bluuebunny/crossref_metadata_2025_split huggingface dataset:
Introgressive hybridization and the evolutionary history of the herring gull complex revealed by mitochondrial and nuclear DNA
Authors: Sternkopf Viviane , Liebers-Helbig Dorit , Ritz Markus S , Zhang Jun , Helbig Andreas J , de Knijff Peter 
Published: November 2010

Abstract

Background
Based on extensive mitochondrial DNA (mtDNA) sequence data, we previously showed that the model of speciation among species of herring gull (Larus argentatus) complex was not that of a ring species, but most likely due more complex speciation scenario's. We also found that two species, herring gull and glaucous gull (L. hyperboreus) displayed an unexpected biphyletic distribution of their mtDNA haplotypes. It was evident that mtDNA sequence data alone were far from sufficient to obtain a more accurate and detailed insight into the demographic processes that underlie speciation of this complex, and that extensive autosomal genetic analysis was warranted.

Results
For this reason, the present study focuses on the reconstruction of the phylogeographic history of a limited number of gull species by means of a combined approach of mtDNA sequence data and 230 autosomal amplified fragment length polymorphism (AFLP) loci. At the species level, the mtDNA and AFLP genetic data were largely congruent. Not only for argentatus and hyperboreus, but also among a third species, great black-backed gull (L. marinus) we observed two distinct groups of mtDNA sequence haplotypes. Based on the AFLP data we were also able to detect distinct genetic subgroups among the various argentatus, hyperboreus, and marinus populations, supporting our initial hypothesis that complex demographic scenario's underlie speciation in the herring gull complex.

Conclusions
We present evidence that for each of these three biphyletic gull species, extensive mtDNA introgression could have taken place among the various geographically distinct subpopulations, or even among current species. Moreover, based on a large number of autosomal AFLP loci, we found evidence for distinct and complex demographic scenario's for each of the three species we studied. A more refined insight into the exact phylogeographic history within the herring gull complex is still impossible, and requires detailed autosomal sequence information, a topic of our future studies.
Contemporary temperature-driven divergence in a Nordic freshwater fish under conditions commonly thought to hinder adaptation
Authors: Kavanagh Kathryn D , Haugen Thrond O , Gregersen Finn , Jernvall Jukka , Vøllestad L Asbjørn 
Published: November 2010

AbstractBackgroundEvaluating the limits of adaptation to temperature is important given the IPCC-predicted rise in global temperatures. The rate and scope of evolutionary adaptation can be limited by low genetic diversity, gene flow, and costs associated with adaptive change. Freshwater organisms are physically confined to lakes and rivers, and must therefore deal directly with climate variation and change. In this study, we take advantage of a system characterised by low genetic variation, small population size, gene flow and between-trait trade-offs to study how such conditions affect the ability of a freshwater fish to adapt to climate change. We test for genetically-based differences in developmental traits indicating local adaptation, by conducting a common-garden experiment using embryos and larvae from replicate pairs of sympatric grayling demes that spawn and develop in natural cold and warm water, respectively. These demes have common ancestors from a colonization event 22 generations ago. Consequently, we explore if diversification may occur under severely constraining conditions.ResultsWe found evidence for divergence in ontogenetic rates. The divergence pattern followed adaptation predictions as cold-deme individuals displayed higher growth rates and yolk conversion efficiency than warm-deme individuals at the same temperature. The cold-deme embryos had a higher rate of muscle mass development. Most of the growth- and development differences occurred prior to hatch. The divergence was probably not caused by genetic drift as there was a strong degree of parallelism in the divergence pattern and because phenotypic differentiation (QST) was larger than estimated genetic drift levels (microsatellite FST) between demes from different temperature groups. We also document that these particular grayling populations cannot develop successfully at temperatures above 12°C, whereas other European populations can, and that increasing the muscle mass development rate comes at the cost of some skeletal trait development rates.ConclusionsThis study shows that genetically based phenotypic divergence can prevail even under conditions of low genetic variation and ongoing gene flow. Furthermore, population-specific maximum development temperatures along with musculoskeletal developmental trade-offs may constrain adaptation.
Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence
Authors: Boyle James P , Thompson Theodore J , Gregg Edward W , Barker Lawrence E , Williamson David F 
Published: November 2010

