Institution
University of Hamburg
Education•Hamburg, Germany•
About: University of Hamburg is a education organization based out in Hamburg, Germany. It is known for research contribution in the topics: Population & Laser. The organization has 45564 authors who have published 89286 publications receiving 2850161 citations. The organization is also known as: Hamburg University.
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TL;DR: In this paper, it was shown that the quantum mechanical hamiltonians of a class of supersymmetric matrix models have a continuous spectrum starting at zero, and that supermembranes (which can be regarded as a limit of such models) have no mass gap.
368 citations
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TL;DR: It is proposed that the online game players' physical and social proximity as well as their mutual familiarity influence bridging and bonding social capital, and that both social capital dimensions are positively related to offline social support.
368 citations
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TL;DR: The mechanisms underlying CKD plus diabetes mellitus and how greater appreciation of distinctions between these entities might facilitate the development of new treatments are discussed.
Abstract: The increasing global prevalence of type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) has prompted research efforts to tackle the growing epidemic of diabetic kidney disease (DKD; also known as diabetic nephropathy). The limited success of much of this research might in part be due to the fact that not all patients diagnosed with DKD have renal dysfunction as a consequence of their diabetes mellitus. Patients who present with CKD and diabetes mellitus (type 1 or type 2) can have true DKD (wherein CKD is a direct consequence of their diabetes status), nondiabetic kidney disease (NDKD) coincident with diabetes mellitus, or a combination of both DKD and NDKD. Preclinical studies using models that more accurately mimic these three entities might improve the ability of animal models to predict clinical trial outcomes. Moreover, improved insights into the pathomechanisms that are shared by these entities - including sodium-glucose cotransporter 2 (SGLT2) and renin-angiotensin system-driven glomerular hyperfiltration and tubular hyper-reabsorption - as well as those that are unique to individual entities might lead to the identification of new treatment targets. Acknowledging that the clinical entity of CKD plus diabetes mellitus encompasses NDKD as well as DKD could help solve some of the urgent unmet medical needs of patients affected by these conditions.
367 citations
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National Institutes of Health1, Karolinska Institutet2, University of Helsinki3, University of Cambridge4, University of Copenhagen5, Carlos III Health Institute6, Autonomous University of Madrid7, University of Tübingen8, Bosch9, German Cancer Research Center10, Ruhr University Bochum11, University of Bonn12, Hannover Medical School13, University of Eastern Finland14, Royal Brisbane and Women's Hospital15, Leiden University16, Erasmus University Rotterdam17, University of Hamburg18, University of Ulm19, Mayo Clinic20, Cancer Council Victoria21, University of Melbourne22, University of Southern California23, University of Hawaii at Manoa24, Harvard University25, Curie Institute26, Nofer Institute of Occupational Medicine27, Agency for Science, Technology and Research28, University of Sheffield29, Cancer Research UK30, International Agency for Research on Cancer31
TL;DR: The findings show that common genetic variants influence the pathological subtype of breast cancer and provide further support for the hypothesis that ER-positive and ER-negative disease are biologically distinct.
Abstract: A three-stage genome-wide association study recently identified single nucleotide polymorphisms (SNPs) in five loci (fibroblast growth receptor 2 (FGFR2), trinucleotide repeat containing 9 (TNRC9), mitogen-activated protein kinase 3 K1 (MAP3K1), 8q24, and lymphocyte-specific protein 1 (LSP1)) associated with breast cancer risk. We investigated whether the associations between these SNPs and breast cancer risk varied by clinically important tumor characteristics in up to 23,039 invasive breast cancer cases and 26,273 controls from 20 studies. We also evaluated their influence on overall survival in 13,527 cases from 13 studies. All participants were of European or Asian origin. rs2981582 in FGFR2 was more strongly related to ER-positive (per-allele OR (95%CI) = 1.31 (1.27-1.36)) than ER-negative (1.08 (1.03-1.14)) disease (P for heterogeneity = 10(-13)). This SNP was also more strongly related to PR-positive, low grade and node positive tumors (P = 10(-5), 10(-8), 0.013, respectively). The association for rs13281615 in 8q24 was stronger for ER-positive, PR-positive, and low grade tumors (P = 0.001, 0.011 and 10(-4), respectively). The differences in the associations between SNPs in FGFR2 and 8q24 and risk by ER and grade remained significant after permutation adjustment for multiple comparisons and after adjustment for other tumor characteristics. Three SNPs (rs2981582, rs3803662, and rs889312) showed weak but significant associations with ER-negative disease, the strongest association being for rs3803662 in TNRC9 (1.14 (1.09-1.21)). rs13281615 in 8q24 was associated with an improvement in survival after diagnosis (per-allele HR = 0.90 (0.83-0.97). The association was attenuated and non-significant after adjusting for known prognostic factors. Our findings show that common genetic variants influence the pathological subtype of breast cancer and provide further support for the hypothesis that ER-positive and ER-negative disease are biologically distinct. Understanding the etiologic heterogeneity of breast cancer may ultimately result in improvements in prevention, early detection, and treatment.
367 citations
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TL;DR: Strong genetic dependence between EA and SZ is found that cannot be explained by chance, linkage disequilibrium, or assortative mating, and multiple genes have pleiotropic effects on both without a systematic pattern of sign concordance.
Abstract: Higher educational attainment (EA) is negatively associated with schizophrenia (SZ). However, recent studies found a positive genetic correlation between EA and SZ. We investigate possible causes of this counterintuitive finding using genome-wide association study results for EA and SZ (N = 443,581) and a replication cohort (1169 controls; 1067 cases) with deeply phenotyped SZ patients. We find strong genetic dependence between EA and SZ that cannot be explained by chance, linkage disequilibrium, or assortative mating. Instead, several genes seem to have pleiotropic effects on EA and SZ, but without a clear pattern of sign concordance. Using EA as a proxy phenotype, we isolate FOXO6 and SLITRK1 as novel candidate genes for SZ. Our results reveal that current SZ diagnoses aggregate over at least two disease subtypes: one part resembles high intelligence and bipolar disorder (BIP), while the other part is a cognitive disorder that is independent of BIP.
366 citations
Authors
Showing all 46072 results
Name | H-index | Papers | Citations |
---|---|---|---|
Rudolf Jaenisch | 206 | 606 | 178436 |
Bruce M. Psaty | 181 | 1205 | 138244 |
Stefan Schreiber | 178 | 1233 | 138528 |
Chris Sander | 178 | 713 | 233287 |
Dennis J. Selkoe | 177 | 607 | 145825 |
Daniel R. Weinberger | 177 | 879 | 128450 |
Ramachandran S. Vasan | 172 | 1100 | 138108 |
Bradley Cox | 169 | 2150 | 156200 |
Anders Björklund | 165 | 769 | 84268 |
J. S. Lange | 160 | 2083 | 145919 |
Hannes Jung | 159 | 2069 | 125069 |
Andrew D. Hamilton | 151 | 1334 | 105439 |
Jongmin Lee | 150 | 2257 | 134772 |
Teresa Lenz | 150 | 1718 | 114725 |
Stefanie Dimmeler | 147 | 574 | 81658 |