Relevant bibliographies by topics / Mammalian

Academic literature on the topic 'Mammalian'

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Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Mammalian"

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Kostopoulos, Dimitris S., Kalliopi K. Koliadimou, and George D. Koufos. "The giraffids (Mammalia, Artiodactyla) from the Late Miocene Mammalian localities of Nikiti (Macedonia, Greece)." Palaeontographica Abteilung A 239, no. 1-3 (April 23, 1996): 61–88. http://dx.doi.org/10.1127/pala/239/1996/61.

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Senter, Phil, and John G. Moch. "A critical survey of vestigial structures in the postcranial skeletons of extant mammals." PeerJ 3 (November 24, 2015): e1439. http://dx.doi.org/10.7717/peerj.1439.

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In the Mammalia, vestigial skeletal structures abound but have not previously been the focus of study, with a few exceptions (e.g., whale pelves). Here we use a phylogenetic bracketing approach to identify vestigial structures in mammalian postcranial skeletons and present a descriptive survey of such structures in the Mammalia. We also correct previous misidentifications, including the previous misidentification of vestigial caviid metatarsals as sesamoids. We also examine the phylogenetic distribution of vestigiality and loss. This distribution indicates multiple vestigialization and loss events in mammalian skeletal structures, especially in the hand and foot, and reveals no correlation in such events between mammalian fore and hind limbs.
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Braun, Thomas, and Thilo Borchardt. "Cardiovascular regeneration in non-mammalian model systems: What are the differences between newts and man?" Thrombosis and Haemostasis 98, no. 08 (2007): 311–18. http://dx.doi.org/10.1160/th07-02-0153.

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SummaryThe mammalian heart cannot regenerate substantial cardiac injuries, while certain non-mammalian vertebrates such as certain fish (Danio rerio) and amphibiae (Notophthalmus viridescens) are able to repair the heart without functional impairment. In mammalians, the prevailing repair process is accompanied by fibrosis and scarring, while zebrafish and newts can replace lost contractile tissue by newly formed cardiac muscle with only little or no scar formation.A better understanding of cardiac regeneration in non-mammalian vertebrates might provide new insights for the manipulation of regenerative pathways in the human heart. Here, we summarize the current knowledge in cardiac regeneration of newts and the principal differences to repair processes in mammalian hearts.
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Rogers, Nedra. "Mammalian." Fourth Genre: Explorations in Nonfiction 9, no. 1 (2007): 1–6. http://dx.doi.org/10.1353/fge.2007.0017.

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Armitage, Kenneth B. "Mammalian Function Mammalian Physiology J. Homer Ferguson." BioScience 37, no. 10 (November 1987): 748. http://dx.doi.org/10.2307/1310495.

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Behringer, Richard R., Guy S. Eakin, and Marilyn B. Renfree. "Mammalian diversity: gametes, embryos and reproduction." Reproduction, Fertility and Development 18, no. 2 (2006): 99. http://dx.doi.org/10.1071/rd05137.

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The class Mammalia is composed of approximately 4800 extant species. These mammalian species are divided into three subclasses that include the monotremes, marsupials and eutherians. Monotremes are remarkable because these mammals are born from eggs laid outside of the mother’s body. Marsupial mammals have relatively short gestation periods and give birth to highly altricial young that continue a significant amount of ‘fetal’ development after birth, supported by a highly sophisticated lactation. Less than 10% of mammalian species are monotremes or marsupials, so the great majority of mammals are grouped into the subclass Eutheria, including mouse and human. Mammals exhibit great variety in morphology, physiology and reproduction. In the present article, we highlight some of this remarkable diversity relative to the mouse, one of the most widely used mammalian model organisms, and human. This diversity creates challenges and opportunities for gamete and embryo collection, culture and transfer technologies.
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Ročková, Š., V. Rada, J. Havlík, R. Švejstil, E. Vlková, V. Bunešová, K. Janda, and I. Profousová. "Growth of bifidobacteria in mammalian milk." Czech Journal of Animal Science 58, No. 3 (March 4, 2013): 99–105. http://dx.doi.org/10.17221/6666-cjas.