AbstractBackgroundPeople with diabetes can suffer from diverse complications that seriously erode quality of life. Diabetes, costing the United States more than $174 billion per year in 2007, is expected to take an increasingly large financial toll in subsequent years. Accurate projections of diabetes burden are essential to policymakers planning for future health care needs and costs.MethodsUsing data on prediabetes and diabetes prevalence in the United States, forecasted incidence, and current US Census projections of mortality and migration, the authors constructed a series of dynamic models employing systems of difference equations to project the future burden of diabetes among US adults. A three-state model partitions the US population into no diabetes, undiagnosed diabetes, and diagnosed diabetes. A four-state model divides the state of "no diabetes" into high-risk (prediabetes) and low-risk (normal glucose) states. A five-state model incorporates an intervention designed to prevent or delay diabetes in adults at high risk.ResultsThe authors project that annual diagnosed diabetes incidence (new cases) will increase from about 8 cases per 1,000 in 2008 to about 15 in 2050. Assuming low incidence and relatively high diabetes mortality, total diabetes prevalence (diagnosed and undiagnosed cases) is projected to increase from 14% in 2010 to 21% of the US adult population by 2050. However, if recent increases in diabetes incidence continue and diabetes mortality is relatively low, prevalence will increase to 33% by 2050. A middle-ground scenario projects a prevalence of 25% to 28% by 2050. Intervention can reduce, but not eliminate, increases in diabetes prevalence.ConclusionsThese projected increases are largely attributable to the aging of the US population, increasing numbers of members of higher-risk minority groups in the population, and people with diabetes living longer. Effective strategies will need to be undertaken to moderate the impact of these factors on national diabetes burden. Our analysis suggests that widespread implementation of reasonably effective preventive interventions focused on high-risk subgroups of the population can considerably reduce, but not eliminate, future increases in diabetes prevalence.
Age-dependent changes in TDP-43 levels in a mouse model of Alzheimer disease are linked to Aβ oligomers accumulation
Authors: Caccamo Antonella , Magrí Andrea , Oddo Salvatore 
Published: November 2010

AbstractBackgroundTransactive response DNA-binding protein 43 (TDP-43) is the pathological protein found in frontotemporal lobar degeneration with ubiquitin positive inclusions and in amyotrophic lateral sclerosis. In diseased tissue, TDP-43 translocates from its physiological nuclear location into the cytoplasm, where it accumulates. Additionally, C-terminal fragments of TDP-43 accumulate in affected brain regions and are sufficient to cause TDP-43 mislocalization and cytoplasmic accumulationin vitro. TDP-43 also accumulates in 30% of Alzheimer disease (AD) cases, a finding that has been highly reproducible. The role of TDP-43 in AD and its relation with Aβ and tau pathology, the two neuropathological hallmarks of AD, remains to be elucidated.ResultsHere we show that levels of TDP-43 and its ~35 kDa C-terminal fragment are significantly increased in the 3×Tg-AD mice, an animal model of AD that develops an age-dependent cognitive decline linked to the accumulation of Aβ and tau. We also report that the levels of TDP-43 and its C-terminal fragment correlate with the levels of soluble Aβ oligomers, which play a key role in AD pathogenesis. Notably, genetically reducing Aβ42production restores the levels of TDP-43 and its ~35 kDa C-terminal fragment to control levels.ConclusionsThese data suggest a possible relation between Aβ oligomers and TDP-43.
Urokinase-type plasminogen activator and arthritis progression: contrasting roles in systemic and monoarticular arthritis models
Authors: De Nardo Christine M , Lenzo Jason C , Pobjoy Jarrad , Hamilton John A , Cook Andrew D 
Published: November 2010

Abstract
Introduction
Urokinase-type plasminogen activator (u-PA) has been implicated in tissue destruction/remodeling. The absence of u-PA results in resistance of mice to systemic immune complex-driven arthritis models; monoarticular arthritis models involving an intra-articular (i.a.) antigen injection, on the other hand, develop more severe arthritis in its absence. The aims of the current study are to investigate further these contrasting roles that u-PA can play in the pathogenesis of inflammatory arthritis and to determine whether u-PA is required for the cartilage and bone destruction associated with disease progression.

