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Mary McGlohon, Stephen Bay, Markus G. Anderle, David M. Steier, Christos Faloutsos
2009 Proceedings of the 15th ACM SIGKDD international conference on Knowledge discovery and data mining - KDD '09  
GL2 The second set of G/L data contained 1, 678 nodes, 18, 720 edges, and 11, 401 red flags.  ...  Manipulation of records can be found by experts on both the G/L and financial statement level.  ... 
doi:10.1145/1557019.1557155 dblp:conf/kdd/McGlohonBASF09 fatcat:zl6mwtqbevhitlcvrodc6b5mmi

Helicobacter pylori HP0231 Influences Bacterial Virulence and Is Essential for Gastric Colonization

Yu Zhong, Florian Anderl, Tobias Kruse, Franziska Schindele, Elżbieta Katarzyna Jagusztyn-Krynicka, Wolfgang Fischer, Markus Gerhard, Raquel Mejías-Luque, Ivo G. Boneca
2016 PLoS ONE  
μg/mL cefsulodin.  ...  Gastric homogenate dilutions were plated on WC dent plates containing 200 μg/mL bacitracin, 10 μg/mL nalidixic acid and 3 μg/mL polymyxin B and antibiotics for selection.  ... 
doi:10.1371/journal.pone.0154643 pmid:27138472 pmcid:PMC4854439 fatcat:yb7s4mp5mzampozoazdu6gnr2e

Pittsburgh compound B imaging and cerebrospinal fluid amyloid-β in a multicentre European memory clinic study

