Relevant bibliographies by topics / Mitosis

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Mitosis'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 June 2025

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Journal articles on the topic "Mitosis"

1

Stratton, Miranda, and Tim Stearns. "Mitosis sans Mitosis: The Mitotic Oscillator in Differentiation." Developmental Cell 43, no. 4 (2017): 385–86. http://dx.doi.org/10.1016/j.devcel.2017.11.001.

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Kantsavaya, I., and O. Alekseenko. "Effect of Beta-lactam Antibiotics on Microscopic Parameters in the Allium-test." Bulletin of Science and Practice 5, no. 10 (2019): 25–31. http://dx.doi.org/10.33619/2414-2948/47/03.

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The work examines the effect of beta-lactam antibiotics (cefotaxime, ampicillin, augmentin) on the pathology of mitosis in the Allium–test. Research methods: Allium–test, cytogenetic analysis, statistical analysis. It was established that the use of individual tested beta-lactam antibiotics increases the percentage of pathological mitoses in the cell by 1.8–3.3 times compared with the value in the control. With the combined use of cefotaxime and Augmentin, synergism appeared, as a result, the value of mitosis pathology turned out to be at the level of the number in the control; minimally represented pathologies indicating damage to the mitotic apparatus. It was revealed that all three beta-lactam antibiotics tested had a pronounced statmokinetic effect. At the same time, with the joint use of cefotaxime and Augmentin, k-mitosis was not registered in dividing cells. Comparison of the spectrum of pathological mitoses in the variants of the experiment showed that the pathology ‘chromosome runaway/backlog’ in anaphase of mitosis dominates in all variants. An increase in the concentration of Augmentin and ampicillin caused the suppression of pathological processes in onion meristematic cells, a decrease in PM values was observed. An increase in Augmentin concentration does not affect the composition and spectrum of pathological mitoses; ampicillin has a decrease in the level of most of the recorded pathologies of mitosis.
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Solnica-Krezel, L., T. G. Burland, and W. F. Dove. "Variable pathways for developmental changes of mitosis and cytokinesis in Physarum polycephalum." Journal of Cell Biology 113, no. 3 (1991): 591–604. http://dx.doi.org/10.1083/jcb.113.3.591.

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The development of a uninucleate ameba into a multinucleate, syncytial plasmodium in myxomycetes involves a change from the open, astral mitosis of the ameba to the intranuclear, anastral mitosis of the plasmodium, and the omission of cytokinesis from the cell cycle. We describe immunofluorescence microscopic studies of the amebal-plasmodial transition (APT) in Physarum polycephalum. We demonstrate that the reorganization of mitotic spindles commences in uninucleate cells after commitment to plasmodium formation, is completed by the binucleate stage, and occurs via different routes in individual developing cells. Most uninucleate developing cells formed mitotic spindles characteristic either of amebae or of plasmodia. However, chimeric mitotic figures exhibiting features of both amebal and plasmodial mitoses, and a novel star microtubular array were also observed. The loss of the ameba-specific alpha 3-tubulin and the accumulation of the plasmodium-specific beta 2-tubulin isotypes during development were not sufficient to explain the changes in the organization of mitotic spindles. The majority of uninucleate developing cells undergoing astral mitoses (amebal and chimeric) exhibited cytokinetic furrows, whereas cells with the anastral plasmodial mitosis exhibited no furrows. Thus, the transition from astral to anastral mitosis during the APT could be sufficient for the omission of cytokinesis from the cell cycle. However, astral mitosis may not ensure cytokinesis: some cells undergoing amebal or chimeric mitosis contained unilateral cytokinetic furrows or no furrow at all. These cells would, most probably, fail to divide. We suggest that a uninucleate committed cell undergoing amebal or chimeric mitosis can either divide or else form a binucleate cell. In contrast, a uninucleate cell with a mitotic spindle of the plasmodial type gives rise only to a binucleate cells. Further, the decision to enter mitosis after commitment to the APT is independent of the developmental changes in the organization of the mitotic spindle and cytokinesis.
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Douglas, Pauline, Ruiqiong Ye, Nicholas Morrice, Sébastien Britton, Laura Trinkle-Mulcahy, and Susan P. Lees-Miller. "Phosphorylation of SAF-A/hnRNP-U Serine 59 by Polo-Like Kinase 1 Is Required for Mitosis." Molecular and Cellular Biology 35, no. 15 (2015): 2699–713. http://dx.doi.org/10.1128/mcb.01312-14.

