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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: This review provides a systematic review of the literature and outlines the current controversies involving different glaucoma drainage devices and their design, overall surgical success, and complications following glau coma drainage device insertion.

292 citations

Journal ArticleDOI
TL;DR: The current state of knowledge regarding the mechanisms underlying mobile element-based genetic instability in mammals is surveyed and recent evidence suggesting that the endonuclease products of TEs may also play a key role in instigating mammalian genomic instability is considered.
Abstract: The ubiquity of mobile elements in mammalian genomes poses considerable challenges for the maintenance of genome integrity. The predisposition of mobile elements towards participation in genomic rearrangements is largely a consequence of their interspersed homologous nature. As tracts of nonallelic sequence homology, they have the potential to interact in a disruptive manner during both meiotic recombination and DNA repair processes, resulting in genomic alterations ranging from deletions and duplications to large-scale chromosomal rearrangements. Although the deleterious effects of transposable element (TE) insertion events have been extensively documented, it is arguably through post-insertion genomic instability that they pose the greatest hazard to their host genomes. Despite the periodic generation of important evolutionary innovations, genomic alterations involving TE sequences are far more frequently neutral or deleterious in nature. The potentially negative consequences of this instability are perhaps best illustrated by the >25 human genetic diseases that are attributable to TE-mediated rearrangements. Some of these rearrangements, such as those involving the MLL locus in leukemia and the LDL receptor in familial hypercholesterolemia, represent recurrent mutations that have independently arisen multiple times in human populations. While TE-instability has been a potent force in shaping eukaryotic genomes and a significant source of genetic disease, much concerning the mechanisms governing the frequency and variety of these events remains to be clarified. Here we survey the current state of knowledge regarding the mechanisms underlying mobile element-based genetic instability in mammals. Compared to simpler eukaryotic systems, mammalian cells appear to have several modifications to their DNA-repair ensemble that allow them to better cope with the large amount of interspersed homology that has been generated by TEs. In addition to the disruptive potential of nonallelic sequence homology, we also consider recent evidence suggesting that the endonuclease products of TEs may also play a key role in instigating mammalian genomic instability.

