bluuebunny/crossref_metadata_2025_split huggingface dataset:
Use of NCPA to understanding genetic sub-structuring of Podarcis lilfordi from the Balearic archipelago
Authors: Terrasa Bàrbara , Pérez-Mellado Valentín , Picornell Antònia , Castro José , Brown Richard , Rodríguez Virginia , Ramon M. Misericordia 
Published: October 2009

AbstractPodarcis lilfordi is an endemic lizard found on islands and islets off the coast of Mallorca and Menorca (including the Cabrera archipelago) in the Balearic Islands, which is extinct on the two main islands themselves. Analyses of mtDNA revealed four unconnected parsimony networks. These represented (I) all Menorcan populations, (II) Dragonera, Malgrats and Toro islands (Western Mallorca), (III and IV) the remaining populations from Cabrera and Mallorca. We applied NCPA to evaluate its utility in understanding the genetic sub-structure. Within network I, contiguous range expansion was inferred for both main clades. Populations from western Mallorca (II) have undergone historical allopatric fragmentation events following isolation around the start of the Pleistocene. Clades within networks III and IV showed some allopatric fragmentation and restricted gene flow (isolation by distance) among islands from Cabrera, as well as long distance dispersal between the Cabrera archipelago and southern Mallorca. The NCPA strongly supports the importance of allopatric fragmentation, with some additional support for range expansion. The primary advantage of the NCPA approach was to provide statistical support for these inferences.
Natural interspecific hybridization in Odontophrynus (Anura: Cycloramphidae)
Authors: Lescano Julián , Marti Dardo , Baldo Diego , Pereyra Martín , Rosset Sergio 
Published: October 2009

AbstractThe frog genus Odontophrynus is a composite of diploid and tetraploid populations and species that are widely distributed in South America. Some of the several genetic studies on this group report the production of artificial hybrids but only a single case of natural hybridization has been documented, in southern Brazil. In this study we report the finding of an interspecific natural hybrid specimen in central Argentina. We present morphological and cytogenetical evidence that the diploid taxa Odontophrynus cordobae and O. occidentalis are the parental species. The hybrid genome exhibited problematic pairing and segregation of homeologue chromosomes during meiosis, and the production of non-reduced gametes.
Olfactory cues and breeding habitat selection in the natterjack toad, Bufo calamita
Authors: Joly Pierre , Sanuy Delfi 
Published: October 2009

AbstractWhereas many amphibians use olfactory cues to detect aquatic habitats, less attention has been paid to the specificity of the information carried by these cues with respect to breeding habitat quality. In the present work, we address this question by taking advantage of the selectivity for specific breeding habitats exhibited by the natterjack toad (temporary waters, gravel pits). Toads were sampled from two populations located in semi-arid regions of the Iberic peninsula experiencing Mediterranean climate, and one population in a temperate region of France experiencing oceanic-continental climate. The choice was given in a maze between waters coming either from habitats known to be suitable for the species (temporary waters on an inorganic-dominated substratum) or from unsuitable habitats (ponds with eutrophic water or permanent water on organic-rich substratum). The toads from the temperate region exhibited a clear selection for water from the suitable habitat. In contrast, toads from the Mediterranean region did not show any preference, either when the waters came from their original region or when they came from the other region. These results show that toads can use chemical cues to discriminate specific habitats, allowing them to quickly find suitable habitat patches that are temporary and often spatially unpredictable. Variation between the two populations in the ability to select water quality is likely to be connected with habitat availability at the regional scale.
Morphological traits affect escape behaviour of the Balearic lizards (Podarcis lilfordi)
Authors: Cooper Jr. William , Pérez-Mellado Valentín , Hawlena Dror 
Published: October 2009

AbstractEscape theory predicts that a prey should start escaping (flight initiation distance = FID) from a predator when the costs of fleeing and the cost staying are equal or until future fitness is maximized. Consequently, prey escape performances and current reproductive asset can affect FID. We tested effects of body condition, morphology, and whether the tail was regenerated or original on FID in the Balearic lizard (Podarcis lilfordi) by ourselves simulating predators. Lizards with better body condition had longer FID and lizards with longer intact tails had shorter FID. Lizards with regenerated tail presented shorter FID than lizards with intact tails. These results suggest that impaired escape performance is counterbalanced by fitness costs of tail regeneration or by alteration of escape behaviour. The weak association between morphology, body condition and FID suggest that escape performances and asset protection have relatively small effect on P. lilfordi escape decisions.
Parasitic infracommunities of the Aegean wall lizard Podarcis erhardii (Lacertidae, Sauria): isolation and impoverishment in small island populations
Authors: Foufopoulos  , Roca  , Valakos  , Pafilis  
Published: October 2009