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Scaffold attachment factor A (SAF-A), also called heterogenous nuclear ribonuclear protein U (hnRNP-U), is phosphorylated on serine 59 by the DNA-dependent protein kinase (DNA-PK) in response to DNA damage. Since SAF-A, DNA-PK catalytic subunit (DNA-PKcs), and protein phosphatase 6 (PP6), which interacts with DNA-PKcs, have all been shown to have roles in mitosis, we asked whether DNA-PKcs phosphorylates SAF-A in mitosis. We show that SAF-A is phosphorylated on serine 59 in mitosis, that phosphorylation requires polo-like kinase 1 (PLK1) rather than DNA-PKcs, that SAF-A interacts with PLK1 in nocodazole-treated cells, and that serine 59 is dephosphorylated by protein phosphatase 2A (PP2A) in mitosis. Moreover, cells expressing SAF-A in which serine 59 is mutated to alanine have multiple characteristics of aberrant mitoses, including misaligned chromosomes, lagging chromosomes, polylobed nuclei, and delayed passage through mitosis. Our findings identify serine 59 of SAF-A as a new target of both PLK1 and PP2A in mitosis and reveal that both phosphorylation and dephosphorylation of SAF-A serine 59 by PLK1 and PP2A, respectively, are required for accurate and timely exit from mitosis.
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Nasuda, Shuhei, Bernd Friebe, and Bikram S. Gill. "Gametocidal Genes Induce Chromosome Breakage in the Interphase Prior to the First Mitotic Cell Division of the Male Gametophyte in Wheat." Genetics 149, no. 2 (1998): 1115–24. http://dx.doi.org/10.1093/genetics/149.2.1115.

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Abstract Male gametogenesis was cytologically analyzed in wheat lines homozygous or hemizygous for gametocidal (Gc) factors with different modes of action. The first and second meiotic divisions in all lines were cytologically normal. The postmeiotic mitoses were normal in the homozygous lines; however, chromosome fragments and bridges were observed in the mitoses of the hemizygous lines. The morphology of the chromosome fragments suggests that the Gc genes induce chromosome breaks in the G1 phase prior to DNA synthesis of the first postmeiotic mitosis. The age of an anther was correlated with the frequency of aberrant second mitosis. Younger anthers contained a higher number of pollen undergoing normal second mitosis. This observation suggests that the arresting of the cell cycle occurs as the result of chromosome breaks during the first mitosis. Because chromosome bridges were more frequent than fragments in the second mitosis, breakage-fusion-bridge cycles possibly occurred during gametogenesis, which led to further chromosomal rearrangements. The Gc factors located on chromosomes 2S of Aegilops speltoides and 4Ssh of Ae. sharonensis induce severe chromosome breakage in pollen lacking them. However, the Gc factor on telosome 2CcL of Ae. cylindrica only induced chromosome breaks at a low frequency. The observed partial fertility of Gc lines is presumably due to cell cycle arrest and the competition among gametes with and without chromosome breakage.
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Brinkley, William (B R. ). "Romancing mitosis and the mitotic apparatus." Molecular Biology of the Cell 25, no. 21 (2014): 3270–72. http://dx.doi.org/10.1091/mbc.e14-06-1123.

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One of the earliest lessons students learn in biology is the process of mitosis and how cells divide to produce daughter cells. Although first described more than a century ago by early investigators such as E. B. Wilson, many aspects of mitosis and cell division remain the subject of considerable research today. My personal investigations and research contributions to the study of mitosis were made possible by recent developments in the field when I began my career, including access to novel mammalian cell culture models and electron and fluorescence microscopy. Building upon those innovations, my laboratory and other contemporary investigators first charted the ultrastructure and molecular organization of mitosis and chromosome movement and the assembly and function of the cytoskeleton. This field of research remains a significant challenge for future investigators in cell biology and medicine.
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Sturm, Bart, David Creytens, Jan Smits, et al. "Computer-Aided Assessment of Melanocytic Lesions by Means of a Mitosis Algorithm." Diagnostics 12, no. 2 (2022): 436. http://dx.doi.org/10.3390/diagnostics12020436.

