Kamrowski-Kruck, Heike

[["dc.bibliographiccitation.firstpage","60"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Liver International"],["dc.bibliographiccitation.lastpage","65"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Nolte, Wilhelm"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Pahl, Karoline"],["dc.contributor.author","Unterberg, Knut"],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Schindler, Christian G."],["dc.contributor.author","Figulla, Hans Reiner"],["dc.contributor.author","Buchwald, Arnd B."],["dc.contributor.author","Hartmann, Heinz"],["dc.contributor.author","Ramadori, Giuliano"],["dc.date.accessioned","2017-09-07T11:44:24Z"],["dc.date.available","2017-09-07T11:44:24Z"],["dc.date.issued","2000"],["dc.description.abstract","Aims/Background: Endothelin-1 (ET-1) may be a mediator for portal hypertension in liver cirrhosis. The aim of the present study was to determine the concentrations of ET-1 in the systemic and splanchnic circulation before and after reduction of portal hypertension by transjugular intrahepatic portosystemic shunt implantation (TIPS). Methods: Plasma concentrations of immunoreactive ET-1 were measured in peripheral venous blood samples from 25 patients with liver cirrhosis before and at 1, 3, 9 and 15 months after TIPS. Furthermore, acute effects of TIPS on ET-1 were studied in plasma samples from the hepatic vein, the portal vein 30 minutes before and after TIPS and in the femoral artery (only after TIPS) in a subgroup of 15 patients. In addition, the portocaval pressure gradient was determined before and after TIPS. Results: Before TIPS peripheral venous plasma ET-1 concentrations (n=25; median 4.2 pg/ml; range 1.9–14.7) were significantly increased in patients with refractory ascites (n=7; median 7.8, range 3.5–14.7) compared to patients with repetitive bleeding (n=18; median 3.4; range 1.9–7.1) (p=0.003). Furthermore, peripheral ET-1 concentrations correlated with the degree of liver dysfunction according to the Child-Pugh classification (Spearman's r=0.46; p=0.02). Following TIPS, peripheral ET-1 concentrations remained unchanged during a follow-up of 15 months. Before TIPS, a positive gradient of ET-1 concentrations from portalvenous to hepatovenous and peripheral venous levels was found (p<0.03). Immediately after TIPS, arterial ET-1 concentrations reached markedly increased levels in individual patients (88, 92 and 103 pg/ml). Severe systemic reactions to these high levels were not observed. Peripheral venous, hepatovenous and portalvenous ET-1 concentrations did not correlate with portocaval pressure gradients. Conclusion: Cirrhotic patients demonstrated unchanged peripheral venous ET-1 concentrations up to 15 months after TIPS. Portal congestion was associated with increased ET-1 levels in the prehepatic splanchnic area. The effect of portal decompression on splanchnic and systemic ET-1 levels deserves further investigation."],["dc.identifier.doi","10.1034/j.1600-0676.2000.020001060.x"],["dc.identifier.gro","3151647"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8464"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","1478-3223"],["dc.title","Systemic and splanchnic endothelin-1 plasma levels in liver cirrhosis before and after transjugular intrahepatic portosystemic shunt (TIPS)"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","613"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","622"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Klafki, Hans-Wolfgang"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Mueller, Katharina"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Popp, Julius"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Wolf, Stefanie"],["dc.contributor.author","Prinz, Berit"],["dc.contributor.author","Luckhaus, Christian"],["dc.contributor.author","Schroeder, Johannes"],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Gertz, Hermann-Josef"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Mueller, Bernhard W."],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T08:34:46Z"],["dc.date.available","2018-11-07T08:34:46Z"],["dc.date.issued","2009"],["dc.description.abstract","The clinical diagnosis of neurodegenerative disorders can be supported by soluble biomarkers in cerebrospinal fluid (CSF), such as tau protein, phospho-tau, and amyloid-beta peptides. In particular, increased CSF levels of phospho-tau in Alzheimer's disease appear to reflect disease specific pathological processes. We report here evidence for the presence of soluble MAP-kinase ERK1/2 in a small set of human CSF samples from patients with Alzheimer's disease, frontotemporal degeneration, and mild cognitive impairment. The level of total ERK1/2 in CSF as measured by electrochemiluminescent assay was correlated with that of total tau and phospho-tau. A small