Relevant bibliographies by topics / Polymorphismus

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Polymorphismus'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Polymorphismus"

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Strobel, Alexander, Burkhard Brocke, and Richard P. Ebstein. "Interaktionseffekte Monoamin-relevanter genetischer Polymorphismen mit Traits des TPQ." Zeitschrift für Differentielle und Diagnostische Psychologie 21, no. 3 (September 2000): 191–99. http://dx.doi.org/10.1024//0170-1789.21.3.191.

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Zusammenfassung: Fortschritte in der Molekulargenetik ermöglichen es, den Erklärungsbeitrag genetischer Polymorphismen mit funktioneller Relevanz zum genetischen Hintergrund der Erblichkeitskomponente einiger Persönlichkeitstraits zu untersuchen. Bisherige Befunde sprechen für potentielle Assoziationen eines Polymorphismus im Dopamin-D4-Rezeptor-Gen (DRD4 Exon 3) mit der Dimension Novelty Seeking (NS) des Tridimensional Personality Questionnaire (TPQ) sowie eines Polymorphismus des Serotonin-Transporter-Gens (5-HTTLPR) mit TPQ Harm Avoidance (HA). Die Betrachtung von Interaktionen dieser Polymorphismen kann einen Beitrag zur Klärung von Inkonsistenzen in bisherigen Assoziationsstudien leisten. In der vorliegenden Arbeit wurden für 134 Personen Interaktionen von DRD4 Exon 3 und 5-HTTLPR sowie einem Polymorphismus des Gens für COMT auf die Faktorwerte der TPQ-Subskalen überprüft. Es zeigten sich Tendenzen zu Interaktionen zwischen DRD4 Exon 3 und 5-HTTLPR bei dem HA-Faktor sowie zwischen DRD4 Exon 3 und dem COMT-Polymorphismus bei dem NS-Faktor.
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Khaw, A. V., and Ch Kessler. "Schlaganfall." Hämostaseologie 26, no. 04 (2006): 287–97. http://dx.doi.org/10.1055/s-0037-1616973.

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ZusammenfassungDer Schlaganfall stellt eine große globale gesundheitspolitische und ökonomische Herausforderung dar. Die Eindämmung des Schlaganfalls kann nur durch genaue Kenntnis der Risikofaktoren und ggf. präventive Intervention erfolgen. Es werden unbeeinflussbare biologische Faktoren (z. B. Geschlecht, Lebensalter, ethnische Herkunft) von proatherosklerotischen bzw. prothrombotischen Risikofaktoren (Hypertonie, Diabetes mellitus, Fettstoffwechselstörungen, serologische und hämostaseologische Faktoren) und kardialer Komorbidität unterschieden. Immer wichtiger werden so genannte Lifestyle-Faktoren (z. B. Rauchen, körperliche Inaktivität und Alkoholkonsum). Neben diesen traditionellen Risikofaktoren hat in den vergangenen Jahren die Beschäftigung mit den genetischen Grundlagen des Schlaganfalls enorm zugenommen. Bei der Suche nach Kandidatengenen werden genetische Varianten (Polymorphismen) funktionell relevanter Gene in Fallkontrollstudien untersucht. Metaanalysen haben eine signifikante Assoziation des Faktor-V-Leiden-Arg506Gln-Polymorphismus, des MTHFR-C677T-Polymorphismus und des ACE-Insertions- Deletions-Polymorphismus zum Schlaganfall gezeigt. Große Hoffnung wird auf populationsbasierte, genomweite Linkage-Analysen gesetzt.
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Annamalai, Karthikeyan, Karl-Heinz Gührs, Rolf Koehler, Matthias Schmidt, Henri Michel, Cornelia Loos, Patricia M. Gaffney, et al. "Polymorphismus von Amyloidfibrillen in vivo." Angewandte Chemie 128, no. 15 (March 8, 2016): 4903–6. http://dx.doi.org/10.1002/ange.201511524.

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Eisenhardt, A., A. Scherag, M. Kempin, K. H. Jöckel, and H. Rübben. "Genotyp des GNB3-C825T-Polymorphismus." Der Urologe 50, no. 9 (July 8, 2011): 1137–42. http://dx.doi.org/10.1007/s00120-011-2621-8.

