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Institution

Indiana University

EducationBloomington, Indiana, United States
About: Indiana University is a education organization based out in Bloomington, Indiana, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 64480 authors who have published 150058 publications receiving 6392902 citations. The organization is also known as: Indiana University system & indiana.edu.


Papers
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Journal ArticleDOI
TL;DR: To explore how the problem of antibiotic resistance might best be addressed, a group of 30 scientists from academia and industry gathered at the Banbury Conference Centre in Cold Spring Harbor, New York, USA, from 16 to 18 May 2011.
Abstract: The development and spread of antibiotic resistance in bacteria is a universal threat to both humans and animals that is generally not preventable but can nevertheless be controlled, and it must be tackled in the most effective ways possible. To explore how the problem of antibiotic resistance might best be addressed, a group of 30 scientists from academia and industry gathered at the Banbury Conference Centre in Cold Spring Harbor, New York, USA, from 16 to 18 May 2011. From these discussions there emerged a priority list of steps that need to be taken to resolve this global crisis.

929 citations

Journal ArticleDOI
TL;DR: Multiple doses of rhuMAb VEGF were well tolerated, and pharmacokinetic studies indicate that doses of > or = 0.3 mg/kg have a half-life similar to that of other humanized antibodies.
Abstract: PURPOSE: We investigated the safety and pharmacokinetics of a recombinant human monoclonal antibody to vascular endothelial growth factor (rhuMAb VEGF) in patients with cancer. PATIENTS AND METHODS: Cohorts of patients with metastatic cancer having failed prior therapy entered a phase I trial of rhuMAb VEGF administered by a 90-minute intravenous infusion at doses from 0.1 to 10.0 mg/kg on days 0, 28, 35, and 42. Patients underwent pharmacokinetic sampling on day 0 and had serum samples obtained during the subsequent 28 days. Response assessment was carried out on days 49 and 72. RESULTS: Twenty-five patients with a median Eastern Cooperative Oncology Group performance status of 0 were accrued. There were no grade III or IV adverse events definitely related to the antibody. There were three episodes of tumor-related bleeding. Infusions of rhuMAb VEGF were well tolerated without significant toxicity. Grades I and II adverse events possibly or probably related to study drug included asthenia, headache, and ...

928 citations

Journal ArticleDOI
07 Apr 1995-Cell
TL;DR: An enzymatic rather than a structural protein defect causing a muscular dystrophy is demonstrated, a defect that may have regulatory consequences, perhaps in signal transduction.

927 citations

Journal ArticleDOI
TL;DR: KCNQ2, KCNQ3 and undiscovered genes of the same family of K+ channels are strong candidates for other IGEs, and a missense mutation in the critical pore region in perfect co-segregation with the BFNC phenotype is found.
Abstract: Epileptic disorders affect about 20-40 million people worldwide, and 40% of these are idiopathic generalized epilepsies (IGEs; ref. 1). Most of the IGEs that are inherited are complex, multigenic diseases. To address basic mechanisms for epilepsies, we have focused on one well-defined class of IGEs with an autosomal-dominant mode of inheritance: the benign familial neonatal convulsions (BFNC; refs 2,3). Genetic heterogeneity of BFNC has been observed. Two loci, EBN1 and EBN2, have been mapped by linkage analysis to chromosome 20q13 (refs 5,6) and chromosome 8q24 (refs 7,8), respectively. By positional cloning, we recently identified the gene for EBN1 as KCNQ2 (ref. 9). This gene, a voltage-gated potassium channel, based on homology, is a member of the KQT-like family. Here we describe an additional member, KCNQ3. We mapped this new gene to chromosome 8, between markers D8S256 and D8S284 on a radiation hybrid map. We screened KCNQ3 for mutations in the large BFNC family previously linked to chromosome 8q24 in the same marker interval. We found a missense mutation in the critical pore region in perfect co-segregation with the BFNC phenotype. The same conserved amino acid is also mutated in KVLQT1 (KCNQ1) in an LQT patient. KCNQ2, KCNQ3 and undiscovered genes of the same family of K+ channels are strong candidates for other IGEs.

927 citations

Journal ArticleDOI
Michael Lynch1
TL;DR: Support is presented for the hypothesis that natural selection pushes mutation rates down to a lower limit set by the power of random genetic drift rather than by intrinsic physiological limitations, and that this has resulted in reduced levels of replication, transcription, and translation fidelity in eukaryotes relative to prokaryotes.

925 citations


Authors

Showing all 64884 results

NameH-indexPapersCitations
Frank B. Hu2501675253464
Stuart H. Orkin186715112182
Bruce M. Spiegelman179434158009
David R. Williams1782034138789
D. M. Strom1763167194314
Markus Antonietti1761068127235
Lei Jiang1702244135205
Brenda W.J.H. Penninx1701139119082
Nahum Sonenberg167647104053
Carl W. Cotman165809105323
Yang Yang1642704144071
Jaakko Kaprio1631532126320
Ralph A. DeFronzo160759132993
Gavin Davies1592036149835
Tyler Jacks158463115172
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023127
2022694
20217,273
20207,310
20196,943
20186,496