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  • 1
    ISSN: 1432-1211
    Keywords: Key words Chicken ; Major histocompatibility complex ; Class I ; Class II ; Haplotypes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract  Although the major histocompatibility complex of chickens (encoded in the B complex) has been studied for a number of years, almost all work has focused on the White Leghorn breed. Broiler (meat-type) chickens were derived from other breeds, including Cornish and Plymouth Rock. It was our hypothesis that new B haplotypes, not previously identified in White Leghorns, might be present in lines of broiler chickens. Furthermore, alloantisera used to identify B serotypes in Leghorn lines reportedly do not work well outside the line in which they were raised, with the result that broiler B haplotypes have not been incorporated into the universal nomenclature system. Our approach was to use a panel of B alloantisera produced to identify B serotypes within a commercial broiler breeder line (designated line A). B homozygotes identified serologically were compared by B-G genotyping using restriction fragment length polymorphism analysis. Furthermore, reverse transcription-polymerase chain reaction was used to amplify variable domains of expressed B-LB and B-F genes of homozygotes of most of the B serotypes in Line A, followed by cloning and nucleotide sequence determination. Comparison of B-LB and B-F sequences with standard Leghorn haplotypes demonstrated the existence of new alleles of B-L and B-F in a broiler breeder line, as well as the presence of alleles previously identified in Leghorns. In some cases, Leghorn-type alleles were in linkage with different B-G alleles in the broiler line than the common haplotypic associations found in Leghorn lines.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2012-06-16
    Description: We learn complex skills such as speech and dance through a gradual process of trial and error. Cortical-basal ganglia circuits have an important yet unresolved function in this trial-and-error skill learning; influential 'actor-critic' models propose that basal ganglia circuits generate a variety of behaviours during training and learn to implement the successful behaviours in their repertoire. Here we show that the anterior forebrain pathway (AFP), a cortical-basal ganglia circuit, contributes to skill learning even when it does not contribute to such 'exploratory' variation in behavioural performance during training. Blocking the output of the AFP while training Bengalese finches to modify their songs prevented the gradual improvement that normally occurs in this complex skill during training. However, unblocking the output of the AFP after training caused an immediate transition from naive performance to excellent performance, indicating that the AFP covertly gained the ability to implement learned skill performance without contributing to skill practice. In contrast, inactivating the output nucleus of the AFP during training completely prevented learning, indicating that learning requires activity within the AFP during training. Our results suggest a revised model of skill learning: basal ganglia circuits can monitor the consequences of behavioural variation produced by other brain regions and then direct those brain regions to implement more successful behaviours. The ability of the AFP to identify successful performances generated by other brain regions indicates that basal ganglia circuits receive a detailed efference copy of premotor activity in those regions. The capacity of the AFP to implement successful performances that were initially produced by other brain regions indicates precise functional connections between basal ganglia circuits and the motor regions that directly control performance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3377745/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3377745/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Charlesworth, Jonathan D -- Warren, Timothy L -- Brainard, Michael S -- P50 MH077970/MH/NIMH NIH HHS/ -- P50 MH077970-05/MH/NIMH NIH HHS/ -- R01 DC006636/DC/NIDCD NIH HHS/ -- R01 DC006636-09/DC/NIDCD NIH HHS/ -- England -- Nature. 2012 May 20;486(7402):251-5. doi: 10.1038/nature11078.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉W. M. Keck Center for Integrative Neuroscience, Department of Physiology, University of California, San Francisco, California 94143, USA. jcharles@phy.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699618" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Basal Ganglia/drug effects/*physiology ; Excitatory Amino Acid Antagonists/pharmacology ; Finches/anatomy & histology/*physiology ; Learning/drug effects/*physiology ; Male ; Prosencephalon/physiology ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors ; Vocalization, Animal/drug effects/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2012-05-19
