Institution
Tel Aviv University
Education•Tel Aviv, Israel•
About: Tel Aviv University is a education organization based out in Tel Aviv, Israel. It is known for research contribution in the topics: Population & Medicine. The organization has 47791 authors who have published 115959 publications receiving 3904391 citations. The organization is also known as: TAU & Universiṭat Tel-Aviv.
Topics: Population, Medicine, Poison control, Context (language use), Cancer
Papers published on a yearly basis
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TL;DR: In this article, the problem of estimating the regression coefficient matrix having known (reduced) rank for the multivariate linear model when both sets of variates are jointly stochastic is discussed.
548 citations
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TL;DR: In this paper, the authors examined the desirability and implications of new venture financing within a principal-agent framework that captures the essence of the relationship between entrepreneurs and venture capitalists.
Abstract: A number of issues that relate to the desirability and implications of new venture financing are examined within a principal-agent framework that captures the essence of the relationship between entrepreneurs and venture capitalists. The model suggests: 1 As long as the skill levels of entrepreneurs are common knowledge, all will choose to involve venture capital investors, since the risk sharing provided by outside participation dominates the agency relationship that is created. 2 The less able entrepreneurs will choose to involve venture capitalists, whereas the more profitable ventures will be developed without external participation because of the adverse selection problem associated with asymmetric information. 3 If a costly signal is available that conveys the entrepreneur's ability, some entrepreneurs will invest in such a signal and then sell to investors; these entrepreneurs, however, need not be the more able ones. The implications for new venture financing of these and other findings are discussed and illustrated by example.
547 citations
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National Institutes of Health1, University of California, Los Angeles2, Royal Brisbane and Women's Hospital3, Cambridge University Hospitals NHS Foundation Trust4, Tel Aviv University5, University of Southern California6, Cedars-Sinai Medical Center7, Katholieke Universiteit Leuven8, University of Cambridge9, Claude Bernard University Lyon 110, Carlos III Health Institute11, City of Hope National Medical Center12, The Royal Marsden NHS Foundation Trust13, University of Kansas14, Fox Chase Cancer Center15, University of Hong Kong16, University of Copenhagen17, Mayo Clinic18, Cancer Care Ontario19, University of Toronto20, Ohio State University21, University of Edinburgh22, Stanford University23, Lund University24, Memorial Sloan Kettering Cancer Center25, University of California, San Francisco26, Roswell Park Cancer Institute27
TL;DR: Among patients with invasive EOC, having a germline mutation in BRCA1 or BRC a2 was associated with improved 5-year overall survival and BRCa2 carriers had the best prognosis.
Abstract: Results The 5-year overall survival was 36% (95% CI, 34%-38%) for noncarriers, 44% (95% CI, 40%-48%) for BRCA1 carriers, and 52% (95% CI, 46%-58%) for BRCA2 carriers. After adjusting for study and year of diagnosis, BRCA1 and BRCA2 mutation carriers showed a more favorable survival than noncarriers (for BRCA1: hazard ratio [HR], 0.78; 95% CI, 0.68-0.89; P.001; and for BRCA2: HR, 0.61; 95% CI, 0.50-0.76; P.001). These survival differences remained after additional adjustment for stage, grade, histology, and age at diagnosis (for BRCA1: HR, 0.73; 95% CI, 0.640.84; P.001; and for BRCA2: HR, 0.49; 95% CI, 0.39-0.61; P.001). The BRCA1 HR estimate was significantly different from the HR estimated in the adjusted model (P for heterogeneity=.003). Conclusion Among patients with invasive EOC, having a germline mutation inBRCA1 or BRCA2 was associated with improved 5-year overall survival. BRCA2 carriers had the best prognosis.
545 citations
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TL;DR: This work uses recently released sequences from the 1000 Genomes Project to identify two western African-specific missense mutations in the neighboring APOL1 gene, and demonstrates that these are more strongly associated with ESKD than previously reported MYH9 variants.