Antoine Leuzy, Konstantinos Chiotis, Steen G. Hasselbalch, Juha O. Rinne, Alexandre de Mendonça, Markus Otto, Alberto Lleó, Miguel Castelo-Branco, Isabel Santana, Jarkko Johansson, Sarah Anderl-Straub, Christine A. F. von Arnim (+9 others)
2016 Brain  
The aim of this study was to assess the agreement between data on cerebral amyloidosis, derived using Pittsburgh compound B positron emission tomography and (i) multi-laboratory INNOTEST enzyme linked immunosorbent assay derived cerebrospinal fluid concentrations of amyloid-b 42 ; (ii) centrally measured cerebrospinal fluid amyloid-b 42 using a Meso Scale Discovery enzyme linked immunosorbent assay; and (iii) cerebrospinal fluid amyloid-b 42 centrally measured using an antibody-independent mass
more » ... spectrometry-based reference method. Moreover, we examined the hypothesis that discordance between amyloid biomarker measurements may be due to interindividual differences in total amyloid-b production, by using the ratio of amyloid-b 42 to amyloid-b 40 . Our study population consisted of 243 subjects from seven centres belonging to the Biomarkers for Alzheimer's and Parkinson's Disease Initiative, and included subjects with normal cognition and patients with mild cognitive impairment, Alzheimer's disease dementia, frontotemporal dementia, and vascular dementia. All had Pittsburgh compound B positron emission tomography data, cerebrospinal fluid INNOTEST amyloid-b 42 values, and cerebrospinal fluid samples available for reanalysis. Cerebrospinal fluid samples were reanalysed (amyloid-b 42 and amyloid-b 40 ) using Meso Scale Discovery electrochemiluminescence enzyme linked immunosorbent assay technology, and a novel, antibody-independent, mass spectrometry reference method. Pittsburgh compound B standardized uptake value ratio results were scaled using the Centiloid method. Concordance between Meso Scale Discovery/mass spectrometry reference measurement procedure findings and Pittsburgh compound B was high in subjects with mild cognitive impairment and Alzheimer's disease, while more variable results were observed for cognitively normal and non-Alzheimer's disease groups. Agreement between Pittsburgh compound B classification and Meso Scale Discovery/mass spectrometry reference measurement procedure findings was further improved when using amyloid-b 42/40 . Agreement between Pittsburgh compound B visual ratings and Centiloids was near complete. Despite improved agreement between Pittsburgh compound B and centrally analysed cerebrospinal fluid, a minority of subjects showed discordant findings. While future studies are needed, our results suggest that amyloid biomarker results may not be interchangeable in some individuals. Abbreviations: AD-100 = amyloid-b-positive Alzheimer's disease subjects used as part of Centiloid standardization; FTD = frontotemporal dementia; MCI = mild cognitive impairment; MSD = Meso Scale Discovery ELISA; MS-RMP = mass spectrometrybased candidate reference measurement procedure; PiB = Pittsburgh compound B; SUVr = standardized uptake value ratio; VaD = vascular dementia; YC-0 = amyloid-b-negative young controls used as part of Centiloid standardization 2 | BRAIN 2016: Page 2 of 14 A. Leuzy et al. by guest on August 5, 2016 http://brain.oxfordjournals.org/ Downloaded from Determination of CSF amyloid-b cut-offs Local amyloid-b 42 values (pooled) were classified as positive (abnormal) or negative (normal) using an optimized cut-off of 557 pg/ml, established in a recent study using a large cohort of BIOMARKAPD subjects (Zwan et al., 2016). Unbiased cutoffs for MSD-and MS-RMP-derived amyloid-b 42 and amyloid-b 42/40 ratios were determined by mixture modelling (Benaglia et al., 2009), implemented in R (v.3.2.3, R Foundation for Statistical Computing, Vienna, Austria, 2015). Association between PiB PET and CSF Ab peptides BRAIN 2016: Page 3 of 14 | 3 by guest on August 5, 2016 http://brain.oxfordjournals.org/ Downloaded from Association between PiB PET and CSF Ab peptides BRAIN 2016: Page 5 of 14 | 5 by guest on August 5, 2016 http://brain.oxfordjournals.org/ Downloaded from Values are reported as median (quartile3, quartile 1), or as n (%). Ab = amyloid-b; AD = Alzheimer's disease; CN = cognitively normal older individuals; MMSE = Mini-Mental State Examination. Cut-offs used to determine positivity were as follows: INNOTEST amyloid-b 42 , 5557 pg/ml; MSD amyloid-b 42 , 5515 pg/ml; MSD amyloid-b 42/40 , 50.72; MS amyloid-b 42 , 5896 pg/ ml; MS amyloid-b 42/40 , 5 0.76. 6 | BRAIN 2016: Page 6 of 14 A. Leuzy et al. by guest on August 5, 2016 http://brain.oxfordjournals.org/ Downloaded from INNOTEST and MSD amyloid-b 42 ; (B) INNOTEST and MS-RMP amyloid-b 42 ; (C) MSD and MS-RMP amyloid-b 42 ; and (D) MSD and MS-RMP amyloid-b 42/40 .
doi:10.1093/brain/aww160 pmid:27401520 pmcid:PMC4995359 fatcat:lpqj7tqlmnhnblsuavh3e5btri

Page 2787 of Psychological Abstracts Vol. 90, Issue 8 [page]

2003 Psychological Abstracts  
Rachel G., 22939 Kleinplatz, Peggy J., 23010 Joa 22182 23861 >) 284 Lacey Klinkenberg, M., 22290 Klock.  ...  S., 22903 an, Pei-Chia Krist, Horst, 21826 andau, Barbar Kroesbergen, Evely 23824 indau, Yael E Kroeze, Wesley K., 2315¢ anderl, Karin Kromm, Alexander, 217¢ andheim, A.  ... 

Page 1647 of Psychological Abstracts Vol. 90, Issue 5 [page]

2003 Psychological Abstracts  
14538, 14538 Amick, Benjamin C. 33, 11869, 13707, 14566 Amico, Janet A., 12428 Amoroso, Paul J., 14790, 14793, 14795 Amsterdam, Jay D., 13289 An, Sylvia, 11905 An, Wen-Lin, 13796 Anda, Robert F., 13517 Anderle  ...  Bacharach, Verne R., 13465 Bachelor, Jonathan, 13007 Bachorowski, Jo-Anne, 12999 Back, Sudie E., 14144 Backer, Thomas E., 14362 Backman, Lars, 12716 Backmund, H., 14345 Baddeley, Alan D., 12691 Bader, Markus  ... 

