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  1. Book ; Thesis: Gestaltung intra-organisationaler Produktionsnetzwerke mit standortübergreifender Kooperation zwischen Entwicklung und Produktion

    Dietrich, Axel Maximilian

    (Wissenschaftliche Schriftenreihe des Instituts für Betriebswissenschaften und Fabriksysteme ; 75)

    2009  

    Author's details Autor: A. M. Dietrich
    Series title Wissenschaftliche Schriftenreihe des Instituts für Betriebswissenschaften und Fabriksysteme ; 75
    Language German
    Size VII, 147 S., A5, Abb., graph. Darst., Tab.
    Publisher IBF
    Publishing place Chemnitz
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Techn. Univ., Diss.--Chemnitz, 2009
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  2. Book: Automarkt Internet 00/01

    Dietrich, Axel

    der Kfz-Handel im Umbruch ; Analysen, Trends, Umfrageergebnisse

    2000  

    Author's details [Autoren: Axel Dietrich ...]
    Keywords Marktübersicht ; Kraftfahrzeughandel ; Internet ; Electronic Commerce ; Kfz-Markt ; Kfz-Gewerbe ; E-Business ; Deutschland
    Language German
    Size 338 S., graph. Darst., 30 cm
    Document type Book
    ISBN 3933814189 ; 9783933814180
    Database ECONomics Information System

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  3. Book ; Online: Consciousness and Learning based on DNA Recombination and Memristor Quality of Microtubules

    Dietrich, Axel / Been, Willem

    2014  

    Abstract: This paper is a completion of an earlier model proposed by us. In the model different memories are attached at cell surface determinants which are the result of DNA recombination. Our earlier experiments strongly suggest that DNA recombination actually ... ...

    Abstract This paper is a completion of an earlier model proposed by us. In the model different memories are attached at cell surface determinants which are the result of DNA recombination. Our earlier experiments strongly suggest that DNA recombination actually takes place during a short period of early development in the brain in a limited number of neurons. In the present paper a model is presented in which switchboard neurons play a key role in the storage and retrieving of memory. And as a consequence, they play a major role in the process of learning and form the basic material for consciousness. In the original model there was insufficient explanation for the realization of the internal connection of one cell surface determinant to the other. We realized that tubulin should play a role in these intracellular connections. The tubulin molecules can form a connective wire because of a change of shape of the individual tubulin dimers. This way the fast switch is realized by the switch of the tubulin dimer configuration. Because the cell should remember which switch was activated and which one was not or less activated, we postulate the memristor quality of microtubules.

    Comment: 11 pages, 3 figures
    Keywords Quantitative Biology - Neurons and Cognition
    Subject code 612
    Publishing date 2014-01-17
    Publishing country us
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: The role of insulin resistance in experimental diabetic retinopathy-Genetic and molecular aspects.

    Järgen, Patrick / Dietrich, Axel / Herling, Andreas W / Hammes, Hans-Peter / Wohlfart, Paulus

    PloS one

    2017  Volume 12, Issue 6, Page(s) e0178658

    Abstract: Background: Diabetic retinopathy is characterized by defects in the retinal neurovascular unit. The underlying mechanisms of impairment-including reactive intermediates and growth-factor dependent signalling pathways and their possible interplay are ... ...

