Kermer, Pawel

[["dc.bibliographiccitation.firstpage","1013"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","1023"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Deeg, S."],["dc.contributor.author","Voigt, A."],["dc.contributor.author","Voßfeldt, H."],["dc.contributor.author","Dohm, C. P."],["dc.contributor.author","Karch, A."],["dc.contributor.author","Weishaupt, Jochen"],["dc.contributor.author","Schulz, J. B."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Kermer, P."],["dc.date.accessioned","2017-09-07T11:46:13Z"],["dc.date.available","2017-09-07T11:46:13Z"],["dc.date.issued","2014"],["dc.description.abstract","Spinocerebellar ataxia type 3 (SCA3) is one of at least nine inherited neurodegenerative diseases caused by an expansion of a polyglutamine tract within corresponding disease-specific proteins. In case of SCA3, mutation of Ataxin-3 results in aggregation of misfolded protein, formation of intranuclear as well as cytosolic inclusion bodies and cell death in distinct neuronal populations. Since cyclin-dependent kinase-5 (CDK5) has been shown to exert beneficial effects on aggregate formation and cell death in various polyglutamine diseases, we tested its therapeutic potential for SCA3. Our data show increased caspase-dependent Ataxin-3 cleavage, aggregation, and neurodegeneration in the absence of sufficient CDK5 activity. This disease-propagating effect could be reversed by mutation of the caspase cleavage site in Ataxin-3. Moreover, reduction of CDK5 expression levels by RNAi in vivo enhances SCA3 toxicity as assayed in a Drosophila model for SCA3. In summary, we present CDK5 as a potent neuroprotectant, regulating cleavage and thereby toxicity of Ataxin-3 and other polyglutamine proteins. We propose that increased caspase-dependent cleavage of mutated Ataxin-3, because of missing CDK5 shielding, leads to aggregation and cell death. Moreover, reduction of CDK5 expression levels by RNAi in vivo enhances SCA3 toxicity as assayed in a Drosophila model for SCA3. We think that CDK5 functions as a shield against cleavage-induced toxification and thereby is an interesting target for therapeutic intervention in polyQ disease in general."],["dc.identifier.doi","10.1111/jnc.12684"],["dc.identifier.gro","3142111"],["dc.identifier.isi","000337760500011"],["dc.identifier.pmid","24548080"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4666"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","CDK5 protects from caspase-induced Ataxin-3 cleavage and neurodegeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","21"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","26"],["dc.bibliographiccitation.volume","1198"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Faida, Lena"],["dc.contributor.author","Dohm, Christoph P."],["dc.contributor.author","Reed, John C."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2017-09-07T11:48:46Z"],["dc.date.available","2017-09-07T11:48:46Z"],["dc.date.issued","2008"],["dc.description.abstract","BAG1 is a potent neuroprotectant as well as a marker of differentiation in neuronal cells. It is known that BAG1 mainly localizes to the nucleus during neuronal development, whereas BAG1 shifts to the cytosol upon neuronal differentiation suggesting that distinct BAG1 functions depend on its subcellular localization. Here, we show that forced BAG1 expression within the nucleus when compared to full-length BAG1 expression and to control cells completely abolishes the neuroprotective effects of BAG1 supporting the notion that cytosolic interaction with Hsp70 is mandatory for BAG1 mediated neuroprotection. At the same time, we observed that cells can no longer differentiate into post-mitotic neurons when BAG1 is only present in the nucleus. In addition, phospho-Erk levels are decreased in those cells indicating that BAG1 has to translocate to the cytosol for Raf-dependent MAPK activation. (C) 2008 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.brainres.2008.01.010"],["dc.identifier.gro","3143337"],["dc.identifier.isi","000254106400003"],["dc.identifier.pmid","18242589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/840"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0006-8993"],["dc.title","Subcellular distribution affects BAG1 function"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","190"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Medical Case Reports"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","von Gottberg, Philipp"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2018-03-08T09:21:27Z"],["dc.date.available","2018-03-08T09:21:27Z"],["dc.date.issued","2011"],["dc.description.abstract","Introduction Infectious ileopectineal bursitis is a rare complication after total hip replacement