1,721,053 research outputs found
Going Beyond Counting First Authors in Author Co-citation Analysis
The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Contribution of mutations in low density lipoprotein receptor (LDLR) and lipoprotein lipase (LPL) genes to familial combined hyperlipidemia (FCHL): A reappraisal by using a resequencing approach
Background:Defective low-density lipoprotein receptor (LDLR) and lipoprotein lipase (LPL) alleles havebeen implicated in familial combined hyperlipidemia (FCHL). However, their contribution might havebeen influenced by diagnostic criteria. This study was aimed to reassess the frequency of rare andcommon variants inLDLRandLPLin FCHL individuals classified with stringent criteria.Methods: LDLRandLPLwere resequenced in 208 FHCL and 171 controls. Variants were classified as loss-(LOF) or gain-of-function (GOF) based uponin silicoprediction, familial segregation and availablefunctional data.Results:Eight LOF variants were detected inLDLR, 6 of which were missense and 2 were predicted todisrupt normal splicing; all were present at heterozygous state. They were found in 10 FCHL but not incontrols, thus indicating that 4.8% of FCHL individuals should be reclassified as FH. LDL-C (positive) andBMI (negative) were the strongest predictors ofLDLRmutations with LDL-C 181 mg/dl being the bestthreshold for diagnosing the presence of dysfunctionalLDLRalleles. The cumulative prevalence of def-initeLPLdefective alleles (1 rare and 2 common heterozygous missense variants) was comparable be-tween FCHL and controls (10.1% vs. 10.5%). Conversely, theLPLGOF variant p.Ser474* showed a lowerfrequency in FCHL than in controls (13.5% vs. 24.0%, p1⁄40.008). Overall, LOFLPLvariants did not show aTG-modulating effect.Conclusions:Ourfindings indicate that, in well characterized FCHL individuals, variants inLDLRandLPLprovide a small contribution to this dyslipidemia, thus limiting the need for such genetic testing.©2015 Elsevier Ireland Ltd. All rights reserve
Effect of exogenous triglyceride administration on plasma free fatty acids and free tryptophan levels in cancer bearing patients
EFFECT OF SOMATOSTATIN ON NEUTRAL AMINO ACID TRANSPORT IN ISOLATED BOVINE BRAIN MICROVESSELS
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