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Search Results: 1 - 10 of 14825 matches for " Christian Hagel "
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Recycling of gold from electronics: Cost-effective use through ‘Design for Recycling’
Christian Hagelüken,Christopher W Corti
Gold Bulletin , 2010, DOI: 10.1007/BF03214988
Abstract: The importance of the gold content of scrap electronics to the economics of recovery of gold and many other valuable metals is not always appreciated and this impacts on the “design for recycling” approach in selecting materials for new products, particularly in the European Union where the WEEE Directive aims to provide a closed loop economy. With a lower carbon footprint than primary-mined gold, recycled gold represents an important “green” source. The challenges faced in recycling electronic scrap to achieve a closed loop economy are discussed.
Nestin Modulates Glucocorticoid Receptor Function by Cytoplasmic Anchoring
Rudolph Reimer, Heike Helmbold, Beata Szalay, Christian Hagel, Heinrich Hohenberg, Wolfgang Deppert, Wolfgang Bohn
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0006084
Abstract: Nestin is the characteristic intermediate filament (IF) protein of rapidly proliferating progenitor cells and regenerating tissue. Nestin copolymerizes with class III IF-proteins, mostly vimentin, into heteromeric filaments. Its expression is downregulated with differentiation. Here we show that a strong nestin expression in mouse embryo tissue coincides with a strong accumulation of the glucocorticoid receptor (GR), a key regulator of growth and differentiation in embryonic development. Microscopic studies on cultured cells show an association of GR with IFs composed of vimentin and nestin. Cells lacking nestin, but expressing vimentin, or cells expressing vimentin, but lacking nestin accumulate GR in the nucleus. Completing these networks with an exogenous nestin, respectively an exogenous vimentin restores cytoplasmic anchoring of GR to the IF system. Thus, heteromeric filaments provide the basis for anchoring of GR. The reaction pattern with phospho-GR specific antibodies and the presence of the chaperone HSC70 suggest that specifically the unliganded receptor is anchored to the IF system. Ligand addition releases GR from IFs and shifts the receptor into the nucleus. Suppression of nestin by specific shRNA abolishes anchoring of GR, induces its accumulation in the nucleus and provokes an irreversible G1/S cell cycle arrest. Suppression of GR prior to that of nestin prevents entry into the arrest. The data give evidence that nestin/vimentin specific anchoring modulates growth suppression by GR. We hypothesize that expression of nestin is a major determinant in suppression of anti-proliferative activity of GR in undifferentiated tissue and facilitates activation of this growth control in a precise tissue and differentiation dependent manner.
Cancer Stem Cell-Like Cells Derived from Malignant Peripheral Nerve Sheath Tumors
Melanie Spyra,Lan Kluwe,Christian Hagel,Rosa Nguyen,Jens Panse,Andreas Kurtz,Victor Felix Mautner,Samuel David Rabkin,Maria Demestre
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0021099
Abstract: This study aims to examine whether or not cancer stem cells exist in malignant peripheral nerve sheath tumors (MPNST). Cells of established lines, primary cultures and freshly dissected tumors were cultured in serum free conditions supplemented with epidermal and fibroblast growth factors. From one established human MPNST cell line, S462, cells meeting the criteria for cancer stem cells were isolated. Clonal spheres were obtained, which could be passaged multiple times. Enrichment of stem cell-like cells in these spheres was also supported by increased expression of stem cell markers such as CD133, Oct4, Nestin and NGFR, and decreased expression of mature cell markers such as CD90 and NCAM. Furthermore, cells of these clonal S462 spheres differentiated into Schwann cells, smooth muscle/fibroblast and neurons-like cells under specific differentiation-inducing cultural conditions. Finally, subcutaneous injection of the spheres into immunodeficient nude mice led to tumor formation at a higher rate compared to the parental adherent cells (66% versus 10% at 2.5×105). These results provide evidence for the existence of cancer stem cell-like cells in malignant peripheral nerve sheath tumors.