and is associated mainly with rheumatoid arthritis. The main complications are local swelling and pain, but communication of the inflamed bursa with the joint can occur, leading to subsequent cartilage damage and bone destruction. Case presentation We report a case of a 47-year-old Caucasian woman without rheumatoid arthritis who reported pain and palsy in her left leg almost one year after total hip replacement. She was diagnosed with an ileopectineal bursitis after total hip replacement, leading to femoral nerve palsy. The diagnosis was obtained by thorough clinical examination, the results of focused computed tomography and magnetic resonance imaging. Conclusion To the best of our knowledge, this is the first report of non-infectious ileopectineal bursitis in a patient without rheumatoid arthritis as a complication of total hip replacement. This rare case underlines the importance of proper neurologic examination of persistent conditions after orthopedic intervention in otherwise healthy individuals. We believe this case should be useful for a broad spectrum of medical specialties, including orthopedics, neurology, radiology, and general practice."],["dc.identifier.doi","10.1186/1752-1947-5-190"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6375"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12889"],["dc.language.iso","en"],["dc.notes.intern","GRO-Li-Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.doi","10.1186/1752-1947-5-190"],["dc.relation.issn","1752-1947"],["dc.relation.issn","1752-1947"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Femoral nerve palsy caused by ileopectineal bursitis after total hip replacement: a case report"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1859"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Current Medical Research and Opinion"],["dc.bibliographiccitation.lastpage","1866"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Diekmann, Sandra"],["dc.contributor.author","Hörster, Laura"],["dc.contributor.author","Evers, Silvia"],["dc.contributor.author","Hiligsmann, Mickaël"],["dc.contributor.author","Gelbrich, Götz"],["dc.contributor.author","Gröschel, Klaus"],["dc.contributor.author","Wachter, Rolf"],["dc.contributor.author","Hamann, Gerhard F."],["dc.contributor.author","Kermer, Pawel"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Weber-Krüger, Mark"],["dc.contributor.author","Wasem, Jürgen"],["dc.contributor.author","Neumann, Anja"],["dc.date.accessioned","2020-12-10T18:14:50Z"],["dc.date.available","2020-12-10T18:14:50Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1080/03007995.2019.1646000"],["dc.identifier.eissn","1473-4877"],["dc.identifier.issn","0300-7995"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74635"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Economic evaluation of prolonged and enhanced ECG Holter monitoring in acute ischemic stroke patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0216530"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Wasser, Katrin"],["dc.contributor.author","Weber-Krüger, Mark"],["dc.contributor.author","Jürries, Falko"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Hamann, Gerhard F."],["dc.contributor.author","Kermer, Pawel"],["dc.contributor.author","Uphaus, Timo"],["dc.contributor.author","Protsenko, Evgeny"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Mende, Meinhard"],["dc.contributor.author","Gröschel, Klaus"],["dc.contributor.author","Wachter, Rolf"],["dc.date.accessioned","2019-07-09T11:51:30Z"],["dc.date.available","2019-07-09T11:51:30Z"],["dc.date.issued","2019"],["dc.description.abstract","BACKGROUND: The cardiac diagnostic workup of stroke patients, especially the value of echocardiography and enhanced and prolonged Holter-ECG monitoring, is still a matter of debate. We aimed to analyse the impact of pathologies detected by echocardiography and ECG monitoring on therapeutic decisions and prognosis. METHODS: Find-AFRANDOMISED was a prospective multicenter study which randomised 398 acute ischemic stroke patients ≥ 60 years to enhanced and prolonged Holter-ECG monitoring or usual stroke unit care. This substudy compared therapeutic consequences of echocardiography and routine Holter-ECG or enhanced and prolonged Holter-ECG monitoring, respectively, and prognosis of patients with or without pathologic findings in echocardiography or Holter-ECG monitoring. RESULTS: 50.3% received enhanced and prolonged Holter-ECG monitoring and 49.7% routine ECG monitoring. 82.9% underwent transthoracic echocardiography (TTE), 38.9% transesophageal echocardiography (TEE) and 25.6% both procedures. 