Hasselblatt, Martin

[["dc.bibliographiccitation.firstpage","427"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow and Metabolism"],["dc.bibliographiccitation.lastpage","430"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Heyer, Andrea"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Häfner, Heinz"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:18Z"],["dc.date.available","2017-09-07T11:46:18Z"],["dc.date.issued","2005"],["dc.description.abstract","Gender differences in neuropsychiatric disease are recognized but not well understood. Investigating the survival of primary rat hippocampal neurons in culture, we found significant and inverted gender differences on normoxia versus hypoxia. Male cells were more resistant under normoxia but more vulnerable under hypoxia than female cells. Male vulnerability pattern was acquired in cells from neonatally testosterone-primed females. Estrogens, acting via membrane receptors, had a higher neuroprotective power in male neurons, explained at least in part by the pronounced increase in estrogen receptor beta/alpha ratio during hypoxia in male cells only."],["dc.identifier.doi","10.1038/sj.jcbfm.9600056"],["dc.identifier.gro","3150469"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7237"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0271-678X"],["dc.subject","aromatase; estrogen receptor alpha; estrogen receptor beta; hippocampus; sex; testosterone"],["dc.title","In vitro gender differences in neuronal survival on hypoxia and in 17 beta-estradiol-mediated neuroprotection"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","239"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Alcohol and Alcoholism"],["dc.bibliographiccitation.lastpage","242"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Krieg-Hartig, Christian"],["dc.contributor.author","Hüfner, Michael"],["dc.contributor.author","Halaris, Angelos"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:45:48Z"],["dc.date.available","2017-09-07T11:45:48Z"],["dc.date.issued","2003"],["dc.description.abstract","Aims: Testosterone synthesis in chronic alcoholics is affected by a variety of mechanisms. Little is known about the reversibility of these changes upon abstinence and available data on circulating hormone levels are incomplete and inconsistent. Methods: Serum concentrations of free testosterone, total testosterone, and luteinizing hormone (LH) were determined in 18 male non-cirrhotic chronic alcoholics on days 2, 22, 82 and 127 of strictly controlled abstinence, as well as in a group of 20 healthy age-matched controls. Results: Higher total testosterone concentrations were found in alcoholics on the second day of abstinence, as compared to controls (7.1 ± 1.9 vs 5.6 ± 1.4 ng/ml) and throughout the whole observation period. Correspondingly, free testosterone concentrations were increased over control levels on day 2 (40.0 ± 12.1 vs 29.7 ± 8.1 pg/ml) and stayed elevated in the presence of augmented concentrations of LH [4.5 U/l (range 1.6–9.5 U/l) vs 2.0 U/l (range 0.8–8.1 U/l)] for up to 127 days of strictly controlled abstinence. Conclusions: Sustained increases in serum free and total testosterone levels in the presence of inadequately raised LH concentrations point towards persisting disturbances of the hypothalamic–pituitary–gonadal axis in male alcoholics upon cessation of drinking."],["dc.identifier.gro","3150460"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7226"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0735-0414"],["dc.subject","testosterone; hormone; luteinizing hormone; persistence; hypothalamic-pituitary-gonadal axis; testosterone measurement; serum; alcoholics"],["dc.title","Persistent disturbance of the hypothalamic-pituitary-gonadal axis in abstinent alcoholic men"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","42"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","54"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Degner, D."],["dc.contributor.author","Meller, Johannes"],["dc.contributor.author","Brines, Michael"],["dc.contributor.author","Behe, M."],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Woldt, Helge"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Knerlich, Friederike"],["dc.contributor.author","Jacob, Silke"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Brück, W."],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Cerami, A."],["dc.contributor.author","Becker, Wolfgang"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:26Z"],["dc.date.available","2017-09-07T11:46:26Z"],["dc.date.issued","2004"],["dc.description.abstract","Erythropoietin (EPO) is a candidate compound for neuroprotection in human brain disease capable of combating a spectrum of pathophysiological processes operational during the progression of schizophrenic psychosis. The purpose of the present study was to prepare the ground for its application in a first neuroprotective add-on strategy in schizophrenia, aiming at improvement of cognitive brain function as well as prevention/slowing of degenerative processes. Using rodent studies, primary hippocampal neurons in culture, immunohistochemical