Methods
To determine how the different pathogenic mechanisms leading to arthritis development in the different models may explain the contrasting requirement for u-PA, the systemic, polyarticular, immune complex-driven K/BxN arthritis model was modified to include an i.a. injection of saline as a local trauma in u-PA-/- mice. This modified model and the antigen-induced arthritis (AIA) model were also used in u-PA-/- mice to determine the requirement for u-PA in joint destruction. Disease severity was determined by clinical and histologic scoring. Fibrin(ogen) staining and the matrix metalloproteinase (MMP)-generated neoepitope DIPEN staining were performed by immunohistochemistry. Gene expression of inflammatory and destructive mediators was measured in joint tissue by quantitative PCR.

Results
In our modified arthritis model, u-PA-/- mice went from being resistant to arthritis development following K/BxN serum transfer to being susceptible following the addition of an i.a. injection of saline. u-PA-/- mice also developed more sustained AIA compared with C57BL/6 mice, including reduced proteoglycan levels and increased bone erosions, fibrin(ogen) deposition and DIPEN expression. Synovial gene expression of the proinflammatory mediators (TNF and IL-1β), aggrecanases (ADAMTS-4 and -5) and MMPs (MMP3 and MMP13) were all sustained over time following AIA induction in u-PA-/- mice compared with C57BL/6 mice.

Conclusions
We propose that u-PA has a protective role in arthritis models with 'wound healing-like' processes following local trauma, possibly through u-PA/plasmin-mediated fibrinolysis, but a deleterious role in systemic models that are critically dependent on immune complex formation and complement activation. Given that cartilage proteoglycan loss and bone erosions were present and sustained in u-PA-/- mice with monoarticular arthritis, it is unlikely that u-PA/plasmin-mediated proteolysis is contributing directly to this tissue destruction/remodeling.
17β-Estradiol Regulates Rat Growth Plate Chondrocyte Apoptosis Through a Mitochondrial Pathway Not Involving Nitric Oxide or MAPKs
Authors: Zhong M. , Carney D. H. , Boyan B. D. , Schwartz Z. 
Published: November 2010

AbstractEstrogens cause growth plate closure in both males and females, by decreasing proliferation and inducing apoptosis of postproliferative growth plate chondrocytes. In vitro studies using 17β-estradiol (E2) conjugated to bovine serum albumin (E2-BSA) show that rat costochondral growth plate resting zone chondrocytes also respond to E2. Moreover, they are regulated by E2-BSA via a protein kinase C and ERK MAPK signaling pathway that is functional only in female cells. To better understand how E2 regulates apoptosis of growth plate chondrocytes, rat resting zone chondrocytes cells were treated with E2 or E2-BSA. E2 caused apoptosis in male and female resting zone and growth zone chondrocytes in a dose-dependent manner, based on elevated DNA fragmentation, terminal deoxynucleotidyl transferase dUTP nick end labeling staining and caspase-3 activation. E2 also up-regulated p53 and Bax protein (Bcl-2-associated X protein) levels and induced release of cytochrome C from the mitochondria, indicating a mitochondrial apoptotic pathway. The apoptotic effect of E2 did not involve elevated nitric oxide production or MAPKs. It was reduced by ICI 182780, which is an estrogen receptor (ER) antagonist and blocked by antibodies to Erα36, a membrane-associated ER. E2-BSA reduced cell viability and increased caspase-3 activity; ICI 182780 had no effect, but anti-ERα36 antibodies blocked the effect. The results indicate that estrogen is able to directly affect the cell population kinetics of growth plate chondrocytes by regulating apoptosis, as well as proliferation and differentiation in both resting zone and growth zone cells. They also have provided further information about the physiological functions of estrogen on longitudinal bone growth.
GPR119 Regulates Murine Glucose Homeostasis Through Incretin Receptor-Dependent and Independent Mechanisms
Authors: Flock Grace , Holland Dianne , Seino Yutaka , Drucker Daniel J. 
Published: November 2010