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An increasing number of pathology laboratories are now fully digitised, using whole slide imaging (WSI) for routine diagnostics. WSI paves the road to use artificial intelligence (AI) that will play an increasing role in computer-aided diagnosis (CAD). In melanocytic skin lesions, the presence of a dermal mitosis may be an important clue for an intermediate or a malignant lesion and may indicate worse prognosis. In this study a mitosis algorithm primarily developed for breast carcinoma is applied to melanocytic skin lesions. This study aimed to assess whether the algorithm could be used in diagnosing melanocytic lesions, and to study the added value in diagnosing melanocytic lesions in a practical setting. WSI’s of a set of hematoxylin and eosin (H&E) stained slides of 99 melanocytic lesions (35 nevi, 4 intermediate melanocytic lesions, and 60 malignant melanomas, including 10 nevoid melanomas), for which a consensus diagnosis was reached by three academic pathologists, were subjected to a mitosis algorithm based on AI. Two academic and six general pathologists specialized in dermatopathology examined the WSI cases two times, first without mitosis annotations and after a washout period of at least 2 months with mitosis annotations based on the algorithm. The algorithm indicated true mitosis in lesional cells, i.e., melanocytes, and non-lesional cells, i.e., mainly keratinocytes and inflammatory cells. A high number of false positive mitosis was indicated as well, comprising melanin pigment, sebaceous glands nuclei, and spindle cell nuclei such as stromal cells and neuroid differentiated melanocytes. All but one pathologist reported more often a dermal mitosis with the mitosis algorithm, which on a regular basis, was incorrectly attributed to mitoses from mainly inflammatory cells. The overall concordance of the pathologists with the consensus diagnosis for all cases excluding nevoid melanoma (n = 89) appeared to be comparable with and without the use of AI (89% vs. 90%). However, the concordance increased by using AI in nevoid melanoma cases (n = 10) (75% vs. 68%). This study showed that in general cases, pathologists perform similarly with the aid of a mitosis algorithm developed primarily for breast cancer. In nevoid melanoma cases, pathologists perform better with the algorithm. From this study, it can be learned that pathologists need to be aware of potential pitfalls using CAD on H&E slides, e.g., misinterpreting dermal mitoses in non-melanotic cells.
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Cancel, Limary M., and John M. Tarbell. "The role of mitosis in LDL transport through cultured endothelial cell monolayers." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 3 (2011): H769—H776. http://dx.doi.org/10.1152/ajpheart.00445.2010.

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We ( 7 ) have previously shown that leaky junctions associated with dying or dividing cells are the dominant pathway for LDL transport under convective conditions, accounting for >90% of the transport. We ( 8 ) have also recently shown that the permeability of bovine aortic endothelial cell monolayers is highly correlated with their rate of apoptosis and that inhibiting apoptosis lowers the permeability of the monolayers to LDL. To explore the role of mitosis in the leaky junction pathway, the microtubule-stabilizing agent paclitaxel was used to alter the rate of mitosis, and LDL flux and water flux ( Jv) were measured. Control monolayers had an average mitosis rate of 0.029%. Treatment with paclitaxel (2.5 μM) for 1.5, 3, 4.5, or 6 h yielded increasing rates of mitosis ranging from 0.099% to 1.03%. The convective permeability of LDL (Pe) increased up to fivefold, whereas Jv increased up to threefold, over this range of mitosis rates. We found strong correlations between the mitosis rate and both Pe and Jv. However, compared with our previous apoptosis study ( 8 ), we found that mitosis was only half as effective as apoptosis in increasing Pe. The results led us to conclude that while mitotsis-related leaky junctions might play a role in the initial infiltration of LDL into the artery wall, the progression of atherosclerosis might be more closely correlated with apoptosis-related leaky junctions.
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Helfer, Hanspeter, and Amy S. Gladfelter. "AgSwe1p Regulates Mitosis in Response to Morphogenesis and Nutrients in Multinucleated Ashbya gossypii Cells." Molecular Biology of the Cell 17, no. 10 (2006): 4494–512. http://dx.doi.org/10.1091/mbc.e06-03-0215.

