Academic literature on the topic 'Division of Biological Effects'
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Journal articles on the topic "Division of Biological Effects"
Stamatakis, Michail, and Nikos V. Mantzaris. "Intrinsic noise and division cycle effects on an abstract biological oscillator." Chaos: An Interdisciplinary Journal of Nonlinear Science 20, no. 3 (September 2010): 033118. http://dx.doi.org/10.1063/1.3484868.
Full textCOX, D. L., R. ENDRES, R. V. KULKARNI, M. LABUTE, and R. R. P. SINGH. "ELECTRON CORRELATION EFFECTS IN BIOLOGICAL MOLECULES." International Journal of Modern Physics B 16, no. 20n22 (August 30, 2002): 3377. http://dx.doi.org/10.1142/s0217979202014462.
Full textSokolova, Ekaterina, Natalia Menzorova, Victoria Davydova, Alexandra Kuz’mich, Anna Kravchenko, Natalya Mishchenko, and Irina Yermak. "Effects of Carrageenans on Biological Properties of Echinochrome." Marine Drugs 16, no. 11 (November 1, 2018): 419. http://dx.doi.org/10.3390/md16110419.
Full textLock, Judith E. "Transgenerational effects of parent and grandparent gender on offspring development in a biparental beetle species." Biology Letters 8, no. 3 (November 16, 2011): 408–11. http://dx.doi.org/10.1098/rsbl.2011.0920.
Full textSchlimpert, Susan, Sebastian Wasserstrom, Govind Chandra, Maureen J. Bibb, Kim C. Findlay, Klas Flärdh, and Mark J. Buttner. "Two dynamin-like proteins stabilize FtsZ rings duringStreptomycessporulation." Proceedings of the National Academy of Sciences 114, no. 30 (July 7, 2017): E6176—E6183. http://dx.doi.org/10.1073/pnas.1704612114.
Full textHelanterä, Heikki, Oliver Aehle, Maurice Roux, Jürgen Heinze, and Patrizia d'Ettorre. "Family-based guilds in the ant Pachycondyla inversa." Biology Letters 9, no. 3 (June 23, 2013): 20130125. http://dx.doi.org/10.1098/rsbl.2013.0125.
Full textDong, Ren G., John Z. Wu, Xueyan S. Xu, Daniel E. Welcome, and Kristine Krajnak. "A Review of Hand–Arm Vibration Studies Conducted by US NIOSH since 2000." Vibration 4, no. 2 (June 15, 2021): 482–528. http://dx.doi.org/10.3390/vibration4020030.
Full textHynd, PI. "Effects of nutrition on wool follicle cell kinetics in sheep differing in efficiency of wool production." Australian Journal of Agricultural Research 40, no. 2 (1989): 409. http://dx.doi.org/10.1071/ar9890409.
Full textYuan, Jintao, Zhiping Wei, Xinwei Xu, Dickson Kofi Wiredu Ocansey, Xiu Cai, and Fei Mao. "The Effects of Mesenchymal Stem Cell on Colorectal Cancer." Stem Cells International 2021 (July 24, 2021): 1–14. http://dx.doi.org/10.1155/2021/9136583.
Full textGeniole, Shawn N., Valentina Proietti, Brian M. Bird, Triana L. Ortiz, Pierre L. Bonin, Bernard Goldfarb, Neil V. Watson, and Justin M. Carré. "Testosterone reduces the threat premium in competitive resource division." Proceedings of the Royal Society B: Biological Sciences 286, no. 1903 (May 29, 2019): 20190720. http://dx.doi.org/10.1098/rspb.2019.0720.
Full textDissertations / Theses on the topic "Division of Biological Effects"
Kisiday, John D. (John David) 1970. "In vitro culture of a chondrocyte-seeded peptide hydrogel and the effects of dynamic compression." Thesis, Massachusetts Institute of Technology, 2003. http://hdl.handle.net/1721.1/29614.
Full textIncludes bibliographical references.
