Hermann, Peter

[["dc.bibliographiccitation.firstpage","761"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Expert Review of Neurotherapeutics"],["dc.bibliographiccitation.lastpage","772"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Hermann, Peter"],["dc.date.accessioned","2020-12-10T18:15:09Z"],["dc.date.available","2020-12-10T18:15:09Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1080/14737175.2018.1519397"],["dc.identifier.eissn","1744-8360"],["dc.identifier.issn","1473-7175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/74764"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Diagnostic challenges in rapidly progressive dementia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","743"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","MINERVA ANESTESIOLOGICA"],["dc.bibliographiccitation.lastpage","750"],["dc.bibliographiccitation.volume","82"],["dc.contributor.author","Harnisch, Lars-Olav"],["dc.contributor.author","Zippel, Carsten"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Quintel, Michael"],["dc.contributor.author","Moerer, Onnen"],["dc.date.accessioned","2018-11-07T10:11:48Z"],["dc.date.available","2018-11-07T10:11:48Z"],["dc.date.issued","2016"],["dc.description.abstract","BACKGROUND: Patient-ventilator asynchrony that prolongs weaning and increases morbidity and mortality is common during invasive ventilation of patients with chronic obstructive pulmonary disease (COPD). In this context, the inspiratory cycling criteria (iCC) of the ventilator during assisted pressure support (PS) ventilation is a poorly acknowledged key factor. We investigated the changes of flow and pressure parameters that resulted from varying the iCC in a simulated COPD lung model. METHODS: A lung simulator was connected to an ICU ventilator through an endotracheal tube. We studied iCC settings from 10% to 70% at different respiratory rates (RR) (15 and 30 bpm) and pressure support (PS) (5 and 15 cmH(2)O) settings and registered asynchrony-index, double-triggering, expiratory trigger latency (TLEXP), intrinsic PEEP (PEEPi), expiratory pressure time product (PTPEXP) and tidal volume. RESULTS: At iCC <= 20%, asynchrony occurred in 50% of all recordings in high RR/high PS. At a low RR, double triggering occurred at high iCC settings. It appeared at 50% iCC with low PS and at 60% iCC with high PS. TLEXP was positive at iCC 10% to 30% but decreased with increasing iCC (P< 0.001). At low RR/high PS settings, PEEPi decreased at iCC <= 40% but increased at iCC >= 50%. High RR/low PS constantly reduced PTPEXP up to 60% iCC. Changes in iCC strongly influenced the resulting tidal volume. CONCLUSIONS: Non-adapted ventilator iCC can cause patient-ventilator asynchrony. The success of assisted invasive ventilation and weaning relies on meticulous adjustments."],["dc.description.sponsorship","Faron Pharm."],["dc.identifier.isi","000386888700006"],["dc.identifier.pmid","26630027"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40114"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Edizioni Minerva Medica"],["dc.relation.issn","1827-1596"],["dc.relation.issn","0375-9393"],["dc.title","Adjusting ventilator off-cycling in invasively ventilated COPD patients needs comprehensive adjustments"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Nature Reviews Neurology"],["dc.contributor.author","Watson, Neil"],["dc.contributor.author","Brandel, Jean-Philippe"],["dc.contributor.author","Green, Alison"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Lindsay, Terri"],["dc.contributor.author","Mackenzie, Janet"],["dc.contributor.author","Pocchiari, Maurizio"],["dc.contributor.author","Smith, Colin"],["dc.contributor.author","Pal, Suvankar"],["dc.date.accessioned","2021-06-01T09:41:41Z"],["dc.date.available","2021-06-01T09:41:41Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1038/s41582-021-00488-7"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85003"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1759-4766"],["dc.relation.issn","1759-4758"],["dc.title","The importance of ongoing international surveillance for Creutzfeldt–Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Nature Reviews Neurology"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2022-06-01T09:39:09Z"],["dc.date.available","2022-06-01T09:39:09Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1038/s41582-022-00659-0"],["dc.identifier.pii","659"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108401"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","1759-4766"],["dc.relation.issn","1759-4758"],["dc.rights.uri","https://www.springer.com/tdm"],["dc.title","Rapidly progressive dementias — aetiologies, diagnosis and