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Microbial colonization of the mammalian intestine begins at birth, when from a sterile state a newborn infant is exposed to an external environment rich in various bacterial species. An important group of intestinal bacteria comprises bifidobacteria. Bifidobacteria represent major intestinal microbiota during the breast-feeding period. Animal milk contains all crucial nutrients for babies’ intestinal microflora. The aim of our work was to test the influence of different mammalian milk on the growth of bifidobacteria. The growth of seven strains of bifidobacteria in human milk, the colostrum of swine, cow’s milk, sheep’s milk, and rabbit’s milk was tested. Good growth accompanied by the production of lactic acid was observed not only in human milk, but also in the other kinds of milk in all three strains of Bifidobacterium bifidum of different origin. Human milk selectively supported the production of lactic acid of human bifidobacterial isolates, especially the Bifidobacterium bifidum species. The promotion of bifidobacteria by milk is species-specific. Human milk contains a key factor for the growth of specific species or strains of human-origin bifidobacteria compared to other kinds of milk. In contrast, some components (maybe lysozyme) of human milk inhibited the growth of Bifidobacterium animalis. Animal-origin strains of bifidobacteria were not able to significantly grow even in milk of animal origin, with the exception of B. animalis subsp. lactis 1,2, which slightly grew in sheep’s milk.
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Folin, Marcella, and Eva Contiero. "Electrophoretic analysis of mammalian hair keratins." Anthropologischer Anzeiger 54, no. 4 (December 12, 1996): 331–39. http://dx.doi.org/10.1127/anthranz/54/1996/331.

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Conley, A. "Mammalian aromatases." Reproduction 121, no. 5 (May 1, 2001): 685–95. http://dx.doi.org/10.1530/reprod/121.5.685.

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Salamat, Muhammad Khalid, Carola Munoz-Montesino, Mohammed Moudjou, Human Rezaei, Hubert Laude, Vincent Béringue, and Michel Dron. "Mammalian prions." Prion 7, no. 2 (March 2013): 131–35. http://dx.doi.org/10.4161/pri.23110.

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Dissertations / Theses on the topic "Mammalian"

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Godliman, N. I. "Mammalian transsulphuration." Thesis, Bucks New University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378101.

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Meijaard, Erik, and emeijaard@tnc org. "Solving Mammalian Riddles." The Australian National University. Faculty of Arts, 2004. http://thesis.anu.edu.au./public/adt-ANU20050924.221423.

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Since the mid 19th century, the biogeography of island South-East Asia has been the subject of much study. Early researchers explained many of the species distribution patterns by the rise and fall of sea levels and land. This and the work of other researchers culminated in a theory that emphasized the role of Pleistocene sea level low stands in species evolution. With the advent of newly developed molecular techniques, however, it became clear that many species divergence events had taken place before the Pleistocene and a biogeographical theory focusing on Pleistocene sea level changes was inadequate. In this research, I have developed a new biogeographic model that explains present-day distribution patterns and evolutionary relationships between species. I use this new model to explain 10 ‘mammalian riddles’, i.e. evolutionary or distribution patterns in selected mammal species groups that could not be explained with the existing theories. I developed the new model by analyzing the geological literature for this region, and by mapping palaeogeographical and palaeoenvironmental changes for the last 20 million years. In addition I compiled information on the palaeontological record for the region and on divergence times between taxa using a molecular clock assumption. These phylogenetic data were compared with the palaeomaps to assess whether particular divergence events could be correlated with certain palaeogeographical or palaeoenvironmental changes. The combination of these two information sources has resulted in a much-improved understanding of mammalian evolution in island SE Asia. Using this model it is now possible to relate important palaeoenvironmental events, such as the Late Miocene cooling, an Early–Middle Pliocene highstand, or the emergence and submergence of a land bridge between the Malay Peninsula and Java to evolutionary changes in species. I test the accuracy of the new model by analysing the relationships within several mammal groups using craniometric and molecular analysis. The observed relationships and deduced timing of divergence between taxa could in many cases be explained by the model, which indicates that it is relatively accurate. In addition, with the new model I have been able to find solutions to most mammalian riddles, although these results require further testing. Overall, I therefore believe I have made a significant contribution to the biogeographical understanding of island SE Asia.
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Whitford, C. "Mammalian somatostatin receptors." Thesis, University of Newcastle Upon Tyne, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356818.

