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  • 2015-2019  (144)
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  • 1
    Online Resource
    Online Resource
    Voice Quality : The Laryngeal Articulator Model. (2019)
    Cambridge :Cambridge University Press,
    Details
    Keywords: Voice-Physiological aspects. ; Electronic books.
    Description / Table of Contents: Examines how accents differ in 'voice quality' across languages and presents a new framework for its analysis with a revised model of lower-vocal-tract articulation, focusing on the larynx in speech. It will appeal to students and researchers in linguistics, phonetics, child language, speech science, clinical linguistics, and forensic phonetics.
    Type of Medium: Online Resource
    Pages: 1 online resource (328 pages)
    Edition: 1st ed.
    ISBN: 9781108597685
    Series Statement: Cambridge Studies in Linguistics Series ; v.Series Number 162
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=5797324
    DDC: 612.7/8
    Language: English
    Note: Cover -- Half-title -- Series information -- Title page -- Copyright information -- Contents -- Figures -- Tables -- Preface -- Acknowledgements -- Abbreviations -- 1 Voice and Voice Quality -- 1.1 Voice Quality Defined -- 1.2 The Laryngeal Articulator -- 1.3 Origins of Voice Quality Theory -- 1.4 Articulatory Parameters -- 1.4.1 Phonation Types -- 1.4.2 Elaborations of the Laryngeal Articulator -- 1.5 Supralaryngeal Categories -- 1.5.1 Velopharyngeal Settings -- 1.5.2 Lingual Settings -- 1.5.3 Mandibular Settings -- 1.5.4 Labial Settings -- 1.6 The Pharyngeal Argument -- 1.6.1 How the Pharynx Relates to the Larynx -- 1.6.2 Methods of Observing the Pharynx and Larynx -- 1.6.3 Categorization of Pharyngeals and Their Relationship to the Larynx -- 2 Laryngeal Voice Quality Classification -- 2.1 States of the Larynx and Phonation Types -- 2.2 Canonical States and Movements -- 2.3 Laryngeal Categories -- 2.3.1 Breathing/Inspiration -- 2.3.2 Breath -- 2.3.3 Modal Voice -- 2.3.4 Prephonation -- 2.3.5 Glottal Stop -- 2.3.6 Epiglottal Stop -- 2.3.7 Whisper -- 2.3.8 Breathy Voice -- 2.3.9 Whispery Voice -- 2.3.10 Falsetto -- 2.3.11 Creaky Voice -- 2.3.12 Harsh Voice -- 2.3.13 Ventricular Voice -- 2.3.14 Aryepiglottic Trilling -- 2.3.15 Laryngeal Constriction at High Pitch -- 2.4 Tense Voice and Lax Voice -- 2.5 Unconstricted vs. Constricted Laryngeal States -- 3 Instrumental Case Studies and Computational Simulations of Voice Quality -- 3.1 Techniques to Examine Long-Term Voice Qualities -- 3.2 Techniques to Image the Larynx -- 3.2.1 Laryngoscopy: The Example of Aryepiglottic Trilling -- 3.2.2 Cineradiography -- 3.2.3 Laryngoscopy + Laryngeal Ultrasound -- 3.2.4 Magnetic Resonance Imaging -- 3.3 Computer Models of the Larynx and Laryngeal Constriction -- 3.3.1 A 3D Laryngeal Constrictor Model -- 3.3.2 A Two-Trapdoor Model of Aryepiglottic Trilling. , 3.3.3 A Model of Vocal-Ventricular Fold Contact -- 3.3.4 The ArtiSynth Model of the Larynx -- 4 Linguistic, Paralinguistic, and Extralinguistic Illustrations of Voice Quality -- 4.1 Laryngeal Categories -- 4.1.1 Glottal Phonation Types -- 4.1.1.1 Breath -- 4.1.1.2 Modal Voice -- 4.1.1.3 Breathy Voice -- 4.1.1.4 Falsetto -- 4.1.2 Phonation Types with Laryngeal Constrictor Effects -- 4.1.2.1 Whisper -- 4.1.2.2 Whispery Voice -- 4.1.2.3 Creaky Voice (Creak) -- 4.1.2.4 Harsh Voice (Mid Pitch) -- 4.1.2.5 Ventricular Voice -- 4.1.2.6 Harsh Voice (Low