management"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","841"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","859"],["dc.bibliographiccitation.volume","141"],["dc.contributor.author","Diaz-Lucena, Daniela"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Thüne, Katrin"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","da Cunha, Jose Eriton Gomes"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","López-Pérez, Óscar"],["dc.contributor.author","Andrés-Benito, Pol"],["dc.contributor.author","Llorens, Franc"],["dc.date.accessioned","2021-06-01T09:42:50Z"],["dc.date.available","2021-06-01T09:42:50Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune cell surface receptor that regulates microglial function and is involved in the pathophysiology of several neurodegenerative diseases. Its soluble form (sTREM2) results from shedding of the TREM2 ectodomain. The role of TREM2 in prion diseases, a group of rapidly progressive dementias remains to be elucidated. In the present study, we analysed the expression of TREM2 and its main sheddase ADAM10 in the brain of sporadic Creutzfeldt-Jakob disease (sCJD) patients and evaluated the role of CSF and plasma sTREM2 as a potential diagnostic marker of prion disease. Our data indicate that, compared to controls, TREM2 is increased in sCJD patient brains at the mRNA and protein levels in a regional and subtype dependent fashion, and expressed in a subpopulation of microglia. In contrast, ADAM10 is increased at the protein, but not the mRNA level, with a restricted neuronal expression. Elevated CSF sTREM2 is found in sCJD, genetic CJD with mutations E200K and V210I in the prion protein gene ( PRNP ), and iatrogenic CJD, as compared to healthy controls (HC) (AUC = 0.78–0.90) and neurological controls (AUC = 0.73–0.85), while CSF sTREM2 is unchanged in fatal familial insomnia. sTREM2 in the CSF of cases with Alzheimer’s disease, and multiple sclerosis was not significantly altered in our series. CSF sTREM2 concentrations in sCJD are PRNP codon 129 and subtype-related, correlate with CSF 14-3-3 positivity, total-tau and YKL-40, and increase with disease progression. In plasma, sTREM2 is increased in sCJD compared with HC (AUC = 0.80), displaying positive correlations with plasma total-tau, neurofilament light, and YKL-40. We conclude that comparative study of TREM2 in brain and biological fluids of prion diseases reveals TREM2 to be altered in human prion diseases with a potential value in target engagement, patient stratification, and disease monitoring."],["dc.identifier.doi","10.1007/s00401-021-02296-1"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85371"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","TREM2 expression in the brain and biological fluids in prion diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e125"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","e134"],["dc.bibliographiccitation.volume","93"],["dc.contributor.author","Minikel, Eric Vallabh"],["dc.contributor.author","Vallabh, Sonia M."],["dc.contributor.author","Orseth, Margaret C."],["dc.contributor.author","Brandel, Jean-Philippe"],["dc.contributor.author","Haïk, Stéphane"],["dc.contributor.author","Laplanche, Jean-Louis"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Parchi, Piero"],["dc.contributor.author","Capellari, Sabina"],["dc.contributor.author","Safar, Jiri"],["dc.contributor.author","Kenny, Janna"],["dc.contributor.author","Fong, Jamie C."],["dc.contributor.author","Takada, Leonel T."],["dc.contributor.author","Ponto, Claudia"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Knipper, Tobias"],["dc.contributor.author","Stehmann, Christiane"],["dc.contributor.author","Kitamoto, Tetsuyuki"],["dc.contributor.author","Ae, Ryusuke"],["dc.contributor.author","Hamaguchi, Tsuyoshi"],["dc.contributor.author","Sanjo, Nobuo"],["dc.contributor.author","Tsukamoto, Tadashi"],["dc.contributor.author","Mizusawa, Hidehiro"],["dc.contributor.author","Collins, Steven J."],["dc.contributor.author","Chiesa, Roberto"],["dc.contributor.author","Roiter, Ignazio"],["dc.contributor.author","de Pedro-Cuesta, Jesús"],["dc.contributor.author","Calero, Miguel"],["dc.contributor.author","Geschwind, Michael D."],["dc.contributor.author","Yamada, Masahito"],["dc.contributor.author","Nakamura, Yosikazu"],["dc.contributor.author","Mead, Simon"],["dc.date.accessioned","2020-12-10T18:41:46Z"],["dc.date.available","2020-12-10T18:41:46Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1212/WNL.0000000000007745"],["dc.identifier.eissn","1526-632X"],["dc.identifier.issn","0028-3878"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77669"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Age at onset in genetic prion disease and the design of preventive clinical