AbstractThe Aegean wall lizard Podarcis erhardii, is widely distributed across the islands of the Aegean Sea (Greece). While there exists a relatively substantial body of knowledge on the ecology and life history of the species, the parasite communities of the taxon remain almost completely unknown. Quantifying the composition of these communities in P. erhardii is not only important for autoecological reasons, but also because inter-island comparisons of this lizard's parasite communities can shed light on the factors that structure parasite diversity in general. Here we investigate the gastrointestinal parasite communities of P. erhardii populations occurring on 16 landbridge islands of the Sporades group in the NW Aegean Sea by examining the gastrointestinal tracts of 113 lizards. In all, 8 species of helminths were found: 1 Trematode (Paradistomum mutabile), 1 Cestode (Oochoristica sp.) and 6 Nematodes (Parapharyngodon micipsae, Parapharyngodon bulbosus, Parapharyngodon echinatus, Spauligodon sp., Abbreviata sp., and Skrjabinelazia sp.). The prevalence, mean intensity, and mean abundance of infection were respectively 63.71%; 6.01 (±11.71; range 1-90); and 3.57 (±9.5; range 0-90). Brillouin's index of diversity for the Sporades was 0.048 (±0.13; range 0-0.142). These values were lower than for most other mainland and insular lacertid populations, and suggest that the investigated island populations harbor very depauperate helminth communities. The severe impoverishment of the parasite communities and the differential persistence of generalist parasite species with simple life cycles is most likely the result of a combination of insular environmental conditions (spatial and temporal isolation, arid climate, small host population sizes) and host life history characteristics (diet, simple gastrointestinal tract architecture). The paucity of parasites in these relictual island populations suggests that small reptile populations fragmented by anthropogenic activities may not be able to sustain their native parasite communities over the long term.
Defining the Outer Limits of the Continental Shelf across the Arctic Basin: The Russian Submission, States' Rights, Boundary Delimitation and Arctic Regional Cooperation
Authors: Weber Mel 
Published: October 2009

AbstractThe Russian submission to the Commission on the Limits of the Continental Shelf (CLCS) provides an excellent example of the difficulty faced by Arctic states in relation to their rights and claims as coastal states. The geology and geography of the Arctic submarine environment are complex and poorly understood. Political maritime boundaries for this semi-enclosed sea are incomplete. The agreed boundaries do not take into consideration the full potential of the legal continental shelves. Viewed against continental shelf issues, possible maritime boundary delimitations and the rights of states to engage in regional initiatives, it is apparent that the Russian submission has not prejudiced the rights of other states. Although the two functions are inherently related, the ability to delimit boundaries with adjacent and opposite states remains separate from the process undertaken by the CLCS.
Identification of early growth response protein 1 (EGR-1) as a novel target for JUN-induced apoptosis in multiple myeloma
Authors: Chen Lijuan , Wang Siqing , Zhou Yiming , Wu Xiaosong , Entin Igor , Epstein Joshua , Yaccoby Shmuel , Xiong Wei , Barlogie Bart , Shaughnessy John D. , Zhan Fenghuang 
Published: October 2009