Pitch, with Aryepiglottic Fold Trilling) -- 4.1.2.7 Laryngeal Constriction at High Pitch (Pressed Voice) -- 4.1.3 Laryngeal Constrictor and Larynx Height Settings -- 4.1.3.1 Constricted (Aryepiglottic Sphinctering, Retracted Lingual Setting, Raised Larynx Height) -- 4.1.3.1.1 Raised-Larynx Voice -- 4.1.3.1.2 Pharyngealized Voice -- 4.1.3.2 Unconstricted -- 4.1.3.2.1 Lowered-Larynx Voice -- 4.1.3.2.2 Faucalized Voice -- 4.2 Supralaryngeal (Oral) Categories -- 4.2.1 Velopharyngeal Port Settings -- 4.2.1.1 Nasal Voice -- 4.2.1.2 Denasal Voice -- 4.2.2 Tongue-Body Lingual Settings -- 4.2.2.1 Fronted Lingual Settings -- 4.2.2.1.1 Dentalized Voice -- 4.2.2.1.2 Alveolarized Voice -- 4.2.2.1.3 Palato-Alveolarized Voice -- 4.2.2.1.4 Palatalized Voice -- 4.2.2.2 Raised Lingual Settings -- 4.2.2.2.1 Velarized Voice -- 4.2.2.2.2 Uvularized Voice -- 4.2.3 Tongue-Front Lingual Settings -- 4.2.3.1 Tongue Tip Articulation (Apical) -- 4.2.3.2 Tongue Blade Articulation (Laminal) -- 4.2.3.3 Retroflex Articulation -- 4.2.4 Jaw Settings -- 4.2.4.1 Close Jaw -- 4.2.4.2 Open Jaw -- 4.2.4.3 Protruded Jaw -- 4.2.4.4 Labiodentalization -- 4.2.4.5 Laterally Offset Jaw -- 4.2.5 Labial Settings -- 4.2.5.1 Close Rounding -- 4.2.5.2 Open Rounding -- 4.2.5.3 Labial Spreading (Spread Lips) -- 4.2.5.4 Upper-Lip Effects. , 4.3 Other Realizations of Laryngeal Constriction -- 4.3.1 Glottalization and Laryngealization -- 4.3.2 Laryngeal Constriction in Segmental Contrast -- 4.3.3 Laryngeal Constriction in Syllabic Contrast -- 4.3.4 Throat Singing -- 5 Phonological Implications of Voice Quality Theory -- 5.1 Voice Quality in Phonological Theory: Previous Approaches -- 5.2 Phonological Potentials, the Laryngeal Articulator, and Voice Quality -- 5.3 Synergistic Relations Network -- 5.4 Voice Quality and Register Contrasts: A Unified Approach -- 5.5 Voice Quality in Sound Change: The Case of Southern Wakashan Pharyngeal Genesis -- 5.6 Voice Quality in Phonology -- 6 Infant Acquisition of Speech and Voice Quality -- 6.1 The Infant Vocal Tract -- 6.2 Vocal Exploration in Infancy -- 6.3 Laryngeal Voice Quality in the First Year of Life -- 6.3.1 Laryngeal Quality -- 6.3.2 Utterance Types -- 6.3.3 Distribution of Laryngeal Constriction by Utterance Type -- 6.4 Laryngeal Components of Early Babbling -- 6.5 Early Laryngeal Sounds as Foundations of Speech Development -- 7 Clinical Illustrations of Voice Quality -- 7.1 Vocal Fold Vibration -- 7.1.1 Human Laryngeal Tissues -- 7.1.2 The Vibratory Pattern at the Glottis (Oscillatory-Impedance Theories) -- 7.1.3 Nonlinear Dynamic Theories -- 7.2 Benign Pathology of the Vocal Folds with Dysphonia -- 7.2.1 Functional: Muscle Tension Dysphonia, Hyper- or Hypofunction -- 7.2.2 Anterior Vocal Fold Lesions: Benign Lesions: Reinke's Edema, Vocal Nodules, Polyps, Cysts, Sulci -- 7.2.3 Posterior Vocal Fold Lesions: Contact Ulcers, Granulomata, Laryngopharyngeal Reflux -- 7.3 Malignant Laryngopharyngeal Lesions -- 7.3.1 Total Laryngectomy -- 7.3.2 Partial Laryngectomies and Laryngopharyngeal Surgery -- 7.3.2.1 Horizontal Supracricoid Partial Laryngectomy (SCPL) -- 7.3.2.2 The Neoglottis and 'Substitution Voice'. , 7.3.2.3 Supraglottic Partial Laryngectomy (SGPL) -- 7.3.2.4 Vertical Partial Laryngectomies -- 7.3.3 Endoscopic Laser Surgery (Cordectomy) -- 7.4 Movement Disorders -- 7.4.1 Vocal Fold Paralysis -- 7.4.2 Parkinson's Disease -- 7.4.3 Tremor, Dystonia, Spasmodic Dysphonia, Myoclonus -- 7.5 The Professional Voice: Adaptive Laryngeal Articulator Possibilities -- 7.5.1 Mongolian Long Song -- 7.5.2 Human Beatboxing -- 8 Laryngeal Articulation and Voice Quality in Sound Change, Language Ontogeny and Phylogeny -- 8.1 Salience and Context -- 8.2 The Axis of [e/o] -- 8.3 Sound Change -- 8.4 Phylogeny -- References -- Multimedia References -- Author/Artist Index -- Subject Index.