14/89 TEE pathologies and 1/90 TTE pathology led to a change in therapy, resulting in a number needed to change decision (NNCD) of 12 and 330 (p < 0.001), respectively. In comparison, enhanced and prolonged Holter-ECG monitoring found atrial fibrillation (AF) in 27 of 200 patients, and routine ECG monitoring in twelve of 198 patients, leading to therapeutic changes in all patients (NNCD 8 and 17, respectively, p < 0.001). CONCLUSIONS: Most changes in therapeutic decisions were triggered by enhanced and prolonged Holter-ECG monitoring, which should therefore play a more prominent role in future guidelines. Echocardiography identifies a patient group at high cardiovascular risk, but rarely result in therapeutic changes. Whether this patient group requires further cardiovascular workup remains unknown. This should be further investigated by interdisciplinary neurocardiologic teams and in appropriate future trials."],["dc.identifier.doi","10.1371/journal.pone.0216530"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16141"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59961"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The cardiac diagnostic work-up in stroke patients—A subanalysis of the Find-AFRANDOMISED trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","282"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Lancet. Neurology"],["dc.bibliographiccitation.lastpage","290"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Wachter, Rolf"],["dc.contributor.author","Gröschel, Klaus"],["dc.contributor.author","Gelbrich, Götz"],["dc.contributor.author","Hamann, Gerhard F"],["dc.contributor.author","Kermer, Pawel"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Wasser, Katrin"],["dc.contributor.author","Schulte, Anna"],["dc.contributor.author","Jürries, Falko"],["dc.contributor.author","Messerschmid, Anna"],["dc.contributor.author","Behnke, Nico"],["dc.contributor.author","Gröschel, Sonja"],["dc.contributor.author","Uphaus, Timo"],["dc.contributor.author","Grings, Anne"],["dc.contributor.author","Ibis, Tugba"],["dc.contributor.author","Klimpe, Sven"],["dc.contributor.author","Wagner-Heck, Michaela"],["dc.contributor.author","Arnold, Magdalena"],["dc.contributor.author","Protsenko, Evgeny"],["dc.contributor.author","Heuschmann, Peter U"],["dc.contributor.author","Conen, David"],["dc.contributor.author","Weber-Krüger, Mark"],["dc.date.accessioned","2020-12-10T15:22:02Z"],["dc.date.available","2020-12-10T15:22:02Z"],["dc.date.issued","2017"],["dc.description.abstract","Background Atrial fibrillation is a major risk factor for recurrent ischaemic stroke, but often remains undiagnosed in patients who have had an acute ischaemic stroke. Enhanced and prolonged Holter-electrocardiogram-monitoring might increase detection of atrial fibrillation. We therefore investigated whether enhanced and prolonged rhythm monitoring was better for detection of atrial fibrillation than standard care procedures in patients with acute ischaemic stroke. Methods Find-AF(RANDOMISED) is an open-label randomised study done at four centres in Germany. We recruited patients with acute ischaemic stroke (symptoms for 7 days or less) aged 60 years or older presenting with sinus rhythm and without history of atrial fibrillation. Patients were included irrespective of the suspected cause of stroke, unless they had a severe ipsilateral carotid or intracranial artery stenosis, which were the exclusion criteria. We used a computer-generated allocation sequence to randomly assign patients in a 1: 1 ratio with permuted block sizes of 2, 4, 6, and 8, stratified by centre, to enhanced and prolonged monitoring (ie, 10-day Holter-electrocardiogram [ECG]-monitoring at baseline, and at 3 months and 6 months of follow-up) or standard care procedures (ie, at least 24 h of rhythm monitoring). Participants and study physicians were not masked to group assignment, but the expert committees that adjudicated endpoints were. The primary endpoint was the occurrence of atrial fibrillation or atrial flutter (30 sec or longer) within 6 months after randomisation and before stroke recurrence. Because Holter ECG is a widely used procedure and not known to harm patients, we chose not to assess safety in detail. Analysis was by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT01855035. Findings Between May 8, 2013, and Aug 31, 2014, we recruited 398 patients. 