analysis of human post-mortem brain tissue and nuclear imaging technology in man, we demonstrate that: (1) peripherally applied recombinant human (rh) EPO penetrates into the brain efficiently both in rat and humans, (2) rhEPO is enriched intracranially in healthy men and more distinctly in schizophrenic patients, (3) EPO receptors are densely expressed in hippocampus and cortex of schizophrenic subjects but distinctly less in controls, (4) rhEPO attenuates the haloperidol-induced neuronal death in vitro, and (4) peripherally administered rhEPO enhances cognitive functioning in mice in the context of an aversion task involving cortical and subcortical pathways presumably affected in schizophrenia. These observations, together with the known safety of rhEPO, render it an interesting compound for neuroprotective add-on strategies in schizophrenia and other human diseases characterized by a progressive decline in cognitive performance."],["dc.identifier.doi","10.1038/sj.mp.4001442"],["dc.identifier.gro","3150503"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7274"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1359-4184"],["dc.subject","recombinant human erythropoietin; EPO; schizophrenia; clinical; rodent; SPECT"],["dc.title","Erythropoietin: a candidate compound for neuroprotection in schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","862"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","867"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Knerlich, Friederike"],["dc.contributor.author","von Ahsen, N."],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Sperling, S."],["dc.contributor.author","Woldt, H."],["dc.contributor.author","Vehmeyer, K."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Sirén, A.-L."],["dc.contributor.author","Ehrenreich, H."],["dc.date.accessioned","2017-09-07T11:46:36Z"],["dc.date.available","2017-09-07T11:46:36Z"],["dc.date.issued","2005"],["dc.description.abstract","Central nervous and hematopoietic systems share developmental features. We report that thrombopoietin (TPO), a stimulator of platelet formation, acts in the brain as a counterpart of erythropoietin (EPO), a hematopoietic growth factor with neuroprotective properties. TPO is most prominent in postnatal brain, whereas EPO is abundant in embryonic brain and decreases postnatally. Upon hypoxia, EPO and its receptor are rapidly reexpressed, whereas neuronal TPO and its receptor are down-regulated. Unexpectedly, TPO is strongly proapoptotic in the brain, causing death of newly generated neurons through the Ras-extracellular signal-regulated kinase 1/2 pathway. This effect is not only inhibited by EPO but also by neurotrophins. We suggest that the proapoptotic function of TPO helps to select for neurons that have acquired target-derived neurotrophic support."],["dc.identifier.doi","10.1073/pnas.0406008102"],["dc.identifier.gro","3150545"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7318"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0027-8424"],["dc.subject","astrocytes; erythropoietin; neurons; differentiation; development"],["dc.title","A hematopoietic growth factor, thrombopoietin, has a proapoptotic role in the brain"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","85"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","100"],["dc.bibliographiccitation.volume","141"],["dc.contributor.author","Suwala, Abigail K."],["dc.contributor.author","Stichel, Damian"],["dc.contributor.author","Schrimpf, Daniel"],["dc.contributor.author","Kloor, Matthias"],["dc.contributor.author","Wefers, Annika K."],["dc.contributor.author","Reinhardt, Annekathrin"],["dc.contributor.author","Maas, Sybren L. N."],["dc.contributor.author","Kratz, Christian P."],["dc.contributor.author","Schweizer, Leonille"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Snuderl, Matija"],["dc.contributor.author","Abedalthagafi, Malak Sameer J."],["dc.contributor.author","Abdullaev, Zied"],["dc.contributor.author","Monoranu, Camelia M."],["dc.contributor.author","Bergmann, Markus"],["dc.contributor.author","Pekrun, Arnulf"],["dc.contributor.author","Freyschlag, Christian"],["dc.contributor.author","Aronica, Eleonora"],["dc.contributor.author","Kramm, Christof M."],["dc.contributor.author","Hinz, Felix"],["dc.contributor.author","Sievers, Philipp"],["dc.contributor.author","Korshunov, Andrey"],["dc.contributor.author","Kool, Marcel"],["dc.contributor.author","Pfister, Stefan M."],["dc.contributor.author","Sturm, Dominik"],["dc.contributor.author","Jones, David T. W."],["dc.contributor.author","Wick, Wolfgang"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Hartmann, Christian"],["dc.contributor.author","Dodgshun, Andrew"],["dc.contributor.author","Tabori, Uri"],["dc.contributor.author","Wesseling, Pieter"],["dc.contributor.author","Sahm, Felix"],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Reuss, David E."],["dc.date.accessioned","2021-04-14T08:30:48Z"],["dc.date.available","2021-04-14T08:30:48Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00401-020-02243-6"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83379"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Primary mismatch repair deficient IDH-mutant astrocytoma (PMMRDIA) is a distinct type with a poor prognosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Piotr, L."],["dc.contributor.author","Dembowski, C."