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  • 2
    Online Resource
    Online Resource
    The Complement FactsBook. (2017)
    San Diego :Elsevier Science & Technology,
    Details
    Keywords: Complement (Immunology). ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (514 pages)
    Edition: 2nd ed.
    ISBN: 9780128104217
    Series Statement: Factsbook Series
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=5106108
    Language: English
    Note: Front Cover -- The Complement FactsBook -- The Complement FactsBook -- Copyright -- Contents -- List of Contributors -- Preface -- 1 - Introduction -- AIMS AND SCOPE OF THE BOOK -- ORGANISATION OF THE DATA -- Other Names -- Physicochemical Properties -- Structure -- Function -- Degradation Pathway -- Tissue Distribution -- Regulation of Expression -- Human Protein Sequence -- Protein Modules -- Chromosomal Location -- cDNA Sequence -- Genomic Structure -- Accession Numbers -- Deficiency -- Polymorphic Variants -- Mutant Animals -- REFERENCE -- 2 - The Complement System -- HISTORICAL PERSPECTIVE -- MODULAR STRUCTURE OF THE COMPONENTS -- The Collectins -- Serine Proteases -- C3 Family -- Terminal Pathway -- Regulatory Proteins -- The Leucocyte Receptors -- PATHWAYS -- Classical Pathway -- Lectin Pathway -- Alternative Pathway -- Terminal Pathway -- REFERENCES -- I - Collectins -- 3 - C1q -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- DEGRADATION PATHWAY -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- HUMAN CDNA SEQUENCE -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- FURTHER READING -- 4 - Mannose-Binding Lectin -- OTHER NAMES OF MANNOSE-BINDING LECTIN -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- PROTEIN SEQUENCE -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- CDNA SEQUENCE -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 5 - Ficolins -- OTHER NAMES FOR FICOLINS -- PHYSICOCHEMICAL PROPERTIES -- FICOLIN-1 -- FICOLIN-2 -- FICOLIN-3 -- STRUCTURE -- FUNCTION -- Lectin and Binding Activities -- Binding of Ficolins to Microorganisms -- Lectin Pathway Activation. , Cross Talk and Collaboration of Ficolins With Noncomplement Proteins -- Roles in Homeostasis -- TISSUE DISTRIBUTION -- PROTEIN SEQUENCE -- PROTEIN MODULES -- Splicing Variants of Ficolins -- CHROMOSOMAL LOCATION -- CDNA SEQUENCE -- GENOMIC STRUCTURE -- Accession Numbers -- POLYMORPHIC VARIANTS -- FICOLIN-DEFICIENT MOUSE -- REFERENCES -- 6 - The Collectins -- OTHER NAMES -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- CRYSTAL STRUCTURE -- FUNCTION -- Sugar Specificity -- Ligand Specificity -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- HUMAN CDNA SEQUENCE -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- II - Serine Proteases -- 7 - MASP-1 -- PHYSICOCHEMICAL PROPERTIES -- Immature Protein -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE -- PROTEIN MODULES -- CHROMOSOMAL LOCATION16 -- HUMAN CDNA SEQUENCE -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 8 - MASP-2 -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE -- PROTEIN MODULES -- CHROMOSOMAL LOCATION14 -- HUMAN