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Nuclei in the filamentous, multinucleated fungus Ashbya gossypii divide asynchronously. We have investigated what internal and external signals spatially direct mitosis within these hyphal cells. Mitoses are most common near cortical septin rings found at growing tips and branchpoints. In septin mutants, mitoses are no longer concentrated at branchpoints, suggesting that the septin rings function to locally promote mitosis near new branches. Similarly, cells lacking AgSwe1p kinase (a Wee1 homologue), AgHsl1p (a Nim1-related kinase), and AgMih1p phosphatase (the Cdc25 homologue that likely counteracts AgSwe1p activity) also have mitoses distributed randomly in the hyphae as opposed to at branchpoints. Surprisingly, however, no phosphorylation of the CDK tyrosine 18 residue, the conserved substrate of Swe1p kinases, was detected in normally growing cells. In contrast, abundant CDK tyrosine phosphorylation was apparent in starving cells, resulting in diminished nuclear density. This starvation-induced CDK phosphorylation is AgSwe1p dependent, and overexpressed AgSwe1p is sufficient to delay nuclei even in rich nutrient conditions. In starving cells lacking septins or AgSwe1p negative regulators, the nuclear density is further diminished compared with wild type. We have generated a model in which AgSwe1p may regulate mitosis in response to cell intrinsic morphogenesis cues and external nutrient availability in multinucleated cells.
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Wang, Richard R. C., Xiaomei Li, and N. Jerry Chatterton. "Cytological evidence for assortment mitosis leading to loss of heterozygosity in rice." Genome 49, no. 5 (2006): 556–57. http://dx.doi.org/10.1139/g06-015.

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In the root meristem cells of the rice line AMR, which causes loss of heterozygosity in its hybrids, both normal and assortment mitoses were observed. During normal mitosis, chromosomes did not form homologous pairs at metaphase; all chromosomes lined up at the equatorial plate and 2 chromatids of each chromosome disjoined at the centromere and moved toward opposite poles. During assortment mitosis, varying numbers of paired homologues were observed at mitotic metaphase. Two groups of 12 chromosomes separated and moved towards the opposite poles of daughter cells with few chromosomes having their chromatids separated at anaphase. These observations support the proposed mechanism that is responsible for early genotype fixation in rice hybrids involving AMR.Key words: mitosis, homologous chromosome, genotype fixation, loss of heterozygosity, rice.
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Dissertations / Theses on the topic "Mitosis"

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Ducháček, Ladislav. "Mitosis." Master's thesis, Vysoké učení technické v Brně. Fakulta výtvarných umění, 2016. http://www.nusl.cz/ntk/nusl-240615.

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Mitosis diploma work is figurative sculpture created by duplication statues. These duplicates to form pairs at each mitotic bind. Couples are composed into complex system, and thus form a spherical object. Against the background of this work is to introduce perspective on the human population and its culture as an independent organic whole.
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Breeden, Lauren N. "Mitosis : a collection." Honors in the Major Thesis, University of Central Florida, 2003. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/409.

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This item is only available in print in the UCF Libraries. If this is your Honors Thesis, you can help us make it available online for use by researchers around the world by following the instructions on the distribution consent form at http://library.ucf.edu/Systems/DigitalInitiatives/DigitalCollections/InternetDistributionConsentAgreementForm.pdf You may also contact the project coordinator, Kerri Bottorff, at kerri.bottorff@ucf.edu for more information.<br>Bachelors<br>Arts and Sciences<br>English
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Daniels, M. J. "Mechanisms regulating eukaryotic mitosis." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598272.

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The fertilised egg gives rise to the entire organism through the coordination of high fidelity chromosome replication and then segregation. When this mechanism is corrupted cells acquire stable genetic mutations that absolve them from the normal proliferative impediments at work to keep the organism healthy. This is the basis of cancer. In order to understand and then rationally treat cancer we must understand the process of cell division. In this thesis I elucidate novel information pertaining to three mechanisms that guide a cell through the process of mitosis. Firstly as cells enter mitosis I have identified the requirement of the Promyelocytic Leukaemia (PML) tumour suppressor for the integrity of the antephase checkpoint. PML limits the intracellular distribution and mobility of the CHFR checkpoint protein previously known to be required for the antephase checkpoint. During mitotic progression the RanGTPase orchestrates several distinct events. By showing that the principle GTPase activating protein (RanGAP1) is the subject of multiple mitotic phosphorylations that regulate its activity I have identified part of the mechanism that allows the cell cycle to control the actions of the RanGTPase in mitosis. Finally I have provided evidence that the tumour suppressor BRCA2 is required during the process of cytokinesis, and that in its absence cells frequently become aneuploid. Thus I have identified a new route of genetic instability in a hereditary form of cancer.
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Sochaj, Alicja Maria. "Dissecting roles and regulation of the fission yeast kinetochore protein Spc7." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/7763.