Abstract
G protein-coupled receptor 119 (GPR119) was originally identified as a β-cell receptor. However, GPR119 activation also promotes incretin secretion and enhances peptide YY action. We examined whether GPR119-dependent control of glucose homeostasis requires preservation of peptidergic pathways in vivo. Insulin secretion was assessed directly in islets, and glucoregulation was examined in wild-type (WT), single incretin receptor (IR) and dual IR knockout (DIRKO) mice. Experimental endpoints included plasma glucose, insulin, glucagon, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), and peptide YY. Gastric emptying was assessed in WT, Glp1r−/−, DIRKO, Glp2r−/−, and GPR119−/− mice treated with the GPR119 agonist AR231453. AR231453 stimulated insulin secretion from WT and DIRKO islets in a glucose-dependent manner, improved glucose homeostasis, and augmented plasma levels of GLP-1, GIP, and insulin in WT and Gipr−/−mice. In contrast, although AR231453 increased levels of GLP-1, GIP, and insulin, it failed to lower glucose in Glp1r−/− and DIRKO mice. Furthermore, AR231453 did not improve ip glucose tolerance and had no effect on insulin action in WT and DIRKO mice. Acute GPR119 activation with AR231453 inhibited gastric emptying in Glp1r−/−, DIRKO, Glp2r−/−, and in WT mice independent of the Y2 receptor (Y2R); however, AR231453 did not control gastric emptying in GPR119−/− mice. Our findings demonstrate that GPR119 activation directly stimulates insulin secretion from islets in vitro, yet requires intact IR signaling and enteral glucose exposure for optimal control of glucose tolerance in vivo. In contrast, AR231453 inhibits gastric emptying independent of incretin, Y2R, or Glp2 receptors through GPR119-dependent pathways. Hence, GPR119 engages multiple complementary pathways for control of glucose homeostasis.
The Jumping SHOX Gene—Crossover in the Pseudoautosomal Region Resulting in Unusual Inheritance of Leri-Weill Dyschondrosteosis
Authors: Kant Sarina G. , van der Kamp Hetty J. , Kriek Marjolein , Bakker Egbert , Bakker Boudewijn , Hoffer Mariette J. V. , van Bunderen Patrick , Losekoot Monique , Maas Saskia M. , Wit Jan M. , Rappold Gudrun , Breuning Martijn H. 
Published: November 2010

abstract

Context:
During meiosis I, the recombination frequency in the pseudoautosomal region on Xp and Yp (PAR1) in males is very high. As a result, mutated genes located within the PAR1 region can be transferred from the Y-chromosome to the X-chromosome and vice versa.

Patients:
Here we describe three families with SHOX abnormalities resulting in Leri-Weill dyschondrosteosis or Langer mesomelic dysplasia.

Results:
In about half of the segregations investigated, a transfer of the SHOX abnormality to the alternate sex chromosome was demonstrated.

Conclusions:
Patients with an abnormality of the SHOX gene should receive genetic counseling as to the likelihood that they may transmit the mutation or deletion to a son as well as to a daughter.
Nanoaggregate Formation of Amphiphilic Alternating and Random Copolyimides in Water
Authors: Hamada Takashi , Kudo Kazuaki 
Published: November 2010

Abstract
Amphiphilic alternating/random copolyimides (coPIs) formed nanoaggregates in water. The diameter of the aggregates were ca. 90 nm for the alternating coPIs and 35 nm for the random coPI. The difference in the aggregate-forming behavior was attributed to the difference in the mode of association of hydrophobic units.
Magnetic Resonance-visible Coating for Endovascular Device Visualization: Gadolinium(III)–Diethylenetriaminepentaacetic Acid-based Insoluble Polymer Coating
Authors: Kurita Tomoka , Kuroda Kagayaki , Ohsaka Takeo 
Published: November 2010

Abstract
A gadolinium(III)–diethylenetriaminepentaacetic acid-based MR (magnetic resonance)-visible polymer composed of hydrophilic and hydrophobic subunits was developed. A catheter and guidewire coated with the polymer yielded strong MR signal, high stability of Gd3+, and excellent surface lubricity, which were essentially required for the devices used for MR-guided endovascular interventions.
Development of a Flux Stabilizer for Solid-state Nuclear Magnetic Resonance with a Hybrid Magnet
Authors: Hashi Kenjiro , Shimizu Tadashi , Fujito Teruaki , Goto Atsushi , Ohki Shinobu , Asano Toshihisa , Nimori Shigeki , Kido Giyuu , Kida Jun 
Published: November 2010