trials"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Canaslan, Sezgi"],["dc.contributor.author","Espinosa, Juan Carlos"],["dc.contributor.author","Fernández-Borges, Natalia"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Varges, Daniela"],["dc.contributor.author","Maass, Fabian"],["dc.contributor.author","Torres, Juan Maria"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2022-07-01T07:35:38Z"],["dc.date.available","2022-07-01T07:35:38Z"],["dc.date.issued","2022"],["dc.description.sponsorship"," Fundació La Marató de TV3 http://dx.doi.org/10.13039/100008666"],["dc.description.sponsorship"," Alzheimer Forschung Initiative http://dx.doi.org/10.13039/100010146"],["dc.description.sponsorship","Robert Koch-Institute through funds of the Federal Ministry of Health"],["dc.description.sponsorship","CJD Foundation"],["dc.identifier.doi","10.1007/s12035-022-02891-7"],["dc.identifier.pii","2891"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112222"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","1559-1182"],["dc.relation.issn","0893-7648"],["dc.rights.uri","https://www.springer.com/tdm"],["dc.title","Validation of Plasma and CSF Neurofilament Light Chain as an Early Marker for Sporadic Creutzfeldt-Jakob Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e2146319"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","JAMA Network Open"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Watson, Neil"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Denouel, Angeline"],["dc.contributor.author","Baiardi, Simone"],["dc.contributor.author","Colaizzo, Elisa"],["dc.contributor.author","Giaccone, Giorgio"],["dc.contributor.author","Glatzel, Markus"],["dc.contributor.author","Green, Alison J. E."],["dc.contributor.author","Haïk, Stéphane"],["dc.contributor.author","Pal, Suvankar"],["dc.date.accessioned","2022-04-01T10:02:09Z"],["dc.date.available","2022-04-01T10:02:09Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1001/jamanetworkopen.2021.46319"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105834"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2574-3805"],["dc.title","Validation of Revised International Creutzfeldt-Jakob Disease Surveillance Network Diagnostic Criteria for Sporadic Creutzfeldt-Jakob Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Brain"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Villar-Piqué, Anna"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Escaramís, Geòrgia"],["dc.contributor.author","Calero, Miguel"],["dc.contributor.author","Chen, Cao"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Golanska, Ewa"],["dc.contributor.author","Sikorska, Beata"],["dc.contributor.author","Llorens, Franc"],["dc.date.accessioned","2022-04-01T10:00:37Z"],["dc.date.available","2022-04-01T10:00:37Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Genetic prion diseases are a rare and diverse group of fatal neurodegenerative disorders caused by pathogenic sequence variations in the prion protein gene, PRNP. Data on CSF biomarkers in patients with genetic prion diseases are limited and conflicting results have been reported for unclear reasons. Here, we aimed to analyse the diagnostic accuracy of CSF biomarkers currently used in prion clinical diagnosis in 302 symptomatic genetic prion disease cases from 11 prion diagnostic centres, encompassing a total of 36 different pathogenic sequence variations within the open reading frame of PRNP. CSF samples were assessed for the surrogate markers of neurodegeneration, 14-3-3 protein (14-3-3), total-tau protein (t-tau) and α-synuclein and for prion seeding activity through the real-time quaking-induced conversion assay. Biomarker results were compared with those obtained in healthy and neurological controls. For the most prevalent PRNP pathogenic sequence variations, biomarker accuracy and associations between biomarkers, demographic and genetic determinants were assessed. Additionally, the prognostic value of biomarkers for predicting total disease duration from symptom onset to death was investigated. High sensitivity of the four biomarkers was detected for genetic Creutzfeldt–Jakob disease associated with the E200K and V210I mutations, but low sensitivity was observed for mutations associated with Gerstmann–Sträussler–Scheinker syndrome and fatal familial insomnia. All biomarkers showed good to excellent specificity using the standard cut-offs often used for sporadic Creutzfeldt–Jakob disease. In genetic prion diseases related to octapeptide repeat insertions, the biomarker sensitivity correlated with the number of repeats. New genetic prion disease-specific cut-offs for 14-3-3, t-tau and α-synuclein were calculated. Disease duration in genetic Creutzfeldt–Jakob