    Abstract Background: Diabetic retinopathy is characterized by defects in the retinal neurovascular unit. The underlying mechanisms of impairment-including reactive intermediates and growth-factor dependent signalling pathways and their possible interplay are incompletely understood. This study aims to assess the relative role of hyperglycemia and hyperinsulinemia alone or in combination on the gene expression patterning in the retina of animal models of diabetes.
    Material and methods: As insulinopenic, hyperglycemic model reflecting type 1 diabetes, male STZ-Wistar rats (60mg/kg BW; i.p. injection at life age week 7) were used. Male obese ZDF rats (fa/fa) were used as type-2 diabetes model characterized by persisting hyperglycemia and transient hyperinsulinemia. Male obese ZF rats (fa/fa) were used reflecting euglycemia and severe insulin resistance. All groups were kept till an age of 20 weeks on respective conditions together with appropriate age-matched controls. Unbiased gene expression analysis was performed per group using Affymetrix gene arrays. Bioinformatics analysis included analysis for clustering and differential gene expression, and pathway and upstream activator analysis. Gene expression differences were confirmed by microfluidic card PCR technology.
    Results: The most complex genetic regulation in the retina was observed in ZDF rats with a strong overlap to STZ-Wistar rats. Surprisingly, systemic insulin resistance alone in ZF rats without concomitant hyperglycemia did not induce any significant change in retinal gene expression pattern. Pathway analysis indicate an overlap between ZDF rats and STZ-treated rats in pathways like complement system activation, acute phase response signalling, and oncostatin-M signalling. Major array gene expression changes could be confirmed by subsequent PCR. An analysis of upstream transcriptional regulators revealed interferon-γ, interleukin-6 and oncostatin-M in STZ and ZDF rats. CONCLUSIONS: Systemic hyperinsulinaemia without hyperglycemia does not result in significant gene expression changes in retina. In contrast, persistent systemic hyperglycemia boosts much stronger expression changes with a limited number of known and new key regulators.
    MeSH term(s) Acute-Phase Proteins ; Animals ; Complement Activation ; Diabetes Mellitus, Experimental/genetics ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/physiopathology ; Diabetic Retinopathy/genetics ; Diabetic Retinopathy/metabolism ; Eye Proteins/biosynthesis ; Eye Proteins/genetics ; Gene Expression Profiling ; Gene Expression Regulation ; Hyperglycemia/complications ; Hyperglycemia/genetics ; Hyperglycemia/metabolism ; Hyperinsulinism/complications ; Hyperinsulinism/genetics ; Hyperinsulinism/metabolism ; Insulin Resistance ; Male ; Oncostatin M/biosynthesis ; Oncostatin M/genetics ; Rats, Mutant Strains ; Rats, Wistar ; Retina/metabolism ; Signal Transduction
    Chemical Substances Acute-Phase Proteins ; Eye Proteins ; Oncostatin M (106956-32-5)
    Language English
    Publishing date 2017-06-02
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0178658
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Sample Size Calculations for Detecting Disease-Modifying Osteoarthritis Drug Effects on Knee Replacement Incidence in Clinical Trials: Data From the Osteoarthritis Initiative.

    Ried, Janina S / Flechsenhar, Klaus / Bartnik, Eckart / Crowther, Daniel / Dietrich, Axel / Eckstein, Felix

    Arthritis & rheumatology (Hoboken, N.J.)

    2015  Volume 67, Issue 12, Page(s) 3174–3183

    Abstract: Objective: To evaluate the extent to which the current designs of clinical trials in knee osteoarthritis (OA) permit detection of a therapeutic effect of disease-modifying OA drugs (DMOADs) on the incidence of knee replacement, and to provide estimates ... ...

