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  • 1
    Call number: QZ50:2
    Keywords: Genetics, Medical
    Pages: ix, 160 p. : ill.
    ISBN: 3894123583
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  • 2
    Call number: YY Diss Haer/Mag
    Keywords: DKFZ-publications / academic dissertations
    Pages: 96, XI S.
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  • 3
    Call number: QZ200:473
    Keywords: Neoplasms ; Research ; Neoplasms / history ; Research / history ; History of Medicine, 20th Cent
    Notes: Proceedings of a symposium organised by the Institut für Geschichte der Medizin in Heildelberg, Feb. 2000.
    Pages: xx, 201 p.
    ISBN: 3131056614
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  • 4
    Call number: QH308:6(4)
    Keywords: Biology
    Pages: viii, 391 p. : ill.
    Edition: Vierte, völlig neu bearbeitete und erweiterte Auflage.
    ISBN: 3-7945-1786-5
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  • 5
    Keywords: Medicine ; Human Genetics ; Biomedicine ; Human Genetics ; Springer eBooks
    Description / Table of Contents: A New Method to Predict Ion Effects in RNA Folding -- Computational Generation of RNA Nanorings -- Protocols for Molecular Dynamics Simulations of RNA Nanostructures -- Rolling Circle Transcription for the Self-Assembly of Multimeric RNAi Structures and its Applications in Nanomedicine -- Computational Prediction of the Immunomodulatory Potential of RNA Sequences -- Co-Transcriptional Production of Chemically Modified RNA Nanoparticles -- Supported Fluid Lipid Bilayer as a Scaffold to Direct Assembly of RNA Nanostructures -- Evaluation of Thermal Stability of RNA Nanoparticles by Temperature Gradient Gel Electrophoresis (TGGE) in Native Condition -- Design and Crystallography of Self-Assembling RNA Nanostructures -- X-Aptamer Selection and Validation -- Design and Preparation of Aptamer-siRNA Chimeras (AsiCs) for Targeted Cancer Therapy -- Cellular Delivery of siRNAs using Bolaamphiphiles -- Preparation and Optimization of Lipid-Like Nanoparticles for mRNA Delivery -- Chitosan Nanoparticles for miRNA Delivery -- Synthesis of PLGA/Lipid Hybrid Nanoparticles for siRNA Delivery using the Emulsion Method PLGA-PEG/Lipid Nanoparticles for siRNA Delivery -- Oxime Ether Lipids as Transfection Agents: Assembly and Complexation with siRNA -- Polycationic Probe-Guided Nanopore Single-Molecule Counter for Selective miRNA Detection -- Intracellular Re-Association of RNA-DNA Hybrids that Activates RNAi in HIV-Infected Cells -- Construction and In Vivo Testing of Prokaryotic Riboregulators -- Preparation of a Conditional RNA Switch -- Rational Engineering of a Modular Group I Ribozyme to Control its Activity by Self-Dimerization -- CRISPR-Cas RNA Scaffolds for Transcriptional Programming in Yeast -- Using Planar Phi29 pRNA Three-Way Junction to Control Size and Shape of RNA Nanoparticles for Biodistribution Profiling in Mice
    Abstract: This volume presents a collection of computational and experimental protocols pertaining to the creation, characterization, and utilization of RNA nanostructures. The chapters in this book cover topics such as ion effects in RNA folding; design and crystallography of self-assembling RNA nanostructures; x-aptamer selection and validation; RNAi in HIV-infected cells; and preparation of a conditional RNA switch. Written in the highly successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Cutting-edge and thorough, RNA Nanostructures: Methods and Protocols is a valuable resource for the design and production of RNA nanostructures. Researchers and scientists sharing these detailed protocols is important for sustained progress in the field
    Pages: XV, 383 p. 95 illus., 75 illus. in color. : online resource.