Abstract
A flux stabilizer has been developed for solid-state NMR measurements with a hybrid magnet installed at the National Institute for Materials Science. The stabilizer consists of an electric circuit, a pickup, and a feedback coils to cancel out the fluctuating magnetic field at a sample by inductive field regulation. Stability of the magnetic field was improved from 6.3 ppmrms to 1.4 ppmrms by the flux stabilizer. Advantages of the flux stabilizer are demonstrated by 79Br magic-angle-spinning NMR measurements of KBr at 28 T.
Submodular Maximization over Multiple Matroids via Generalized Exchange Properties
Authors: Lee Jon , Sviridenko Maxim , Vondrák Jan 
Published: November 2010

Submodular function maximization is a central problem in combinatorial optimization, generalizing many important NP-hard problems including max cut in digraphs, graphs, and hypergraphs; certain constraint satisfaction problems; maximum entropy sampling; and maximum facility location problems. Our main result is that for any k ≥ 2 and any ε > 0, there is a natural local search algorithm that has approximation guarantee of 1/(k + ε) for the problem of maximizing a monotone submodular function subject to k matroid constraints. This improves upon the 1/(k + 1)-approximation of Fisher, Nemhauser, and Wolsey obtained in 1978 [Fisher, M., G. Nemhauser, L. Wolsey. 1978. An analysis of approximations for maximizing submodular set functions—II. Math. Programming Stud. 8 73–87]. Also, our analysis can be applied to the problem of maximizing a linear objective function and even a general nonmonotone submodular function subject to k matroid constraints. We show that, in these cases, the approximation guarantees of our algorithms are 1/(k − 1 + ε) and 1/(k + 1 + 1/(k − 1) + ε), respectively. Our analyses are based on two new exchange properties for matroids. One is a generalization of the classical Rota exchange property for matroid bases, and another is an exchange property for two matroids based on the structure of matroid intersection.
Modulated Branching Processes, Origins of Power Laws, and Queueing Duality
Authors: Jelenković Predrag R. , Tan Jian 
Published: November 2010

Power law distributions have been repeatedly observed in a wide variety of socioeconomic, biological, and technological areas. In many of the observations, e.g., city populations and sizes of living organisms, the objects of interest evolve because of the replication of their many independent components, e.g., births and deaths of individuals and replications of cells. Furthermore, the rates of replications are often controlled by exogenous parameters causing periods of expansion and contraction, e.g., baby booms and busts, economic booms and recessions, etc. In addition, the sizes of these objects often have reflective lower boundaries, e.g., cities do not fall below a certain size, low-income individuals are subsidized by the government, companies are protected by bankruptcy laws, etc. Hence, it is natural to propose reflected modulated branching processes as generic models for many of the preceding observations. Indeed, our main results show that the proposed mathematical models result in power law distributions under quite general polynomial Gärtner-Ellis conditions, the generality of which could explain the ubiquitous nature of power law distributions. In addition, on a logarithmic scale, we establish an asymptotic equivalence between the reflected branching processes and the corresponding multiplicative ones. The latter, as recognized by Goldie [Goldie, C. M. 1991. Implicit renewal theory and tails of solutions of random equations. Ann. Appl. Probab. 1(1) 126–166], is known to be dual to queueing/additive processes. We emphasize this duality further in the generality of stationary and ergodic processes.
Buprenorphine Transdermal System
Authors: Cada Dennis J. , Levien Terri L. , Baker Danial E. 
Published: November 2010

Each month, subscribers to The Formulary Monograph Service receive 5 to 6 well-documented monographs on drugs that are newly released or are in late phase 3 trials. The monographs are targeted to Pharmacy & Therapeutics Committees. Subscribers also receive monthly 1-page summary monographs on agents that are useful for agendas and pharmacy/nursing inservices. A comprehensive target drug utilization evaluation/medication use evaluation (DUE/MUE) is also provided each month. With a subscription, the monographs are sent in print and are also available online. Monographs can be customized to meet the needs of a facility. Subscribers to The Formulary Monograph Service also receive access to a pharmacy bulletin board, The Formulary Information Exchange (The F.I.X.). All topics pertinent to clinical and hospital pharmacy are discussed on The F.I.X. Through the cooperation of The Formulary, Hospital Pharmacy publishes selected reviews in this column. For more information about The Formulary Monograph Service or The F.I.X., call The Formulary at 800-322-4349. The November 2010 monograph topics are on pegloticase, ulipristal, incobotulinumtoxinA, eribulin, and ipilimumab. The DUE/MUE is on denosumab.