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Baier, Monika, Ekkehard Haen, and Peter Lauer. "COMT-Polymorphismus und GST-Mangel." NeuroTransmitter 24, no. 4 (April 2013): 49–52. http://dx.doi.org/10.1007/s15016-013-0140-0.

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Schmid, D. O., and D. R. Osterhoff. "Über den Hämoglobin-Polymorphismus beim Zebra." Zentralblatt für Veterinärmedizin Reihe A 14, no. 1 (May 13, 2010): 91–92. http://dx.doi.org/10.1111/j.1439-0442.1967.tb00218.x.

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Mayer, Björn, and Heribert Schunkert. "ACE-Gen-Polymorphismus und kardiovaskuläre Erkrankungen." Herz 25, no. 1 (February 2000): 1–6. http://dx.doi.org/10.1007/bf03044118.

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Pfeilschifter, J. "Genetik der Osteoporose: Der COLIA1-Sp1-Polymorphismus. Genetics of Osteoporosis: The COLIA1-Sp1-Polymorphism." Laboratoriums Medizin 27, no. 3-4 (May 2003): 92–99. http://dx.doi.org/10.1046/j.1439-0477.2003.03016.x.

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Pfeilschifter, J. "Genetik der Osteoporose: Der COLIA1-Sp1-Polymorphismus/Genetics of Osteoporosis: The COLIA1-Sp1-Polymorphism." LaboratoriumsMedizin 27, no. 3/4 (January 1, 2003): 92–99. http://dx.doi.org/10.1515/labmed.2003.015.

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Rohrbacher, H., and K. Zetner. "Blutgruppen und biochemischer Polymorphismus in österreichischen Rinderrassen." Zeitschrift für Tierzüchtung und Züchtungsbiologie 88, no. 1-4 (April 26, 2010): 279–90. http://dx.doi.org/10.1111/j.1439-0388.1971.tb01375.x.

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Dissertations / Theses on the topic "Polymorphismus"

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Kaes, Stefan. "Parametrischer Polymorphismus, Überladungen und Konversionen." [S.l.] : [s.n.], 2005. http://elib.tu-darmstadt.de/diss/000544.

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Ehlers, Anke. "HLA-gekoppelte olfaktorische Rezeptorgene: Polymorphismus- und Expressionsanalyse." [S.l. : s.n.], 2001. http://www.diss.fu-berlin.de/2002/48/index.html.

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Gick, Claudia. "Polymorphismus der Chicken Ig-like Receptors (CHIRs)." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-96779.

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Storz, Kristina Ulrike Anna. "Polymorphismen des IL-6-Rezeptor-Gens ( +24013 A/G: Ala31Ala; +48892 A/C: Asp358Ala ), des IL-8-Rezeptor-Gens ( +2607G/C:Ser/Thr )und des TNFalpha-Gens -238 ( G/A ) bei M. Behçet." [S.l. : s.n.], 2006.

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Hummel, Thomas. "Methylen-Tetrahydrofolat-Reduktase-Polymorphismus, Hyperhomocysteinämie und Morbus Parkinson." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=962689394.

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Büeler, Thomas. "Casein-Polymorphismus und gerinnungsrelevante Eigenschaften von Milch Schweizerischer Ziegenrassen /." [S.l.] : [s.n.], 2002. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=14876.

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Bourakkadi, Zarrouki Driss. "Die Wirkung des BDNF-Polymorphismus auf trankraniell induzierte Neuroplastizität." Doctoral thesis, Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2013. http://hdl.handle.net/11858/00-1735-0000-000D-F681-8.

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Groß, Andreas [Verfasser]. "Polymorphismus biologischer Makromoleküle in Zellen : Eine Elektronenspinresonanzspektroskopiestudie / Andreas Groß." Konstanz : Bibliothek der Universität Konstanz, 2015. http://d-nb.info/1109923236/34.

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Wang, Yean. "Phylogeny, pedigree, and population structure studies application of molecular polymorphisms." Saarbrücken VDM Verlag Dr. Müller, 2007. http://d-nb.info/98875634X/04.

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Lauer, Nadine. "Assoziation von Genpolymorphismen mit der Cholelithiasis." [S.l. : s.n.], 2009. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-67027.