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Palczewski, Grzegorz. "Mammalian Carotenoid Metabolism." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1467993233.

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Yurttas, Piraye. "Peptidylarginine deiminase 6 and the cytoplasmic lattices : mammalian regulators of maternal factor storage and localization necessary for embryonic genome activation and development /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1528353791&sid=6&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Croft, S. M. "Mammalian-wide interspersed repeats (MIRs) and their role in mammalian gene function and evolution." Thesis, Nottingham Trent University, 2009. http://irep.ntu.ac.uk/id/eprint/104/.

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Transposable elements (TEs) are ubiquitous components of plant and animal genomes and constitute more than ~45% of the human genome. Though originally considered as 'parasitic' or 'junk' DNA, TEs are now thought to have played a role in shaping genomes during evolution, contributing to genome plasticity and diversity. All classes of retrotransposons accumulate in the genome via a process termed retrotransposition, wherein the elements are reverse transcribed into RNA and inserted into the genome as DNA. Exaptation of these elements can provide additional or novel function for endogenous genes. Mammalian-wide interspersed repeats (MIRs) are short interspersed nuclear elements (SINEs), belonging to the non-autonomous class of retroelements and are found in all mammals. The recruitment of an MIR element by a gene may provide insight into mammalian evolution and gene function. The human genome was screened for genes that have exaptated MIR elements and the compiled dataset was analysed to determine any commonality which may suggest conserved function(s). Subsequently 1359 genes were identified that have exaptated MIR elements, constituting 5% of the total genes in the human genome. MIR elements may be multifunctional, as 1% of the total human genes contain MIRs that are spliced and/or are contributing to protein coding sequences. Subsequently sequence motifs were identified in the MIR consensus sequences which resemble canonical mammalian splice sites; therefore MIR elements recruited in the 5'-UTR and coding sequence may be a result of the exonisation of intronic elements. The MIR-containing transcripts are frequently expressed in neurological tissue, suggesting a role in neuronal function. Moreover a number of MIR-containing mRNA transcripts are known to be localised to the dendritic compartment of the neurone, and ciliated region of photoreceptors. Some of the localised mRNAs contain putative microRNA binding sites within the MIR sequence, and possible dsRNA structures were noted between MIR elements. It is proposed that exaptated MIR elements may be a source of cis-acting regulatory elements, involved in post-transcriptional control of gene expression, including localisation of mRNA to distinct intracellular compartments.
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Marcet, Ortega Marina. "Surveillance mechanisms in mammalian meiosis." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/387429.