Page 3130 of Mathematical Reviews Vol. , Issue 2003d [page]

2003 Mathematical Reviews  
G.  ...  Brown, Nonlinear thoughts about linear signal processing (99-111); Markus Anderle and Michael Kirby [Michael Joseph Kirby], An application of the maximum noise fraction method to filtering noisy time series  ... 

VIRUS. Beiträge zur Sozialgeschichte der Medizin Band 10

Elisabeth Dietrich-Daum, Werner Matt, Wolfgang Weber, Carlos Watzka
2020 VIRUS - Beiträge zur Sozialgeschichte der Medizin  
Apart from Freud and some other university professors, a few doctors were dealing with sexology like e. g. Helene Stourzh-Anderle (1890-1966).  ...  Markus Rachbauer, Begleiter am Lern-und Gedenkort Schloss Hartheim und in der KZ-Gedenkstätte Mauthausen.  ... 
doi:10.1553/virus10s001 fatcat:3y3r2qdfubhczngbjkgpjluope

Age at symptom onset and death and disease duration in genetic frontotemporal dementia: an international retrospective cohort study

Katrina M Moore, Jennifer Nicholas, Murray Grossman, Corey T McMillan, David J Irwin, Lauren Massimo, Vivianna M Van Deerlin, Jason D Warren, Nick C Fox, Martin N Rossor, Simon Mead, Martina Bocchetta (+159 others)
2019 Lancet Neurology  
Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. In this international, retrospective cohort study, we collected data on age at
more » ... om onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49·5 years (SD 10·0; onset) and 58·5 years (11·3; death) in the MAPT group, 58·2 years (9·8; onset) and 65·3 years (10·9; death) in the C9orf72 group, and 61·3 years (8·8; onset) and 68·8 years (9·7; death) in the GRN group. Mean disease duration was 6·4 years (SD 4·9) in the C9orf72 group, 7·1 years (3·9) in the GRN group, and 9·3 years (6·4) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0·45 between individual and parental age at onset, r=0·63 between individual and mean family age at onset, r=0·58 between individual and parental age at death, and r=0·69 between individual and mean family age at death) than in either the C9orf72 group (r=0·32 individual and parental age at onset, r=0·36 individual and mean family age at onset, r=0·38 individual and parental age at death, and r=0·40 individual and mean family age at death) or the GRN group (r=0·22 individual and parental age at onset, r=0·18 individual and mean family age at onset, r=0·22 individual and parental age at death, and r=0·32 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35-62, for age at onset; 61%, 47-73, for age at death), and even more by family membership (66%, 56-75, for age at onset; 74%, 65-82, for age at death). In the GRN group, only 2% (0-10) of the variability of age at onset and 9% (3-21) of that of age of death was explained by the specific mutation, whereas 14% (9-22) of the variability of age at onset and 20% (12-30) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11-26) of the variability of age at onset and 19% (12-29) of that of age at death. Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society.
doi:10.1016/s1474-4422(19)30394-1 pmid:31810826 pmcid:PMC7007771 fatcat:jrjh3znksveg3ezjgviojmoyaa

Reactive oxygen species-dependent Toll/NF-κB activation in the Drosophila hematopoietic niche confers resistance to wasp parasitism

Isabelle Louradour, Anurag Sharma, Ismael Morin-Poulard, Manon Letourneau, Alain Vincent, Michèle Crozatier, Nathalie Vanzo
2017 eLife  
., 2011; Márkus et al., 2009) .  ...  (D, G, J, L).  ... 
doi:10.7554/elife.25496 pmid:29091025 pmcid:PMC5681226 fatcat:g447wno7ofdzpn4ncxkhybwc5e

A single-cell survey of Drosophila blood [article]