200 patients were randomly assigned to the enhanced and prolonged monitoring group and 198 to the standard care group. After 6 months, we detected atrial fibrillation in 14% of 200 patients in the enhanced and prolonged monitoring group (27 patients) versus 5% in the control group (nine of 198 patients, absolute difference 9.0%; 95% CI 3.4-14.5, p=0.002; number needed to screen 11). Interpretation Enhanced and prolonged monitoring initiated early in patients with acute ischaemic stroke aged 60 years or older was better than standard care for the detection of atrial fibrillation. These findings support the consideration of all patients aged 60 years or older with stroke for prolonged monitoring if the detection of atrial fibrillation would result in a change in medical management (eg, initiation of anticoagulation)."],["dc.identifier.doi","10.1016/S1474-4422(17)30002-9"],["dc.identifier.isi","000396336600017"],["dc.identifier.issn","1474-4422"],["dc.identifier.pmid","28187920"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73251"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1474-4465"],["dc.relation.issn","1474-4422"],["dc.title","Holter-electrocardiogram-monitoring in patients with acute ischaemic stroke (Find-AF RANDOMISED ): an open-label randomised controlled trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","438"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","American Heart Journal"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","168"],["dc.contributor.author","Weber-Krueger, Mark"],["dc.contributor.author","Gelbrich, Goetz"],["dc.contributor.author","Stahrenberg, Raoul"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Kermer, Pawel"],["dc.contributor.author","Hamann, Gerhard F."],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Groeschel, Klaus"],["dc.contributor.author","Wachter, R. Rolf"],["dc.date.accessioned","2018-11-07T09:34:27Z"],["dc.date.available","2018-11-07T09:34:27Z"],["dc.date.issued","2014"],["dc.description.abstract","Background Detecting paroxysmal atrial fibrillation (AF) in patients with ischemic strokes presenting in sinus rhythm is challenging because episodes are often short, occur randomly, and are frequently asymptomatic. If AF is detected, recurrent thromboembolism can be prevented efficiently by oral anticoagulation. Numerous uncontrolled studies using various electrocardiogram (ECG) devices have established that prolonged ECG monitoring increases the yield of AF detection, but most established procedures are time-consuming and costly. The few randomized trials are mostly limited to cryptogenic strokes. The optimal method, duration, and patient selection remain unclear. Repeated prolonged continuous Holter ECG monitoring to detect paroxysmal AF within an unspecific stroke population may prove to be a widely applicable, effective secondary prevention strategy. Study Design Find-AF(RANDOMISED) is a randomized and controlled prospective multicenter trial. Four hundred patients 60 years or older with manifest (symptoms >= 24 hours or acute computed tomography/magnetic resonance imaging lesion) and acute (symptoms <= 7 days) ischemic strokes will be included at 4 certified stroke centers in Germany. Those with previously diagnosed AF/flutter, indications/contraindications for oral anticoagulation, or obvious causative blood vessel pathologies will be excluded. Patients will be randomized 1:1 to either enhanced and prolonged Holter ECG monitoring (10 days at baseline and after 3 and 6 months) or standard of care (>= 24-hour continuous ECG monitoring, according to current stroke guidelines). All patients will be followed up for at least 12 months. Outcomes The primary end point is newly detected AF (>= 30 seconds) after 6 months, confirmed by an independent adjudication committee. We plan to complete recruitment in autumn 2014. First results can be expected by spring 2016."],["dc.description.sponsorship","Boehringer Ingelheim; Pfizer; Medtronic"],["dc.identifier.doi","10.1016/j.ahj.2014.06.018"],["dc.identifier.isi","000343096900008"],["dc.identifier.pmid","25262252"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32171"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Mosby-elsevier"],["dc.relation.issn","1097-5330"],["dc.relation.issn","0002-8703"],["dc.title","Finding atrial fibrillation in stroke patients: Randomized evaluation of enhanced and prolonged Holter monitoring-Find-AF(RANDOMISED) -rationale and design"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","175"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Journal of Paediatric Neurology"],["dc.bibliographiccitation.lastpage","178"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Wellmer, Andreas"],["dc.contributor.author","Rostasy, Kevin"],["dc.contributor.author","Baehr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2017-09-07T11:48:57Z"],["dc.date.available","2017-09-07T11:48:57Z"],["dc.date.issued","2012"],["dc.description.abstract","NBIA/HSS is a neurodegenerative disorder associated with iron accumulation in specific brain regions. To date, the diagnosis is obtained by typical MRI changes followed by genetic mutation analysis. This procedure is laborious and limited to a few specially equipped medical centres. Since