fraction of ERK1/2 in a pooled CSF sample was found to be in the doubly phosphorylated (activated) state. Our findings suggest that i) MAP kinase ERK1/2 is apparently released under neurodegenerative conditions in parallel with tau and phospho-tau and ii) in the future, it might be possible to find in CSF samples evidence for disease related alterations in brain kinase signaling pathways by use of highly sensitive and activation-state specific anti-kinase antibodies."],["dc.identifier.doi","10.3233/JAD-2009-1167"],["dc.identifier.isi","000272860100013"],["dc.identifier.pmid","19625747"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17898"],["dc.notes.claim","Wed Nov 07 12:36:41 UTC 2018:dc_contributor_author:Hallo Sabine, das ist nicht mein Artikel.... :-)"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1387-2877"],["dc.title","Measurement of ERK 1/2 in CSF from Patients with Neuropsychiatric Disorders and Evidence for the Presence of the Activated Form"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","18"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","26"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Loffler, B. M."],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","von Ahsen, N."],["dc.contributor.author","Siren, A. L."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T09:12:33Z"],["dc.date.available","2018-11-07T09:12:33Z"],["dc.date.issued","2001"],["dc.description.abstract","Astrocytes are known to possess an effective endothelin (ET) eliminatory system which involves astrocytic ETA and ETB receptors and may become particularly relevant under pathophysiological conditions. The present study has therefore been designed to explore the effect of standardized hypoxia on extracellular concentrations of endothelin-1 (ET-1) and on endothelin-converting enzyme (ECE) activity in primary rat astrocytes genetically (sl/sl) or experimentally (dexamethasone) deficient in ETB receptors. The results revealed (1) a hypoxia-mediated decrease of extracellular ET-1 in wildtype astrocytes (+/+) that was not observed in ETB-deficient (sl/sl) cultures; (2) an ET receptor antagonist-induced increase in ET-1 in the media of both genotypes with further elevation upon hypoxia in +/+ cultures only; (3) augmentation of the dexamethasone-induced increase in extracellular ET-1 by hypoxia in +/+, but not in sl/sl cultures; (4) synergistic reduction of ETB gene transcription by hypoxia and dexamethasone; and (5) significant increases in endothelin-converting enzyme activity in the presence of hypoxia. To conclude, hypoxia stimulates astrocytic release of mature ET-1, This stimulation is (over)compensated for by increased ET-1 binding to functional ETB receptors. ETB deficiency, whether genetic or experimentally induced, impairs elimination of extracellular (C) 2001 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/glia.1036"],["dc.identifier.isi","000167958400003"],["dc.identifier.pmid","11284016"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26960"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Role of the astrocytic ETB receptor in the regulation of extracellular endothelin-1 during hypoxia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","957"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Neurochemical Research"],["dc.bibliographiccitation.lastpage","969"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Siren, A. L."],["dc.contributor.author","Knerlich, F."],["dc.contributor.author","Schilling, L."],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Hahn, A."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T10:42:23Z"],["dc.date.available","2018-11-07T10:42:23Z"],["dc.date.issued","2000"],["dc.description.abstract","We characterized the time-course, intensity of expression and cellular origin of components of the endothelin (ET) system in the rat brain after a standardized neurotrauma (cryogenic lesion of the parietal cortex). ET mRNAs were expressed at sham level after neurotrauma, whereas immunoreactivity for ET-1 was enhanced in glia and endothelium of the lesioned hemisphere and both hippocampi. The number of ET-3 positive mononuclear cells in the lesion perimeter increased starting at 24h after injury. At 48h after neurotrauma, ET-receptor immunoreactivity was increased in astrocytes. In basilar artery endothelium, ETB-immunoreactivity was reduced at 48h to 72h recovering at 7 days whereas ETA-receptor and ET-peptide immunoreactivities were not altered. In summary, neurotrauma leads to a multicellular stimulation of endothelins in the brain along with a delayed selective loss of vascular ETB-receptors. These changes seem to be posttranscriptional and cell type specific. They favor vasoconstriction increasing the risk of late vasospasm and ischemia."],["dc.identifier.doi","10.1023/A:1007552408463"],["dc.identifier.isi","000088734500008"],["dc.identifier.pmid","10959492"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46784"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Kluwer Academic/plenum Publ"],["dc.relation.issn","0364-3190"],["dc.title","Differential glial and vascular expression of endothelins and their receptors in rat brain after neurotrauma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3485"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Neuroreport"],["dc.bibliographiccitation.lastpage","3488"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Heyer, A."],["dc.contributor.author","Unzicker, C."],["dc.contributor.author","Siren, A. L."