Institution
University of Alabama
Education•Tuscaloosa, Alabama, United States•
About: University of Alabama is a education organization based out in Tuscaloosa, Alabama, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 27323 authors who have published 48609 publications receiving 1565337 citations. The organization is also known as: Alabama & Bama.
Topics: Population, Poison control, Large Hadron Collider, Galaxy, Health care
Papers published on a yearly basis
Papers
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TL;DR: These recent developments in DNA-based species delimitation methods are reviewed, and it is discussed how they have changed and continue to change the authors' understanding of algal species boundaries.
Abstract: Given the problems of species delimitation in algae using morphology or sexual compatibility, molecular data are becoming the standard for delimiting species and testing their traditional boundaries. The idea that species are separately evolving metapopulation lineages, along with theoretical progress in phylogenetic and population genetic analyses, has led to the development of new methods of species delimitation. We review these recent developments in DNA-based species delimitation methods, and discuss how they have changed and continue to change our understanding of algal species boundaries. Although single-locus approaches have proven effective for a first rapid and large-scale assessment of species diversity, species delimitation based on single gene trees falls short due to gene tree–species tree incongruence, caused by confounding processes like incomplete lineage sorting, trans-species polymorphism, hybridization and introgression. Data from unlinked loci and multi-species coalescent methods, whic...
290 citations
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TL;DR: Retinal nerve fiber layer (RNFL) thickness is significantly decreased in multiple sclerosis (MS) optic neuritis (ON) eyes, unaffected fellow eyes of patients with MS ON, and MS eyes not affected by ON in the authors' cohort.
Abstract: Objective: To examine retinal nerve fiber layer (RNFL) thickness, macular volumes (MV), and visual acuity in multiple sclerosis (MS) eyes, with and without history of acute optic neuritis (ON). Methods: RNFL thickness was measured in 326 MS and 94 control eyes using optical coherence tomography (OCT). MV and vision testing were done in a subset of the cohort. MS subtype was classified as relapsing-remitting (RRMS, n = 135), primary progressive (PPMS, n = 12), and secondary progressive (SPMS, n = 16). Results: MS ON eyes had decreased RNFL thickness (84.2 μm) compared to controls (102.7 μm) ( p p p p p p 3 ) ( p 3 ) ( p 3 ). Conclusion: Retinal nerve fiber layer (RNFL) is significantly decreased in multiple sclerosis (MS) optic neuritis (ON) eyes, unaffected fellow eyes of patients with MS ON, and MS eyes not affected by ON in our cohort. Macular volumes (MV) showed a significant decrease in MS ON eyes. Progressive MS cases showed more marked decreases in RNFL and MV than relapsing-remitting MS. OCT is a promising tool to detect subclinical changes in RNFL and MV in patients with MS and should be examined in longitudinal studies as a potential biomarker of retinal pathology in MS.
290 citations
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TL;DR: Although there has been much debate about whether democratization causes ethnic conflict, and many comparativists have argued about which kinds of political institutions are best for managing commu....
Abstract: Although there has been much debate about whether democratization causes ethnic conflict, and many comparativists have argued about which kinds of political institutions are best for managing commu...
290 citations
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TL;DR: In this article, drug susceptibility was determined by a phenotypic assay and genotypic evidence of resistance assessed by nucleotide sequencing of protease and reversetranscriptase, compared among the three patient groups.