transcranial sonography (TCS) is widely used for the early diagnosis of PD in adults displaying parenchymal metal deposits, it is likely to be a reliable diagnostic tool for the early diagnosis of NBIA. In 7 patients with proven NBIA and 13 age-matched controls without record of neurological disease TCS was performed by an experienced ultrasound examiner. Data were analysed by two blinded investigators regarding hyperechogenicity and size of the substantia nigra (SN). SN size and hyperechogenicity was significantly increased in patients with NBIA compared to controls (students t-test: p < 0.001). TCS appears to be a non-invasive and inexpensive screening technique in patients with suspected NBIA. Performed by an experienced physician, it could enable an earlier diagnosis and pre-selection of patients for the MRI scan and genetic testing, which are still the diagnostic gold standard. (C) 2011 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.ejpn.2011.07.009"],["dc.identifier.gro","3142571"],["dc.identifier.isi","000301216700011"],["dc.identifier.pmid","21816641"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8936"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1090-3798"],["dc.title","Transcranial ultrasound in neurodegeneration with brain iron accumulation (NBIA)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Molecular Neuroscience"],["dc.bibliographiccitation.lastpage","8"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Dohm, Christoph P."],["dc.contributor.author","Siedenberg, Sandra"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Esposito, Alessandro"],["dc.contributor.author","Wouters, Fred S."],["dc.contributor.author","Reed, John C."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2017-09-07T11:53:38Z"],["dc.date.available","2017-09-07T11:53:38Z"],["dc.date.issued","2006"],["dc.description.abstract","Bax ihibitor-1 (BI-1) has been characterized as an inhibitor of Bax-induced cell death in plants and various mammalian cell systems. To explore the function of BI-1 in neurons, we overexpressed BI-1 tagged to HA or GFP in rat nigral CSM14.1 and human SH-SY5Y neuroblastoma cells. Stable BI-1 expression proved marked protection from cell death induced by thapsigargine, a stress agent blocking the Call-ATPase of the endoplasmic reticulum (ER) but failed to inhibit cell death induced by staurosporine, a kinase inhibitor initiating mitochondria-dependent apoptosis. Moreover, BI-1 was neuroprotective in a paradigm mimicking ischemia, namely oxygen-glucose as well as serum deprivation. Examination of the subcellular distribution revealed that BI-1 predominantly locates to the ER and nuclear envelope but not mitochondria. Taken together, BI-1 overexpression in the ER is protective in neurons, making BI-1 an interesting target for future studies aiming at the inhibition of neuronal cell death during neurodegenerative diseases and stroke."],["dc.identifier.doi","10.1385/JMN:29:1:1"],["dc.identifier.gro","3143760"],["dc.identifier.isi","000237933400001"],["dc.identifier.pmid","16757804"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1309"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: NCI NIH HHS [CA67329]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0895-8696"],["dc.title","Bax inhibitor-1 protects neurons from oxygen-glucose deprivation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","349"],["dc.bibliographiccitation.issue","1-12"],["dc.bibliographiccitation.journal","Perspectives in Medicine"],["dc.bibliographiccitation.lastpage","352"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kermer, Pawel"],["dc.date.accessioned","2019-07-09T11:40:54Z"],["dc.date.available","2019-07-09T11:40:54Z"],["dc.date.issued","2012"],["dc.description.abstract","Since the first discovery, that ultrasound can overcome the skull allowing examination of the intracranial blood-flow as well as the first description of substantia nigra (SN) signal alterations via B-mode sonography, a plethora of applications especially in the field of movement disorders have been fostered. Up to now, however, most studies investigated adult individuals, even though numerous of the diseases studied have their onset already during childhood or adolescence. This overview summarizes recent studies of transcranial B-mode sonography (TCS) within the movement disorder field and outlines potential implications for pediatric applications."],["dc.identifier.doi","10.1016/j.permed.2012.02.003"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11472"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58293"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Transcranial ultrasound in adults and children with movement disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]