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Per tal de protegir les cèl·lules germinals de sofrir inestabilitat genòmica, diversos mecanismes de control s’encarreguen de que la progressió de la meiosis sigui correcte. En mamífers, els espermatòcits que presenten defectes de recombinació o de la formació de la vesícula sexual pateixen un bloqueig a l’estadi de paquitè. Estudis previs del nostre laboratori descriuen que la via complex MRE11-ATM-CHK2 activa l’arrest dependent de recombinació en presència de trencaments de doble cadena (DSBs) no reparats. L’objectiu d’aquest treball ha estat identificar si els membres de la família p53, els quals són possibles substrats de ATM i CHK2, participen en l’activació del arrest depenent de recombinació. En una aproximació genètica, hem obtingut ratolins doble mutants portadors d’una mutació de un membre de la família p53 (p53, Tap63 o p73) en un fons defectiu per Trip13. La mutació de Trip13 causa defectes de recombinació, el qual activa l’arrest depenent de recombinació en els espermatòcits a l’estadi de paquitè. Per tant, hem estudiat com l’absència d’algun membre de la família p53 afectava aquest fenotip d’arrest el espermatòcits Trip13mod/mod. Els nostres resultats demostren que tant la deficiència de p53 com Tap63, però no p73, permeten que els espermatòcits progressin més enllà i arribin a l’estadi de paquitè tardà tot i acumular nombrosos DSBs no reparats. Addicionalment, l’absència de p53 o Tap63 resulta en una disminució del nombre d’espermatòcits apoptòtics a l’estadi de paquitè primerenc. Així, els nostres resultats indiquen que p53 i TAp63 són responsables d’activar l’arrest dependent de recombinació en els espermatòcits de ratolí. Tot i així, els espermatòcits doble mutants encara presenten un bloqueig a l’estadi de paquitè. Per tal d’estudiar si els espermatòcits doble mutants arresten a causa de l’activació de l’arrest depenent de la correcta formació de la vesícula sexual, hem analitzat la funcionalitat del MSCI en els mutants Trip13. Per tant, el fet de saltar-se l’arrest dependent de recombinació ens ha permès elucidar el paper de TRIP13 en el silenciament meiòtic, de manera que al fallar la vesícula sexual es desencadena l’apoptosi i bloqueig dels mutants Trip13. Aquests resultats infereixen que el bloqueig depenent de recombinació i el depenent de la correcta formació de la vesícula sexual, són mecanismes que s’activen per mecanismes genèticament separats. A partir de l’observació que TRIP13 és necessari per implementar el silenciament del MSCI, he dut a terme un anàlisis exhaustiu de la transcripció en els mutants de Trip13. Els nostres resultats de marcatge de RNA amb EU i activació de la RNA polimerasa II fosforilada (S2) suggereixen que la expressió de RNA en els espermatòcits mutants per Trip13 es troba incrementada en els estadis inicials de la meiosis. Addicionalment, la seqüenciació del RNA ha permès observar que els gens dels cromosomes sexuals i gens pre-meiòtics es troben sobre expressats en els mutants de Trip13, suggerint que TRIP13 és necessari per mantenir l’expressió d’aquests gens a nivells baixos. En conjunt, els resultats presentats en aquest treball contribueixen a entendre com els mecanismes de control regulen diversos passes crucials de la progressió de la profase meiòtica en els espermatòcits de mamífer.
In order to protect germinal cells from genomic instability, surveillance mechanisms ensure that meiosis occurs properly. In mammals, spermatocytes that display recombination or sex body defects experience an arrest at pachytene stage. Previous studies from our lab described that the MRE11 complex-ATM-CHK2 pathway activates the recombination-dependent arrest in the presence of unrepaired double strand breaks (DSBs). In this work we aimed to identify if p53 family members, which are putative targets of ATM and CHK2, participate in the activation of the recombination-dependent arrest. As a genetic approach, we bred double mutant mice carrying a mutation of a member of the p53 family (p53, TAp63, p73) in a Trip13 defective background. Trip13 mutation causes recombination defects, which activate the recombination-dependent arrest in pachytene-stage spermatocytes. Thus, we studied how the absence of p53 family members affected the arrest phenotype of Trip13mod/mod spermatocytes. Our data showed that p53 and TAp63 deficiency, but not p73, allowed spermatocytes to progress further into late pachynema, despite accumulating numerous unrepaired DBSs. In addition, lack of p53 or TAp63 resulted in a decrease of apoptotic spermatocytes at early pachytene stage. Therefore, our results indicate that p53 and TAp63 are responsible to activate the recombination-dependent arrest in mouse spermatocytes. Even though, double mutant spermatocytes still arrested at pachytene stage. To study if double mutant spermatocytes were arresting due to the activation of the sex body deficient arrest we analyzed MSCI functionality in Trip13 mutants. Thus, by bypassing the recombination-dependent arrest has allowed us to elucidate a role for TRIP13 protein in meiotic silencing, which consequently triggers apoptosis in double mutants at late pachytene stage due to sex body impairment. These results infer that the recombination-dependent and the sex-body deficient arrest are activated by two genetically separated mechanisms. From the observation that TRIP13 is required to implement MSCI silencing, we performed an exhaustive analysis of transcription in Trip13 mutants. Our results suggested that RNA expression in Trip13 mutants was increased in early meiotic stage spermatocytes, assessed by EU-labeling RNA and phosphorylated(S2)-RNA polymerase II. Moreover, RNA sequencing data highlighted the observation that sex chromosome genes and pre-meiotic genes are overexpressed in Trip13 mutants, suggesting that TRIP13 is required to maintain the expression of these genes at low levels. Overall, the data presented in this work contributes to the understanding on how surveillance mechanisms control several crucial steps of meiotic prophase progression in mammalian spermatocytes.
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Tsirigotis, Maria. "Mutational analysis of mammalian ubiquitin." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/29267.