Sudhir Gopal Tattikota, Yanhui Hu, Yifang Liu, Bumsik Cho, Victor Barrera, Michael Steinbaugh, Sang-Ho Yoon, Aram Comjean, Fangge Li, Franz Dervis, Ruei-Jiun Hung, Jin-Wu Nam (+3 others)
2019 bioRxiv   pre-print
et al., 2016; Leitão and Sucena, 2015; Márkus et al., 2009) .  ...  G-G'') Expression validation of E(spl)m3-HLH in vivo.  ... 
doi:10.1101/2019.12.20.884999 fatcat:bulrkk6ojzhknphxjkiuo2pu2e

Monitoring of Pathogen-Specific T-Cell Immune Reconstitution after Allogeneic Hematopoietic Stem Cell Transplantation

Shigeo Fuji, Markus Kapp, Hermann Einsele
2013 Frontiers in Immunology  
Neudorfer J, Schmidt B, Huster KM, Anderl F, Schiemann M, Holzapfel G, et al.  ...  Potenza L, Barozzi P, Rossi G, Palazzi G, Vallerini D, Riva G, et al. Assessment of Aspergillus-Scheinberg P, Barrett AJ, et al.  ... 
doi:10.3389/fimmu.2013.00276 pmid:24062744 pmcid:PMC3775001 fatcat:7xav45jtifa7xfxl4gff4u5oz4

Enhancer of Polycomb/Tip60 represses hematological tumor initiation by negatively regulating JAK/STAT pathway activity

Alessandro A. Bailetti, Lenny J. Negrón-Piñeiro, Vishal Dhruva, Sneh Harsh, Sean Lu, Aisha Bosula, Erika A. Bach
2019 Disease Models & Mechanisms  
et al., 2009; Honti et al., 2010; Stofanko et al., 2010; Avet-Rochex et al., 2010; Anderl et al., 2016) .  ...  However, they can be mobilized en masse in response to infection (Markus et al., 2009; Makhijani et al., 2011; Gold and Brückner, 2015) .  ... 
doi:10.1242/dmm.038679 pmid:31072879 pmcid:PMC6550037 fatcat:wdnm2iyktjetlm6fvnj2eyc73i

Host JAK/Stat activity is a target of endoparasitoid wasp virulence strategies [article]

Susanna E. Brantley, Nathan T. Mortimer, Todd A. Schlenke
2018 bioRxiv   pre-print
and they signal pro-hemocytes in the lymph gland (the larval hematopoietic organ) as well as other circulating plasmatocytes (via the intermediate podocyte form) to differentiate into lamellocytes (Anderl  ...  GFP expression in 10XStat92E-GFP larval tissues 48 hours following infection by the avirulent wasp L. clavipes (LcNet; a-f) compared to age-matched uninfected larvae (g-l).  ... 
doi:10.1101/423335 fatcat:wy3okhjg35fuhgbv2xic2z46ga

Page 143 of Psychological Abstracts Vol. 90, Issue Author & Book Title Index [page]

Psychological Abstracts  
., G.  ...  ., 28762 Lam, Amy G., 1511 Lam, Andrew, 17182 Lam, Chi-Chung, 11520 Lam, Cindy L.  ... 

Cerebrospinal Fluid Levels of Prodynorphin-Derived Peptides Are Decreased in Huntington's Disease

Mhd Rami Al Shweiki, Patrick Oeckl, Adrian Pachollek, Petra Steinacker, Peggy Barschke, Steffen Halbgebauer, Sarah Anderl-Straub, Jan Lewerenz, Albert C Ludolph, Georg Bernhard Landwehrmeyer, Markus Otto
2020 Movement Disorders  
0.48 (0.38-0.56) 0.25 (0.16-0.31) 0.47 (0.36-0.63) 0.48 (0.36-0.56) 0.39 (0.32-0.45) 0.31 (0.26-0.64) Movement Disorders, Vol. 36, No. 2, 2021 P R O D Y N O R P H I N I N H U N T I N G  ...  (G) Receiver operating characteristic (ROC) curves of CSF NfL and CSF PDYN for differentiation between HD patients and controls (NfL in blue, PDYN in orange) as well as HD and other neurodegenerative conditions  ... 
doi:10.1002/mds.28300 pmid:33006791 fatcat:rkc5qtwlfnhyhhkcz34zweuf4e
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