    ISBN: 9781493971381
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  • 6
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Trauma ; Stoffwechsel ; totale parenterale Ernährung ; Glukose ; Fruktose ; Fettemulsionen ; Glukose-/Fettsäuren-Zyklus ; Key words Trauma ; Metabolism ; Total parenteral nutrition ; Glucose ; Fructose ; Lipid emulsions ; Glucose-Fatty-Acid-Cycle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract Parenteral nutrition required following surgery or injury should not only meet post-aggression caloric requirements but also match the specific metabolic needs so as not to worsen the metabolic disruptions already present in this situation. The primary objective of parenteral nutrition is body protein maintenance or restoration by reduction of protein catabolism or promotion of protein synthesis or both. Whether all parenteral energy donors, i.e., glucose, fructose, other polyols, and lipid emulsions, are equally capable of achieving this objective continues to be a controversial issue. The objective of the present study was to answer the following questions: (1) Do glucose and fructose differ in their effects on the metabolic changes seen following surgery or injury, the changes in glucose metabolism in particular? (2) Can the observation of poorer glucose utilization in the presence of lipids be confirmed in ICU patients? Patients, materials and methods. A prospective, randomized clinical trial has been conducted in 20 aseptic surgical ICU patients to generate an objective database along these lines by performing a detailed analysis of the metabolic responses to different parenteral nutrition protocols. The effects of a glucose solution+lipid emulsion regimen vs fructose solution+lipid emulsion regimen on a number of carbohydrate and lipid metabolism variables were evaluated for an isocaloric (carbohydrates: 0.25 g/kg body weight/h; lipids: 0.166 g/kg body weight/h) and isonitrogenous (amino acids: 0.0625 g/kg body weight/h) total nutrient supply over a 10-h study period. Results. A significantly smaller rise in blood glucose concentrations (increase from baseline: glucose+lipids P〈0.001 vs fructose+lipids n.s.) suggested that fructose had a small effect, if any at all, on glucose metabolism. Serum insulin activity showed significant differences as a function of carbohydrate regimen, i.e. infusion of fructose instead of glucose produced a less pronounced increase in insulin activity (increase from baseline: glucose+lipids P〈0.001 vs fructose+lipids P〈0.01). Impairment of glucose utilization by concomitant administration of lipids was observed neither in patients who first received glucose nor in those who first received fructose. Conclusions. As demonstrated, parenteral fructose, unlike parenteral glucose, has a significantly less adverse impact than glucose on the glucose balance, which is disrupted initially in the post-aggression state. In addition, the less pronounced increase in insulin activity during fructose infusion than during glucose infusion can be assumed to facilitate mobilization of endogenous lipid stores and lipid oxidation. Earlier workers pointed out that any rise in free fatty acid and ketone body concentrations in the serum produces inhibition of muscular glucose uptake and oxidation, and of glycolysis. These findings were recorded in a rat model and could not be confirmed in our post-aggression state patients receiving lipid doses commensurate with the usual clinical infusion rates. The serious complications that can result from hereditary fructose intolerance are completely avoidable if a careful patient history is taken before the first parenteral use of fructose. If the patient or family members and close friends, are simply asked whether he/she can tolerate fruit and sweet dishes, hereditary fructose intolerance can be ruled out beyond all reasonable doubt. Only in the extremely rare situations in which it is not possible to question either the patient or any significant other, a test dose will have to be administered to exclude fructose intolerance. The benefits of fructose-specific metabolic effects reported in the literature and corroborated by the results of our own study suggest that fructose is an important nutrient that contributes to metabolic stabilization, especially in the post-aggression phase and in septic patients. Hyperglycaemic states are largely prevented, and fewer patients require exogenous insulin, thus avoiding the frequently underestimated risk of hypoglycaemic states.