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Much of what is known about the ubiquitin/proteasome pathway has been deduced from mutational analysis performed in the yeast model system. From the high level of conservation between yeast and mammalian ubiquitin it would be expected that expression of analogous ubiquitin isoforms in higher eukaryotes would result in similar phenotypes. A site directed mutagenesis approach was employed to investigate the phenotypes of expression of mutant ubiquitin in higher eukaryotes and in the in vivo setting of novel ubiquitin transgenic mice. It was found that Ub-EGFP fusion proteins are efficiently recognized and processed by ubiquitin specific proteases both in mammalian cells and in transgenic mice; the transgene-derived ubiquitin moiety was found to substitute for endogenous ubiquitin in poly-Ub chain assembly and ubiquitinated conjugates were recovered using standard purification methodologies. The expression of chain-terminating ubiquitin derivatives (K48R and K63R) predisposed cells to the toxic effects of misfolded proteins and sensitized cells to DNA damaging agents. In transgenic mice, the expression of K48R mutant ubiquitin was found to confer protective effects and delay the deterioration of Purkinje neurons in a mouse model of SCA-1. The neuroprotective effect of K48R mutant ubiquitin may be mediated though stabilization of key transcription factors whose loss figured in the normal course of the SCA1 disease. The expression of C-terminal variants in yeast has been proposed to have profound effects on ubiquitin metabolism. A mechanistically related mechanism has been proposed to contribute to the pathogenesis of Alzheimer's disease wherein transcriptional frameshifting of the ubiquitin B mRNA generates an aberrant ubiquitin protein (termed UBB+1) with an altered C-terminus. To investigate the constraints with regard to processing/conjugation and recycling of ubiquitin in higher eukaryotes a plethora of C-terminal ubiquitin variants were generated and introduced in mammalian cells as linear fusions with EGFP. Mutations that inactivate yeast ubiquitin did not abolish the function of ubiquitin in higher eukaryotes; C-terminal ubiquitin variants were processed by deubiquitinating enzymes and in some cases were found to conjugate to cellular proteins. The tolerance of mammalian cells to mutant ubiquitin may be attributable to loosened constraints that exist at the C-terminus due to mechanisms that couple deubiquitination, targeting and destruction of Ub-EGFP fusion proteins. Preliminary data suggest that prolonged exposure of cells of neuronal lineage to C-terminal ubiquitin variant as assessed in transgenic mice may result in perturbed ubiquitin homeostasis, a feature observed in the pathogenesis of Alzheimer's disease.
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Lau, Stephen S. K. "Gene silencing in mammalian cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ28435.pdf.

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Lee, Douglas P. "Glycerolipid metabolism in mammalian tissues." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2002. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ62649.pdf.

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Books on the topic "Mammalian"

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Ferguson, J. Homer. Mammalian physiology. Columbus: C.E. Merrill Pub. Co., 1985.

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Naaktgeboren, C. Mammalian birth. Basel: Roche, Information Service, Animal Nutrition Department, 1997.

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Peter, Lonai, ed. Mammalian development. Amsterdam, The Netherlands: Harwood Academic Publishers, 1996.