Emerging medical technologies for effective and lasting repair of articular cartilage include delivery of cells or cell-seeded scaffolds to a defect site to initiate de novo tissue regeneration. Biocompatible scaffolds assist in providing a template for cell distribution and extracellular matrix accumulation in a three-dimensional geometry. In these studies, a self-assembling peptide hydrogel is evaluated as a potential scaffold for cartilage repair using a model bovine cell source. A seeding technique is developed for 3-D encapsulation of chondrocytes in a peptide hydrogel. The chondrocyte-seeded peptide hydrogel was then evaluated cellular activities in vitro under standard culture conditions and also when subjected to dynamic compression. During 4 weeks of culture in vitro, chondrocytes seeded within the peptide hydrogel retained their morphology and developed a cartilage-like ECM rich in proteoglycans and type II collagen, indicative of a stable chondrocyte phenotype. Time dependent accumulation of this ECM was paralleled by increases in material stiffness, indicative of deposition of mechanically-functional neo-tissue. Culture of chondrocyte-seeded peptide hydrogels in ITS-supplemented medium was investigated as an alternative to high serum culture. Low serum (0.2%), ITS-supplemented medium was found to maintain high levels of cell division and extracellular matrix synthesis and accumulation, as seen in high serum culture. Furthermore, low serum, ITS medium induced minimal chondrocyte de-differentiation on the surface of the hydrogel. This is in contrast to high serum culture, where surface de-differentiation and subsequent proliferation led to a 5-10 cell thick layer that stained positive for type I collagen.
(cont.) The effects of dynamic compression of chondrocyte-seeded peptide hydrogels were evaluated over long-term culture. A non-continuous loading protocol was identified in which proteoglycan, but not protein, synthesis increased over static, free-swelling culture. Increases in GAG matrix accumulation were observed after at least 8 days of loading, while hydroxyproline accumulation was unaffected by dynamic compression. These data demonstrated dynamic compression differentially regulated the synthesis of proteoglycans. Analysis of GAG loss to the medium indicated peak proteoglycan catabolism occurred immediately after the initiation of loading. This phenomenon was further explored using a modified loading protocol that increased GAG loss to the medium. Peak GAG loss to the medium was 2-fold higher than previously observed, resulting in GAG accumulation values significantly less than controls. Hydroxyproline accumulation was minimally affected by loading, demonstrating that dynamic compression also differentially regulated the catabolism of proteoglycans. Proteoglycan catabolism was not predominantly due to physical disruption accumulated extracellular matrix or loss of newly-synthesized molecules. Instead, the presence of MMPs in the medium that coincided with GAG loss suggest a potential enzymatic mechanism. These results demonstrate the potential of a self-assembling peptide hydrogel as a scaffold for the synthesis and accumulation of a true cartilage-like extracellular matrix ...
John D. Kisiday.
Ph.D.in Bioengineering
Szafranski, Jon D. (Jon David). "Cartilage mechanobiology : the effects of loading on the fine structure and function of chondroitin sulfate glycosaminoglycans." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/33871.
Full textIncludes bibliographical references.
Chondroitin sulfate is a critical component of articular cartilage due to its contribution to the tissue's resistance to compressive deformation. Alterations in the biosynthesis of this molecule over time could impact the ability of the tissue to perform its necessary functions. Several factors have been shown to alter the biosynthesis of chondroitin sulfate in cartilage; among them are age, disease, depth of tissue, and mechanical compression. Specifically, mechanical compression has been shown to have a significant effect on the sulfation pattern and chain length and number in cartilage explant studies. The mechanisms that govern these alterations, however, have not been determined. The purpose of this study is to examine the effects of mechanical compression on chondroitin sulfate biosynthesis and analyze the roles of two possible mechanisms; enzyme transcription and organelle deformation. The effects of mechanical compression on the transcription rates of enzymes associated with the biosynthesis of chondroitin sulfate have not been previously studied. To perform this study in a bovine model, portions of the bovine genome had to be sequenced, PCR primers designed, and bulk expression levels determined. Static compression resulted in the significant up-regulation of two genes of interest: chondroitin sulfate and GalNAc 4S,6-sulfotransferase.