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T11:00:45Z"],["dc.date.available","2018-11-07T11:00:45Z"],["dc.date.issued","2000"],["dc.description.abstract","The potential of erythropoietin (EPO) to reduce hypoxia-induced cell death has been investigated in 5-day-old primary cultures of rat postnatal hippocampal neurons. Application of EPO (100 pM) at the start of hypoxia resulted in a significant reduction of neuronal death (33.0 +/- 7.5% in cells incubated with EPO vs 56.75 +/- 7.3% in non-treated cells; n = 4, p < 0.021). Similiar results were obtained upon application of cycloheximide (CHX; 1 M) simultaneously with hypoxia (34.75 +/- 5.6% vs 56.75 +/- 7.3% with and without CHX, respectively, n = 4, p < 0.035), indicating that hypoxia-induced neuronal death is an active, protein synthesis-dependent process. Both, EPO and EPO receptor (EPOR) were found to; be expressed after hypoxia in hippocampal neurons in vitro and in vivo. These results demonstrate for the first time that EPO can reverse hypoxia-induced neuronal death when applied simultaneously with the hypoxic stimulus. NeuroReport 11:3485-3488 (C) 2000 Lippincott Williams & Wilkins."],["dc.identifier.doi","10.1097/00001756-200011090-00017"],["dc.identifier.isi","000165301600017"],["dc.identifier.pmid","11095504"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50997"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0959-4965"],["dc.title","Survival of hippocampal neurons in culture upon hypoxia: effect of erythropoietin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","127"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuroscience Research"],["dc.bibliographiccitation.lastpage","134"],["dc.contributor.author","Jordan, Wolfgang"],["dc.contributor.author","Deckers, Markus"],["dc.contributor.author","Kamrowski, H."],["dc.contributor.author","Brunner, Edgar"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Hajak, G."],["dc.date.accessioned","2017-09-07T11:45:34Z"],["dc.date.available","2017-09-07T11:45:34Z"],["dc.date.issued","2002"],["dc.description.abstract","Plasma endothelin elevations have been associated with cerebrovascular pathology. Mechanisms of stimulation, however, are unknown. Therefore, in healthy subjects a marked physiological cerebrovascular response was experimentally provoked by hypercapnia, hypocapnia, and alternating capneic conditions. During these challenges plasma immunoreactive- endothelin-1 (ir-ET-1) concentrations were determined using a radioimmunassay. Physiological effects were continuously recorded for pCO(2), cerebral blood flow velocity, pulse frequency, and arterial blood pressure. No alterations in plasma ET-1 levels were found upon any of the cerebrovascular stimuli. We conclude that massive cerebrovascular challenges in healthy individuals do not lead to high circulating ET-I levels. (C) 2002 Elsevier Science Ireland Ltd and the Japan Neuroscience Society. All rights reserved."],["dc.identifier.gro","3150393"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7152"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0168-0102"],["dc.title","Effects of cerebrovascular challenges on plasma endothelin"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","480"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Pediatric Surgery"],["dc.bibliographiccitation.lastpage","488"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Dembowski, C."],["dc.contributor.author","Hofmann, Peter J."],["dc.contributor.author","Koch, T."],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Riedesel, H."],["dc.contributor.author","Krammer, H. J."],["dc.contributor.author","Kaup, F. J."