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Accurate chromosome segregation is critical as unequal distribution of the genomic DNA results in impaired cell function or cell death. Kinetochores, the multi-protein structures assembled on centromeric DNA, drive chromosome segregation. Chromosome segregation is under supervision of mitotic spindle checkpoint. The mitotic spindle checkpoint is a surveillance mechanism ensuring that cells enter anaphase with all kinetochores properly attached to spindle microtubules and thereby preventing missegregation. Some checkpoint proteins are localised at kinetochore where they generate and enhance the checkpoint signal. Mps1 (Mph1 in S. pombe) and Aurora B (Ark1 in S. pombe) kinases are required for precise chromosome segregation and mitotic spindle checkpoint in fission yeast. In this study we investigate the roles of Mph1 and Ark1 in regulating the S. pombe kinetochore protein Spc7, which is the homologue of human Blinkin/KNL1. We demonstrated that both kinases target the N-terminus of Spc7. Loss of phosphorylation on the candidate phosphosites results in sensitivity to microtubule depolymerizing drugs indicating mitotic defects. As Blinkin has been proposed to be a docking platform for checkpoint proteins, we tested the possibility that Mph1 kinase is involved in kinetochore targeting of checkpoint proteins, Bub1 and Bub3. Our results demonstrate that Mph1-dependent phosphorylation of Spc7 at conserved MELT motifs is required for Bub1 and Bub3 kinetochore localisation. We were able to reconstitute the interaction between Spc7 and the Bub proteins in vitro demonstrating that the Spc7 phosphorylation is sufficient for Bub1 and Bub3 association with Spc7, most likely with Bub3 making the Spc7 contact. Mimicking phosphorylation at the MELT motifs leads to constitutive Bub1 localisation at kinetochores. We also showed that the N-terminus of Spc7 has microtubule binding activity regulated by Ark1 kinase. Mimicking phosphorylation at Ark1 sites results in reduced amount of recombinant Spc7 co-precipitating with microtubules in microtubule binding assays. Moreover, two stretches of basic residues, that contribute to Spc7 microtubule binding activity, have been mapped in the extreme Nterminus of Spc7. Spc7 also interacts with PP1 phosphatase, Dis2 in S. pombe, which is required for checkpoint silencing, but the mechanism of this interactions remains to be determined. These findings allow us to speculate on Spc7 role(s) in coupling microtubule binding with spindle checkpoint activation and silencing.
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Madriles, Gimeno Carles. "Mitosis based speculative multithreaded architectures." Doctoral thesis, Universitat Politècnica de Catalunya, 2012. http://hdl.handle.net/10803/124709.

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In the last decade, industry made a right-hand turn and shifted towards multi-core processor designs, also known as Chip-Multi-Processors (CMPs), in order to provide further performance improvements under a reasonable power budget, design complexity, and validation cost. Over the years, several processor vendors have come out with multi-core chips in their product lines and they have become mainstream, with the number of cores increasing in each processor generation. Multi-core processors improve the performance of applications by exploiting Thread Level Parallelism (TLP) while the Instruction Level Parallelism (ILP) exploited by each individual core is limited. These architectures are very efficient when multiple threads are available for execution. However, single-thread sections of code (single-thread applications and serial sections of parallel applications) pose important constraints on the benefits achieved by parallel execution, as pointed out by Amdahl’s law. Parallel programming, even with the help of recently proposed techniques like transactional memory, has proven to be a very challenging task. On the other hand, automatically partitioning applications into threads may be a straightforward task in regular applications, but becomes much harder for irregular programs, where compilers usually fail to discover sufficient TLP. In this scenario, two main directions have been followed in the research community to take benefit of multi-core platforms: Speculative Multithreading (SpMT) and Non-Speculative Clustered architectures. The former splits a sequential application into speculative threads, while the later partitions the instructions among the cores based on data-dependences but avoid large degree of speculation. Despite the large amount of research on both these approaches, the proposed techniques so far have shown marginal performance improvements. In this thesis we propose novel schemes to speed-up sequential or lightly threaded applications in multi-core processors that effectively address the main unresolved challenges of previous approaches. In particular, we propose a SpMT architecture, called Mitosis, that leverages a powerful software value prediction technique to manage inter-thread dependences, based on pre-computation slices (p-slices). Thanks to the accuracy and low cost of this technique, Mitosis is able to effectively parallelize applications even in the presence of frequent dependences among threads. We also propose a novel architecture, called Anaphase, that combines the best of SpMT schemes and clustered architectures. Anaphase effectively exploits ILP, TLP and Memory Level Parallelism (MLP), thanks to its unique finegrain thread decomposition algorithm that adapts to the available parallelism in the application.
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Chakraborty, Papia. "Regulation of Nucleoporins in Mitosis." Scholarly Repository, 2007. http://scholarlyrepository.miami.edu/oa_dissertations/54.