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Books on the topic "Polymorphismus"

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NATO Advanced Research Workshop on DNA Polymorphisms as Disease Markers (1990 London, England). DNA polymorphisms as disease markers. New York: Plenum Press, 1991.

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D, Varfolomeyev S., and Zaikov Gennadiĭ Efremovich, eds. Molecular polymorphism of man: Structural and functional individual multiformity of biomacromolecules. Hauppauge, NY: Nova Science Publishers, 2009.

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Kwok, Pui-Yan. Single Nucleotide Polymorphisms. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592593275.

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Sauna, Zuben E., and Chava Kimchi-Sarfaty, eds. Single Nucleotide Polymorphisms. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-05616-1.

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Komar, Anton A., ed. Single Nucleotide Polymorphisms. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-411-1.

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Hannan, Anthony J., ed. Tandem Repeat Polymorphisms. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5434-2.

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Roychoudhury, Arun K. Human polymorphic genes: World distribution. New York: Oxford University Press, 1988.

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Masatoshi, Nei, ed. Humanpolymorphic genes. New York: Oxford University Press, 1988.

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Single nucleotide polymorphisms: Methods and protocols. 2nd ed. New York: Humana, 2009.

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Stanley, H. Eugene, ed. Liquid Polymorphism. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118540350.

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Book chapters on the topic "Polymorphismus"

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Aupperle, Martin. "Polymorphismus." In Programmierhandbuch Visual C++ Version 1.5, 487–502. Wiesbaden: Vieweg+Teubner Verlag, 1994. http://dx.doi.org/10.1007/978-3-322-87231-9_21.

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Arnemann, J. "Polymorphismus." In Springer Reference Medizin, 1913. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_3559.

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Arnemann, J. "Polymorphismus." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_3559-1.

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Dankert, Jürgen. "Polymorphismus." In Informatik & Praxis, 106–42. Wiesbaden: Vieweg+Teubner Verlag, 1998. http://dx.doi.org/10.1007/978-3-322-92730-9_5.

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Duschl, Dieter. "Polymorphismus." In Softwareentwicklung mit C++, 305–24. Wiesbaden: Springer Fachmedien Wiesbaden, 2017. http://dx.doi.org/10.1007/978-3-658-18123-9_10.

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Duschl, Dieter. "Polymorphismus." In Softwareentwicklung mit C++, 293–312. Wiesbaden: Springer Fachmedien Wiesbaden, 2014. http://dx.doi.org/10.1007/978-3-658-01586-2_10.

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Toepfer, Georg. "Polymorphismus." In Historisches Wörterbuch der Biologie, 111–13. Stuttgart: J.B. Metzler, 2011. http://dx.doi.org/10.1007/978-3-476-00461-1_6.

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Aupperle, Martin. "Fallstudie „Polymorphismus“." In Die Kunst der objektorientierten Programmierung mit C++, 645–67. Wiesbaden: Vieweg+Teubner Verlag, 1997. http://dx.doi.org/10.1007/978-3-322-96868-5_23.

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Aupperle, Martin. "Fallstudie Polymorphismus." In Die Kunst der Programmierung mit C++, 787–820. Wiesbaden: Vieweg+Teubner Verlag, 2002. http://dx.doi.org/10.1007/978-3-663-07766-4_34.

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Aupperle, Martin. "Polymorphismus: Zwei Fallstudien." In Objektorientiert mit TURBO C++, 341–79. Wiesbaden: Vieweg+Teubner Verlag, 1992. http://dx.doi.org/10.1007/978-3-322-93857-2_11.

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Conference papers on the topic "Polymorphismus"

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Mederacke, YS, M. Kirstein, S. Marhenke, F. Metzler, MP Manns, A. Vogel, and I. Mederacke. "PNPLA3 Polymorphismus ist bei Patienten mit Autoimmunhepatitis mit einem schwereren Krankheitsverlauf assoziiert." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695581.

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Fischer, J., E. Koukoulioti, T. Müller, B. Fueloep, R. Heyne, T. Berg, and F. van Bömmel. "Assoziation des Polymorphismus rs7000921 im INTS10-Gen mit der Leberzirrhose bei kaukasischen Patienten mit chronischer Hepatitis B." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695325.