    Notes: Zusammenfassung Wie kritisch kranke Patienten im Postaggressionsstoffwechsel parenteral ernährt werden sollen ist nach wie vor Gegenstand zahlreicher Diskussionen. Insbesondere wird kontrovers erörtert, ob Glukose allein oder zusammen mit Fruktose bzw. anderen Polyolen unter Berücksichtigung der traumabedingten Veränderungen im Glukosestoffwechsel als Kalorienträger appliziert werden soll und ob Fett als Bestandteil jedes parenteralen Ernährungsprogramms verabreicht werden kann. Zur Objektivierung dieser Fragestellung wurde im Rahmen einer prospektiv, randomisierten Studie bei 20 aseptischen Patienten einer operativen Intensivstation das Stoffwechselverhalten unter differenten Ernährungsbedingungen eingehend untersucht. In einem zehnstündigen Untersuchungszeitraum wurde bei isokalorischer (Kohlenhydrate: 0,25 g/kg KG/h, Fett: 0,166 g/kg KG/h) und isonitrogener (Aminosäuren: 0,0625 g/kg KG/h) Gesamtzufuhr der unterschiedliche Einfluß eines Glukose-/Fett- vs. Fruktose-/Fett-Regimes auf verschiedene Parameter des Kohlenhydrat- und Fettstoffwechsels verglichen. Anhand eines signifikant geringeren Blutglukose- (Anstieg gegenüber Ausgangswert: Glukose-/Fett: p〈0,001; Fruktose-/Fett: n.s.) und Insulinanstiegs (Anstieg gegenüber Ausgangswert: Glukose-/Fett: p〈0,001; Fruktose-/Fett: p〈0,01) ließ sich eine den Glukosestoffwechsel kaum beeinflussende Wirkung der Fruktose nachweisen. Eine Beeinträchtigung der Glukoseverwertung durch gleichzeitige Fettapplikation ließ sich unabhängig davon, ob die Patienten primär Glukose oder Fruktose erhielten, nicht beobachten. Die Untersuchungsergebnisse haben gezeigt, daß während des sog. Postaggressionsstoffwechsels die gleichzeitige Verabreichung von Fruktose und Fett die Glukosehomöostase signifikant weniger beeinflußt als die Applikation von Glukose als Energieträger.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 0030-493X
    Keywords: Chemistry ; Analytical Chemistry and Spectroscopy
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Additional Material: 14 Ill.
    Type of Medium: Electronic Resource
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  • 8
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Jahrestagung der Gesellschaft für Medizinische Ausbildung (GMA); 20140925-20140927; Hamburg; DOCV221 /20140911/
    Publication Date: 2014-09-12
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 9
    Keywords: brain ; EXPRESSION ; Germany ; DEATH ; PROTEIN ; METABOLISM ; MICE ; DNA ; MECHANISM ; animals ; mechanisms ; fibroblasts ; DISORDER ; ALZHEIMERS-DISEASE ; GLUTATHIONE ; PLASMA ; MUTATION ; REPAIR ; RATES ; PATHOGENESIS ; DIET ; DEMENTIA ; BEHAVIOR ; ANTIOXIDANT ; MEMORY IMPAIRMENT ; DENTATE GYRUS ; STROKE ; DEFICIENCY ; DISORDERS ; ADULT ; review ; fibroblast ; MICE LACKING ; NEURONS ; neurogenesis ; LEVEL ; NUCLEAR ; INDUCE ; GENOTYPE ; PSYCHIATRIC-DISORDERS ; USA ; HOMOCYSTEINE ; depression ; neurodegeneration ; animal ; DEGENERATION ; base excision repair ; DYSFUNCTION ; ADULT HIPPOCAMPAL NEUROGENESIS ; despair ; folate deficiency ; FOLIC-ACID DEFICIENCY ; MAJOR DEPRESSIVE DISORDER ; MILD CEREBRAL-ISCHEMIA ; MITOCHONDRIAL-DNA ; NEURAL-TUBE DEFECTS ; NEURONAL CELL-DEATH ; OXYGEN SPECIES PRODUCTION ; PLASMA HOMOCYSTEINE LEVELS
    Abstract: Folate deficiency and resultant increased homocysteine levels have been linked experimentally and epidemiologically with neurodegenerative conditions like stroke and dementia. Moreover, folate deficiency has been implicated in the pathogenesis of psychiatric disorders, most notably depression. We hypothesized that the pathogenic mechanisms include uracil misincorporation and, therefore, analyzed the effects of folate deficiency in mice lacking uracil DNA glycosylase (Ung(-/-)) versus wild-type controls. Folate depletion increased nuclear mutation rates in Ung(-/-) embryonic fibroblasts, and conferred death of cultured Ung(-/-) hippocampal neurons. Feeding animals a folate-deficient diet (FD) for 3 months induced degeneration of CA3 pyramidal neurons in Ung(-/-) but not Ung(-/-) mice along with decreased hippocampal expression of brain-derived neurotrophic factor protein and decreased brain levels of antioxidant glutathione. Furthermore, FD induced cognitive deficits and mood alterations such as anxious and despair-like behaviors that were aggravated in Ung(-/-) mice. Independent of Ung genotype, FD increased plasma homocysteine levels, altered brain monoamine metabolism, and inhibited adult hippocampal neurogenesis. These results indicate that impaired uracil repair is involved in neurodegeneration and neuropsychiatric dysfunction induced by experimental folate deficiency
    Type of Publication: Journal article published
    PubMed ID: 18614692
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  • 10
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