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Book ; Thesis: Zur Bedeutung des neuronalen Energiemetabolismus und mitochondrialer Funktionen während epileptiformer Aktivität

Schuchmann, Sebastian

Untersuchungen an In-vitro-Epilepsiemodellen

2003

Author's details	von Sebastian Schuchmann
Language	German
Size	123 Bl. : Ill., graph. Darst.
Edition	[Mikrofiche-Ausg.]
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Berlin, Humboldt-Univ., Diss., 2003
HBZ-ID	HT013758823
Database	Catalogue ZB MED Medicine, Health

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2002 MB 5349	order for loan	Magazin

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Article: Antiphospholipid-Syndrom 2007. Aktuelle Aspekte in der Labordiagnostik und deren therapeutische Konsequenzen.

Schuchmann, S / Dörner, T

Zeitschrift fur Rheumatologie

2007 Volume 66, Issue 3, Page(s) 198–200, 202–5

Abstract: Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent vascular thrombosis and loss of pregnancy in association with the presence of antiphospholipid antibodies (APA) detectable as lupus anticoagulants, anticardiolipin ... ...

Title translation	Antiphospholipid syndrome 2007. Current aspects of laboratory diagnostics and their therapeutic consequences.
Abstract	Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent vascular thrombosis and loss of pregnancy in association with the presence of antiphospholipid antibodies (APA) detectable as lupus anticoagulants, anticardiolipin antibodies or anti-beta2 glycoprotein I antibodies. The pathophysiological importance of APA in APS is accepted, however, the mechanisms leading to thrombosis are likely to be multifactorial and are so far unclear. Without a prior thrombosis, the risk of developing a new thrombosis in healthy patients with APA is slightly increased (<1% per year). However, the risk of a recurrent thrombosis increases considerably (>10% per year) in patients with a history of thrombosis without anticoagulation. The careful and correct identification of patients with APS is important because prophylactic anticoagulation can reduce the risk of recurrent thrombotic events, and during pregnancy can improve fetal and maternal outcome.
MeSH term(s)	Antiphospholipid Syndrome/diagnosis ; Antiphospholipid Syndrome/therapy ; Clinical Laboratory Techniques/trends ; Female ; Germany ; Humans ; Practice Guidelines as Topic ; Practice Patterns, Physicians'/trends ; Pregnancy ; Pregnancy Complications/diagnosis ; Pregnancy Complications/therapy ; Thrombosis/diagnosis ; Thrombosis/therapy
Language	German
Publishing date	2007-05
Publishing country	Germany
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	124985-x
ISSN	1435-1250 ; 0340-1855 ; 0301-6382
ISSN (online)	1435-1250
ISSN	0340-1855 ; 0301-6382
DOI	10.1007/s00393-007-0155-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book: Pilotprojekt DV-gestuetztes Informationssystem 'Konversion' fuer das Land Brandenburg, Deutschland

Schuchmann, S.

Abstract: Im Rahmen eines Pilotprojektes wurde Lahmeyer International beauftragt, einen Prototypen fuer das Informationssystem 'Konversion' zu erstellen. Dabei wurden alle relevanten Daten (Raumordnung, Regionalplanung, Naturschutz und Naturhaushalt etc.) fuer die ...

Title variant	Pilot Project Computer Aided Information System 'Conversion', Federal State of Brandenburg
Institution	Lahmeyer International GmbH - Beratende Ingenieure, 60496, 60496, Frankfurt am Main, DE
Abstract	Im Rahmen eines Pilotprojektes wurde Lahmeyer International beauftragt, einen Prototypen fuer das Informationssystem 'Konversion' zu erstellen. Dabei wurden alle relevanten Daten (Raumordnung, Regionalplanung, Naturschutz und Naturhaushalt etc.) fuer die Nachnutzung der Liegenschaften zusammengetragen und fuer den Einsatz in ARC/INFO aufbereitet. Als Visualisierungs- und Abfragetool dient eine mit Avenue aufbereitete ArcView 2.0-Benutzeroberflaeche. Ziel des Projektes ist es, am Beispiel der ehemaligen WGT-Standorte Stadtkaserne Perleberg, Flugplatz Finderwalde und Nuhnenkaserne Frankfurt/Oder Angaben fuer die Liegenschaftskataster zusammenzutragen, einen Prototypen fuer ein funktionales Abfrage- und Darstellungsmodell abzuleiten.
Keywords	Benutzeroberflaeche ; Umweltinformationssystem ; Geographisches Informationssystem ; Raumordnung ; Naturschutz ; Umweltplanung ; Visualisierung (Umweltinformation) ; Regionalplanung ; Prototyp ; Naturhaushalt ; Liegenschaft ; Computerprogramm ; Software ; Kataster ; Datenbank ; Flugplatz ; Pilotprojekt ; Informationssystem ; Raumbezogene Information ; Brandenburg (Land) ; Bundesrepublik Deutschland ; Frankfurt (Oder)
Language	German
Document type	Book
Remark	Projektbeginn: 01.01.1994 Projektende: 31.12.1995 Foerdernummer:
Database	Environmental research database (UFORDAT) of the German Federal Environment Agency (UBA)

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Article: Antiphospholipid-Syndrom 2007. Aktuelle Aspekte in der Labordiagnostik und deren therapeutische Konsequenzen

Schuchmann, S. / Dörner, T.