Abstract
Tumor–bone marrow microenvironment interactions in multiple myeloma (MM) are documented to play crucial roles in plasma-cell growth/survival. In vitro coculture of MM cells with osteoclasts supported cell survival and significantly down-regulated JUN expression. JUN expression in myeloma cells from late-stage and high-risk MM was significantly lower than in plasma cells from healthy donors, monoclonal gammopathy of undetermined significance, smoldering MM, and low-risk MM; patients with low-JUN–expressing MM cells had earlier disease-related deaths. JUN overexpression in MM cells induced cell death and growth inhibition and up-regulated expression of early growth response protein 1 (EGR-1), whose low expression also carried unfavorable clinical implications. EGR-1 knockdown in MM cells abrogated JUN overexpression-induced MM cell death and growth inhibition, indicating that EGR-1 acts directly downstream of JUN. JUN modulates myeloma cell apoptosis through interacting with EGR-1, which down-regulates Survivin and triggers caspase signaling. Importantly, high JUN or EGR-1 expression was associated with improved outcome in Total Therapy 3, in which bortezomib is given throughout therapy, versus Total Therapy 2, in which bortezomib is given only at relapse. Consistently, JUN or EGR-1 knockdown in cultured MM cells enhanced their resistance to bortezomib, demonstrating the crucial role of low JUN/EGR-1 expression in MM resistance to bortezomib.
A gene expression signature of CD34+ cells to predict major cytogenetic response in chronic-phase chronic myeloid leukemia patients treated with imatinib
Authors: McWeeney Shannon K. , Pemberton Lucy C. , Loriaux Marc M. , Vartanian Kristina , Willis Stephanie G. , Yochum Gregory , Wilmot Beth , Turpaz Yaron , Pillai Raji , Druker Brian J. , Snead Jennifer L. , MacPartlin Mary , O'Brien Stephen G. , Melo Junia V. , Lange Thoralf , Harrington Christina A. , Deininger Michael W. N. 
Published: October 2009

Abstract
In chronic-phase chronic myeloid leukemia (CML) patients, the lack of a major cytogenetic response (< 36% Ph+ metaphases) to imatinib within 12 months indicates failure and mandates a change of therapy. To identify biomarkers predictive of imatinib failure, we performed gene expression array profiling of CD34+ cells from 2 independent cohorts of imatinib-naive chronic-phase CML patients. The learning set consisted of retrospectively selected patients with a complete cytogenetic response or more than 65% Ph+ metaphases within 12 months of imatinib therapy. Based on analysis of variance P less than .1 and fold difference 1.5 or more, we identified 885 probe sets with differential expression between responders and nonresponders, from which we extracted a 75-probe set minimal signature (classifier) that separated the 2 groups. On application to a prospectively accrued validation set, the classifier correctly predicted 88% of responders and 83% of nonresponders. Bioinformatics analysis and comparison with published studies revealed overlap of classifier genes with CML progression signatures and implicated β-catenin in their regulation, suggesting that chronic-phase CML patients destined to fail imatinib have more advanced disease than evident by morphologic criteria. Our classifier may allow directing more aggressive therapy upfront to the patients most likely to benefit while sparing good-risk patients from unnecessary toxicity.
EMMPRIN promotes angiogenesis through hypoxia-inducible factor-2α–mediated regulation of soluble VEGF isoforms and their receptor VEGFR-2
Authors: Bougatef Faten , Quemener Cathy , Kellouche Sabrina , Naïmi Benyoussef , Podgorniak Marie-Pierre , Millot Guy , Gabison Eric E. , Calvo Fabien , Dosquet Christine , Lebbé Céleste , Menashi Suzanne , Mourah Samia 
Published: October 2009

AbstractExtracellular matrix metalloproteinase inducer (EMMPRIN/CD147) is thought to promote tumor angiogenesis mostly through its protease-inducing function and more recently by its ability to increase tumor cell expression of vascular endothelial growth factor (VEGF). In this study, we present evidence that EMMPRIN can promote angiogenesis by a direct effect on endothelial cells through a paracrine regulation of the VEGF/VEGF-receptor (VEGFR) system. Using human microvascular endothelial cell line–1 endothelial cells, we show that EMMPRIN selectively increased the soluble VEGF isoforms (121 and 165), but not the matrix-bound VEGF 189 form. In addition, EMMPRIN up-regulated the expression of VEGFR-2 without an effect on VEGFR-1. This increase in VEGFR-2 was responsible for the observed EMMPRIN stimulation of the migratory and tube formation capacity of endothelial cells. EMMPRIN′s effects, which were matrix metalloproteinase and urokinase-type plasminogen activator independent, were mediated primarily through hypoxia-inducible factor-2α expression, also up-regulated by EMMPRIN. VEGFR-2 increase was also observed in vivo in a mouse model of xenograph tumors overexpressing EMMPRIN. These results suggest that in addition to increasing protease production, EMMPRIN may contribute to the formation of a reactive stroma also through the up-regulation of hypoxia-inducible factor-2α, VEGFR-2, and the soluble forms of VEGF in endothelial cells, thus directly regulating the angiogenic process.
Migrating monocytes recruited to the spleen play an important role in control of blood stage malaria
Authors: Sponaas Anne-Marit , Freitas do Rosario Ana Paula , Voisine Cecile , Mastelic Beatris , Thompson Joanne , Koernig Sandra , Jarra William , Renia Laurent , Mauduit Marjorie , Potocnik Alexandre J. , Langhorne Jean 
Published: October 2009