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Miles, Gilbert B., ed. Mammalian osteology. Columbia, Mo: Missouri Archaeological Society, 1990.

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Smith, Robert Elijah. Mammalian homeostasis. Burlington, N.C: Carolina Biological Supply Co., 1987.

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Ruvinsky, A., and J. A. Marshall Graves, eds. Mammalian genomics. Wallingford: CABI, 2005. http://dx.doi.org/10.1079/9780851999104.0000.

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Rozman, Damjana, and Rolf Gebhardt, eds. Mammalian Sterols. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39684-8.

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Mohamed B., Abou-Donia, ed. Mammalian Toxicology. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118683484.

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Malven, Paul V. Mammalian neuroendocrinology. Boca Raton, Fla: CRC Press, 1993.

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Janigro, Damir. Mammalian Brain Development. Totowa, NJ: Humana Press, 2009.

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Book chapters on the topic "Mammalian"

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Krietenstein, Nils, and Oliver J. Rando. "Mammalian." In Methods in Molecular Biology, 321–32. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2140-0_17.

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Skubic, Cene, and Damjana Rozman. "Sterols from the Post-Lanosterol Part of Cholesterol Synthesis: Novel Signaling Players." In Mammalian Sterols, 1–22. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39684-8_1.

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Smith, Caitlin J., John M. Dagle, and Kelli K. Ryckman. "Genetic Variability in Cholesterol Metabolism." In Mammalian Sterols, 23–40. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39684-8_2.

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Björkhem, Ingemar, and Ulf Diczfalusy. "Side-Chain Oxidized Oxysterols in Health and Disease." In Mammalian Sterols, 41–79. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39684-8_3.

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Keitel, Verena, Christoph G. W. Gertzen, Sven Schäfer, Caroline Klindt, Christina Wöhler, Kathleen Deutschmann, Maria Reich, Holger Gohlke, and Dieter Häussinger. "Bile Acids and TGR5 (Gpbar1) Signaling." In Mammalian Sterols, 81–100. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39684-8_4.

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Matz-Soja, Madlen. "Bile Acids as Regulatory Signalling Molecules." In Mammalian Sterols, 101–16. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39684-8_5.

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Fon Tacer, Klementina. "Oxysterols and Bile Acid Act as Signaling Molecules That Regulate Cholesterol Homeostasis: Nuclear Receptors LXR, FXR, and Fibroblast Growth Factor 15/19." In Mammalian Sterols, 117–43. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39684-8_6.

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Guengerich, F. Peter, and Francis K. Yoshimoto. "Cytochrome P450 Metabolism Leads to Novel Biological Sterols and Other Steroids." In Mammalian Sterols, 145–71. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39684-8_7.

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Abou-Donia, Mohamed B. "General Principles." In Mammalian Toxicology, 1–14. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118683484.ch1.

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Abou-Donia, Mohamed B. "Gases." In Mammalian Toxicology, 219–32. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118683484.ch10.

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Conference papers on the topic "Mammalian"

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Smith, Sonya T., and Richard Chadwick. "Nanofluidics of Mammalian Hearing." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-64729.

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The inner hair cell stereocilia bundle performs the role of transducer in mammalian hearing. Acoustic stimuli deflect the hair bundle to open ion channels, resulting in cation influx and the subsequent release of a neurotransmitter at the base of the cell. Hypotheses for this transduction include fluid shear-driven motion between the tectorial membrane and the reticular lamina to deflect the bundle. It is presumed that ‘molecular gates’ sense tension in tip-links that connect adjacent stepped rows of stereocilia to open the channels. However, almost nothing is known about the endolymphatic flow in the micron-sized gap surrounding the bundle and the nanoscale sized gaps between individual stereocilia rows and between individual bundles. Here we show with nanometer resolution, how each row of stereocilia, their associated tip links and gates and the corresponding flow patterns move in response to acoustical input.
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Lohmueller, Jason J. "Mammalian Synthetic Gene Networks." In GLSVLSI '15: Great Lakes Symposium on VLSI 2015. New York, NY, USA: ACM, 2015. http://dx.doi.org/10.1145/2742060.2743764.