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Schiergens, T., S. Zehl, R. Al-Sayegh, P. Ganschow, F. Beigel, T. Olzsak, M. Siebeck, et al. "Relevanz des NOD2 Polymorphismus sowie inter-enterischer Fisteln für das Auftreten postoperativer Komplikationen nach Ileozökalresektion bei Morbus Crohn." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604811.

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Roth, A., J. Muth, G. Piontek, M. Buchberger, M. Wirth, and A. Pickhard. "Einfluss des Phe31-Ile Polymorphismus der AurkA als prädiktiver Marker auf die Empfänglichkeit von HNSCC-Patienten für eine Cetuximabtherapie." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685910.

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Koukoulioti, E., J. Fischer, E. Schott, B. Fülöp, R. Heyne, T. Berg, and F. van Bömmel. "Assoziation eines Polymorphismus im Toll-like-Rezeptor 5-Gen mit der Entwicklung von hepatozellulären Karzinomen bei Patienten mit chronischer Hepatitis B-Virusinfektion." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1605019.

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Chan, Vivian, V. W. S. Liu, A. C. K. Wong, and T. K. Chan. "DNA POLYMORPHISMS IN OR LINKED TO THE FACTOR VIII GENE IN CHINESE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644049.

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78 unrelated X chromosomes from Southern Chinese (56 normal and 22 haemophiliac) were studied. DNA was restricted by Bel I, Bgl I or Taq I and hybridized to 3' factor VIII:C cDNA probe (5 kb, Chiron) or St 14.1 probe(3 kb, Oberle &Mandel) by standard techniques. The intragenic Bel I polymorphic site was positive in 82%, while Bgl I polymorphic site was positive in all. Thus, 29.5%(2 x×0.82 × 0.18) of Chinese females carried the Bel I polymorphism. Asto the Taq I polymorphism in the closely linked DXS52 DNA segment, the incidences for the various alleles were :System I - allele (3) 10.2%, (4) 2.6%, (5) 2.6%,(6) 17.9%, (7) 21.8% and (8) 44.9% System II - α a allele 56%, 6 allele 44%. Approximately 80% of females were heterozygous for two different alleles. Hence the Bel I and Taq I polymorphisms can be used to track the defective factor VIII gene for carrier detection and prenatal diagnosis. Furthermore, their frequencies in the Chinese are different from those previously reported in other ethnic groups.
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Rezende, Rubens Barbosa, and Larissa Teodoro. "Presence of genetic polymorphisms may impact on predisposition to Parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.004.

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Introduction: Parkinson’s disease (PD) is characterized by the degeneration and loss of dopaminergic neurons in the black substantia and the formation of Lewy bodies, thus being considered a neurodegenerative disease. Thus, the objective was to understand the impact of polymorphisms in the predisposition to PD. Methods: It’s a narrative review of literature in the PubMed and SciELO databases, using the descriptors: “Polymorphism, Single Nucleotide” and “Parkinson disease”, registered in DeCS/MeSH, and using the Boolean operator AND. The inclusion criteria were: complete articles and made available free of charge, published in English, Spanish and Portuguese, between 2016 and January 2021. Results: After the research, 167 publications were found and seven were included. The data from the first study indicate that the rs33949390 of the LRRK2 gene helps in predisposition to PD in Asian populations, mainly Chinese. The second study indicated that the NFE2L2 rs6721961 allele was linked to a reduced risk of PD. The third study found that the GSK3B rs1732170, STK11 rs8111699, SNCA rs356219 and FCHSD1 rs456998 polymorphisms were linked to a high risk of PD. The fourth study found that the SNCA variants rs7684318, rs356220, rs356203 and rs2736990 were linked to the disease and were at high risk of developing PD in the Mexican population. The fifth and sixth study are meta-analyzes, the fifth confirming the lower allele rs11558538 of HNMT is associated with a reduced risk of developing PD. And the sixth assumes a possible link between CCDC62 rs12817488 and the risk of PD in the Chinese population. Conclusion: However, the analyzed data indicate that the polymorphisms contributed to the susceptibility to PD, however further studies related to the polymorphisms and their relationship to PD are still needed for more ethnic groups, and thus early diagnosis is possible.
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Greverath, LM, E. Leicht, N. Wald de Chamorro, ACB Wilde, LM Pohlan, D. Paclik, J. Fischer, T. Berg, F. Tacke, and T. Müller. "Assoziation des rs4620530 Single Nucleotide Polymorphismus im muskarinergen Acetylcholinrezeptor Typ 3 Gen mit der primär biliären Cholangitis – eine retrospektive Analyse aus zwei universitären Zentren." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695246.