AbstractHost responses controlling blood-stage malaria include both innate and acquired immune effector mechanisms. During Plasmodium chabaudi infection in mice, a population of CD11bhighLy6C+ monocytes are generated in bone marrow, most of which depend on the chemokine receptor CCR2 for migration from bone marrow to the spleen. In the absence of this receptor mice harbor higher parasitemias. Most importantly, splenic CD11bhighLy6C+ cells from P chabaudi–infected wild-type mice significantly reduce acute-stage parasitemia in CCR2−/− mice. The CD11bhighLy6C+ cells in this malaria infection display effector functions such as production of inducible nitric oxide synthase and reactive oxygen intermediates, and phagocytose P chabaudi parasites in vitro, and in a proportion of the cells, in vivo in the spleen, suggesting possible mechanisms of parasite killing. In contrast to monocyte-derived dendritic cells, CD11bhighLy6C+ cells isolated from malaria-infected mice express low levels of major histocompatibility complex II and have limited ability to present the P chabaudi antigen, merozoite surface protein-1, to specific T-cell receptor transgenic CD4 T cells and fail to activate these T cells. We propose that these monocytes, which are rapidly produced in the bone marrow as part of the early defense mechanism against invading pathogens, are important for controlling blood-stage malaria parasites.
How I treat age-related morbidities in elderly persons with hemophilia
Authors: Mannucci Pier M. , Schutgens Roger E. G. , Santagostino Elena , Mauser-Bunschoten Evelien P. 
Published: October 2009

Abstract
In persons with hemophilia, life expectancy is now approaching that of the general male population, at least in countries that can afford regular replacement therapy with coagulation factor concentrates. The new challenges for comprehensive treatment centers are thus to provide optimal health care for this aging population of patients, who often present not only with the comorbidities typically associated with hemophilia (arthropathy, chronic pain, blood-borne infections), but also with common age-related illnesses such as cardiovascular disease and cancer. There are no evidence-based guidelines for the management of these conditions, which often require drugs that interfere with hemostasis, enhance the bleeding tendency, and warrant more intensive replacement therapy. At the moment, elderly patients with hemophilia affected by other diseases should be managed like their age-group peers without hemophilia, provided replacement therapy is tailored to the heightened risk of bleeding associated with the need for invasive procedures and drugs that further compromise the deranged hemostasis. More detailed advice is provided on the schedules of replacement therapy needed to tackle cardiovascular diseases, such as acute coronary syndromes and nonvalvular atrial fibrillation, because these conditions will become more and more frequent challenges for the comprehensive treatment centers.
Costs and Benefits of the National Cancer Institute Central Institutional Review Board
Authors: Wagner Todd H. , Murray Christine , Goldberg Jacquelyn , Adler Jeanne M. , Abrams Jeffrey 
Published: October 2009

PurposeIn 2001, the National Cancer Institute (NCI) formed the Central Institutional Review Board (CIRB) to conduct a single human subjects review for its multisite phase III oncology trials. The goal of this study was to assess whether NCI's CIRB was associated with lower effort, time, and cost in processing adult phase III oncology trials.MethodsWe conducted an observational study and compared sites affiliated with the NCI CIRB to unaffiliated sites that used their local IRB for review. Oncology research staff and IRB staff were surveyed to understand effort and timing. Response rates were 60% and 42%, respectively. Analysis of these survey data yielded information on effort, timing, and costs. We combined these data with CIRB operational data to determine the net savings of the CIRB using a societal perspective.ResultsCIRB affiliation was associated with faster reviews (33.9 calendar days faster on average), and 6.1 fewer hours of research staff effort. CIRB affiliation was associated with a savings of $717 per initial review. The estimated cost of running the CIRB was $161,000 per month. The CIRB yielded a net cost of approximately $55,000 per month from a societal perspective. Whether the CIRB results in higher or lower quality reviews was not assessed because there is no standard definition of review quality.ConclusionThe CIRB was associated with decreases in investigator and IRB staff effort and faster protocol reviews, although savings would be higher if institutions used the CIRB as intended.
Ubiquitin Carboxyl-Terminal Hydrolase L3 Promotes Insulin Signaling and Adipogenesis
Authors: Suzuki Mari , Setsuie Rieko , Wada Keiji 
Published: October 2009

