magdeburg; DOCP 055 /20170609/
    Publication Date: 2017-06-09
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 6
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  17. Grazer Konferenz - Qualität der Lehre 2013: Teaching medical skills; 20130404-20130406; Wien, Österreich; DOCP03 /20131129/
    Publication Date: 2013-11-30
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 7
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  130. Kongress der Deutschen Gesellschaft für Chirurgie; 20130430-20130503; München; DOC13dgch564 /20130426/
    Publication Date: 2013-04-27
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 8
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  83. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; 20120516-20120520; Mainz; DOC12hnod482 /20120404/
    Publication Date: 2012-04-05
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 9
    Keywords: CELLS ; EXPRESSION ; carcinoma ; Germany ; LUNG ; PATHWAY ; DEATH ; PROTEIN ; PROTEINS ; TUMOR-NECROSIS-FACTOR ; MECHANISM ; TRANSCRIPTION FACTOR ; DOMAIN ; CONTRAST ; mechanisms ; SEQUENCE ; VARIANTS ; MOLECULE ; NUCLEI ; MALIGNANCIES ; PATTERNS ; CARCINOMA CELLS ; CELL-DEATH ; DAMAGE ; LOCALIZATION ; MITOCHONDRIA ; LENGTH ; targeting ; SINGLE ; MALIGNANCY ; HUMAN LUNG ; cell death ; DEPENDENT APOPTOSIS ; HEPATOCYTE APOPTOSIS ; HUMAN-PROSTATE ; LYSOSOMAL PATHWAY ; MATURE ; SUBCELLULAR-DISTRIBUTION
    Abstract: Background: Splicing variants of human cathepsinB primary transcripts ( CB(- 2,3)) result in an expression product product which lacks the signal peptide and parts of the propeptide. This naturally truncated Delta(51)CB is thus unable to follow the regular CB processing and sorting pathway. It is addressed to the mitochondria through an activated N-terminal mitochondrial targeting signal instead. Although Delta(51)CB is supposed to be devoid of the typical CB enzymatic activity, it might play a role in malignancies and trigger cell death/apoptosis independent from the function of the regular enzyme. Cytoplasmic presence of the mature CB might occur as a result of lysosomal damage. Results: We investigated such "aberrant" proteins by artificial CB-GFP chimeras covering various sequence parts in respect to their enzymatic activity, their localization in different cell types, and the effects on the cell viability. Unlike the entire full length CB form, the artificial single chain form was not processed and did not reveal typical enzymatic CB activity during transient overexpression in large cell lung carcinoma cells.. Delta(51)CB was found predominantly in mitochondria. In contrast, the shorter artificial CB constructs localized in the cytoplasm, inside the cell nucleus, and in the midbodies of dividing cells. Bleaching experiments revealed both mobile and immobile fractions of these constructs in the nucleus. Nuclear accumulation of artificially truncated CB variants led to disintegration of nuclei, followed by cell death. Conclusion: We propose that cell death associated with CB is not necessarily triggered by its regular enzymatic activity but alternatively by a yet unknown activity profile of truncated CB. Cytoplasmic CB might be able to enter the cell nucleus. According to a mutational analysis, the part of CB that mediates its nuclear import is a signal patch within its heavy chain domain. The results suggest that besides the N-terminal signal peptide also other CB domains contain patterns which are responsible for a differentiated targeting of the molecule, e. g. to the mitochondria, to the nucleus, or to vesicles. We propose a hierarchy of targeting signals depending on their strength and availability. This implies other possible transport mechanisms besides the usual trafficking via the mannose-6-pathway
    Type of Publication: Journal article published
    PubMed ID: 15807897
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  • 10
    Keywords: CANCER ; CELLS ; SURVIVAL ; carcinoma ; CELL ; LUNG ; INFORMATION ; lung cancer ; LUNG-CANCER ; GENE ; PROTEIN ; TISSUE ; PATIENT ; MACROPHAGES ; MARKER ; prognosis ; CONTRAST ; LYMPH-NODES ; STAGE ; PROGRESSION ; HIGH-RISK ; LOCALIZATION ; HEAD ; HIGH-LEVEL ; non-small cell lung cancer ; CATHEPSIN-B ; STEFIN-A ; TUMOR TISSUE ; LEVEL ; IMMUNOHISTOCHEMICAL ANALYSIS ; NSCLC ; CYSTEINE PROTEASE ; RELEVANCE ; macrophage ; PREDICTOR ; inflammatory cells ; biological markers ; cystatin ; cathepsin ; CYSTEINE PROTEINASE-INHIBITOR ; ENDOGENOUS INHIBITORS ; PROTEASE INHIBITORS ; stefin
    Abstract: Cystatins regulate tumour-associated cysteine proteases, however, their role in tumour progression is not clear yet. To assess their relevance in the progression of nonsmall cell lung cancer (NSCLC) the protein level, cysteine protease activity (CPI) and localization of type I (stefins A and B) and type H (C, E/M and F) cystatins were defined in tumours and control lung counterparts from 165 patients. The medians of CPI activity, stefins A and B were significantly greater in tumour than in lung tissue (2.1-fold, 1.7-fold, 1.2-fold, respectively, all p 〈 0.001). The median levels of cystatin C and cystatin E/M were lower in tumour tissue (0.9-fold, p=0.06; 0.6-fold, p 〈 0.01). In all the samples the levels of cystatin F were below the detection limit. Immunohistochemical analysis revealed the presence of all cystatins in tumour cells and infiltrated inflammatory cells such as macrophages and neutrophils. In univariate survival analysis patients with high levels of stefin A, stefin B and CPI activity exhibited a better survival probability (p=0.05, p=0.05, p 〈 0.01, respectively). In contrast, cystatins C and E/M provided no prognostic information. In multivariate analysis the most powerful predictor of survival was the pTNM stage (p 〈 0.0001; RR 3.5), followed by stefin A, stefin B and CPI activity (all p=0.03; RR 1.5). Our results suggest that only stefins A and B, i.e. type I cystatins, are up-regulated in lung tumours and thus able to counteract harmful tumour-associated proteolytic activity. As biological markers they may add independent prognostic information for better assessment of low- and high-risk patients with NSCLC
    Type of Publication: Journal article published
    PubMed ID: 16969475
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