An Individual Patient Data Meta-Analysis on Characteristics and Outcome of Patients with Papillary Glioneuronal Tumor, Rosette Glioneuronal Tumor with Neuropil-Like Islands and Rosette Forming Glioneuronal Tumor of the Fourth Ventricle
Annika Schlamann, André O. von Bueren, Christian Hagel, Isabella Zwiener, Clemens Seidel, Rolf-Dieter Kortmann, Klaus Müller
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0101211
Abstract: Background and Purpose In 2007, the WHO classification of brain tumors was extended by three new entities of glioneuronal tumors: papillary glioneuronal tumor (PGNT), rosette-forming glioneuronal tumor of the fourth ventricle (RGNT) and glioneuronal tumor with neuropil-like islands (GNTNI). Focusing on clinical characteristics and outcome, the authors performed a comprehensive individual patient data (IPD) meta-analysis of the cases reported in literature until December 2012. Methods PubMed, Embase and Web of Science were searched for peer-reviewed articles reporting on PGNT, RGNT, and GNTNI using predefined keywords. Results 95 publications reported on 182 patients (PGNT, 71; GNTNI, 26; RGNT, 85). Median age at diagnosis was 23 years (range 4–75) for PGNT, 27 years (range 6–79) for RGNT, and 40 years (range 2–65) for GNTNI. Ninety-seven percent of PGNT and 69% of GNTNI were located in the supratentorial region, 23% of GNTNI were in the spinal cord, and 80% of RGNT were localized in the posterior fossa. Complete resection was reported in 52 PGNT (73%), 36 RGNT (42%), and 7 GNTNI (27%) patients. Eight PGNT, 3 RGNT, and 12 GNTNI patients were treated with chemo- and/or radiotherapy as the primary postoperative treatment. Follow-up data were available for 132 cases. After a median follow-up time of 1.5 years (range 0.2–25) across all patients, 1.5-year progression-free survival rates were 52±12% for GNTNI, 86±5% for PGNT, and 100% for RGNT. The 1.5-year overall-survival were 95±5%, 98±2%, and 100%, respectively. Conclusions The clinical understanding of the three new entities of glioneuronal tumors, PGNT, RGNT and GNTNI, is currently emerging. The present meta-analysis will hopefully contribute to a delineation of their diagnostic, therapeutic, and prognostic profiles. However, the available data do not provide a solid basis to define the optimum treatment approach. Hence, a central register should be established.
Surgical Treatment for Neonatal Hydrocephalus: Catheter-Based Cerebrospinal Fluid Diversion or Endoscopic Intervention?  [PDF]
Matthias Krause, Christos P. Panteliadis, Christian Hagel, Franz W. Hirsch, Ulrich H. Thome, Jürgen Meixensberger, Ulf Nestler
Open Journal of Modern Neurosurgery (OJMN) , 2018, DOI: 10.4236/ojmn.2018.81002
Abstract: Neonatal hydrocephalus can arise from a multitude of disturbances, among them congenital aqueductal stenosis, myelomeningocele or posthemorrhagic complications in preterm infants. Diagnostic work-up comprises transfontanellar ultrasonography, T2 weighted MRI and clinical assessment for rare inherited syndromes. Classification of hydrocephalus and treatment guidelines is based on detailed consensus statements. The recent evidence favors catheter-based cerebrospinal fluid diversion in children below 6 months, but emerging techniques such as neuroendoscopic lavage carry the potential to lower shunt insertion rates. More long-term study results will be needed to allow for individualized, multidisciplinary decision making. This article gives an overview regarding contemporary pathophysiological concepts, the latest consensus statements and most recent technical developments.
Expression of Eukaryotic Initiation Factor 5A and Hypusine Forming Enzymes in Glioblastoma Patient Samples: Implications for New Targeted Therapies
Michael Preukschas, Christian Hagel, Alexander Schulte, Kristoffer Weber, Katrin Lamszus, Henning Sievert, Nora P?llmann, Carsten Bokemeyer, Joachim Hauber, Melanie Braig, Stefan Balabanov
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0043468
Abstract: Glioblastomas are highly aggressive brain tumors of adults with poor clinical outcome. Despite a broad range of new and more specific treatment strategies, therapy of glioblastomas remains challenging and tumors relapse in all cases. Recent work demonstrated that the posttranslational hypusine modification of the eukaryotic initiation factor 5A (eIF-5A) is a crucial regulator of cell proliferation, differentiation and an important factor in tumor formation, progression and maintenance. Here we report that eIF-5A as well as the hypusine-forming enzymes deoxyhypusine synthase (DHS) and deoxyhypusine hydroxylase (DOHH) are highly overexpressed in glioblastoma patient samples. Importantly, targeting eIF-5A and its hypusine modification with GC7, a specific DHS-inhibitor, showed a strong antiproliferative effect in glioblastoma cell lines in vitro, while normal human astrocytes were not affected. Furthermore, we identified p53 dependent premature senescence, a permanent cell cycle arrest, as the primary outcome in U87-MG cells after treatment with GC7. Strikingly, combined treatment with clinically relevant alkylating agents and GC7 had an additive antiproliferative effect in glioblastoma cell lines. In addition, stable knockdown of eIF-5A and DHS by short hairpin RNA (shRNA) could mimic the antiproliferative effects of GC7. These findings suggest that pharmacological inhibition of eIF-5A may represent a novel concept to treat glioblastomas and may help to substantially improve the clinical course of this tumor entity.