    Description: Rare genetic variants contribute to complex disease risk; however, the abundance of rare variants in human populations remains unknown. We explored this spectrum of variation by sequencing 202 genes encoding drug targets in 14,002 individuals. We find rare variants are abundant (1 every 17 bases) and geographically localized, so that even with large sample sizes, rare variant catalogs will be largely incomplete. We used the observed patterns of variation to estimate population growth parameters, the proportion of variants in a given frequency class that are putatively deleterious, and mutation rates for each gene. We conclude that because of rapid population growth and weak purifying selection, human populations harbor an abundance of rare variants, many of which are deleterious and have relevance to understanding disease risk.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4319976/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4319976/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Matthew R -- Wegmann, Daniel -- Ehm, Margaret G -- Kessner, Darren -- St Jean, Pamela -- Verzilli, Claudio -- Shen, Judong -- Tang, Zhengzheng -- Bacanu, Silviu-Alin -- Fraser, Dana -- Warren, Liling -- Aponte, Jennifer -- Zawistowski, Matthew -- Liu, Xiao -- Zhang, Hao -- Zhang, Yong -- Li, Jun -- Li, Yun -- Li, Li -- Woollard, Peter -- Topp, Simon -- Hall, Matthew D -- Nangle, Keith -- Wang, Jun -- Abecasis, Goncalo -- Cardon, Lon R -- Zollner, Sebastian -- Whittaker, John C -- Chissoe, Stephanie L -- Novembre, John -- Mooser, Vincent -- T32 HG002536/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2012 Jul 6;337(6090):100-4. doi: 10.1126/science.1217876. Epub 2012 May 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Quantitative Sciences, GlaxoSmithKline (GSK), Research Triangle Park, NC 27709, USA. matthew.r.nelson@gsk.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22604722" target="_blank"〉PubMed〈/a〉
    Keywords: African Americans/genetics ; Asian Continental Ancestry Group ; Disease/*genetics ; European Continental Ancestry Group/genetics ; Gene Frequency ; Genetic Association Studies ; Genetic Predisposition to Disease ; *Genetic Variation ; *Genome, Human ; Geography ; High-Throughput Nucleotide Sequencing ; Humans ; Molecular Targeted Therapy ; Multifactorial Inheritance ; Mutation Rate ; Pharmacogenetics ; Phenotype ; Polymorphism, Single Nucleotide ; Population Growth ; Sample Size ; Selection, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2018-10-16
    Description: Late-onset toxicity is common for novel molecularly targeted agents and immunotherapy. It causes major logistic difficulty for existing adaptive phase I trial designs, which require the observance of toxicity early enough to apply dose-escalation rules for new patients. The same logistic difficulty arises when the accrual is rapid. We propose the time-to-event Bayesian optimal interval (TITE-BOIN) design to accelerate phase I trials by allowing for real-time dose assignment decisions for new patients while some enrolled patients’ toxicity data are still pending. Similar to the rolling six design, the TITE-BOIN dose-escalation/deescalation rule can be tabulated before the trial begins, making it transparent and simple to implement, but is more flexible in choosing the target dose-limiting toxicity (DLT) rate and has higher accuracy to identify the MTD. Compared with the more complicated model-based time-to-event continuous reassessment method (TITE-CRM), the TITE-BOIN has comparable accuracy to identify the MTD but is simpler to implement with substantially better overdose control. As the TITE-CRM is more aggressive in dose escalation, it is less likely to underdose patients. When there are no pending data, the TITE-BOIN seamlessly reduces to the BOIN design. Numerical studies show that the TITE-BOIN design supports continuous accrual without sacrificing patient safety or the accuracy of identifying the MTD, and therefore has great potential to accelerate early-phase drug development. Clin Cancer Res; 24(20); 4921–30. ©2018 AACR .
    Print ISSN: 1078-0432
    Electronic ISSN: 1557-3265
    Topics: Medicine
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  • 6
    Publication Date: 2018-03-07
    Description: Trade-offs associated with sexual size dimorphism (SSD) are well documented across the Tree of Life. However, studies of SSD often do not consider potential investment trade-offs between metabolically expensive structures under sexual selection and other morphological modules. Based on the expectations of the expensive tissue hypothesis, investment in one metabolically expensive structure should come at the direct cost of investment in another. Here, we examine allometric trends in the ontogeny of oyster toadfish ( Opsanus tau ) to test whether investment in structures known to have been influenced by strong sexual selection conform to these expectations. Despite recovering clear changes in the ontogeny of a sexually selected trait between males and females, we find no evidence for predicted ontogenetic trade-offs with metabolically expensive organs. Our results are part of a growing body of work demonstrating that increased investment in one structure does not necessarily drive a wholesale loss of mass in one or more organs. Organisms are faced with a finite energy budget with which to accumulate biomass in developing tissues, raising the question of how sexual selection imposes trade-offs in organ investment. We test the expectations of the expensive tissue hypothesis (ETH) across the ontogeny of oyster toadfishes, a species in which males are under strong sexual selection for a metabolically expensive acoustic repertoire that involves maintaining the fastest twitching muscles of any vertebrates. However, despite finding clear evidence of sexual dimorphism, we failed to recover any evidence supporting the expectations of the ETH.
    Electronic ISSN: 2045-7758
    Topics: Biology
    Published by Wiley-Blackwell
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  • 7
    ISSN: 0167-4838
    Keywords: (Murine hybridoma) ; Gel filtration chromatography ; Glycopeptide ; Glycosylation ; IgG
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 0167-4889
    Keywords: (Leukemia cell) ; Differentiation ; Sialic acid lyase ; Tumor promoter
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 0304-4165
    Keywords: (Species comparison) ; Glycopeptide ; Glycoprotein
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 0273-1177
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Type of Medium: Electronic Resource
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