(cont.) Dynamic compression resulted in the significant up-regulation of the three sulfotransferases responsible for the bulk of sulfation in cartilage tissue. These results indicate a transient mechanotransduction reaction that differs based on the load regime. The effect of mechanical loading on the biosynthesis of chondroitin sulfate has been studied previously, however, this study seeks to examine more comprehensive loading regimes. Static compression and release resulted in an increase in 6-sulfation and a decrease in 4-sulfation that lasted to 48 hours after release of compression. Dynamic compression and release had the opposite effect on sulfation ratio, with an increase in 4-sulfation compared to 6-sulfation. The transcription changes seen in this study do not indicate the changes that occur in the end products of synthesis. Other factors may play a larger role, such as precursor availability or transport through the Golgi apparatus. Intracellular organelles react to static compression of the surrounding tissue in one of two manners. The majority of organelles deform much as the nucleus, proportionally in volume and shape to the cell. The Golgi apparatus appears to retain a significant portion of its volume relative to the cell and other organelles. In addition, it reforms structurally into a highly ordered stacked appearance.
(cont.) Osmotic forces within the Golgi may allow it to balance the osmotic load in the cytoplasm and resist compression and altered trafficking of the Golgi may in turn produce the altered appearance. Recent microscopy experiments on the Golgi apparatus utilizing two-photon microscopy have allowed us to examine the reaction of live tissue to static compression. These results illustrate the significant, but differing, effects of static and dynamic compression on the biosynthesis of chondroitin sulfate. The effects of these compression types on the transcription of enzymes responsible for this biosynthesis cannot fully explain the changes seen in newly synthesized chondroitin sulfate. Organelle reorganization has been shown to occur in response to static load and it is possible that altered organelle trafficking plays a role in this altered biosynthesis. Further studies are necessary to determine the final effect of the altered transcription and organelle structure on the manufacture of this important cartilage molecule.
by Jon D. Szafranski.
Ph.D.
Wheeler, Cameron 1978. "Cartilage mechanobiology and transcriptional effects of combined mechanical compression and IGF-1 stimulation on bovine cartilage explants." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/38613.
Full textIncludes bibliographical references.
Background: Investigators have focused on mechano-regulation of upstream signaling and responses at the level of gene transcription, protein translation and post-translational modifications. Intracellular pathways including those involving integrin signaling, mitogen activated protein kinases (MAPKs), and release of intracellular calcium have been confirmed in several laboratories. Studies with IGF-1: Insulin-like growth factor-I (IGF-1) is a potent anabolic factor capable of endocrine and paracrine/autocrine signaling. Previous studies have demonstrated that mechanical compression can regulate the action of IGF-1 on chondrocyte biosynthesis in intact tissue; when applied simultaneously, these stimuli act by distinct cell activation pathways. Our objectives were to elucidate the extent and kinetics of the chondrocyte transcriptional response to combined IGF-1 and static compression in cartilage explants. Discussion: Clustering analysis revealed five distinct groups. TIMP-3 and ADAMTS-5, MMP-l and IGF-2, and IGF-1 and Collagen II, were all robustly co-expressed under all conditions tested. In comparing gene expression levels to previously measured aggrecan biosynthesis levels, aggrecan synthesis is shown to be transcriptionally regulated by IGF- 1, whereas inhibition of aggrecan synthesis by compression is not transcriptionally regulated.
(cont.) Conclusion: Many genes measured are responsive the effects of IGF-1 under 0% compression and 50% compression. Clustering analysis revealed strong co-expressed gene pairings. IGF-1 stimulates aggrecan biosynthesis in a transcriptionally regulated manner, whereas compression inhibits aggrecan synthesis in a manner not regulated by transcriptional activity.
by Cameron A. Wheeler.
S.M.
Villasenor, Jose Fernando. "HABITAT USE AND THE EFFECTS OF DISTURBANCE ON WINTERING BIRDS USING RIPARIAN HABITATS IN SONORA, MEXICO." The University of Montana, 2007. http://etd.lib.umt.edu/theses/available/etd-03282007-165836/.