CDNA SEQUENCE -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 9 - MASP-3 -- PHYSICOCHEMICAL PROPERTIES -- Immature Protein -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE -- PROTEIN MODULES -- CHROMOSOMAL LOCATION18 -- HUMAN CDNA SEQUENCE -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 10 - C1r -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- 3D Structure -- FUNCTION. , TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE20-23 -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- HUMAN CDNA SEQUENCE22 -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 11 - C1s -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- 3D STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE26-28 -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- HUMAN CDNA SEQUENCE26 -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 12 - Factor D -- OTHER NAMES -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- DEGRADATION PATHWAY -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- CDNA SEQUENCES -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- FURTHER READING -- 13 - C2 -- PHYSIOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- EXPRESSION AND REGULATION -- PROTEIN SEQUENCE12,13 -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- CDNA SEQUENCE -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 14 - Factor B -- OTHER NAMES -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- PROTEIN SEQUENCES -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- CDNA SEQUENCE -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 15 - Factor I -- OTHER NAMES -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- PROTEIN SEQUENCES -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- CDNA SEQUENCES AND GENOMIC STRUCTURE. , POLYMORPHIC VARIANTS, DEFICIENCY AND DISEASE-RELATED SINGLE NUCLEOTIDE POLYMORPHISMS -- FI KNOCKOUT MICE -- REFERENCES -- III - C3 Family -- 16 - C3 -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- DEGRADATION PATHWAY -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- HUMAN CDNA SEQUENCE -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 17 - C4 -- OTHER NAMES -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- PROTEIN SEQUENCE31 -- PROTEIN MODULES -- CHROMOSOMAL LOCATION33 -- CDNA SEQUENCE31,34 -- cDNA Sequence-Continued -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- Naturally Occurring C4 Deficiency -- C4 KNOCKOUT MOUSE PHENOTYPES -- REFERENCES -- 18 - C5 -- OTHER NAMES -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- DEGRADATION PATHWAY -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE3 -- HUMAN PROTEIN SEQUENCE-CONTINUED -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- HUMAN CDNA SEQUENCE -- HUMAN CDNA SEQUENCE-CONTINUED -- HUMAN CDNA SEQUENCE-CONTINUED -- Genomic Structure26,27 -- ACCESSION NUMBERS -- DEFICIENCY -- African-American Families28 -- Western Cape, South African Families29 -- Saudi Family30 -- Spanish Families31,32 -- Italian Family31 -- Brazilian Family33 -- Turkish Family34 -- Norwegian Family35 -- Danish Family35 -- Dutch Family36 -- Morocco Families37 -- POLYMORPHIC VARIANTS38 -- MUTANT ANIMALS -- REFERENCES -- IV - Terminal Pathway Components -- 19 - C6 -- PHYSIOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE1,2 -- CHROMOSOMAL LOCATION -- HUMAN CDNA SEQUENCE1,2. , GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 20 - C7 -- PHYSIOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE1 -- CHROMOSOMAL LOCATION -- HUMAN CDNA SEQUENCE1 -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 21 - C8 -- PHYSIOCHEMICAL PROPERTIES -- STRUCTURE -- CRYSTAL STRUCTURES -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE -- C8α19 -- C8β20, 21 -- C8γ22 -- CHROMOSOMAL LOCATION -- HUMAN CDNA SEQUENCE -- C8α19 -- C8β20, 21 -- C8γ22 -- GENOMIC STRUCTURE -- C8α24 -- C8β25 -- C8γ26 -- Polymorphic Variants -- MUTANT ANIMALS -- REFERENCES -- 22 - C9 -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- HUMAN CDNA SEQUENCE -- HUMAN CDNA SEQUENCE-CONTINUED -- GENOMIC STRUCTURE -- ACCESSION NUMBERS -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- V - Regulatory Proteins -- 23 - C1 Inhibitor -- PHYSICOCHEMICAL PROPERTIES -- Immature Protein -- Mature Protein -- STRUCTURE -- FUNCTIONS -- DEGRADATION PATHWAY -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- HUMAN PROTEIN SEQUENCE -- PROTEIN MODULES -- CHROMOSOMAL LOCATION -- CDNA SEQUENCE -- GENOMIC STRUCTURE -- DEFICIENCY -- POLYMORPHIC VARIANTS -- MUTANT ANIMALS -- REFERENCES -- 24 - C4b-Binding Protein -- OTHER NAMES -- PHYSICOCHEMICAL PROPERTIES -- STRUCTURE -- FUNCTION -- TISSUE DISTRIBUTION -- REGULATION OF EXPRESSION -- PROTEIN SEQUENCES -- PROTEIN MODULES -- CHROMOSOMAL LOCATION AND GENOMIC STRUCTURE -- CDNA SEQUENCES -- DEFICIENCY -- POLYMORPHIC VARIANTS AND DISEASE-RELATED SINGLE NUCLEOTIDE POLYMORPHISMS. , C4BP KNOCKOUT AND TRANSGENIC MICE.
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  • 3
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    Evidence of a Causal Association Between Insulinemia and Endometrial Cancer: A Mendelian Randomization Analysis (2015)
    Oxford University Press
    Details
    Publication Date: 2015-07-03
    Description: Background: Insulinemia and type 2 diabetes (T2D) have been associated with endometrial cancer risk in numerous observational studies. However, the causality of these associations is uncertain. Here we use a Mendelian randomization (MR) approach to assess whether insulinemia and T2D are causally associated with endometrial cancer. Methods: We used single nucleotide polymorphisms (SNPs) associated with T2D (49 variants), fasting glucose (36 variants), fasting insulin (18 variants), early insulin secretion (17 variants), and body mass index (BMI) (32 variants) as instrumental variables in MR analyses. We calculated MR estimates for each risk factor with endometrial cancer using an inverse-variance weighted method with SNP-endometrial cancer associations from 1287 case patients and 8273 control participants. Results: Genetically predicted higher fasting insulin levels were associated with greater risk of endometrial cancer (odds ratio [OR] per standard deviation = 2.34, 95% confidence internal [CI] = 1.06 to 5.14, P = .03). Consistently, genetically predicted higher 30-minute postchallenge insulin levels were also associated with endometrial cancer risk (OR = 1.40, 95% CI = 1.12 to 1.76, P = .003). We observed no associations between genetic risk of type 2 diabetes (OR = 0.91, 95% CI = 0.79 to 1.04, P = .16) or higher fasting glucose (OR = 1.00, 95% CI = 0.67 to 1.50, P = .99) and endometrial cancer. In contrast, endometrial cancer risk was higher in individuals with genetically predicted higher BMI (OR = 3.86, 95% CI = 2.24 to 6.64, P = 1.2x10 -6 ). Conclusion: This study provides evidence to support a causal association of higher insulin levels, independently of BMI, with endometrial cancer risk.