Disruption of the Autophagy-Lysosome Pathway Is Involved in Neuropathology of the nclf Mouse Model of Neuronal Ceroid Lipofuscinosis
Melanie Thelen, Markus Daμμe, Michaela Schweizer, Christian Hagel, Andrew M.S. Wong, Jonathan D. Cooper, Thomas Braulke, Giovanna Galliciotti
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035493
Abstract: Variant late-infantile neuronal ceroid lipofuscinosis, a fatal lysosomal storage disorder accompanied by regional atrophy and pronounced neuron loss in the brain, is caused by mutations in the CLN6 gene. CLN6 is a non-glycosylated endoplasmic reticulum (ER)-resident membrane protein of unknown function. To investigate mechanisms contributing to neurodegeneration in CLN6 disease we examined the nclf mouse, a naturally occurring model of the human CLN6 disease. Prominent autofluorescent and electron-dense lysosomal storage material was found in cerebellar Purkinje cells, thalamus, hippocampus, olfactory bulb and in cortical layer II to V. Another prominent early feature of nclf pathogenesis was the localized astrocytosis that was evident in many brain regions and the more widespread microgliosis. Expression analysis of mutant Cln6 found in nclf mice demonstrated synthesis of a truncated protein with a reduced half-life. Whereas the rapid degradation of the mutant Cln6 protein can be inhibited by proteasomal inhibitors, there was no evidence for ER stress or activation of the unfolded protein response in various brain areas during postnatal development. Age-dependent increases in LC3-II, ubiquitinated proteins, and neuronal p62-positive aggregates were observed, indicating a disruption of the autophagy-lysosome degradation pathway of proteins in brains of nclf mice, most likely due to defective fusion between autophagosomes and lysosomes. These data suggest that proteasomal degradation of mutant Cln6 is sufficient to prevent the accumulation of misfolded Cln6 protein, whereas lysosomal dysfunction impairs constitutive autophagy promoting neurodegeneration.
Targeting Class IA PI3K Isoforms Selectively Impairs Cell Growth, Survival, and Migration in Glioblastoma
Katrin H?land, Danielle Boller, Christian Hagel, Silvia Dolski, András Treszl, Olivier E. Pardo, Paulina ?wiek, Fabiana Salm, Zaira Leni, Peter R. Shepherd, Beata Styp-Rekowska, Valentin Djonov, André O. von Bueren, Karl Frei, Alexandre Arcaro
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0094132
Abstract: The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is frequently activated in human cancer and plays a crucial role in glioblastoma biology. We were interested in gaining further insight into the potential of targeting PI3K isoforms as a novel anti-tumor approach in glioblastoma. Consistent expression of the PI3K catalytic isoform PI3K p110α was detected in a panel of glioblastoma patient samples. In contrast, PI3K p110β expression was only rarely detected in glioblastoma patient samples. The expression of a module comprising the epidermal growth factor receptor (EGFR)/PI3K p110α/phosphorylated ribosomal S6 protein (p-S6) was correlated with shorter patient survival. Inhibition of PI3K p110α activity impaired the anchorage-dependent growth of glioblastoma cells and induced tumor regression in vivo. Inhibition of PI3K p110α or PI3K p110β also led to impaired anchorage-independent growth, a decreased migratory capacity of glioblastoma cells, and reduced the activation of the Akt/mTOR pathway. These effects were selective, because targeting of PI3K p110δ did not result in a comparable impairment of glioblastoma tumorigenic properties. Together, our data reveal that drugs targeting PI3K p110α can reduce growth in a subset of glioblastoma tumors characterized by the expression of EGFR/PI3K p110α/p-S6.
Active stabilization of a chaotic urban system
Günter Haag,Tilo Hagel,Timm Sigg
Discrete Dynamics in Nature and Society , 1996, DOI: 10.1155/s1026022697000137
Abstract: A new method to stabilize dynamical systems by forcing the system variables into the desired unstable stationary point is proposed. The key conception of the method is based on parametric perturbation. This means that the equations of motion are influenced by continuous variation of some selected parameters. Thus ¢ € “ without using any external forces ¢ € “ the motion of the system approaches the chosen unstable stationary point. The variation of the parameters will vanish after the successful stabilization. Therefore, the system and its parameters are changed during the control process only. The algorithm is applied to an urban system within a metropolitan area obeying a Lorenz-type dynamics as well as to the H non attractor as an example for a discrete scenario.
Biochemistry and Occurrence of O-Demethylation in Plant Metabolism
Jillian M. Hagel,Peter J. Facchini
Frontiers in Physiology , 2010, DOI: 10.3389/fphys.2010.00014
Abstract: Demethylases play a pivitol role in numerous biological processes from covalent histone modification and DNA repair to specialized metabolism in plants and microorganisms. Enzymes that catalyze O- and N-demethylation include 2-oxoglutarate (2OG)/Fe(II)-dependent dioxygenases, cytochromes P450, Rieske-domain proteins and flavin adenine dinucleotide (FAD)-dependent oxidases. Proposed mechanisms for demethylation by 2OG/Fe(II)-dependent enzymes involve hydroxylation at the O- or N-linked methyl group followed by formaldehyde elimination. Members of this enzyme family catalyze a wide variety of reactions in diverse plant metabolic pathways. Recently, we showed that 2OG/Fe(II)-dependent dioxygenases catalyze the unique O-demethylation steps of morphine biosynthesis in opium poppy, which provides a rational basis for the widespread occurrence of demethylases in benzylisoquinoline alkaloid metabolism.
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