disease-E200K, Gerstmann–Sträussler–Scheinker-P102L and fatal familial insomnia was highly dependent on PRNP codon 129 MV polymorphism and was significantly associated with biomarker levels. In a large cohort of genetic prion diseases, the simultaneous analysis of CSF prion disease biomarkers allowed the determination of new mutation-specific cut-offs improving the discrimination of genetic prion disease cases and unveiled genetic prion disease-specific associations with disease duration."],["dc.identifier.doi","10.1093/brain/awab350"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105472"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","Diagnostic accuracy of cerebrospinal fluid biomarkers in genetic prion diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1844"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Critical Care Medicine"],["dc.bibliographiccitation.lastpage","1851"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Muench, Elke"],["dc.contributor.author","Horn, Peter"],["dc.contributor.author","Bauhuf, Christian"],["dc.contributor.author","Roth, Harry"],["dc.contributor.author","Philipps, Mark"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Quintel, Michael"],["dc.contributor.author","Schmiedek, Peter"],["dc.contributor.author","Vajkoczy, Peter"],["dc.date.accessioned","2018-11-07T10:59:50Z"],["dc.date.available","2018-11-07T10:59:50Z"],["dc.date.issued","2007"],["dc.description.abstract","Objective: Hypertensive, hypervolemic, hemodilution therapy (triple-H therapy) is a generally accepted treatment for cerebral vasospasm after subarachnoid hemorrhage. However, the particular role of the three components of triple-H therapy remains controversial. The aim of the study was to investigate the influence of the three arms of triple-H therapy on regional cerebral blood flow and brain tissue oxygenation. Design: Animal research and clinical intervention study. Setting: Surgical intensive care unit of a university hospital. Subjects and Patients: Experiments were carried out in five healthy pigs, followed by a clinical investigation of ten patients with subarachnoid hemorrhage. Interventions: First, we investigated the effect of the three components of triple-H therapy under physiologic conditions in an experimental pig model. In the next step we applied the same study protocol to patients following aneurysmal subarachnoid hemorrhage. Mean arterial pressure, intracranial pressure, cerebral perfusion pressure, cardiac output, regional cerebral blood flow, and brain tissue oxygenation were continuously recorded. Intrathoracic blood volume and central venous pressure were measured intermittently. Vasopressors and/or colloids and crystalloids were administered to stepwise establish the three components of triple-H therapy. Measurements and Main Results: In the animals, neither induced hypertension nor hypervolemia had an effect on intracranial pressure, brain tissue oxygenation, or regional cerebral blood flow. In the patient population, induction of hypertension (mean arterial pressure 143 +/- 10 mm Hg) resulted in a significant (P <.05) increase of regional cerebral blood flow and brain tissue oxygenation at all observation time points. In contrast, hypervolemia/hemodilution (intrathoracic blood volume index 1123 :L 152 mL/m(2)) induced only a slight increase of regional cerebral blood flow while brain tissue oxygenation did not improve. Finally, triple-H therapy failed to improve regional cerebral blood flow more than hypertension alone and was characterized by the drawback that the hypervolemia/hemodilution component reversed the effect of induced hypertension on brain tissue oxygenation. Conclusions: Vasopressor-induced elevation of mean arterial pressure caused a significant increase of regional cerebral blood flow and brain tissue oxygenation in all patients with subarachnoid hemorrhage. Volume expansion resulted in a slight effect on regional cerebral blood flow only but reversed the effect on brain tissue oxygenation. In view of the questionable benefit of hypervolemia on regional cerebral blood flow and the negative consequences on brain tissue oxygenation together with the increased risk of complications, hypervolemic therapy as a part of triple-H therapy should be applied with utmost caution."],["dc.identifier.doi","10.1097/01.CCM.0000275392.08410.DD"],["dc.identifier.isi","000248251600005"],["dc.identifier.pmid","17581487"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50788"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0090-3493"],["dc.title","Effects of hypervolemia and hypertension on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation after subarachnoid hemorrhage"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]