    Electronic ISSN: 1460-2105
    Topics: Medicine
    Published by Oxford University Press
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  • 4
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    A meta-analysis of 120 246 individuals identifies 18 new loci for fibrinogen concentration (2016)
    de Vries, P. S., Chasman, D. I., Sabater-Lleal, M., Chen, M.-H., Huffman, J. E., Steri, M., Tang, W., Teumer, A., Marioni, R. E., Grossmann, V., Hottenga, J. J., Trompet, S., Müller-Nurasyid, M., Zhao, J. H., Brody, J. A., Kleber, M. E., Guo, X., Wang, J. J., Auer, P. L., Attia, J. R., Yanek, L. R., Ahluwalia, T. S., Lahti, J., Venturini, C., Tanaka, T., Bielak, L. F., Joshi, P. K., Rocanin-Arjo, A., Kolcic, I., Navarro, P., Rose, L. M., Oldmeadow, C., Riess, H., Mazur, J., Basu, S., Goel, A., Yang, Q., Ghanbari, M., Willemsen, G., Rumley, A., Fiorillo, E., de Craen, A. J. M., Grotevendt, A., Scott, R., Taylor, K. D., Delgado, G. E., Yao, J., Kifley, A., Kooperberg, C., Qayyum, R., Lopez, L. M., Berentzen, T. L., Räikkönen, K., Mangino, M., Bandinelli, S., Peyser, P. A., Wild, S., Tregouët, D.-A., Wright, A. F., Marten, J., Zemunik, T., Morrison, A. C., Sennblad, B., Tofler, G., de Maat, M. P. M., de Geus, E. J. C., Lowe, G. D., Zoledziewska, M., Sattar, N., Binder, H., Völker, U., Waldenberger, M., Khaw, K.-T., Mcknight, B., Huang, J., Jenny, N. S., Holliday, E. G., Qi, L., Mcevoy, M. G., Becker, D. M., Starr, J. M., Sarin, A.-P., Hysi, P. G., Hernandez, D. G., Jhun, M. A., Campbell, H., Hamsten, A., Rivadeneira, F., Mcardle, W. L., Slagboom, P. E., Zeller, T., Koenig, W., Psaty, B. M., Haritunians, T., Liu, J., Palotie, A., Uitterlinden, A. G., Stott, D. J., Hofman, A., Franco, O. H., Polasek, O., Rudan, I., Morange, P.-E., Wilson, J. F., Kardia, S. L. R., Ferrucci, L., Spector, T. D., Eriksson, J. G., Hansen, T., Deary, I. J., Becker, L. C., Scott, R. J., Mitchell, P., März, W., Wareham, N. J., Peters, A., Greinacher, A., Wild, P. S., Jukema, J. W., Boomsma, D. I., Hayward, C., Cucca, F., Tracy, R., Watkins, H., Reiner, A. P., Folsom, A. R., Ridker, P. M., O'Donnell, C. J., Smith, N. L., Strachan, D. P., Dehghan, A.
    Oxford University Press
    Details
    Publication Date: 2016-01-09
    Description: Genome-wide association studies have previously identified 23 genetic loci associated with circulating fibrinogen concentration. These studies used HapMap imputation and did not examine the X-chromosome. 1000 Genomes imputation provides better coverage of uncommon variants, and includes indels. We conducted a genome-wide association analysis of 34 studies imputed to the 1000 Genomes Project reference panel and including ~120 000 participants of European ancestry (95 806 participants with data on the X-chromosome). Approximately 10.7 million single-nucleotide polymorphisms and 1.2 million indels were examined. We identified 41 genome-wide significant fibrinogen loci; of which, 18 were newly identified. There were no genome-wide significant signals on the X-chromosome. The lead variants of five significant loci were indels. We further identified six additional independent signals, including three rare variants, at two previously characterized loci: FGB and IRF1 . Together the 41 loci explain 3% of the variance in plasma fibrinogen concentration.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 5
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    Biogeochemistry and microbiology of groundwater during acetate and bicarbonate amendment to an alluvial aquifer (2015)
    PANGAEA
    In:  Supplement to: Long, Philip E; Williams, Kenneth H; Davis, James A; Fox, Patricia M; Wilkins, Michael J; Yabusaki, Steven B; Fang, Yilin; Waichler, Scott R; Berman, Elena S F; Gupta, Manish; Chandler, Darrell P; Murray, Chris; Peacock, Aaron D; Giloteaux, Ludovic; Handley, Kim M; Lovley, Derek R; Banfield, Jillian F (2015): Bicarbonate impact on U(VI) bioreduction in a shallow alluvial aquifer. Geochimica et Cosmochimica Acta, 150, 106-124, https://doi.org/10.1016/j.gca.2014.11.013
    Details
    Publication Date: 2024-05-25