Full textAnthropogenic disturbance has imposed significant changes in riparian habitats, and is known to have negative effects on biological communities. To assess the effects of human induced disturbance on wintering bird communities, I recorded community composition, relative abundance of species, and three indicators of bird condition in relatively undisturbed and highly disturbed sites at three river systems in Sonora. There is, in general, little effect of disturbance on the composition of wintering communities, with less than 20% of the most common species having significant differences in their abundances between relatively undisturbed and highly disturbed sites. Condition indicators were similar in the two disturbance levels, but the mean heterophil/lymphocyte ratio in the blood of sampled birds showed increased levels of physiological stress in disturbed sites. A more experimental approach is needed to determine the specific cause of the stress expression in leucocytes.
Modification of natural flooding regimes has modified riparian areas, as has been the case in the Colorado River Delta. I present a summary of the changes experienced by riparian systems and some of the measures implemented for riparian restoration in the southwestern United States, and then I compare the scenario with that in central Sonora, where some of the same stressors exist on riparian systems, but where traditional management practices have also mitigated some of the negative consequences of flow control along mid-sized river systems.
Anderson, Michelle Louise. "The edge effect: lateral habitat ecology of an alluvial river flood plain." The University of Montana, 2008. http://etd.lib.umt.edu/theses/available/etd-10012008-134442/.
Full textSachs, Karen Ph D. Massachusetts Institute of Technology. "Bayesian network models of biological signaling pathways." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/38865.
Full textIncludes bibliographical references (p. 153-165).
Cells communicate with other cells, and process cues from their environment, via signaling pathways, in which extracellular cues trigger a cascade of information flow, causing signaling molecules to become chemically, physically or locationally modified, gain new functional capabilities, and affect subsequent molecules in the cascade, culminating in a phenotypic cellular response. Mapping the influence connections among biomolecules in a signaling cascade aids in understanding of the underlying biological process and in development of therapeutics for diseases involving aberrant pathways, such as cancer and autoimmune disease. In this thesis, we present an approach for automatically reverse-engineering the structure of a signaling pathway, from high-throughput data. We apply Bayesian network structure inference to signaling protein measurements performed in thousands of single cells, using a machine called a flow cytorneter. Our de novo reconstruction of a T-cell signaling map was highly accurate, closely reproducing the known pathway structure, and accurately predicted novel pathway connections. The flow cytometry measurements include specific perturbations of signaling molecules, aiding in a causal interpretation of the Bayesian network graph structure.
(cont.) However, this machine can measure only -4-12 molecules per cell, too few for effective coverage of a signaling pathway. To address this problem, we employ a number of biologically motivated assumptions to extend our technique to scale up from the number of molecules measured to larger models, using measurements of overlapping variable subsets. We demonstrate this approach by scaling up to a model of 11 variables, using 15 overlapping 4-variable measurements.
by Karen Sachs.
Ph.D.
Shiva, V. A. "Scalable computational architecture for integrating biological pathway models." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/42384.
Full textMIT Institute Archives copy: DVD inserted in pocket on p. [3] of cover on v. 1.
"c2007"--p. ii.
Includes bibliographical references (v. 2, leaves 292-302).
A grand challenge of systems biology is to model the cell. The cell is an integrated network of cellular functions. Each cellular function, such as immune response, cell division, metabolism or apoptosis, is defined by an interconnected ensemble of biological pathways. Modeling the cell or even one cellular function requires a computational architecture that integrates multiple biological pathway models in a scalable manner while ensuring minimal effort to maintain the resulting integrated model. Scalable is defined as the ease in which more and more biological pathway models can be integrated. Current architectures for integrating biological pathway models are primarily monolithic and involve combining each biological pathway model's software source code to build one large monolithic model that executes on a single computer. Such architectures are not scalable for modeling complex cellular functions or the whole cell. We present Cytosolve, a new computational architecture that integrates a distributed ensemble of biological pathway models and computes solutions in a parallel manner while offering ease of maintenance of the integrated model. The individual biological pathway models can be represented in SBML, CellML or in any number of formats. The EGFR model of Kholodenko with known solutions is used to compare the Cytosolve solution and computational times with a known monolithic approach. A new integrative model of the interferon (IFN) response to virus infection is developed using Cytosolve. Each model within the integrated model, spans different time scales, is created by different authors from four countries and three continents across different disciplines, is written in different software codes, and is built on different hardware platforms.
