Institution
Medical University of Graz
Education•Graz, Steiermark, Austria•
About: Medical University of Graz is a education organization based out in Graz, Steiermark, Austria. It is known for research contribution in the topics: Population & Medicine. The organization has 5684 authors who have published 12349 publications receiving 417282 citations.
Topics: Population, Medicine, Cancer, Transplantation, Vitamin D and neurology
Papers published on a yearly basis
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University of Washington1, University of Texas Health Science Center at Houston2, John P. Hussman Institute for Human Genomics3, Boston University4, Case Western Reserve University5, Baylor College of Medicine6, Icahn School of Medicine at Mount Sinai7, University of Pennsylvania8, Erasmus University Medical Center9, French Institute of Health and Medical Research10, Pasteur Institute11, university of lille12, Vanderbilt University Medical Center13, Washington University in St. Louis14, University of Bordeaux15, Broad Institute16, National Institutes of Health17, University of Helsinki18, University of Eastern Finland19, Harvard University20, McGill University21, University of Tampere22, Columbia University23, Indiana University24, University of Tartu25, University of Nantes26, Oulu University Hospital27, Medical University of Graz28, University of Texas at Austin29
TL;DR: The Alzheimer’s Disease Sequencing Project undertook whole exome sequencing in 5,740 late-onset Alzheimer disease cases and 5,096 cognitively normal controls primarily of European ancestry, identifying novel and predicted functional genetic variants in genes previously associated with AD.
Abstract: The Alzheimer’s Disease Sequencing Project (ADSP) undertook whole exome sequencing in 5,740 late-onset Alzheimer disease (AD) cases and 5,096 cognitively normal controls primarily of European ancestry (EA), among whom 218 cases and 177 controls were Caribbean Hispanic (CH). An age-, sex- and APOE based risk score and family history were used to select cases most likely to harbor novel AD risk variants and controls least likely to develop AD by age 85 years. We tested ~1.5 million single nucleotide variants (SNVs) and 50,000 insertion-deletion polymorphisms (indels) for association to AD, using multiple models considering individual variants as well as gene-based tests aggregating rare, predicted functional, and loss of function variants. Sixteen single variants and 19 genes that met criteria for significant or suggestive associations after multiple-testing correction were evaluated for replication in four independent samples; three with whole exome sequencing (2,778 cases, 7,262 controls) and one with genome-wide genotyping imputed to the Haplotype Reference Consortium panel (9,343 cases, 11,527 controls). The top findings in the discovery sample were also followed-up in the ADSP whole-genome sequenced family-based dataset (197 members of 42 EA families and 501 members of 157 CH families). We identified novel and predicted functional genetic variants in genes previously associated with AD. We also detected associations in three novel genes: IGHG3 (p = 9.8 × 10−7), an immunoglobulin gene whose antibodies interact with β-amyloid, a long non-coding RNA AC099552.4 (p = 1.2 × 10−7), and a zinc-finger protein ZNF655 (gene-based p = 5.0 × 10−6). The latter two suggest an important role for transcriptional regulation in AD pathogenesis.
191 citations
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TL;DR: This study describes an influence of SAT topography on adiponectin serum levels and provides first evidence that incipient atherosclerosis is associated with low serum levels of this adipocytokine.
Abstract: sensitive C-reactive protein (P 0.001), indicating early stages of atherosclerosis. Serum levels of adiponectin were highly significantly negatively correlated with carotid IMT, even after controlling for common cardiovascular risk factors (P 0.001; r 0.34). Furthermore, adiponectin was positively correlated with high-density lipoprotein-free cholesterol and serum apolipoprotein-A1 and negatively with triglycerides, insulin resistance, uric acid, and serum transaminases. By a multiple regression analysis, adiponectin was shown to be the strongest predictive variable for carotid IMT. Finally, adiponectin was found positively correlated with SAT thickness of the rear and inner thigh in boys and negatively with the SAT thickness of the neck in girls. Conclusion: In summary, our study describes an influence of SAT topography on adiponectin serum levels and provides first evidence that incipient atherosclerosis is associated with low serum levels of this adipocytokine. (J Clin Endocrinol Metab 90: 4792–4796, 2005)
190 citations
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TL;DR: The risk of residual or recurrent CIN2+ is significantly greater with involved margins on excisional treatment; however, high-risk HPV post-treatment predicts treatment failure more accurately than margin status.