    Description: Field-scale biostimulation and desorption tracer experiments conducted in a uranium (U) contaminated, shallow alluvial aquifer have provided insight into the coupling of microbiology, biogeochemistry, and hydrogeology that control U mobility in the subsurface. Initial experiments successfully tested the concept that Fe-reducing bacteria such as Geobacter sp. could enzymatically reduce soluble U(VI) to insoluble U(IV) during in situ electron donor amendment (Anderson et al., 2003; Williams et al., 2011). In parallel, in situ desorption tracer tests using bicarbonate amendment demonstrated rate-limited U(VI) desorption (Fox et al., 2012). These results and prior laboratory studies underscored the importance of enzymatic U(VI)-reduction and suggested the ability to combine desorption and bioreduction of U(VI). Here we report the results of a new field experiment in which bicarbonate-promoted uranium desorption and acetate amendment were combined and compared to an acetate amendment-only experiment in the same experimental plot. Results confirm that bicarbonate amendment to alluvial aquifer sediments desorbs U(VI) and increases the abundance of Ca-uranyl-carbonato complexes. At the same time, the rate of acetate-promoted enzymatic U(VI) reduction was greater in the presence of added bicarbonate in spite of the increased dominance of Ca-uranyl-carbonato aqueous complexes. A model-simulated peak rate of U(VI) reduction was ~3.8 times higher during acetate-bicarbonate treatment than under acetate-only conditions. Lack of consistent differences in microbial community structure between acetate-bicarbonate and acetate-only treatments suggest that a significantly higher rate of U(VI) reduction in the bicarbonate-impacted sediment may be due to a higher intrinsic rate of microbial reduction induced by elevated concentrations of the bicarbonate oxyanion. The findings indicate that bicarbonate amendment may be useful in improving the engineered bioremediation of uranium in aquifers.
    Type: Dataset
    Format: application/zip, 3 datasets
    Location Call Number Limitation Availability
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    DATA PANGAEA
  • 6
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    (Tab 3) Signal to noise ratio (SNR) by genus for microarray probes in an alluvial aquifer along the Colorado River in Rifle, Colorado, USA (2015)
    PANGAEA
    Details
    Publication Date: 2024-05-25
    Keywords: Calculated; Colorado, U.S.A., North America; Date; DATE/TIME; Depth, relative; ELEVATION; Elevation 2; LATITUDE; LONGITUDE; Rilfe; Sample code/label; Sampling Well; Signal/noise ratio; WELL
    Type: Dataset
    Format: text/tab-separated-values, 2386 data points
    Location Call Number Limitation Availability
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    DATA PANGAEA
  • 7
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    (Tab 1) Biogeochemistry of groundwater during acetate and bicarbonate amendment to an alluvial aquifer along the Colorado River in Rifle, Colorado, USA (2015)
    PANGAEA
    Details
    Publication Date: 2024-05-25
    Keywords: Acetate; Aluminium; Aluminium, standard deviation; Arsenic; Arsenic, standard deviation; Barium, standard deviation; Barium 2+; Boron; Boron, standard deviation; Bromide; Bromine; Bromine, standard deviation; Calcium; Calcium, standard deviation; Carbon, inorganic, total; Chloride; Chromium; Chromium, standard deviation; Cobalt; Cobalt, standard deviation; Colorado, U.S.A., North America; Conductivity, electrolytic; Damage rate, standard deviation; DATE/TIME; Depth, logging; Depth, relative; ELEVATION; Elevation 2; Iron; Iron, standard deviation; Iron 2+; LATITUDE; Lithium; Lithium, standard deviation; LONGITUDE; Magnesium; Magnesium, standard deviation; Manganese; Manganese, standard deviation; Molybdenum; Molybdenum, standard deviation; pH; Potassium; Rilfe; Rubidium; Rubidium, standard deviation; Sample code/label; Sampling Well; Selenium; Selenium, standard deviation; Silicate; Silicate, standard deviation; Sodium; Sodium, standard deviation; Strontium, standard deviation; Strontium 2+; Sulfate; Sulfide; Thiosulfate; Titanium; Titanium, standard deviation; Uranium; Uranium, standard deviation; Vanadium; Vanadium, standard deviation; Water level; WELL; Zinc; Zinc, standard deviation; δ18O; δ18O, standard deviation; δ34S; δ34S, standard deviation; δ Deuterium; δ Deuterium, standard deviation
    Type: Dataset
    Format: text/tab-separated-values, 58204 data points
    Location Call Number Limitation Availability
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    DATA PANGAEA
  • 8
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    (Tab 2) Average signal to noise ratio (SNR) for individual microarray probes in an alluvial aquifer along the Colorado River in Rifle, Colorado, USA (2015)