    Abstract Objective: To evaluate the extent to which the current designs of clinical trials in knee osteoarthritis (OA) permit detection of a therapeutic effect of disease-modifying OA drugs (DMOADs) on the incidence of knee replacement, and to provide estimates of the required sample sizes.
    Methods: We selected distinct subcohorts of the Osteoarthritis Initiative (OAI), based on available information on eligibility criteria for clinical knee OA trials (ClinicalTrials.gov) and additional subcohorts stratified for age, sex, and the severity of radiographic OA. The observed incidence of knee replacement in these OAI subcohorts was used to estimate the expected incidence of knee replacement in the control group of a clinical trial. Based on this estimate, the sample sizes required to detect hypothetical treatment effects on the incidence of knee replacement were calculated, assuming observation periods of 2, 5, or 7 years.
    Results: The cumulative knee replacement incidence rates in the OAI subcohorts ranged from 0.9% to 12.9%. The corresponding sample sizes required to detect 50% improvement by the DMOAD, with a power of 80% and 95% confidence, were 5,459 and 362, respectively. Including only women with advanced age and radiographic OA increased the incidence of knee replacement and decreased the required sample size.
    Conclusion: The sample sizes that are commonly used in clinical trials do not enable the effects of a DMOAD on incident knee replacement to be detected with sufficient power and confidence. The estimated incidence rates of knee replacement and the corresponding sample sizes are important for informing the design of trials for disease course-modifying effects as well as for socioeconomic evaluation of a DMOAD in terms of preventing knee replacement.
    MeSH term(s) Aged ; Aged, 80 and over ; Arthroplasty, Replacement, Knee/statistics & numerical data ; Clinical Trials as Topic ; Disease Progression ; Female ; Humans ; Incidence ; Knee Joint/diagnostic imaging ; Knee Joint/surgery ; Male ; Middle Aged ; Osteoarthritis, Knee/diagnostic imaging ; Osteoarthritis, Knee/drug therapy ; Osteoarthritis, Knee/surgery ; Radiography ; Sample Size ; Sex Factors
    Language English
    Publishing date 2015-12
    Publishing country United States
    Document type Clinical Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.39334
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 24: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  6. Book ; Online ; Thesis: Tolperison

    Dietrich, Axel

    alter Wirkstoff oder neue Leitstruktur?

    1999  

    Author's details Axel Dietrich
    Language German
    Size Online-Ressource (Online-Ressource)
    Publisher Universitätsbibliothek
    Publishing place Paderborn
    Document type Book ; Online ; Thesis
    Thesis / German Habilitation thesis Paderborn, Universität, Diss., 1999
    Database Former special subject collection: coastal and deep sea fishing

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  7. Article ; Online: Hyperglycaemic memory affects the neurovascular unit of the retina in a diabetic mouse model.

    Friedrichs, Patrick / Schlotterer, Andrea / Sticht, Carsten / Kolibabka, Matthias / Wohlfart, Paulus / Dietrich, Axel / Linn, Thomas / Molema, Grietje / Hammes, Hans-Peter

    Diabetologia

    2017  Volume 60, Issue 7, Page(s) 1354–1358

    Abstract: Aims/hypothesis: The aim of this study was to evaluate damage to the neurovascular unit in a mouse model of hyperglycaemic memory.: Methods: A streptozotocin-induced mouse model of diabetes (C57BL/6J background) received insulin-releasing pellets and ...

    Abstract Aims/hypothesis: The aim of this study was to evaluate damage to the neurovascular unit in a mouse model of hyperglycaemic memory.
    Methods: A streptozotocin-induced mouse model of diabetes (C57BL/6J background) received insulin-releasing pellets and pancreatic islet-cell transplantation. Damage to the neurovascular unit was studied by quantitative retinal morphometry for microvascular changes and microarray analysis, with subsequent functional annotation clustering, for changes of the retinal genome.
    Results: Sustained microvascular damage was confirmed by persistent loss of pericytes in the retinal vasculature (PC/mm
    Conclusions/interpretation: We demonstrated that changes in gene expression and microvascular damage persist after euglycaemic re-entry, indicating memory.
    Data availability: The datasets generated during and/or analysed during the current study are available in the GEO repository, GSE87433, www.ncbi.nlm.nih.gov/geo/query/acc.cgi?token=idmbysgctluxviv&acc=GSE87433 .
    Language English
    Publishing date 2017-07
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1694-9
    ISSN 1432-0428 ; 0012-186X
    ISSN (online) 1432-0428
    ISSN 0012-186X
    DOI 10.1007/s00125-017-4254-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 279: Show issues Location:
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  8. Book ; Online ; Thesis: Tolperison

    Dietrich, Axel [Verfasser]

    alter Wirkstoff oder neue Leitstruktur?

    1999  

    Author's details Axel Dietrich
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language German
    Publisher Universitätsbibliothek
    Publishing place Paderborn
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  9. Article ; Online: High throughput screening of mitochondrial bioenergetics in human differentiated myotubes identifies novel enhancers of muscle performance in aged mice.

