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Institution

Tulane University

EducationNew Orleans, Louisiana, United States
About: Tulane University is a education organization based out in New Orleans, Louisiana, United States. It is known for research contribution in the topics: Population & Blood pressure. The organization has 24478 authors who have published 47205 publications receiving 1944993 citations. The organization is also known as: University of Louisiana.


Papers
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Journal ArticleDOI
TL;DR: In this paper, the authors show that when there are multiple informants who disagree, responses aggregated with confidence- or competence-based weights outperform those with response data based weights, which in turn provide significant gains in estimation accuracy over simply averaging informant reports.
Abstract: Organizational research frequently involves seeking judgmental response data from informants within organizations. This article discusses why using multiple informants improves the quality of response data and thereby the validity of research findings. The authors show that when there are multiple informants who disagree, responses aggregated with confidence- or competence-based weights outperform those with response data–based weights, which in turn provide significant gains in estimation accuracy over simply averaging informant reports. The proposed methods are effective, inexpensive, and easy to use in organizational marketing research.

299 citations

Journal ArticleDOI
TL;DR: The IKMG redefines MGRS as a clonal proliferative disorder that produces a nephrotoxic monoclonal immunoglobulin and does not meet previously defined haematological criteria for treatment of a specific malignancy.
Abstract: The term monoclonal gammopathy of renal significance (MGRS) was introduced by the International Kidney and Monoclonal Gammopathy Research Group (IKMG) in 2012. The IKMG met in April 2017 to refine the definition of MGRS and to update the diagnostic criteria for MGRS-related diseases. Accordingly, in this Expert Consensus Document, the IKMG redefines MGRS as a clonal proliferative disorder that produces a nephrotoxic monoclonal immunoglobulin and does not meet previously defined haematological criteria for treatment of a specific malignancy. The diagnosis of MGRS-related disease is established by kidney biopsy and immunofluorescence studies to identify the monotypic immunoglobulin deposits (although these deposits are minimal in patients with either C3 glomerulopathy or thrombotic microangiopathy). Accordingly, the IKMG recommends a kidney biopsy in patients suspected of having MGRS to maximize the chance of correct diagnosis. Serum and urine protein electrophoresis and immunofixation, as well as analyses of serum free light chains, should also be performed to identify the monoclonal immunoglobulin, which helps to establish the diagnosis of MGRS and might also be useful for assessing responses to treatment. Finally, bone marrow aspiration and biopsy should be conducted to identify the lymphoproliferative clone. Flow cytometry can be helpful in identifying small clones. Additional genetic tests and fluorescent in situ hybridization studies are helpful for clonal identification and for generating treatment recommendations. Treatment of MGRS was not addressed at the 2017 IKMG meeting; consequently, this Expert Consensus Document does not include any recommendations for the treatment of patients with MGRS.

299 citations

Journal ArticleDOI
TL;DR: Results suggest that miR-146a functions in a negative feedback loop to modulate the intensity and/or duration of the interferon response.
Abstract: The Epstein-Barr virus (EBV)-encoded latent membrane protein 1 (LMP1) is a functional homologue of the tumor necrosis factor receptor family and contributes substantially to the oncogenic potential of EBV through activation of nuclear factor κB (NF-κB). MicroRNAs (miRNAs) are a class of small RNA molecules that are involved in the regulation of cellular processes such as growth, development, and apoptosis and have recently been linked to cancer phenotypes. Through miRNA microarray analysis, we demonstrate that LMP1 dysregulates the expression of several cellular miRNAs, including the most highly regulated of these, miR-146a. Quantitative reverse transcription-PCR analysis confirmed induced expression of miR-146a by LMP1. Analysis of miR-146a expression in EBV latency type III and type I cell lines revealed substantial expression of miR-146a in type III (which express LMP1) but not in type I cell lines. Reporter studies demonstrated that LMP1 induces miR-146a predominantly through two NF-κB binding sites in the miR-146a promoter and identified a role for an Oct-1 site in conferring basal and induced expression. Array analysis of cellular mRNAs expressed in Akata cells transduced with an miR-146a-expressing retrovirus identified genes that are directly or indirectly regulated by miR-146a, including a group of interferon-responsive genes that are inhibited by miR-146a. Since miR-146a is known to be induced by agents that activate the interferon response pathway (including LMP1), these results suggest that miR-146a functions in a negative feedback loop to modulate the intensity and/or duration of the interferon response.

298 citations

Journal ArticleDOI
01 May 1998-Peptides
TL;DR: The results show that the permeabilities of these two peptides across the blood-brain barrier differed from each other and among brain regions, suggesting that differential permeability of the BBB for blood-borne peptides could provide a mechanism by which their effects on the CNS are regulated.

298 citations

Journal ArticleDOI
TL;DR: In conclusion, 11βHSD1 inhibition offers a new potential approach to control glucose and cardiovascular risk factors in type 2 diabetes and was efficacious and well tolerated in patients with type 1 diabetes who had inadequate glycemic control with metformin alone.
Abstract: OBJECTIVE 11-β-hydroxysteroid dehydrogenase type 1 (11βHSD1) converts inactive cortisone into active cortisol, thereby amplifying intracellular glucocorticoid action. The efficacy and safety of the 11βHSD1 inhibitor INCB13739 were assessed when added to ongoing metformin monotherapy in patients with type 2 diabetes exhibiting inadequate glycemic control (A1C 7–11%). RESEARCH DESIGN AND METHODS This double-blind placebo-controlled paralleled study randomized 302 patients with type 2 diabetes (mean A1C 8.3%) on metformin monotherapy (mean 1.5 g/day) to receive one of five INCB13739 doses or placebo once daily for 12 weeks. The primary end point was the change in A1C at study end. Other end points included changes in fasting glucose, lipids, weight, adverse events, and safety. RESULTS After 12 weeks, 200 mg of INCB13739 resulted in significant reductions in A1C (−0.6%), fasting plasma glucose (−24 mg/dl), and homeostasis model assessment–insulin resistance (HOMA-IR) (−24%) compared with placebo. Total cholesterol, LDL cholesterol, and triglycerides were all significantly decreased in hyperlipidemic patients. Body weight decreased relative to placebo after INCB13739 therapy. A reversible dose-dependent elevation in adrenocorticotrophic hormone, generally within the normal reference range, was observed. Basal cortisol homeostasis, testosterone in men, and free androgen index in women were unchanged by INCB13739. Adverse events were similar across all treatment groups. CONCLUSIONS INCB13739 added to ongoing metformin therapy was efficacious and well tolerated in patients with type 2 diabetes who had inadequate glycemic control with metformin alone. 11βHSD1 inhibition offers a new potential approach to control glucose and cardiovascular risk factors in type 2 diabetes.

298 citations


Authors

Showing all 24722 results

NameH-indexPapersCitations
Walter C. Willett3342399413322
JoAnn E. Manson2701819258509
Frank B. Hu2501675253464
Eric B. Rimm196988147119
Krzysztof Matyjaszewski1691431128585
Nicholas J. White1611352104539
Tien Yin Wong1601880131830
Tomas Hökfelt158103395979
Thomas E. Starzl150162591704
Geoffrey Burnstock141148899525
Joseph Sodroski13854277070
Glenn M. Chertow12876482401
Darwin J. Prockop12857687066
Kenneth J. Pienta12767164531
Charles Taylor12674177626
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202388
2022372
20212,622
20202,491
20192,038
20181,795