(cont.) A new quantitative methodology and formalism is then derived for evaluating different types of monolithic and distributed architectures for integrating biological pathway models. As more biological pathway models develop in a disparate and decentralized manner, the Cytosolve architecture offers a unique platform to build and test complex models of cellular function, and eventually the whole cell.
by V.A. Shiva Ayyadurai.
Ph.D.
Margolin, Yelena 1977. "Analysis of sequence-selective guanine oxidation by biological agents." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/42381.
Full textVita.
Includes bibliographical references.
Oxidatively damaged DNA has been strongly associated with cancer, chronic degenerative diseases and aging. Guanine is the most frequently oxidized base in the DNA, and generation of a guanine radical cation (G'") as an intermediate in the oxidation reaction leads to migration of a resulting cationic hole through the DNA n-stack until it is trapped at the lowest-energy sites. These sites reside at runs of guanines, such as 5'-GG-3' sequences, and are characterized by the lowest sequence-specific ionization potentials (IPs). The charge transfer mechanism suggests that hotspots of oxidative DNA damage induced by electron transfer reagents can be predicted based on the primary DNA sequence. However, preliminary data indicated that nitrosoperoxycarbonate (ONOOCO2"), a mediator of chronic inflammation and a one-electron oxidant, displayed unusual guanine oxidation properties that were the focus of present work. As a first step in our study, we determined relative levels of guanine oxidation, induced by ONOOCO2 in all possible three-base sequence contexts (XGY) within double-stranded oligonucleotides. These levels were compared to the relative oxidation induced within the same guanines by photoactivated riboflavin, a one-electron reagent. We found that, in agreement with previous studies, photoactivated riboflavin was selective for guanines of lowest IPs located within 5'-GG-3' sequences. In contrast, ONOOCO2" preferentially reacted with guanines located within 5'-GC-3' sequences characterized by the highest IPs. This demonstrated that that sequence-specific IP was not a determinant of guanine reactivity with ONOOCO2". Sequence selectivities for both reagents were double-strand specific. Selectivity of ONOOCO2 for 5'-GC-3' sites was also observed in human genomic DNA after ligation-mediated PCR analysis.
(cont.) Relative yields of different guanine lesions produced by both ONOOCO2" and riboflavin varied 4- to 5-fold across all sequence contexts. To assess the role of solvent exposure in mediating guanine oxidation by ONOOCO2", relative reactivities of mismatched guanines with ONOOCO2" were measured. The majority of the mismatches displayed an increased reactivity with ONOOCO2 as compared to the fully matched G-C base-pairs. The extent of reactivity enhancement was sequence context-dependent, and the greatest levels of enhancement were observed for the conformationally flexible guanine- guanine (G-G) mismatches and for guanines located across from a synthetic abasic site. To test the hypothesis that the negative charge of an oxidant influences its reactivity with guanines in DNA, sequence-selective guanine oxidation by a negatively charged reagent, Fe+2-EDTA, was assessed and compared to guanine oxidation produced by a neutral oxidant, y-radiation. Because both of these agents cause high levels of deoxyribose oxidation, a general method to quantify sequence-specific nucleobase oxidation in the presence of direct strand breaks was developed. This method exploited activity of exonuclease III (Exo III), a 3' to 5' exonuclease, and utilized phosphorothioate-modified synthetic oligonucleotides that were resistant to Exo III activity. This method was employed to determine sequence-selective guanine oxidation by Fe+2-EDTA complex and y-radiation and to show that both agents produced identical guanine oxidation pattems and were equally reactive with all guanines, irrespective of their sequence-specific IPs or sequence context.
(cont.) This showed that negative charge was not a determinant of Fe+2-EDTA-mediated guanine oxidation. Finally, the role of oxidant binding on nucleobase damage was assessed by studying sequence-selective oxidation produced by DNA-bound Fe+2 ions in the presence of H202. We found that the major oxidation targets were thymines located within 5'-TGG-3' motifs, demonstrating that while guanines were a required element for coordination of Fe+2 to DNA, they were not oxidized. Our results suggest that factors other than sequence-specific IPs can act as major determinants of sequence-selective guanine oxidation, and that current models of guanine oxidation and charge transfer in DNA cannot be used to adequately predict the location and identity of mutagenic lesions in the genome.
by Yelena Margolin.