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Graham, J. B., D. B. Lubahn, J. D. Kirshtein, S. T. Lord, I. M. Nilsson, A. Wallmark, R. Ljung, et al. "THE “MALMO“ EPITOPE OF FACTOR IX: PHENOTYPIC EXPRESSION OF THE “VIKING“ GENE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643566.

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The epitope of a mouse monoclonal AB (9.9) which detects a Factor IX (F.IX) polymorphism in the plasma of normal persons (PNAS 82:3839, 1985) has been related to not more than 6 AA residues of F.IX by recombinant DNA technology. The same 6 residues define Smith’s polymorphic epitope (Am. J. Human Genet. 37:688, 1985 and in press). This region of F.IX contains the alanine:threonine dimorphism at residue 148 first suggested by McGraw et al. (PNAS 82: 2847, 1985) and established by Winship and Brownlee with synthetic DNA oligomers (Lancet in press). Using synthetic DNA probes, we have found that the DNA difference between positive and negative reactors to 9.9 is whether base pair 20422, the first pair in the codon for residue 148, is A:T or G:C. We can conclude that 9.9 reacts with F.IX containing threonine but not alanine at position 148.The F.IX immunologic polymorphism-whose epitope we are referring to as “Malmo”-is, not surprisingly, in strong linkage disequilibrium with two F.IX DNA polymorphisms, TaqI and Xmnl. The highest frequency of the rarer Malmo allele in 6 disparate ethnic groups was in Swedes (32%); a lower frequency (14%) was seen in White Americans whose ancestors came overwhelmingly from the Celtic regions of the British Isles; it was at very low frequency or absent in Black Americans, East Indians, Chinese and Malays. A maximum frequency in Swedes and absence in Africans and Orientals suggest that the transition from A:T to G:C occurred in Scandinavia and spread from there. The history of Europe and America plus the geographical distribution of the rare allele lead us to suggest that this locus might be designated: “the Viking gene”.
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Guijun Wang and A. Ambler. "Invocation polymorphism." In Proceedings of Symposium on Visual Languages. IEEE, 1995. http://dx.doi.org/10.1109/vl.1995.520789.

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Reports on the topic "Polymorphismus"

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Zou, Chenghui, Weng Zhang, Mao Li, Dan He, Yujie Han, and Mao Lu. A meta-analysis of association between CCL5、CCL11、CCL17 polymorphisms and AD. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0148.

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Review question / Objective: At present, many studies on the association between CCL5、CCL11、CCL17 polymorphisms and atopic dermatitis（AD）are inconsistent. We conducted this meta-analysis of Case control trial to evaluate the association between CCL5、CCL11、CCL17 polymorphisms and atopic dermatitis（AD). Condition being studied: Since the discovery of cytokines, and in particular the role of chemokines in the progression of AD, many clinical studies have been carried out around the world to explore the association of AD with chemokine polymorphism. However, the quality, type and conclusions of studies on the correlation between chemokine polymorphism and AD are inconsistent. Foreign studies have shown that chemokine polymorphism is statistically significant in relation to AD. Studies by Menzies-Gow A et al have shown that a new therapeutic strategy targeting to block CCL11 signal has been proven to significantly improve patients with moderate to severe AD. However, some foreign studies have also reported that chemokine polymorphism is unrelated to AD.
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Weller, Joel I., Derek M. Bickhart, Micha Ron, Eyal Seroussi, George Liu, and George R. Wiggans. Determination of actual polymorphisms responsible for economic trait variation in dairy cattle. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600017.bard.