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Nucleoporins mediate nucleocytoplasmic trafficking in interphase. In mitosis, upon nuclear envelope breakdown, the role and regulation of Nups remain to be elucidated. An important subcomplex of nucleoporins is the Nup107-160 complex, which, in mitosis, is involved in spindle assembly and nuclear pore re-assembly. Here we show that the level of a key constituent of the Nup107-160 complex- Nup96 is cell cycle regulated. We found that the mechanism involved in regulating Nup96 levels in mitosis is proteolysis by the anaphase-promoting complex (APC). Nup96 interacts with the APC, and its proteolysis can be regulated by Cdc20 and Cdh1. Like the Nup107-160 complex, the APC is localized at kinetochores, centrosomes, and spindles. Disruption of Nup96 levels led to an acceleration of prophase to prometaphase transition and, most importantly, resulted in a delay of G1 progression. Thus, regulation of Nup96 proteolysis in mitosis sets the stage for proper G1 progression. Additionally, we have observed differential regulation of members of the Nup107-160 complex during mitosis and have identified interacting partners of Nup96 at the centrosome which reveal a novel role of nucleoporins in regulating microtubule nucleation.
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Martin, Carol-Anne. "Role of microcephalin at mitosis." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/8734.

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A large brain is one of the most distinguishing features of humans compared to other members of the animal kingdom. During mammalian evolution there has been a disproportionate enlargement of the brain relative to body size and this expansion has been particularly prominent during the past 3 million years of human lineage. This must be the consequence of adaptive genetic alterations during mammalian evolution, but the genes and molecular processes altered are essentially unknown. One approach for identifying candidate genes for brain size regulation is through characterisation of Mendelian disorders of brain development. In particular, primary microcephaly has received considerable interest as a model disease for studying brain size regulators because patients present with a profoundly reduced brain size but have no other malformations. Genetic studies have identified mutations in seven genes that can cause primary microcephaly. All the primary microcephaly proteins localise to the centrosome at some stage during the cell cycle and have roles in a diverse range of functions including centrosome maturation, centriole formation and microtubule organisation at the spindle pole. The precise mechanism leading to primary microcephaly is not known but a prevalent hypothesis is that centrosome dysfunction disrupts mitosis of neural progenitor cells. Despite there being strong evidence in support of this hypothesis for most primary microcephaly genes, MCPH1 (the first primary microcephaly gene to be identified) always appeared to be functionally distinct from other primary microcephaly proteins. Most work on MCPH1 has focussed on its role in the DNA damage response and cell cycle timing rather than on its mitotic role. As a result, the aim of this thesis is to perform a detailed analysis of MCPH1 function during mitosis. In this thesis, three isoforms of MCPH1 were characterised and their localisation, expression and stability examined. It was established that MCPH1 is highly regulated during mitosis. MCPH1 transcript and protein levels vary significantly throughout the cell cycle and MCPH1 protein is targeted for degradation late in mitosis. In addition, MCPH1 is hyperphosphorylated during mitosis (in prometaphase-arrested cells) suggesting that phosphorylation could potentially regulate MCPH1 mitotic function. Twelve mitotic phosphorylation sites were identified by phosphopeptide mapping, many of which were CDK1 and PLK1 consensus sites. Both PLK1 and CDK1 also contribute to MCPH1 phosphorylation in vivo. Although MCPH1 non-phosphorylatable mutants localise normally during mitosis, binding to interaction partners may be affected which may have functional consequences. During mitosis MCPH1 localises to the centrosomes and kinetochores. Consistent with this localisation, RNAi-mediated knockdown of MCPH1 leads to metaphase arrest with multipolar spindles, major defects in chromosome alignment and loss of chromatid cohesion. In addition, MCPH1 deficient mouse embryonic fibroblast cells also demonstrate similar chromosome alignment defects, strengthening this finding in an independent system. Live-imaging of MCPH1 depleted cells demonstrate that a normal bipolar spindle and metaphase plate are initially formed, but subsequently chromosomes and chromatids drop off the metaphase plate and eventually the spindle collapses. This suggests that the primary function of MCPH1 is to allow timely progression through metaphase, possibly by mediating kinetochore-microtubule attachments to satisfy the spindle activated checkpoint. Therefore my work describes several roles for MCPH1 in mitosis (centrosome stability, chromosome alignment and metaphase progression) suggesting that its role in mitosis could result in primary microcephaly in a number of different ways.
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ZUCCA, FEDERICO. "ASTRAL MICROTUBULE REGULATION IN MITOSIS." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/790260.

