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Institution

University of Marburg

EducationMarburg, Germany
About: University of Marburg is a education organization based out in Marburg, Germany. It is known for research contribution in the topics: Population & Virus. The organization has 23195 authors who have published 42907 publications receiving 1506069 citations. The organization is also known as: Philipps University of Marburg & Philipps-Universität.
Topics: Population, Virus, Gene, Exciton, Photoluminescence


Papers
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Journal ArticleDOI
TL;DR: The existence of initially antibody-positive HHCs suggests that mild cases of Ebola virus infection occurred and that the full extent of the EHF epidemic was probably underestimated.
Abstract: A cohort of convalescent Ebola hemorrhagic fever (EHF) patients and their household contacts (HHCs) were studied prospectively to determine if convalescent body fluids contain Ebola virus and if secondary transmission occurs during convalescence. Twenty-nine EHF convalescents and 152 HHCs were monitored for up to 21 months. Blood specimens were obtained and symptom information was collected from convalescents and their HHCs; other body fluid specimens were also obtained from convalescents. Arthralgias and myalgia were reported significantly more often by convalescents than HHCs. Evidence of Ebola virus was detected by reverse transcription-polymerase chain reaction in semen specimens up to 91 days after disease onset; however, these and all other non-blood body fluids tested negative by virus isolation. Among 81 initially antibody negative HHCs, none became antibody positive. Blood specimens of 5 HHCs not identified as EHF patients were initially antibody positive. No direct evidence of convalescent-to-HHC transmission of EHF was found, although the semen of convalescents may be infectious. The existence of initially antibody-positive HHCs suggests that mild cases of Ebola virus infection occurred and that the full extent of the EHF epidemic was probably underestimated.

366 citations

Journal ArticleDOI
TL;DR: The final analysis of a prospective multicentre study by the European MSA Study Group provides new insights into the evolution of MSA based on a follow-up period that exceeds that of previous studies.
Abstract: Summary Background Multiple system atrophy (MSA) is a fatal and still poorly understood degenerative movement disorder that is characterised by autonomic failure, cerebellar ataxia, and parkinsonism in various combinations. Here we present the final analysis of a prospective multicentre study by the European MSA Study Group to investigate the natural history of MSA. Methods Patients with a clinical diagnosis of MSA were recruited and followed up clinically for 2 years. Vital status was ascertained 2 years after study completion. Disease progression was assessed using the unified MSA rating scale (UMSARS), a disease-specific questionnaire that enables the semiquantitative rating of autonomic and motor impairment in patients with MSA. Additional rating methods were applied to grade global disease severity, autonomic symptoms, and quality of life. Survival was calculated using a Kaplan-Meier analysis and predictors were identified in a Cox regression model. Group differences were analysed by parametric tests and non-parametric tests as appropriate. Sample size estimates were calculated using a paired two-group t test. Findings 141 patients with moderately severe disease fulfilled the consensus criteria for MSA. Mean age at symptom onset was 56·2 (SD 8·4) years. Median survival from symptom onset as determined by Kaplan-Meier analysis was 9·8 years (95% CI 8·1–11·4). The parkinsonian variant of MSA (hazard ratio [HR] 2·08, 95% CI 1·09–3·97; p=0·026) and incomplete bladder emptying (HR 2·10, 1·02–4·30; p=0·044) predicted shorter survival. 24-month progression rates of UMSARS activities of daily living, motor examination, and total scores were 49% (9·4 [SD 5·9]), 74% (12·9 [8·5]), and 57% (21·9 [11·9]), respectively, relative to baseline scores. Autonomic symptom scores progressed throughout the follow-up. Shorter symptom duration at baseline (OR 0·68, 0·5–0·9; p=0·006) and absent levodopa response (OR 3·4, 1·1–10·2; p=0·03) predicted rapid UMSARS progression. Sample size estimation showed that an interventional trial with 258 patients (129 per group) would be able to detect a 30% effect size in 1-year UMSARS motor examination decline rates at 80% power. Interpretation Our prospective dataset provides new insights into the evolution of MSA based on a follow-up period that exceeds that of previous studies. It also represents a useful resource for patient counselling and planning of multicentre trials. Funding Fifth Framework Programme of the European Union, the Oesterreichische Nationalbank, and the Austrian Science Fund.

365 citations

Journal ArticleDOI
TL;DR: Ultrafast relaxation processes in poly(p-phenylenevinylene) and its oligomers are investigated using femtosecond luminescence spectroscopy and a quasi-instantaneous luminecence rise and the absence of luminescent near the excitation energy indicate very rapid vibronic relaxation.
Abstract: Ultrafast relaxation processes in poly(p-phenylenevinylene) and its oligomers are investigated using femtosecond luminescence spectroscopy. A quasi-instantaneous luminescence rise and the absence of luminescence near the excitation energy indicate very rapid vibronic relaxation. The subsequent transient redshift of the spectra is attributed to ultrafast energy relaxation of optical excitations within an inhomogeneously broadened density of states.

365 citations

Journal ArticleDOI

365 citations

Journal ArticleDOI
TL;DR: It is reported that mutation in the gene for plectin, a cytoskeleton–membrane anchorage protein, is a cause of autosomal recessive muscular dystrophy associated with skin blistering associated withepidermolysis bullosa simplex.
Abstract: We report that mutation in the gene for plectin, a cytoskeleton–membrane anchorage protein, is a cause of autosomal recessive muscular dystrophy associated with skin blistering (epidermolysis bullosa simplex). The evidence comes from absence of plectin by antibody staining in affected individuals from four families, supportive genetic analysis (localization of the human plectin gene to chromosome 8q24.13–qter and evidence for disease segregation with markers in this region) and finally the identification of a homozygous frameshift mutation detected in plectin cDNA. Absence of the large multifunctional cytoskeleton protein plectin can simultaneously account for structural failure in both muscle and skin.

365 citations


Authors

Showing all 23488 results

NameH-indexPapersCitations
John C. Morris1831441168413
Russel J. Reiter1691646121010
Martin J. Blaser147820104104
Christopher T. Walsh13981974314
Markus Cristinziani131114084538
James C. Paulson12644352152
Markus F. Neurath12493462376
Nicholas W. Wood12361466270
Florian Lang116142166496
Howard I. Maibach116182160765
Thomas G. Ksiazek11339846108
Frank Glorius11366349305
Eberhard Ritz111110961530
Manfred T. Reetz11095942941
Wolfgang H. Oertel11065351147
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023142
2022412
20212,103
20201,918
20191,749
20181,592