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Edwards, D. S., R. Allen, T. Papadopoulos, D. Rowan, S. Y. Kim, and L. Wilmot-Brown. "Investigations of mammalian echolocation." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5335313.

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Guha, S. K. "Electrical effects on mammalian sperm." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1988. http://dx.doi.org/10.1109/iembs.1988.95158.

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Stevenson, David, Ben Agate, Lynn Paterson, Tanya Lake, Muriel Comrie, Tom Brown, Andrew Riches, et al. "Optical transfection of mammalian cells." In Photonics Europe, edited by Romualda Grzymala and Olivier Haeberle. SPIE, 2006. http://dx.doi.org/10.1117/12.662325.

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Etienne, A. S. "Navigation: the mammalian model (discussion)." In IEE Seminar on Self-Learning Robots II: Bio-Robotics. IEE, 1998. http://dx.doi.org/10.1049/ic:19980275.

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Heffner, Henry E., and Rickye S. Heffner. "The evolution of mammalian hearing." In TO THE EAR AND BACK AGAIN - ADVANCES IN AUDITORY BIOPHYSICS: Proceedings of the 13th Mechanics of Hearing Workshop. Author(s), 2018. http://dx.doi.org/10.1063/1.5038516.

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Cho, Sung Hwan, Chun Hao Chen, Frank S. Tsai, Jessica Godin, and Yu-Hwa Lo. "Mammalian Cell Sorting Using μFACS." In Conference on Lasers and Electro-Optics. Washington, D.C.: OSA, 2010. http://dx.doi.org/10.1364/cleo.2010.ctud1.

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Ravosa, Matthew J., Ravinder Kunwar, Elisabeth K. Nicholson, Emily B. Klopp, Jessie Pinchoff, Stuart R. Stock, M. Sharon Stack, and Mark W. Hamrick. "Adaptive plasticity in mammalian masticatory joints." In SPIE Optics + Photonics, edited by Ulrich Bonse. SPIE, 2006. http://dx.doi.org/10.1117/12.680580.

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"Chitosan Microcarriers in Mammalian Cell Culture." In International Conference on Biological, Chemical and Environmental Sciences. International Institute of Chemical, Biological & Environmental Engineering, 2014. http://dx.doi.org/10.15242/iicbe.c614033.

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Reports on the topic "Mammalian"

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Stone, Scot J. Mammalian Diacylglycerol Acyltransferases (DGAT). AOCS, June 2011. http://dx.doi.org/10.21748/lipidlibrary.39186.

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Andrews, Paul W., and Leslie Hill. AS52/GPT Mammalian Mutagenesis Assay. Fort Belvoir, VA: Defense Technical Information Center, May 1996. http://dx.doi.org/10.21236/ada597200.

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Krippaehne, Suzanne. Three Dimensional Mammalian Skull Morphology. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.6485.

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Stern, David F. Mammalian Homologs of Yeast Checkpoint Genes. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada404591.

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Stern, David. Mammalian Homologs of Yeast Checkpoint Genes. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada393426.

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Stern, David F. Mammalian Homologs of Yeast Checkpoint Genes. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada384149.

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Harris, David A. Propagation of Mammalian Prions in Yeast. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada472675.

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Bucan, Maja. A Genetic Approach to Mammalian Circadian Rhythms. Fort Belvoir, VA: Defense Technical Information Center, January 1995. http://dx.doi.org/10.21236/ada330711.

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Hamkalo, B. A., A. Henschen, and M. H. Parseghian. Molecular characterization of flow-sorted mammalian centromeres. Office of Scientific and Technical Information (OSTI), December 1998. http://dx.doi.org/10.2172/560745.

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Taylor, J. H., and J. T. Hare. Repair of mismatched basepairs in mammalian DNA. Office of Scientific and Technical Information (OSTI), August 1991. http://dx.doi.org/10.2172/6614063.

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