Ph.D.
Canton, Bartholomew (Bartholomew John). "Engineering the interface between cellular chassis and synthetic biological systems." Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/44918.
Full textThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Includes bibliographical references (p. 165-176).
The aim of my thesis is to help enable the engineering of biological systems that behave in a predictable manner. Well-established techniques exist to engineer systems that behave as expected. Here, I apply such techniques to two aspects of the engineering of biological systems. First, I address the design and construction of standard biological devices in a manner that facilitates reuse in higher-order systems. I describe the design and construction of an exemplar device, an engineered cell-cell communication receiver using standard biological parts (refined genetic objects designed to support physical and functional composition). I adopt a conventional framework for describing the behavior of engineered devices and use the adopted framework to design and interpret experiments that describe the behavior of the receiver. The output of the device is the activity of a promoter reported in units of Polymerases Per Second (PoPS), a common signal carrier. Second, I begin to address the coupling that exists between engineered biological systems and the host cell, or chassis. I propose that the coupling between engineered biological systems and the cellular chassis might be reduced if fewer resources were shared between the system and the chassis. I describe the construction of cellular chassis expressing both T7 RNA polymerases (RNAP) and orthogonal ribosomes that are unused by the chassis but are available for use by an engineered system. I implement a network in which the orthogonal ribosomal RNA and the gene encoding T7 RNAP are transcribed by T7 RNAP. In turn, the orthogonal ribosomes translate the T7 RNAP message. In addition, the T7 RNAP and orthogonal ribosomes express a repressor that inhibits transcription of both the T7 RNAP and orthogonal ribosomes.
(cont.) As a result, the orthogonal RNAP and ribosomes are auto-generating and self-regulating. The provision of resources unused by the cellular chassis and dedicated to an engineered biological system forms the beginnings of a biological virtual machine.
by Bartholomew Canton.
Ph.D.
Frick, Lauren Elizabeth. "The versatile E. coli adaptive response protein AlkB mitigates toxicity and mutagenicity of etheno-, ethano-, and methyl-modified bases in vivo." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/42382.
Full textVita.
Includes bibliographical references.
The Escherichia coli AlkB protein is an exceptionally versatile DNA repair enzyme. Its expression is induced upon exposure to alkylating agents as part of the Ada-mediated adaptive response. This member of the ac-ketoglutarate/iron(II)-dependent dioxygenase family was originally discovered to reverse directly methylated lesions formed preferentially in single-stranded regions of DNA, such as 1-methyladenine and 3- methylcytosine. Repair proceeds via an oxidative demethylation pathway, in which the aberrant methyl group is hydroxylated and spontaneously lost as formaldehyde. Since these early studies, the list of lesions repaired by AlkB through this pathway has been extended to include 1-methylguanine, 3-methylthymine, 3-ethylcytosine, and 1-ethyladenine. Furthermore, the protein possesses a second, distinct chemical mechanism through which it can repair another class of lesions, the etheno-adducts formed by the reaction of DNA with metabolites of the carcinogen vinyl chloride or with breakdown products generated by lipid oxidation. In this case, direct repair proceeds through epoxidation of the etheno bond, creating an intermediate that hydrolyzes to a glycol form and finally releases the two-carbon bridge as glyoxal, restoring the unadducted adenine or cytosine. Thus, the AlkB protein bridges the repair of alkylative lesions with those induced by oxidative stress and embodies the multi-faceted protection required to preserve genomic stability and coding information despite the constant threats to which organisms are exposed.
(cont.) Herein, we exploit and characterize a pair of E. coli strains differing only in AlkB status to demonstrate the ability of AlkB to repair the etheno-lesions, the structural analog 1,N6-ethanoadenine (EA), and 3-methyluracil in vivo. Additionally, we establish the ability of the EA "repair product" to form interstrand cross-links in certain sequence contexts of duplex DNA. We also show that although the adaptive response proteins repair lesions generated by oxidative stress, oxidative agents do not induce expression of the response. Finally, we establish that certain hypothesized substrates for AlkB are not in fact repaired by the enzyme, nor are they repaired by another adaptive response protein, AidB. This work extends the current knowledge regarding the amazing ability of AlkB to protect cellular nucleic acids from damage arising from a diverse array of both endogenous and exogenous sources.
by Lauren Elizabeth Frick.