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The project’s general objectives were to determine specific polymorphisms at the DNA level responsible for observed quantitative trait loci (QTLs) and to estimate their effects, frequencies, and selection potential in the Holstein dairy cattle breed. The specific objectives were to (1) localize the causative polymorphisms to small chromosomal segments based on analysis of 52 U.S. Holstein bulls each with at least 100 sons with high-reliability genetic evaluations using the a posteriori granddaughter design; (2) sequence the complete genomes of at least 40 of those bulls to 20 coverage; (3) determine causative polymorphisms based on concordance between the bulls’ genotypes for specific polymorphisms and their status for a QTL; (4) validate putative quantitative trait variants by genotyping a sample of Israeli Holstein cows; and (5) perform gene expression analysis using statistical methodologies, including determination of signatures of selection, based on somatic cells of cows that are homozygous for contrasting quantitative trait variants; and (6) analyze genes with putative quantitative trait variants using data mining techniques. Current methods for genomic evaluation are based on population-wide linkage disequilibrium between markers and actual alleles that affect traits of interest. Those methods have approximately doubled the rate of genetic gain for most traits in the U.S. Holstein population. With determination of causative polymorphisms, increasing the accuracy of genomic evaluations should be possible by including those genotypes as fixed effects in the analysis models. Determination of causative polymorphisms should also yield useful information on gene function and genetic architecture of complex traits. Concordance between QTL genotype as determined by the a posteriori granddaughter design and marker genotype was determined for 30 trait-by-chromosomal segment effects that are segregating in the U.S. Holstein population; a probability of <10²⁰ was used to accept the null hypothesis that no segregating gene within the chromosomal segment was affecting the trait. Genotypes for 83 grandsires and 17,217 sons were determined by either complete sequence or imputation for 3,148,506 polymorphisms across the entire genome. Variant sites were identified from previous studies (such as the 1000 Bull Genomes Project) and from DNA sequencing of bulls unique to this project, which is one of the largest marker variant surveys conducted for the Holstein breed of cattle. Effects for stature on chromosome 11, daughter pregnancy rate on chromosome 18, and protein percentage on chromosome 20 met 3 criteria: (1) complete or nearly complete concordance, (2) nominal significance of the polymorphism effect after correction for all other polymorphisms, and (3) marker coefficient of determination >40% of total multiple-regression coefficient of determination for the 30 polymorphisms with highest concordance. The missense polymorphism Phe279Tyr in GHR at 31,909,478 base pairs on chromosome 20 was confirmed as the causative mutation for fat and protein concentration. For effect on fat percentage, 12 additional missensepolymorphisms on chromosome 14 were found that had nearly complete concordance with the suggested causative polymorphism (missense mutation Ala232Glu in DGAT1). The markers used in routine U.S. genomic evaluations were increased from 60,000 to 80,000 by adding markers for known QTLs and markers detected in BARD and other research projects. Objectives 1 and 2 were completely accomplished, and objective 3 was partially accomplished. Because no new clear-cut causative polymorphisms were discovered, objectives 4 through 6 were not completed.
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Raftogianis, Rebecca B. UGT1A9 Genetic Polymorphisms and Raloxifene Pharmacogenetics. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada405339.

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Raftogianis, Rebecca B. UGT1A9 Genetic Polymorphisms and Raloxifene Pharmacogenetics. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada416490.

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Deschamps, J. R., D. A. Parrish, and R. J. Butcher. Polymorphism in Energetic Materials. Fort Belvoir, VA: Defense Technical Information Center, January 2008. http://dx.doi.org/10.21236/ada517861.

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Ma, Long, Gang Jin, Yi Yang, Yao Pang, Wenhao Wang, Hongyi Zhang, Jiawei Liu, et al. Association Between CYP2A13 Polymorphisms and Lung Cancer. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2020. http://dx.doi.org/10.37766/inplasy2020.9.0102.

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Harper, Robert, and Greg Morrisett. Compiling with Non-Parametric Polymorphism. Fort Belvoir, VA: Defense Technical Information Center, February 1994. http://dx.doi.org/10.21236/ada290316.

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Harper, Robert, and Mark Lillibridge. Explicit Polymorphism and CPS Conversion,. Fort Belvoir, VA: Defense Technical Information Center, October 1992. http://dx.doi.org/10.21236/ada258635.

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Adami, Hans-Olov G., and Landegran. Estrogen Receptor Gene Polymorphisms and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, December 2000. http://dx.doi.org/10.21236/ada392392.

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Adami, Habs-Olov G., and Landegran. Estrogen Receptor Gene Polymorphisms and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, December 1999. http://dx.doi.org/10.21236/ada383021.

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