Zeitschrift für Rheumatologie

2007 Volume 66, Issue 3, Page(s) 198

Language	German
Document type	Article
ZDB-ID	124985-x
ISSN	0340-1855 ; 0301-6382
Database	Current Contents Medicine

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Article: Diminished glutathione levels cause spontaneous and mitochondria-mediated cell death in neurons from trisomy 16 mice: a model of Down's syndrome.

Schuchmann, S / Heinemann, U

publication RETRACTED

Journal of neurochemistry

2000 Volume 74, Issue 3, Page(s) 1205–1214

Abstract: It has been suggested that the increased neuronal death in cultures from trisomy 16 (Ts16) mice, a model of Down's syndrome, might result from a diminished concentration of reduced glutathione (GSH). In this study we used microfluorometric techniques to ... ...

Abstract	It has been suggested that the increased neuronal death in cultures from trisomy 16 (Ts16) mice, a model of Down's syndrome, might result from a diminished concentration of reduced glutathione (GSH). In this study we used microfluorometric techniques to investigate the effect of GSH levels on neuronal survival in diploid and Ts16 cultures. Addition of the GSH precursors cysteine and cystine and the antioxidant tocopherol to the culture medium increased the GSH concentration up to 126.0% in diploid and up to 111.9% in Ts16 neurons. Moreover, we observed a reduced spontaneous neuronal death rate in diploid and Ts16 cultures. Following the application of 50-100 microM glutamate to culture medium, we found a GSH increase in the presence of cysteine, cystine, tocopherol, and cyclosporin A, an inhibitor of mitochondrial permeability transition (diploid, 105.8-110.8%; Ts16, 83.1-96.3%). However, only tocopherol and cyclosporin A had a protective effect on glutamate-induced neuronal death. The results suggest that reduced GSH levels affect the increase of a spontaneous and a mitochondria-mediated, cyclosporin A-sensitive type of neuronal cell death. Therefore, elevating intracellular GSH concentration may have neuroprotective effects in Down's syndrome and Alzheimer's disease.
MeSH term(s)	Animals ; Cell Communication ; Cell Death ; Cells, Cultured ; Chromosomes/genetics ; Diploidy ; Disease Models, Animal ; Down Syndrome/genetics ; Down Syndrome/metabolism ; Glutathione/deficiency ; Hippocampus/pathology ; Hippocampus/physiopathology ; Humans ; Mice ; Mice, Inbred Strains ; Mice, Mutant Strains ; Mitochondria/metabolism ; Neuroglia/metabolism ; Neuroglia/pathology ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Trisomy
Chemical Substances	Glutathione (GAN16C9B8O)
Language	English
Publishing date	2000-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Retracted Publication
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1046/j.1471-4159.2000.741205.x
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Article: Increased mitochondrial superoxide generation in neurons from trisomy 16 mice: a model of Down's syndrome.

Schuchmann, S / Heinemann, U

Free radical biology & medicine

2000 Volume 28, Issue 2, Page(s) 235–250

Abstract: Increased neuronal cell death in neurodegenerative diseases has been suggested to result from an increased mitochondrial generation of radical oxygen species (ROS). To test this hypothesis, we investigated superoxide formation in cultured hippocampal ... ...