    PANGAEA
    Details
    Publication Date: 2024-05-25
    Keywords: 20-mer oligonucleotide; Calculated; Colorado, U.S.A., North America; DATE/TIME; Depth, relative; ELEVATION; Elevation 2; Fluorescent dye, Cyanine 3; Hybridization marker; LATITUDE; LONGITUDE; Rilfe; Sample code/label; Sampling Well; Signal/noise ratio; WELL
    Type: Dataset
    Format: text/tab-separated-values, 8480 data points
    Location Call Number Limitation Availability
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    DATA PANGAEA
  • 9
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    Conserving Shells in Kenya. (2015)
    Details
    Publication Date: 2021-05-19
    Description: Over-collecting of shells on the Kenya coast, mainly for sale to tourists, has almost denuded some popular and accessible sites. In some formerly rich areas few molluscs can now be found, and collecting has shifted to more inaccessible sites. The authors describe an investigation they made in 1972 and 1974 into stocks held by dealers and the effects on the wild populations. They emphasise the importance of the marine national parks at Malindi and Watamu, where regular patrolling effectively prevents collecting and there are signs that cowries at least may now be re-establishing themselves. The creation of a third and much larger marine national park, near Shimoni, will protect another area rich in shells.
    Description: Published
    Keywords: Shells ; Animal products ; Marine parks ; Protected areas ; Resource development ; Exploitation
    Repository Name: AquaDocs
    Type: Journal Contribution , Not Known
    Format: pp.480-485
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    PAPER (OA)
  • 10
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    Regenerative capacity in the lamprey spinal cord is not altered after a repeated transection (2019)
    Public Library of Science
    Details
    Publication Date: 2022-05-25
    Description: © The Author(s), 2019. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in PLoS One 14(1), (2019):e0204193, doi: 10.1371/journal.pone.0204193.
    Description: The resilience of regeneration in vertebrates is not very well understood. Yet understanding if tissues can regenerate after repeated insults, and identifying limitations, is important for elucidating the underlying mechanisms of tissue plasticity. This is particularly challenging in tissues, such as the nervous system, which possess a large number of terminally differentiated cells and often exhibit limited regeneration in the first place. However, unlike mammals, which exhibit very limited regeneration of spinal cord tissues, many non-mammalian vertebrates, including lampreys, bony fishes, amphibians, and reptiles, regenerate their spinal cords and functionally recover even after a complete spinal cord transection. It is well established that lampreys undergo full functional recovery of swimming behaviors after a single spinal cord transection, which is accompanied by tissue repair at the lesion site, as well as axon and synapse regeneration. Here we begin to explore the resilience of spinal cord regeneration in lampreys after a second spinal transection (re-transection). We report that by all functional and anatomical measures tested, lampreys regenerate after spinal re-transection just as robustly as after single transections. Recovery of swimming, synapse and cytoskeletal distributions, axon regeneration, and neuronal survival were nearly identical after spinal transection or re-transection. Only minor differences in tissue repair at the lesion site were observed in re-transected spinal cords. Thus, regenerative potential in the lamprey spinal cord is largely unaffected by spinal re-transection, indicating a greater persistent regenerative potential than exists in some other highly regenerative models. These findings establish a new path for uncovering pro-regenerative targets that could be deployed in non-regenerative conditions.
    Description: The authors would like to thank Dr. Cristina Roman-Vendrell and Louie Kerr, Director of the Central Microscopy Facility at the MBL, for technical support. We also thank Dr. Juan Diaz-Quiroz for helpful comments on the manuscript. EG was supported in part by an NSF REU Award (#1659604: Biological Discovery in Woods Hole at the Marine Biological Laboratory).
    Repository Name: Woods Hole Open Access Server
    Type: Article
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