Abstract: ContextLoss of viral suppression in patients infected with human immunodeficiency
virus (HIV), who are receiving potent antiretroviral therapy, has been attributed
to outgrowth of drug-resistant virus; however, resistance patterns are not
well characterized in patients whose protease inhibitor combination therapy
fails after achieving viral suppression.ObjectiveTo characterize drug susceptibility of virus from HIV-infected patients
who are failing to sustain suppression while taking an indinavir-containing
antiretroviral regimen.Design and SettingSubstudy of the AIDS Clinical Trials Group 343, a multicenter clinical
research trial conducted between February 1997 and October 1998.PatientsTwenty-six subjects who experienced rebound (HIV RNA level ≥200 copies/mL)
during indinavir monotherapy (n = 9) or triple-drug therapy (indinavir, lamivudine,
and zidovudine; n = 17) after initially achieving suppression while receiving
all 3 drugs, and 10 control subjects who had viral suppression while receiving
triple-drug therapy.Main Outcome MeasureDrug susceptibility, determined by a phenotypic assay and genotypic
evidence of resistance assessed by nucleotide sequencing of protease and reverse
transcriptase, compared among the 3 patient groups.ResultsIndinavir resistance was not detected in the 9 subjects with viral rebound
during indinavir monotherapy or in the 17 subjects with rebound during triple-drug
therapy, despite plasma HIV RNA levels ranging from 102 to 105 copies/mL. In contrast, lamivudine resistance was detected by phenotypic
assay in rebound isolates from 14 of 17 subjects receiving triple-drug therapy,
and genotypic analyses showed changes at codon 184 of reverse transcriptase
in these 14 isolates. Mean random plasma indinavir concentrations in the 2
groups with rebound were similar to those of a control group with sustained
viral suppression, although levels below 50 ng/mL were more frequent in the
triple-drug group than in the control group (P =
.03).ConclusionsLoss of viral suppression may be due to suboptimal antiviral potency,
and selection of a predominantly indinavir-resistant virus population may
be delayed for months even in the presence of ongoing indinavir therapy. The
results suggest possible value in assessing strategies using drug components
of failing regimens evaluated with resistance testing.
290 citations
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TL;DR: In this paper, the Higgs boson mass was measured in the H → ZZ → 4l (l = e, μ) decay channel and the signal strength modifiers for individual Higgs production modes were also measured.
Abstract: Properties of the Higgs boson are measured in the H → ZZ → 4l (l = e, μ) decay channel. A data sample of proton-proton collisions at $ \sqrt{s}=13 $ TeV, collected with the CMS detector at the LHC and corresponding to an integrated luminosity of 35.9 fb$^{−1}$ is used. The signal strength modifier μ, defined as the ratio of the observed Higgs boson rate in the H → ZZ → 4l decay channel to the standard model expectation, is measured to be μ = 1.05$_{− 0.17}^{+ 0.19}$ at m$_{H}$ = 125.09 GeV, the combined ATLAS and CMS measurement of the Higgs boson mass. The signal strength modifiers for the individual Higgs boson production modes are also measured. The cross section in the fiducial phase space defined by the requirements on lepton kinematics and event topology is measured to be 2. 92$_{− 0.44}^{+ 0.48}$ (stat)$_{− 0.24}^{+ 0.28}$ (syst)fb, which is compatible with the standard model prediction of 2.76 ± 0.14 fb. Differential cross sections are reported as a function of the transverse momentum of the Higgs boson, the number of associated jets, and the transverse momentum of the leading associated jet. The Higgs boson mass is measured to be m$_{H}$ = 125.26 ± 0.21 GeV and the width is constrained using the on-shell invariant mass distribution to be Γ$_{H}$ < 1.10 GeV, at 95% confidence level.
290 citations
Authors
Showing all 27508 results
Name | H-index | Papers | Citations |
---|---|---|---|
Jasvinder A. Singh | 176 | 2382 | 223370 |
Hongfang Liu | 166 | 2356 | 156290 |
Ian J. Deary | 166 | 1795 | 114161 |
Yongsun Kim | 156 | 2588 | 145619 |
Dong-Chul Son | 138 | 1370 | 98686 |
Simon C. Watkins | 135 | 950 | 68358 |
Kenichi Hatakeyama | 134 | 1731 | 102438 |
Conor Henderson | 133 | 1387 | 88725 |
Peter R Hobson | 133 | 1590 | 94257 |
Tulika Bose | 132 | 1285 | 88895 |
Helen F Heath | 132 | 1185 | 89466 |
James Rohlf | 131 | 1215 | 89436 |
Panos A Razis | 130 | 1287 | 90704 |
David B. Allison | 129 | 836 | 69697 |
Eduardo Marbán | 129 | 579 | 49586 |