    Biesemann, Nadine / Ried, Janina S / Ding-Pfennigdorff, Danping / Dietrich, Axel / Rudolph, Christine / Hahn, Steffen / Hennerici, Wolfgang / Asbrand, Christian / Leeuw, Thomas / Strübing, Carsten

    Scientific reports

    2018  Volume 8, Issue 1, Page(s) 9408

    Abstract: Mitochondrial dysfunction is increasingly recognized as a contributor to age-related muscle loss and functional impairment. Therefore, we developed a high throughput screening strategy that enabled the identification of compounds boosting mitochondrial ... ...

    Abstract Mitochondrial dysfunction is increasingly recognized as a contributor to age-related muscle loss and functional impairment. Therefore, we developed a high throughput screening strategy that enabled the identification of compounds boosting mitochondrial energy production in a human skeletal muscle cell model. Screening of 7949 pure natural products revealed 22 molecules that significantly increased oxygen consumption and ATP levels in myotubes. One of the most potent compounds was the flavanone hesperetin. Hesperetin (10 µM) increased intracellular ATP by 33% and mitochondrial spare capacity by 25%. Furthermore, the compound reduced oxidative stress in primary myotubes as well as muscle tissue in vivo. In aged mice administration of hesperetin (50 mg/kg/d) completely reverted the age-related decrease of muscle fiber size and improved running performance of treated animals. These results provide a novel screening platform for the discovery of drugs that can improve skeletal muscle function in patients suffering from sarcopenia or other disorders associated with mitochondrial dysfunction.
    MeSH term(s) Adenosine Triphosphate/metabolism ; Animals ; Cell Differentiation/drug effects ; Energy Metabolism/drug effects ; Hesperidin/pharmacology ; Humans ; Membrane Potential, Mitochondrial ; Mice ; Mitochondria/drug effects ; Mitochondria/metabolism ; Muscle Fibers, Skeletal/cytology ; Muscle, Skeletal/cytology ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Oxidative Stress/drug effects
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE) ; Hesperidin (E750O06Y6O) ; hesperetin (Q9Q3D557F1)
    Language English
    Publishing date 2018-06-20
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-018-27614-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Scaffold-hopping potential of fragment-based de novo design: the chances and limits of variation.

    Krueger, Bjoern A / Dietrich, Axel / Baringhaus, Karl-Heinz / Schneider, Gisbert

    Combinatorial chemistry & high throughput screening

    2009  Volume 12, Issue 4, Page(s) 383–396

    Abstract: The identification of new lead structures is a pivotal task in early drug discovery. Molecular de novo design of ligand structures has been successfully applied in various drug discovery projects. Still, the question of the scaffold hopping potential of ... ...

    Abstract The identification of new lead structures is a pivotal task in early drug discovery. Molecular de novo design of ligand structures has been successfully applied in various drug discovery projects. Still, the question of the scaffold hopping potential of drug design by adaptive evolutionary optimization has been left unanswered. It was unclear whether de novo design is actually able to leap away from given chemotypes ("activity islands"), allowing for rescaffolding of compounds. We have addressed these questions by scrutinizing different scoring functions of our de novo design software Flux for their ability to enable scaffold-hops for various target classes. We evaluated both the potential bioactivity and the scaffold diversity of de novo generated structures. For several target classes, known lead structures were reconstructed by the de novo algorithm ("lead-hopping"). We demonstrate that for one or multiple templates of a given chemotype, other chemotypes are reached during de novo compound generation, thus indicating successful scaffold-hops.
    MeSH term(s) Algorithms ; Computer Simulation ; Drug Design ; Ligands ; Molecular Structure ; Pharmaceutical Preparations/chemical synthesis ; Pharmaceutical Preparations/chemistry ; Software
    Chemical Substances Ligands ; Pharmaceutical Preparations
    Language English
    Publishing date 2009-04-21
    Publishing country United Arab Emirates
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2064785-2
    ISSN 1875-5402 ; 1386-2073
    ISSN (online) 1875-5402
    ISSN 1386-2073
    DOI 10.2174/138620709788167971
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5577: Show issues Location:
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