Institution
University of Groningen
Education•Groningen, Groningen, Netherlands•
About: University of Groningen is a education organization based out in Groningen, Groningen, Netherlands. It is known for research contribution in the topics: Population & Poison control. The organization has 36346 authors who have published 69116 publications receiving 2940370 citations. The organization is also known as: Rijksuniversiteit Groningen & RUG.
Papers published on a yearly basis
Papers
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TL;DR: In this paper, the authors provide a comprehensive overview of the strengths and weaknesses of different spatial econometric model specifications in terms of spillover effects and advocate taking the SLX model as point of departure in case a well-founded theory indicating which model is most appropriate is lacking.
Abstract: We provide a comprehensive overview of the strengths and weaknesses of different spatial econometric model specifications in terms of spillover effects. Based on this overview, we advocate taking the SLX model as point of departure in case a well-founded theory indicating which model is most appropriate is lacking. In contrast to other spatial econometric models, the SLX model also allows for the spatial weights matrix W to be parameterized and the application of standard econometric techniques to test for endogenous explanatory variables. This starkly contrasts commonly used spatial econometric specification strategies and is a complement to the critique of spatial econometrics raised in a special theme issue of the Journal of Regional Science (Volume 52, Issue 2). To illustrate the pitfalls of the standard spatial econometrics approach and the benefits of our proposed alternative approach in an empirical setting, the Baltagi and Li (2004) cigarette demand model is estimated.
443 citations
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TL;DR: Two compounds are structurally related, antiviral compounds that inhibit the replication of rhino (common cold) viruses and related picornaviruses and prevent the pH-mediated uncoating of the viral RNA.
Abstract: WIN 51711 and WIN 52084 are structurally related, antiviral compounds that inhibit the replication of rhino (common cold) viruses and related picornaviruses. They prevent the pH-mediated uncoating of the viral RNA. The compounds consist of a 3-methylisoxazole group that inserts itself into the hydrophobic interior of the VP1 beta-barrel, a connecting seven-membered aliphatic chain, and a 4-oxazolinylphenoxy group (OP) that covers the entrance to an ion channel in the floor of the "canyon." Viral disassembly may be inhibited by preventing the collapse of the VP1 hydrophobic pocket or by blocking the flow of ions into the virus interior.
443 citations
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TL;DR: Results show that catalysis by the dehalogenase proceeds by a two-step mechanism involving an ester intermediate covalently bound at Asp124, and that the alkylated enzyme is hydrolysed by a water molecule activated by the His289–Asp260 pair in the active site.
Abstract: Crystal structures of haloalkane dehalogenase were determined in the presence of the substrate 1,2-dichloroethane. At pH 5 and 4 degrees C, substrate is bound in the active site without being converted; warming to room temperature causes the substrate's carbon-chlorine bond to be broken, producing a chloride ion with concomitant alkylation of the active-site residue Asp124. At pH 6 and room temperature the alkylated enzyme is hydrolysed by a water molecule activated by the His289-Asp260 pair in the active site. These results show that catalysis by the dehalogenase proceeds by a two-step mechanism involving an ester intermediate covalently bound at Asp124.
443 citations
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TL;DR: Hereditary non-polyposis colorectal cancer was shown to be caused by germline mutations in the DNA mismatch repair genes MSH2, MLH1, PMS1,PMS2 and MSH6, and many HNPCC families do not fully comply with the clinical Amsterdam criteria, and the causative mutations are unknown.
Abstract: Hereditary non-polyposis colorectal cancer (HNPCC) is a common autosomal dominant condition characterized by early onset colorectal cancer as well as other tumour types at different anatomical sites1. HNPCC tumours often display a high level of genomic instability, characterized by changes in repeat numbers of simple repetitive sequences (microsatellite instability, MSI), which reflects the malfunction of the DNA mismatch repair machinery2, 3. Accordingly, HNPCC was shown to be caused by germline mutations in the DNA mismatch repair genes (MMR) MSH2, MLH1, PMS1, PMS2 and MSH6 (refs 3, 4, 5, 6). So far, more than 220 predisposing mutations have been identified, most in MSH2 and MLH1 and in families complying with the clinical Amsterdam criteria3, 7, 8 (AMS+). Many HNPCC families, however, do not fully comply with these criteria, and in most cases the causative mutations are unknown.
442 citations
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TL;DR: In patients with infected necrotising pancreatitis, the endoscopic step-up approach was not superior to the surgical step- up approach in reducing major complications or death, and the rate of pancreatic fistulas and length of hospital stay were lower in the endoscopy group.
442 citations
Authors
Showing all 36692 results
Name | H-index | Papers | Citations |
---|---|---|---|
Ronald C. Kessler | 274 | 1332 | 328983 |
Nicholas J. Wareham | 212 | 1657 | 204896 |
André G. Uitterlinden | 199 | 1229 | 156747 |
Lei Jiang | 170 | 2244 | 135205 |
Brenda W.J.H. Penninx | 170 | 1139 | 119082 |
Richard H. Friend | 169 | 1182 | 140032 |
Panos Deloukas | 162 | 410 | 154018 |
Jerome I. Rotter | 156 | 1071 | 116296 |
Christopher M. Dobson | 150 | 1008 | 105475 |
Dirk Inzé | 149 | 647 | 74468 |
Scott T. Weiss | 147 | 1025 | 74742 |
Dieter Lutz | 139 | 671 | 67414 |
Wilmar B. Schaufeli | 137 | 513 | 95718 |
Cisca Wijmenga | 136 | 668 | 86572 |
Arnold B. Bakker | 135 | 506 | 103778 |