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Stiefel, M."],["dc.contributor.author","Rustenbeck, Hans Heino"],["dc.contributor.author","Jacob, S."],["dc.contributor.author","Knerlich, F."],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Siren, A. L."],["dc.date.accessioned","2018-11-07T10:33:49Z"],["dc.date.available","2018-11-07T10:33:49Z"],["dc.date.issued","2002"],["dc.format.extent","354"],["dc.identifier.isi","000173147700143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44705"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0039-2499"],["dc.title","Erythropoietin treatment for acute stroke: A randomized double-blind proof-of concept trial in man"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1634"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1636"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Mooren, F. C."],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Keyvani, Kathy"],["dc.contributor.author","Fromme, A."],["dc.contributor.author","Schwarze-Eicker, K."],["dc.contributor.author","Senner, V."],["dc.contributor.author","Paulus, Walter J."],["dc.date.accessioned","2018-11-07T10:48:57Z"],["dc.date.available","2018-11-07T10:48:57Z"],["dc.date.issued","2004"],["dc.description.abstract","The contribution of extracranial tissue damage to serum S100beta increases was examined in 18 marathon runners without clinical or laboratory signs of brain damage. Postrace serum S100beta and creatine kinase (CK) concentrations increased (p < 0.001), and areas under the curve were highly correlated (p = 0.001). To conclude, serum S100β increases after running originate from extracranial sources. CK determination may improve specificity of S100β as a marker of brain tissue damage in acute trauma."],["dc.identifier.isi","000221350400038"],["dc.identifier.pmid","15136701"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48321"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Serum S100 beta increases in marathon runners reflect extracranial release rather than glial damage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","390"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","397"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Bunte, Marion"],["dc.contributor.author","Dringen, Ralf"],["dc.contributor.author","Tabernero, Arantxa"],["dc.contributor.author","Medina, José M."],["dc.contributor.author","Giaume, Christian"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:45:47Z"],["dc.date.available","2017-09-07T11:45:47Z"],["dc.date.issued","2003"],["dc.description.abstract","The astrocytic endothelin (ET) receptors, ETA and ETB, modulate calcium signaling and the astrocytic gap junctional network. The nonselective ET receptor ligand ET-1 inhibits gap junction permeability, an effect that can be blocked by tolbutamide. This mechanism may play a role in pathophysiological conditions such as ischemic stroke, characterized by elevated tissue ET-1 levels and hypertrophic-appearing reactive astrocytes. Therefore, the effect of ET-1 on cellular protein content was investigated in confluent once-passaged rat astrocyte cultures under serum-free conditions, by the Lowry method. Gap junction permeability was determined by the dye transfer technique. ET-1 prevented the decrease in astrocytic protein content observed in controls. The effect of ET-1 on cellular protein content was most pronounced in cultures seeded at high density, but it was attenuated in ETB-deficient (sl/sl) astrocytes. This effect could be blocked by the nonselective ET antagonist LU 302872 (10 μM), as well as by the protein synthesis inhibitor cycloheximide (10 μM). This increase in astrocytic protein content was inhibited by the ATP-sensitive K+ channel blocker tolbutamide, which also antagonized the ET-1-induced reduction of gap junction permeability and reversed the morphological changes observed in astrocytes upon ET-1 treatment. Cytosine arabinoside (10 μM), a DNA synthesis blocker, inhibited the ET-1-induced BrdU uptake without affecting the ET-1-induced increase in astrocytic protein content. To conclude, ET-1 induces an increase in astrocytic protein content as well as changes in astrocyte morphology in vitro. This hypertrophic response involves uncoupling of the astrocytic gap junctional network and is not dependent on DNA synthesis."],["dc.identifier.doi","10.1002/glia.10224"],["dc.identifier.gro","3150461"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7227"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0894-1491"],["dc.title","Effect of endothelin-1 on astrocytic protein content"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","132"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neurosurgical Anesthesiology"],["dc.bibliographiccitation.lastpage","138"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:18Z"],["dc.date.available","2017-09-07T11:46:18Z"],["dc.date.issued","2006"],["dc.description.abstract","The