Ph.D.
Books on the topic "Division of Biological Effects"
Kiefer, Jürgen. Biological Radiation Effects. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83769-2.
Full textLaboratory, U. S. Army Research. Terminal Effects Division. [Adelphi, Md.?: ARL, 1998.
Find full textNational Research Council of Canada. Division of Biological Sciences. S.l: s.n, 1985.
Find full textHoriguchi, Toshihiro, ed. Biological Effects by Organotins. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56451-5.
Full textStavroulakis, Peter, and Marko Markov. Biological effects of electromagnetic fields: Mechanisms, modeling, biological effects, therapeutic effects, international standards, exposure criteria. Berlin: Springer, 2003.
Find full text1948-, Williams R. Sanders, and Wallace Andrew G. 1935-, eds. Biological effects of physical activity. Champaign, Ill: Human Kinetics Books, 1989.
Find full textStavroulakis, Peter, ed. Biological Effects of Electromagnetic Fields. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-06079-7.
Full textBook chapters on the topic "Division of Biological Effects"
Lytle, Thomas. "Commercial Division." In Drug and Biological Development, 222–39. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-69094-0_10.
Full textShen, Zhenyao, Junfeng Niu, Ying Wang, Hongyuan Wang, and Xin Zhao. "Biological Effects." In Advanced Topics in Science and Technology in China, 67–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-34964-5_4.
Full textAon, M. A., and S. Cortassa. "Dynamics of cell growth and division." In Dynamic Biological Organization, 322–60. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5828-2_9.
Full textWataha, John. "Palladium, Biological Effects." In Encyclopedia of Metalloproteins, 1628–35. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_573.
Full textD’Haese, Patrick C. "Aluminum, Biological Effects." In Encyclopedia of Metalloproteins, 47–53. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_110.
Full textWang, Jiangxue, Ying Hou, and Jiawei Ma. "Titanium, Biological Effects." In Encyclopedia of Metalloproteins, 2250–51. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_200002.
Full textHe, Xiao. "Scandium, Biological Effects." In Encyclopedia of Metalloproteins, 1882–84. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_200024.
Full textHe, Xiao. "Yttrium, Biological Effects." In Encyclopedia of Metalloproteins, 2338–40. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_200039.
Full textLotufo, Guilherme R., G. Allen Burton, Gunther Rosen, and John W. Fleeger. "Assessing Biological Effects." In SERDP/ESTCP Environmental Remediation Technology, 131–75. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6726-7_6.
Full textKiefer, Jürgen. "Late Somatic Effects." In Biological Radiation Effects, 319–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83769-2_20.
Full textConference papers on the topic "Division of Biological Effects"
Ateshian, Gerard A., Kevin D. Costa, Evren U. Azeloglu, Barclay Morrison, and Clark T. Hung. "Continuum Modeling of Biological Tissue Growth by Cell Division." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205495.
Full textZhang, Muheng, and Yongsheng Lian. "Numerical Investigation of the Coulter Principle in a Microfluidic Device." In ASME 2013 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/fedsm2013-16011.
Full textBeal, David N., Stephen Huyer, Daniel L. Macumber, and Anuradha M. Annaswamy. "Blade Tonal Noise Reduction Using Stator Trailing-Edge Articulation." In ASME 2005 Fluids Engineering Division Summer Meeting. ASMEDC, 2005. http://dx.doi.org/10.1115/fedsm2005-77446.
Full textKrishnamoorthi, M., S. Sreedhara, and Pavan Prakash Duvvuri. "Modelling of Soot Formation and Experimental Study for Different Octane Number Fuels in Dual Fuel Combustion Engine With Diesel." In ASME 2020 Internal Combustion Engine Division Fall Technical Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/icef2020-2914.