292 citations

Journal ArticleDOI
Nathan D. Grubaugh1, Jason T. Ladner2, Moritz U. G. Kraemer3, Moritz U. G. Kraemer4, Gytis Dudas5, Amanda L Tan6, Karthik Gangavarapu1, Michael R. Wiley, Stephen White7, Julien Thézé4, Diogo M. Magnani8, Karla Prieto2, Karla Prieto9, Daniel Reyes2, Daniel Reyes9, Andrea M. Bingham10, Lauren M. Paul6, Refugio Robles-Sikisaka1, Glenn Oliveira10, Darryl Pronty7, Carolyn M. Barcellona6, Hayden C. Metsky11, Mary Lynn Baniecki11, Kayla G. Barnes11, Bridget Chak11, Catherine A. Freije11, Adrianne Gladden-Young11, Andreas Gnirke11, Cynthia Y. Luo11, Bronwyn MacInnis11, Christian B. Matranga11, Daniel J. Park11, James Qu11, Stephen F. Schaffner11, Christopher Tomkins-Tinch11, Kendra West11, Sarah M. Winnicki11, Shirlee Wohl11, Nathan L. Yozwiak11, Joshua Quick12, Joseph R. Fauver13, Kamran Khan14, Shannon E Brent14, Robert C. Reiner15, Paola Lichtenberger8, Michael J. Ricciardi8, Varian K. Bailey8, David I. Watkins8, Marshall R. Cone7, Edgar W. Kopp7, Kelly N. Hogan7, Andrew C. Cannons7, Reynald Jean7, Andrew J. Monaghan16, Robert F. Garry17, Nicholas J. Loman12, Nuno R. Faria4, Mario C. Porcelli, Chalmers Vasquez, Elyse R. Nagle9, Elyse R. Nagle2, Derek A. T. Cummings18, Danielle Stanek7, Andrew Rambaut19, Andrew Rambaut20, Mariano Sanchez-Lockhart, Pardis C. Sabeti11, Pardis C. Sabeti3, Pardis C. Sabeti21, Leah D Gillis7, Scott F. Michael6, Trevor Bedford5, Oliver G. Pybus4, Sharon Isern6, Gustavo Palacios2, Kristian G. Andersen1, Kristian G. Andersen10 
24 May 2017-Nature
TL;DR: It is shown that at least 4 introductions, but potentially as many as 40, contributed to the outbreak in Florida and that local transmission is likely to have started in the spring of 2016—several months before its initial detection.
Abstract: Genome sequencing of Zika virus samples from infected patients and Aedes aegypti mosquitoes in Florida shows that the virus was probably introduced into the United States on multiple occasions, and that the Caribbean is the most likely source Three papers in this issue present a wealth of new Zika virus (ZIKV) genome sequences and further insights into the genetic epidemiology of ZIKV Nathan Grubaugh et al provide 39 new ZIKV genome sequences from infected patients and Aedes aegypti mosquitoes in Florida Phylogenetic analysis suggests that the virus has been introduced on multiple separate occasions, probably linked to travel from the Caribbean They find a low probability of long-term persistence of ZIKV transmission chains within Florida, suggesting that the potential for future ZIKV outbreaks there will depend on transmission dynamics in the Americas Nuno Faria et al and Hayden Metsky et al reconstruct the spread of ZIKV in Brazil and the Americas Faria et al provide 54 new ZIKV genomes, several sequenced in real time in a mobile genomics laboratory They trace the spatial origins and spread of ZIKV in Brazil and the Americas and date the timing of the international spread of ZIKV from Brazil They find that northeast Brazil had a crucial role in the establishment of the epidemic and the spread of the virus within Brazil and the Americas Metsky et al generate 110 ZIKV genomes from clinical and mosquito samples from ten regions They also see rapid expansion of the epidemic within Brazil and multiple introductions to other geographic areas In agreement with Faria et al, they find that ZIKV circulated unobserved for many months before transmission was detected Metsky et al additionally describe ZIKV evolution and discuss how the accumulation of mutations might affect the performance of diagnostic tests in the future Zika virus (ZIKV) is causing an unprecedented epidemic linked to severe congenital abnormalities1,2 In July 2016, mosquito-borne ZIKV transmission was reported in the continental United States; since then, hundreds of locally acquired infections have been reported in Florida3,4 To gain insights into the timing, source, and likely route(s) of ZIKV introduction, we tracked the virus from its first detection in Florida by sequencing ZIKV genomes from infected patients and Aedes aegypti mosquitoes We show that at least 4 introductions, but potentially as many as 40, contributed to the outbreak in Florida and that local transmission is likely to have started in the spring of 2016—several months before its initial detection By analysing surveillance and genetic data, we show that ZIKV moved among transmission zones in Miami Our analyses show that most introductions were linked to the Caribbean, a finding corroborated by the high incidence rates and traffic volumes from the region into the Miami area Our study provides an understanding of how ZIKV initiates transmission in new regions