discovery of the broad neuroprotective potential of erythropoietin (EPO), an endogenous hematopoietic growth factor, has opened new therapeutic avenues in the treatment of brain diseases. EPO expression in the brain is induced by hypoxia. Practically all brain cells are capable of production and release of EPO and expression of its receptor. EPO exerts Multifaceted protective effects on brain cells. It protects neuronal cells from noxious stimuli Such as hypoxia, excess glutamate, serum deprivation or kainic acid exposure in vitro by targeting a variety of mechanisms and involves neuronal, glial and endothelial cell functions. In rodent models of ischemic stroke, EPO reduces infarct volume and improves functional outcome, but beneficial effects have also been observed in animal models of subarachnoid hemorrhage, intracerebral hemorrhage, traumatic brain injury, and spinal cord injury. EPO has a convenient therapeutic window upon ischemic stroke and favorable pharmacokinetics. Results from first therapeutic trials in humans are promising, but will need to be validated in larger trials. The safety profile and effectiveness of EPO in a wide variety of neurologic disease models make EPO a candidate compound for a potential first-line therapeutic for neurologic emergencies."],["dc.identifier.gro","3150470"],["dc.identifier.pmid","16628067"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7238"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0898-4921"],["dc.title","The brain erythropoietin system and its potential for therapeutic exploitation in brain disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","495"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","505"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Dembowski, Christoph"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Lewczuk, Pjotr"],["dc.contributor.author","Stiefel, Michael"],["dc.contributor.author","Rustenbeck, Hans-Heino"],["dc.contributor.author","Breiter, Norbert"],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Knerlich, Friederike"],["dc.contributor.author","Bohn, Matthias"],["dc.contributor.author","Poser, Wolfgang"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Kochen, Michael"],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Wessel, Thomas C."],["dc.contributor.author","Ryck, Marc de"],["dc.contributor.author","Itri, Loretta"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Cerami, Anthony"],["dc.contributor.author","Brines, Michael"],["dc.contributor.author","Siren, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:45:41Z"],["dc.date.available","2017-09-07T11:45:41Z"],["dc.date.issued","2002"],["dc.description.abstract","Background: Erythropoietin (EPO) and its receptor play a major role in embryonic brain, are weakly expressed in normal postnatal/adult brain and up-regulated upon metabolic stress. EPO protects neurons from hypoxic/ ischemic injury. The objective of this trial is to study the safety and efficacy of recombinant human EPO (rhEPO) for treatment of ischemic stroke in man. Materials and Methods: The trial consisted of a safety part and an efficacy part. in the safety study, 13 patients received rhEPO intravenously (3.3 x 10(4) IU/50 m/130 min) once daily for the first 3 days after stroke. in the double-blind randomized proof-of-concept trial, 40 patients received either rhEPO or saline. Inclusion criteria were age {.extbackslash}textless80 years, ischemic stroke within the middle cerebral artery territory confirmed by diffusion-weighted MRI, symptom onset {.extbackslash}textless8 hr before drug administration, and deficits on stroke scales. The study endpoints were functional outcome at day 30 (Barthel index, modified Rankin scale), NIH and Scandinavian stroke scales, evolution of infarct size (sequential MRI evaluation using diffusion-weighted [DWI] and fluid-attenuated inversion recovery sequences [FLAIR]) and the damage marker S100ss. Results: No safety concerns were identified. Cerebrospinal fluid EPO increased to 60-100 times that of nontreated patients, proving that intravenously administered rhEPO reaches the brain. in the efficacy trial, patients received rhEPO within 5 hr of onset of symptoms (median, range 2:40-7:55). Admission neurologic scores and serum S100beta concentrations were strong predictors of outcome. Analysis of covariance controlled for these two variables indicated that rhEPO treatment was associated with an improvement in follow-up and outcome scales. A strong trend for reduction in infarct size in rhEPO patients as compared to controls was observed by MRI. Conclusion: intravenous high-dose rhEPO is well tolerated in acute ischemic stroke and associated with an improvement in clinical outcome at 1 month. A larger scale clinical trial is warranted."],["dc.identifier.gro","3150429"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7192"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1076-1551"],["dc.relation.orgunit","Institut für Allgemeinmedizin"],["dc.title","Erythropoietin therapy for acute stroke is both safe and beneficial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]