Abstract: Summary Background Incomplete excision of cervical precancer is associated with therapeutic failure and is therefore considered as a quality indicator of clinical practice. Conversely, the risk of preterm birth is reported to correlate with size of cervical excision and therefore balancing the risk of adequate treatment with iatrogenic harm is challenging. We reviewed the literature with an aim to reveal whether incomplete excision, reflected by presence of precancerous tissue at the section margins, or post-treatment HPV testing are accurate predictors of treatment failure. Methods We did a systematic review and meta-analysis to assess the risk of therapeutic failure associated with the histological status of the margins of the tissue excised to treat cervical precancer. We estimated the accuracy of the margin status to predict occurrence of residual or recurrent high-grade cervical intraepithelial neoplasia of grade two or worse (CIN2+) and compared it with post-treatment high-risk human papillomavirus (HPV) testing. We searched for published systematic reviews and new references from PubMed-MEDLINE, Embase, and CENTRAL and did also a new search spanning the period Jan 1, 1975, until Feb 1, 2016. Studies were eligible if women underwent treatment by excision of a histologically confirmed CIN2+ lesion, with verification of presence or absence of CIN at the resection margins; were tested by cytology or HPV assay between 3 months and 9 months after treatment; and had subsequent follow-up of at least 18 months post-treatment including histological confirmation of the occurrence of CIN2+. Primary endpoints were the proportion of positive section margins and the occurrence of treatment failure associated with the marginal status, in which treatment failure was defined as occurrence of residual or recurrent CIN2+. Information about positive resection margins and subsequent treatment failure was pooled using procedures for meta-analysis of binomial data and analysed using random-effects models. Findings 97 studies were eligible for inclusion in the meta-analysis and included 44 446 women treated for cervical precancer. The proportion of positive margins was 23·1% (95% CI 20·4–25·9) overall and varied by treatment procedure (ranging from 17·8% [12·9–23·2] for laser conisation to 25·9% [22·3–29·6] for large loop excision of the transformation zone) and increased by the severity of the treated lesion. The overall risk of residual or recurrent CIN2+ was 6·6% (95% CI 4·9–8·4) and was increased with positive compared with negative resection margins (relative risk 4·8, 95% CI 3·2–7·2). The pooled sensitivity and specificity to predict residual or recurrent CIN2+ was 55·8% (95% CI 45·8–65·5) and 84·4% (79·5–88·4), respectively, for the margin status, and 91·0% (82·3–95·5) and 83·8% (77·7–88·7), respectively, for high-risk HPV testing. A negative high-risk HPV test post treatment was associated with a risk of CIN2+ of 0·8%, whereas this risk was 3·7% when margins were free. Interpretation The risk of residual or recurrent CIN2+ is significantly greater with involved margins on excisional treatment; however, high-risk HPV post-treatment predicts treatment failure more accurately than margin status. Funding European Federation for Colposcopy and Institut national du Cancer (INCA).
190 citations
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University of Texas Health Science Center at Houston1, Boston University2, University of Washington3, Medical University of Graz4, Erasmus University Rotterdam5, French Institute of Health and Medical Research6, University of Caen Lower Normandy7, McGill University8, University of Vermont9, University of North Carolina at Chapel Hill10, Mayo Clinic11, University of Ferrara12, National Institutes of Health13, University of Pittsburgh14, Pasteur Institute15, Johns Hopkins University16, Group Health Cooperative17, United States Department of Veterans Affairs18, University of Iceland19, Cedars-Sinai Medical Center20, University of Mississippi21, University of California, Davis22
TL;DR: White matter hyperintensities detectable by magnetic resonance imaging are part of the spectrum of vascular injury associated with aging of the brain and are thought to reflect ischemic damage to the small deep cerebral vessels.
Abstract: textObjective: White matter hyperintensities (WMHs) detectable by magnetic resonance imaging are part of the spectrum of vascular injury associated with aging of the brain and are thought to reflect ischemic damage to the small deep cerebral vessels. WMHs are associated with an increased risk of cognitive and motor dysfunction, dementia, depression, and stroke. Despite a significant heritability, few genetic loci influencing WMH burden have been identified. Methods: We performed a meta-analysis of genome-wide association studies (GWASs) for WMH burden in 9,361 stroke-free individuals of European descent from 7 community-based cohorts. Significant findings were tested for replication in 3,024 individuals from 2 additional cohorts. Results: We identified 6 novel risk-associated single nucleotide polymorphisms (SNPs) in 1 locus on chromosome 17q25 encompassing 6 known genes including WBP2, TRIM65, TRIM47, MRPL38, FBF1, and ACOX1. The most significant association was for rs3744028 (pdiscovery= 4.0 × 10-9; preplication= 1.3 × 10-7; pcombined= 4.0 × 10-15). Other SNPs in this region also reaching genome-wide significance were rs9894383 (p = 5.3 × 10-9), rs11869977 (p = 5.7 × 10-9), rs936393 (p = 6.8 × 10-9), rs3744017 (p = 7.3 × 10-9), and rs1055129 (p = 4.1 × 10-8). Variant alleles at these loci conferred a small increase in WMH burden (4-8% of the overall mean WMH burden in the sample). Interpretation: This large GWAS of WMH burden in community-based cohorts of individuals of European descent identifies a novel locus on chromosome 17. Further characterization of this locus may provide novel insights into the pathogenesis of cerebral WMH.
189 citations
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Children's Hospital Oakland Research Institute1, Universidade Federal do Rio Grande do Sul2, University of Porto3, University of Manchester4, University of Mainz5, University of Padua6, Boston Children's Hospital7, Medical University of Graz8, Oregon Health & Science University9, University of Pennsylvania10, BioMarin Pharmaceutical11
TL;DR: RhASB treatment up to 5 years results in sustained improvements in endurance and has an acceptable safety profile.
189 citations
Authors
Showing all 5763 results
Name | H-index | Papers | Citations |
---|---|---|---|
Ian J. Deary | 166 | 1795 | 114161 |
James F. Wilson | 146 | 677 | 101883 |
Nancy L. Pedersen | 145 | 890 | 94696 |
William Wijns | 127 | 752 | 95517 |
Andrew Simmons | 102 | 460 | 36608 |
Franz Fazekas | 101 | 629 | 49775 |
Hans-Peter Hartung | 100 | 810 | 49792 |
Michael Trauner | 98 | 667 | 35543 |
Dietmar Fuchs | 97 | 1119 | 39758 |
Funda Meric-Bernstam | 96 | 753 | 36803 |
Ulf Landmesser | 94 | 564 | 46096 |
Aysegul A. Sahin | 93 | 322 | 30038 |
Frank Madeo | 92 | 269 | 45942 |
Takayoshi Ohkubo | 91 | 631 | 69634 |
Jürgen C. Becker | 90 | 637 | 28741 |