AbstractInsulin is a potent adipogenic hormone that triggers the induction of a series of transcription factors and specific proteins governing the differentiation of preadipocytes into mature adipocytes. Here we report that ubiquitin carboxyl-terminal hydrolase (UCH)-L3, a deubiquitinating enzyme, promotes insulin signaling and adipogenesis. Uchl3−/− mice had less visceral white adipose tissue compared with wild-type mice. In vitro adipogenesis experiments revealed that mouse embryonic fibroblasts (MEFs) and preadipocytes from Uchl3−/− mice had impaired ability to differentiate into mature adipocytes than those from wild-type mice. This difference was diminished by removing insulin from the medium. RT-PCR analysis showed that insulin-regulated expression of srebp1c, fas, glut4, and adiponectin is impaired in Uchl3−/− cells. The phosphorylation of insulin/IGF-I receptor, Akt, glycogen synthase kinase-3β, and FoxO1 was decreased in Uchl3−/− MEFs treated with insulin. Moreover, ectopic expression of wild-type UCH-L3 restored the phosphorylation of insulin/IGF-I receptor and adipocyte differentiation in Uchl3−/− MEFs. In contrast, hydrolase activity-deficient UCH-L3 did not enhance insulin signaling and the expression of glut4, fabp4, and adiponectin, resulting in impaired formation of large lipid droplets. These results suggest that UCH-L3 promotes adipogenesis by enhancing insulin signaling in a hydrolase activity-dependent manner.
Mechanisms Involved in 3′,5′-Cyclic Adenosine Monophosphate-Mediated Inhibition of the Ubiquitin-Proteasome System in Skeletal Muscle
Authors: Gonçalves Dawit A. P. , Lira Eduardo C. , Baviera Amanda M. , Cao Peirang , Zanon Neusa M. , Arany Zoltan , Bedard Nathalie , Tanksale Preeti , Wing Simon S. , Lecker Stewart H. , Kettelhut Isis C. , Navegantes Luiz C. C. 
Published: October 2009

AbstractAlthough it is well known that catecholamines inhibit skeletal muscle protein degradation, the molecular underlying mechanism remains unclear. This study was undertaken to investigate the role of β2-adrenoceptors (AR) and cAMP in regulating the ubiquitin-proteasome system (UPS) in skeletal muscle. We report that increased levels of cAMP in isolated muscles, promoted by the cAMP phosphodiesterase inhibitor isobutylmethylxanthine was accompanied by decreased activity of the UPS, levels of ubiquitin-protein conjugates, and expression of atrogin-1, a key ubiquitin-protein ligase involved in muscle atrophy. In cultured myotubes, atrogin-1 induction after dexamethasone treatment was completely prevented by isobutylmethylxanthine. Furthermore, administration of clenbuterol, a selective β2-agonist, to mice increased muscle cAMP levels and suppressed the fasting-induced expression of atrogin-1 and MuRF-1, atrogin-1 mRNA being much more responsive to clenbuterol. Moreover, clenbuterol increased the phosphorylation of muscle Akt and Foxo3a in fasted rats. Similar responses were observed in muscles exposed to dibutyryl-cAMP. The stimulatory effect of clenbuterol on cAMP and Akt was abolished in muscles from β2-AR knockout mice. The suppressive effect of β2-agonist on atrogin-1 was not mediated by PGC-1α (peroxisome proliferator-activated receptor-γ coactivator 1α known to be induced by β2-agonists and previously shown to inhibit atrogin-1 expression), because food-deprived PGC-1α knockout mice were still sensitive to clenbuterol. These findings suggest that the cAMP increase induced by stimulation of β2-AR in skeletal muscles from fasted mice is possibly the mechanism by which catecholamines suppress atrogin-1 and the UPS, this effect being mediated via phosphorylation of Akt and thus inactivation of Foxo3.