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T09:25:53Z"],["dc.date.available","2018-11-07T09:25:53Z"],["dc.date.issued","2000"],["dc.description.abstract","Background/Purpose: Spotting lethal (sl) rats, a model for Hirschsprung's disease, recently have been found to carry a deletion in the endothelin B (ETB) gene, causing functional lack of ETB receptors. The ETB receptor mediates, together with and in counterbalance to the ETA receptor, endothelin actions on vessels, cell proliferation, and migration. The authors investigated the effect of homozygosity (sl/sl) or heterozygosity (+/sl) on phenotype, intestinal morphology, and survival. Methods: Weight, circumference, and serum albumin were measured. Histological tests of major organs and immunoperoxidase reaction for Peripherin, glial fibrillary acid protein (GFAP), and S-100 in small and large intestine were performed. Peripherin-immunostained sections of colon and jejunum were analyzed morphometrically. Screening for sep sis included search for enterocolitis, bacterial infection, endotoxin, and INOS mRNA. Results: Sl/sl rats died within 4 weeks of life, showing an early and a later death group. Serum albumin levels were de-creased in sl/sl rats, whereas signs of sepsis were rare. Immunostaining uncovered alterations in nerve and glial cells in the whole gut of sl/sl rats, and to a subtle degree also in +/sl rats, which appear clinically normal. Morphometric quantification yielded statistically significant alterations in sl/sl rats only. No obvious abnormalities were found in other organs. Conclusions: Sl/sl rats die from malnutrition rather than sepsis, too early for ischemic complications to occur. Rats of the later death group are a suitable model for studying the ETB receptor in vivo. Subtle abnormalities in the enteric nervous system of heterozygous rats underline the critical role of the \"gene dose\" for functional compensation. Copyright (C) 2000 by W.B. Saunders Company."],["dc.identifier.doi","10.1016/S0022-3468(00)90218-5"],["dc.identifier.isi","000085604600016"],["dc.identifier.pmid","10726693"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30169"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co"],["dc.relation.issn","0022-3468"],["dc.title","Phenotype, intestinal morphology, and survival of homozygous and heterozygous endothelin B receptor-deficient (spotting lethal) rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","138"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","145"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Popp, J."],["dc.contributor.author","Buerger, Katharina"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Prinz, Berit"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, C. H."],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Huell, Michael"],["dc.contributor.author","Schroeder, J."],["dc.contributor.author","Kessler, H."],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Gertz, H-J"],["dc.contributor.author","Klafki, H-W"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Reulbach, Udo"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T08:46:25Z"],["dc.date.available","2018-11-07T08:46:25Z"],["dc.date.issued","2010"],["dc.description.abstract","In this report, we present the results of a multicenter study to test analytic and diagnostic performance of soluble forms of amyloid precursor proteins alpha and beta (sAPP alpha and sAPP beta) in the cerebrospinal fluid (CSF) of patients with different forms of dementing conditions. CSF samples were collected from 188 patients with early dementia (mini-mental state examination >= 20 in majority of cases) and mild cognitive impairment (MCI) in 12 gerontopsychiatric centers, and the clinical diagnoses were supported by neurochemical dementia diagnostic (NDD) tools: CSF amyloid beta peptides, Tau and phospho-Tau. sAPP alpha and sAPP beta were measured with multiplexing method based on electrochemiluminescence. sAPP alpha and sAPP beta CSF concentrations correlated with each other with very high correlation ratio (R= 0.96, P < 0.001). We observed highly significantly increased sAPP alpha and sAPP beta CSF concentrations in patients with NDD characteristic for Alzheimer's disease (AD) compared to those with NDD negative results. sAPP alpha and sAPP beta highly significantly separated patients with AD, whose diagnosis was supported by NDD findings (sAPP alpha: cutoff, 117.4 ng ml(-1), sensitivity, 68%, specificity, 85%, P< 0.001; sAPP beta: cutoff, 181.8 ng ml(-1), sensitivity, 75%, specificity, 85%, P < 0.001), from the patients clinically assessed as having other dementias and supported by NDD untypical for AD. We conclude sAPP alpha and sAPP beta might be regarded as novel promising biomarkers supporting the clinical diagnosis of AD. Molecular Psychiatry (2010) 15, 138-145; doi: 10.1038/mp.2008.84; published online 29 July 2008"],["dc.identifier.doi","10.1038/mp.2008.84"],["dc.identifier.isi","000273876000006"],["dc.identifier.pmid","18663368"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20687"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1359-4184"],["dc.title","Soluble amyloid precursor proteins in the cerebrospinal fluid as novel potential biomarkers of Alzheimer's disease: a multicenter study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]