Abstract: MYH9 has been proposed as a major genetic risk locus for a spectrum of nondiabetic end stage kidney disease (ESKD). We use recently released sequences from the 1000 Genomes Project to identify two western African-specific missense mutations (S342G and I384M) in the neighboring APOL1 gene, and demonstrate that these are more strongly associated with ESKD than previously reported MYH9 variants. The APOL1 gene product, apolipoprotein L-1, has been studied for its roles in trypanosomal lysis, autophagic cell death, lipid metabolism, as well as vascular and other biological activities. We also show that the distribution of these newly identified APOL1 risk variants in African populations is consistent with the pattern of African ancestry ESKD risk previously attributed to MYH9.Mapping by admixture linkage disequilibrium (MALD) localized an interval on chromosome 22, in a region that includes the MYH9 gene, which was shown to contain African ancestry risk variants associated with certain forms of ESKD (Kao et al. 2008; Kopp et al. 2008). MYH9 encodes nonmuscle myosin heavy chain IIa, a major cytoskeletal nanomotor protein expressed in many cell types, including podocyte cells of the renal glomerulus. Moreover, 39 different coding region mutations in MYH9 have been identified in patients with a group of rare syndromes, collectively termed the Giant Platelet Syndromes, with clear autosomal dominant inheritance, and various clinical manifestations, sometimes also including glomerular pathology and chronic kidney disease (Kopp 2010; Sekine et al. 2010). Accordingly, MYH9 was further explored in these studies as the leading candidate gene responsible for the MALD signal. Dense mapping of MYH9 identified individual single nucleotide polymorphisms (SNPs) and sets of such SNPs grouped as haplotypes that were found to be highly associated with a large and important group of ESKD risk phenotypes, which as a consequence were designated as MYH9-associated nephropathies (Bostrom and Freedman 2010). These included HIV-associated nephropathy (HIVAN), primary nonmonogenic forms of focal segmental glomerulosclerosis, and hypertension affiliated chronic kidney disease not attributed to other etiologies (Bostrom and Freedman 2010). The MYH9 SNP and haplotype associations observed with these forms of ESKD yielded the largest odds ratios (OR) reported to date for the association of common variants with common disease risk (Winkler et al. 2010). Two specific MYH9 variants (rs5750250 of S-haplotype and rs11912763 of F-haplotype) were designated as most strongly predictive on the basis of Receiver Operating Characteristic analysis (Nelson et al. 2010). These MYH9 association studies were then also extended to earlier stage and related kidney disease phenotypes and to population groups with varying degrees of recent African ancestry admixture (Behar et al. 2010; Freedman et al. 2009a, b; Nelson et al. 2010), and led to the expectation of finding a functional African ancestry causative variant within MYH9. However, despite intensive efforts including re-sequencing of the MYH9 gene no suggested functional mutation has been identified (Nelson et al. 2010; Winkler et al. 2010). This led us to re-examine the interval surrounding MYH9 and to the detection of novel missense mutations with predicted functional effects in the neighboring APOL1 gene, which are significantly more associated with ESKD than all previously reported SNPs in MYH9.
544 citations
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TL;DR: A theoretical framework is proposed that combines hindered and restricted models of water diffusion (CHARMED) and an experimental methodology that embodies features of diffusion tensor and q‐space MRI that shows promise in determining the orientations of two or more fiber compartments more precisely and accurately than with diffusion Tensor imaging.
Abstract: To characterize anisotropic water diffusion in brain white matter, a theoretical framework is proposed that combines hindered and restricted models of water diffusion (CHARMED) and an experimental methodology that embodies features of diffusion tensor and q-space MRI. This model contains a hindered extra-axonal compartment, whose diffusion properties are characterized by an effective diffusion tensor, and an intra-axonal compartment, whose diffusion properties are characterized by a restricted model of diffusion within cylinders. The hindered model primarily explains the Gaussian signal attenuation observed at low b values; the restricted non-Gaussian model does so at high b. Both high and low b data obtained along different directions are required to estimate various microstructural parameters of the composite model, such as the nerve fiber orientation(s), the T2-weighted extra- and intra-axonal volume fractions, and principal diffusivities. The proposed model provides a description of restricted diffusion in 3D given by a 3D probability distribution (average propagator), which is obtained by 3D Fourier transformation of the estimated signal attenuation profile. The new model is tested using synthetic phantoms and validated on excised spinal cord tissue. This framework shows promise in determining the orientations of two or more fiber compartments more precisely and accurately than with diffusion tensor imaging.
544 citations
Authors
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Name | H-index | Papers | Citations |
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Jing Wang | 184 | 4046 | 202769 |
Aviv Regev | 163 | 640 | 133857 |
Itamar Willner | 143 | 927 | 76316 |
M. Morii | 134 | 1664 | 102074 |
Halina Abramowicz | 134 | 1192 | 89294 |
Joost J. Oppenheim | 130 | 454 | 59601 |
Gideon Bella | 129 | 1301 | 87905 |
Avishay Gal-Yam | 129 | 795 | 56382 |
Erez Etzion | 129 | 1216 | 85577 |
Allen Mincer | 129 | 1040 | 80059 |
Abner Soffer | 129 | 1028 | 82149 |
Gideon Koren | 129 | 1994 | 81718 |
Alex Zunger | 128 | 826 | 78798 |
Odette Benary | 128 | 844 | 74238 |
Gideon Alexander | 128 | 1201 | 81555 |