Full textChen, Larry, and Urmila Ghia. "Composite Solution Procedure for 3-D Flow Simulations on a Multi-Box Grid." In ASME 2006 2nd Joint U.S.-European Fluids Engineering Summer Meeting Collocated With the 14th International Conference on Nuclear Engineering. ASMEDC, 2006. http://dx.doi.org/10.1115/fedsm2006-98441.
Full textWong, Voon-Loong, Katerina Loizou, Phei-Li Lau, Richard S. Graham, and Buddhika N. Hewakandamby. "Numerical Simulation of the Effect of Rheological Parameters on Shear-Thinning Droplet Formation." In ASME 2014 4th Joint US-European Fluids Engineering Division Summer Meeting collocated with the ASME 2014 12th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/fedsm2014-21363.
Full textRivier, Nicolas, Xavier Arcenegui-Siemens, and Gudrun Schliecker. "CELL DIVISION AND EVOLUTION OF BIOLOGICAL TISSUES." In Proceedings of the Workshop. WORLD SCIENTIFIC, 1995. http://dx.doi.org/10.1142/9789814447089_0025.
Full textPineda, Saira F., Arjan M. Kamp, D. Legendre, and Armando J. Blanco. "Axisymmetric Low-Reynolds Motion of Drops Through Circular Microchannels." In ASME 2012 10th International Conference on Nanochannels, Microchannels, and Minichannels collocated with the ASME 2012 Heat Transfer Summer Conference and the ASME 2012 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/icnmm2012-73198.
Full textKumari, Suruchi, and S. Raghavan. "Biological effects of microwave." In 2014 International Conference on Information Communication and Embedded Systems (ICICES). IEEE, 2014. http://dx.doi.org/10.1109/icices.2014.7034127.
Full textBrown, Samuel J. "An Introduction to the ASME HPS Section 6000 “Hazardous Release Protection”: Historical Development of a Means to Reduce Risk From Pressure Systems Failure." In ASME 2003 Pressure Vessels and Piping Conference. ASMEDC, 2003. http://dx.doi.org/10.1115/pvp2003-1814.
Full textReports on the topic "Division of Biological Effects"
Dayton, Thomas, Charles Beason, M. K. Hitt, Walter Rogers, and Michael Cook. Biological Effects of Directed Energy. Fort Belvoir, VA: Defense Technical Information Center, November 2002. http://dx.doi.org/10.21236/ada408809.
Full textSelby, P. (Biological effects of atomic radiation). Office of Scientific and Technical Information (OSTI), June 1990. http://dx.doi.org/10.2172/6867425.
Full textBarr, S. H., ed. Division of Biological and Medical Research research summary 1984-1985. Office of Scientific and Technical Information (OSTI), August 1985. http://dx.doi.org/10.2172/6039516.
Full textSchoenbach, Karl H., Stephen J. Beebe, E. S. Buescher, and Shenggang Liu. Pulsed Electric Field Effects on Biological Cells. Fort Belvoir, VA: Defense Technical Information Center, November 2001. http://dx.doi.org/10.21236/ada399182.
Full textRitchie, Glenn D., Marni Y. Bekkedal, Andrew J. Bobb, and Kenneth R. Still. Biological and Health Effects of JP-8 Exposure. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada399728.
Full textHolman, Peter, and Albert W. Price. Chemical Biological Material Effects Database New User Guide. Fort Belvoir, VA: Defense Technical Information Center, February 2011. http://dx.doi.org/10.21236/ada539856.
Full textReeves, Glen I., and David Auton. Biological Effects of Nuclear Explosions (BENE) Domain Guide. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada570379.
Full textGrabow, Chad L. Implications and Effects of Advanced Biological and Biological/Chemical Weapons at the Operational Planning Level. Fort Belvoir, VA: Defense Technical Information Center, June 1991. http://dx.doi.org/10.21236/ada240460.
Full textMcCarthy, Geraldine. Biological Effects of Calcium Hydroxyapatite Crystals in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada413254.
Full textARMY DUGWAY PROVING GROUND UT. Chemical, Biological, and Radiological Contamination Survivability: Material Effects Testing. Fort Belvoir, VA: Defense Technical Information Center, June 2012. http://dx.doi.org/10.21236/ada565279.
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