Abstract	Increased neuronal cell death in neurodegenerative diseases has been suggested to result from an increased mitochondrial generation of radical oxygen species (ROS). To test this hypothesis, we investigated superoxide formation in cultured hippocampal neurons from diploid and trisomy 16 mice (Ts16), a model of Down's syndrome. Microflurometric techniques were used to measure superoxide-induced oxidation rate of hydroethidine (HEt) to ethidium and reduced nicotinamide adenine dinucleotide (NADH) and reduced nicotinamide adenine dinucleotide phosphate (NADPH) autofluorescence signal to monitor changes in neuronal energy metabolism. We found an increase in superoxide formation by more than 50% in Ts16 neurons in comparison with diploid control neurons. In the presence of the mitochondrial respiratory chain complex I inhibitor rotenone superoxide production was blocked in diploid neurons, but the increased superoxide generation in Ts16 neurons remained. Uncoupling of mitochondrial oxidative phosphorylation using carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) caused irreversible deficiency in the energy metabolism, monitored by NAD(P)H autofluorescence in Ts16 neurons, but not in diploid control neurons. These results suggest an increased basal generation of superoxide in Ts16 neurons, probably caused by a deficient complex I of mitochondrial electron transport chain, which leads to an impaired mitochondrial energy metabolism and finally neuronal cell death.
MeSH term(s)	Animals ; Antimycin A/pharmacology ; Cell Death ; Cells, Cultured ; Chromosome Mapping ; Cyanides/pharmacology ; Diploidy ; Disease Models, Animal ; Down Syndrome/genetics ; Down Syndrome/pathology ; Down Syndrome/physiopathology ; Electron Transport Complex I ; Electron Transport Complex III/metabolism ; Electron Transport Complex IV/metabolism ; Embryonic and Fetal Development/genetics ; Hippocampus/pathology ; Hippocampus/physiopathology ; Humans ; Mice ; Mice, Mutant Strains ; Mitochondria/drug effects ; Mitochondria/physiology ; NADH, NADPH Oxidoreductases/metabolism ; Neurons/cytology ; Neurons/pathology ; Neurons/physiology ; Reactive Oxygen Species/physiology ; Rotenone/pharmacology ; Superoxides/metabolism ; Trisomy
Chemical Substances	Cyanides ; Reactive Oxygen Species ; Rotenone (03L9OT429T) ; Superoxides (11062-77-4) ; Antimycin A (642-15-9) ; Electron Transport Complex III (EC 1.10.2.2) ; NADH, NADPH Oxidoreductases (EC 1.6.-) ; Electron Transport Complex I (EC 1.6.5.3) ; Electron Transport Complex IV (EC 1.9.3.1)
Language	English
Publishing date	2000-12-14
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/s0891-5849(99)00226-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 2109: Show issues

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Article: Coupling of neuronal activity and mitochondrial metabolism as revealed by NAD(P)H fluorescence signals in organotypic hippocampal slice cultures of the rat.

Kann, O / Schuchmann, S / Buchheim, K / Heinemann, U

Neuroscience

2003 Volume 119, Issue 1, Page(s) 87–100

Abstract: During physiological activity neurons may experience localised energy demands which require intracellular signals for stimulation of mitochondrial NADH generation and subsequent delivery of ATP. To elucidate these mechanisms, we applied microfluorimetric ...

Abstract	During physiological activity neurons may experience localised energy demands which require intracellular signals for stimulation of mitochondrial NADH generation and subsequent delivery of ATP. To elucidate these mechanisms, we applied microfluorimetric monitoring of cytoplasmic (Fluo-3) and mitochondrial (Rhod-2) calcium concentration ([Ca(2+)](c), [Ca(2+)](m)), as well as of mitochondrial oxidative metabolism (NAD(P)H), whilst simultaneously measuring changes in extracellular potassium concentration ([K(+)](o)), as an indicator of neuronal activity in hippocampal slice cultures. Changes in neuronal activity were induced by repetitive stimulation at different frequencies (5, 20, 100 Hz) and intensities. Stimulation parameters were chosen to elicit rises in [K(+)](o) of less than 3 mM which is comparable to physiologically occurring rises in [K(+)](o). The mitochondrial uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP) reduced stimulus-induced changes in Rhod-2 fluorescence by 79%, indicating that Rhod-2 signals were primarily of mitochondrial origin. Repetitive stimulation at 20 Hz applied to areas CA1 or CA3 resulted in moderate rises in [K(+)](o) which were associated with stimulus-dependent elevations in [Ca(2+)](c) and [Ca(2+)](m) of up to 15%. The same stimuli also elicited biphasic changes in NAD(P)H fluorescence characterised by an initial decline and a subsequent prolonged elevation of up to 10%. Variation of stimulus parameters revealed close correlations between rises in [K(+)](o), in [Ca(2+)](m) and changes in NAD(P)H fluorescence. To elucidate the role of intracellular Ca(2+) accumulation in induction of NAD(P)H fluorescence signals, the effect of application of Ca(2+)-free solution on these signals evoked by repetitive antidromic stimulation of the alveus during recordings in area CA1 was studied. Lowering extracellular Ca(2+) led to complete blockade of postsynaptic field potential components as well as of rises in [Ca(2+)](c) and [Ca(2+)](m). Amplitudes of NAD(P)H signals were reduced by 59%, though rises in [K(+)](o) were comparable in presence and absence of extracellular Ca(2+). The results suggest i) that mitochondrial oxidative metabolism is fine-tuned to graded physiological activity in neurons and ii) that rapid mitochondrial Ca(2+) signalling represents one of the main determinants for stimulation of oxidative metabolism under physiological conditions.
MeSH term(s)	Aniline Compounds/pharmacokinetics ; Animals ; Animals, Newborn ; Calcium/metabolism ; Calcium/pharmacology ; Carbonyl Cyanide m-Chlorophenyl Hydrazone/pharmacology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Electric Stimulation ; Fluorescent Dyes/pharmacokinetics ; Heterocyclic Compounds, 3-Ring ; Hippocampus/cytology ; Hippocampus/metabolism ; In Vitro Techniques ; Ion-Selective Electrodes ; Ionophores/pharmacology ; Membrane Potentials/physiology ; Mitochondria/metabolism ; NADP/metabolism ; Neurons/physiology ; Potassium/metabolism ; Rats ; Rats, Wistar ; Xanthenes/pharmacokinetics
Chemical Substances	Aniline Compounds ; Fluorescent Dyes ; Heterocyclic Compounds, 3-Ring ; Ionophores ; Xanthenes ; rhod-2 (10I3106D4A) ; Fluo-3 (23D4W0B50Y) ; NADP (53-59-8) ; Carbonyl Cyanide m-Chlorophenyl Hydrazone (555-60-2) ; Potassium (RWP5GA015D) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2003
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/s0306-4522(03)00026-5
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Book ; Thesis: Mikrofluorometrische Untersuchungen zur Bedeutung von Glutathion, Sauerstoffradikalen und mitochondrialen Funktionen für den neuronalen Zelltod bei der Trisomie-16-Maus, einem Modell für das Down-Syndrom und die Alzheimersche Krankheit