292 citations

Journal ArticleDOI
TL;DR: These data confirm previous findings regarding deficits associated with institutional care and extend the understanding of the impact of individual differences in caregiving quality on the development of young children in institutions.
Abstract: Background: We assess individual differences in the caregiving environments of young children being raised in institutions in Romania in relation to developmental characteristics such as physical growth, cognitive development, emotional expression, and problem and competence behaviors. Method: Videotaped observations of the child and favorite caregiver in their ‘home’ environment were coded for caregiving quality, and this was related to child characteristics. Child emotional reactivity was assessed during responses to interactional tasks. Cognitive development was assessed from child responses to the Bayley Scales of Infant Development. Data regarding problem behaviors and competence were obtained from caregiver report. Children reared in institutions were compared on all of these measures to never institutionalized children to assist gauging degree of impairment. Results: Children raised in institutions demonstrated marked delays in cognitive development, poorer physical growth, and marked deficits in competence. Individual differences in caregiving environment were associated with cognitive development, competence, and negative behavior among these young children being reared in institutions. Conclusions: These data confirm previous findings regarding deficits associated with institutional care and extend our understanding of the impact of individual differences in caregiving quality on the development of young children in institutions. Keywords: Infancy, orphans, institutionalization, caregiving quality, cognitive deficits, physical growth, emotional expression, competence. Abbreviations: BEIP, Bucharest Early Intervention Project; BSID-II, Bayley Scales of Infant Development – II; DQ, Developmental Quotient; IG, institution group; ITSEA, Infant–Toddler Social Emotional Assessment; MDI, Mental Development Index; NIG, never institutionalized group; ORCE, Observational Record of the Caregiving Environment.

292 citations

Journal ArticleDOI
TL;DR: The primary objective was to demonstrate non‐inferiority of vildagliptin vs. glimepiride in glycosylated haemoglobin reduction at week 52 of a large, randomized, double‐blind, multicentre study on type 2 diabetes mellitus.
Abstract: To examine the efficacy and safety of vildagliptin vs. glimepiride as add-on therapy to metformin in patients with type 2 diabetes mellitus in a 52-week interim analysis of a large, randomized, double-blind, multicentre study. The primary objective was to demonstrate non-inferiority of vildagliptin vs. glimepiride in glycosylated haemoglobin (HbA(1c)) reduction at week 52. Patients inadequately controlled on metformin monotherapy (HbA(1c) 6.5-8.5%) and receiving a stable dose of metformin (mean dose 1898 mg/day; mean duration of use 36 months) were randomized 1:1 to receive vildagliptin (50 mg twice daily, n = 1396) or glimepiride (titrated up to 6 mg/day; mean dose 4.5 mg/day, n = 1393). Non-inferiority of vildagliptin was demonstrated (97.5% confidence interval 0.02%, 0.16%) with a mean (SE) change from baseline HbA(1c) (7.3% in both groups) to week 52 endpoint of -0.44% (0.02%) with vildagliptin and -0.53% (0.02%) with glimepiride. Although a similar proportion of patients reached a target HbA(1c) level of < 7% with vildagliptin and glimepiride (54.1 and 55.5%, respectively), a greater proportion of patients reached this target without hypoglycaemia in the vildagliptin group (50.9 vs. 44.3%; p < 0.01). Fasting plasma glucose (FPG) reductions were comparable between groups (mean [SE] -1.01 [0.06] mmol/l and -1.14 [0.06] mmol/l respectively). Vildagliptin significantly reduced body weight relative to glimepiride (mean [SE] change from baseline -0.23 [0.11] kg; between-group difference -1.79 kg; p < 0.001) and resulted in a 10-fold lower incidence of hypoglycaemia than glimepiride (1.7 vs. 16.2% of patients presenting at least one hypoglycaemic event; 39 vs. 554 hypoglycaemic events, p < 0.01). No severe hypoglycaemia occurred with vildagliptin compared with 10 episodes with glimepiride (p < 0.01), and no patient in the vildagliptin group discontinued because of hypoglycaemia compared with 11 patients in the glimepiride group. The incidence of adverse events (AEs), serious AEs and adjudicated cardiovascular events was 74.5, 7.1 and 0.9%, respectively, in patients receiving vildagliptin, and 81.1, 9.5 and 1.6%, respectively, in patients receiving glimepiride. When metformin alone fails to maintain sufficient glycaemic control, the addition of vildagliptin provides comparable efficacy to that of glimepiride after 52 weeks and displays a favourable AE profile, with no weight gain and a significant reduction in hypoglycaemia compared with glimepiride. (Less)

292 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