Schuchmann, Sebastian

1998

Author's details	von Sebastian Schuchmann
Language	German
Size	106 S, Ill., graph. Darst
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Humboldt-Univ., Diss.--Berlin, 1998
Database	Former special subject collection: coastal and deep sea fishing

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Book ; Thesis: Mikrofluorometrische Untersuchungen zur Bedeutung von Glutathion, Sauerstoffradikalen und mitochondrialen Funktionen für den neuronalen Zelltod bei der Trisomie-16-Maus, einem Modell für das Down-Syndrom und die Alzheimersche Krankheit

Schuchmann, Sebastian

1998

Author's details	von Sebastian Schuchmann
Language	German
Size	106 S, Ill., graph. Darst
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Humboldt-Univ., Diss.--Berlin, 1998
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Neurobiological and physiological mechanisms of fever-related epileptiform syndromes.

Schuchmann, Sebastian / Vanhatalo, Sampsa / Kaila, Kai

Brain & development

2009 Volume 31, Issue 5, Page(s) 378–382

Abstract: Febrile seizures (FS) are the most common type of convulsive events in children. FS have been extensively studied using animal models, where rat and mice pups are placed in a hyperthermic environment. Such work has largely focused on the consequences ... ...

Abstract	Febrile seizures (FS) are the most common type of convulsive events in children. FS have been extensively studied using animal models, where rat and mice pups are placed in a hyperthermic environment. Such work has largely focused on the consequences rather than on the mechanisms of experimental febrile seizures (eFS). We have recently shown that eFS are preceded by a dramatic rise in the rate of respiration. The consequent respiratory alkalosis affecting the brain and increasing neuronal excitability is a direct cause of the eFS [1]. If a similar mechanism contributes to human FS and other fever-related epileptiform syndromes, a number of factors operating at the molecular, cellular and systems level that have not been previously thought to be involved in their etiology must be considered. These include physiological and pathophysiological factors affecting CO(2) chemosensitivity as well as cellular and systemic mechanisms of acid-base regulation. Furthermore, a critical role for brain pH in FS points to novel types of susceptibility genes, which include genes coding pH-sensitive target proteins (e.g. neuronal ion channels) and pH-regulatory proteins. We will discuss these novel ideas and putative therapies based on them.
MeSH term(s)	Acid-Base Equilibrium/physiology ; Alkalosis, Respiratory/complications ; Alkalosis, Respiratory/physiopathology ; Animals ; Brain/metabolism ; Brain/physiopathology ; Carbon Dioxide/metabolism ; Chemoreceptor Cells/physiology ; Disease Models, Animal ; Genetic Predisposition to Disease/genetics ; Humans ; Hyperventilation/complications ; Hyperventilation/physiopathology ; Infant ; Ion Channels/genetics ; Mice ; Rats ; Seizures, Febrile/etiology ; Seizures, Febrile/metabolism ; Seizures, Febrile/physiopathology
Chemical Substances	Ion Channels ; Carbon Dioxide (142M471B3J)
Language	English
Publishing date	2009-05
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604822-5
ISSN	1872-7131 ; 0387-7604
ISSN (online)	1872-7131
ISSN	0387-7604
DOI	10.1016/j.braindev.2008.11.011
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 1788: Show issues

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