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The faithful generation of two daughter cells genetically identical to each other relies on a complex cellular machinery called the mitotic spindle, which binds to each sister chromatid pair in a bipolar fashion and drives their segregation to the two newly generated daughters. The mitotic spindle is mainly composed of microtubules, microtubule-associated proteins and motor proteins. Spindle microtubules are conventionally divided into three different categories: (i) kinetochore microtubules (kMTs), which connect the spindle poles to chromosomes, (ii) interpolar microtubules (iMTs), which form a bundle that connects the two poles together, and (iii) astral microtubules (aMTs), which connect the poles to the cellular cortex. Proper spindle functions require drastic changes in microtubule dynamics. kMTs are unstable while searching for chromosomes, stabilized upon reaching a correct bipolar attachment and destabilized again soon after sister chromatids separation. iMTs remain unstable up to anaphase, when they become stable to drive spindle elongation. Finally, aMTs are stabilized and destabilized upon binding to different zones of the cellular cortex, to correctly direct the spindle. If differences in microtubules dynamics have been reported, the molecular mechanisms underneath them remain elusive. To gather insights into the machinery controlling spindle microtubules, we took advantage of cdc14 cdc5 double mutant cells. These cells already proved to be precious as they revealed an essential requirement for spindle microtubule regulation – that is the activity of the phosphatase Cdc14 and the polo-like kinase Cdc5 for iMT stabilization in anaphase. We now show that central to the regulation of each type of spindle microtubule is the activity of the Anaphase Promoting Complex or Cyclosome in combination with its activator subunit Cdc20 (APC/C-Cdc20), that via removal of a yet to be identified substrate triggers aMT stabilization. We propose that the signalling cascade initiated by the APC/C-Cdc20 – namely the metaphase to anaphase transition – sets the order of events that finely control the chromosome segregation process through the regulation of specific types of spindle microtubule.
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Cortez, Beatriz de Araujo. "Interação da crisotila com células de carcinoma de pulmão humano em cultura: interferência com a mitose utilizando genes repórteres e microscopia em tempo real e estudo do potencial genotóxico." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/41/41131/tde-05042010-134617/.

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Asbesto é um nome geral dado a seis tipos de fibras minerais encontradas naturalmente na crosta terrestre. Estas fibras vêm sendo exploradas industrialmente desde 1970, porém diversos trabalhadores expostos às fibras apresentaram patologias no trato respiratório, como fibroses e carcinomas. Alguns tipos de fibra foram banidos do mercado, porém o tipo de asbesto crisotila ainda pode ser comercializado na maioria dos países. Estudos in vivo e in vitro tentam elucidar as alterações causadas pela exposição à asbesto nos tecidos e nas células que possam estar relacionadas ao aparecimento de doenças, e foi verificado que a exposição às fibras leva a quebras na dupla fita de DNA, estresse oxidativo, formação de células micronucleadas e células aneuploides. O presente estudo teve como objetivo verificar a presença de alterações causadas em células em cultura expostas à crisotila por 48 h e recuperadas em meio livre de fibras por 48 h, 4 dias e 8 dias, além de observar por microscopia em tempo real divisões aberrantes após a exposição as fibras por 24 e 48h. Foram verificadas alterações que permaneceram na cultura mesmo após 8 dias de recuperação, quando não foram mais observadas fibras na cultura, como formação de células aneuploides, diminuição de frequência de células em G0/G1, aumento de células em G2/M e aumento relativo de células em metáfase quanto à porcentagem de células em fases mais tardias da fase M do ciclo. Já aumento da frequência de células micronucleadas ocorreu apenas nos períodos quando foram observadas fibras na cultura. Para análise da formação de mitoses multipolares e destinos destas células foram construídos vetores para expressão de tubulinas fusionadas a proteínas fluorescentes RFP e GFP, padronizadas as condições de transfecção e de aquisição de imagens para que as células tratadas com crisotila fossem observadas por time-lapse. Alguns destinos de mitoses multipolares causadas pelo tratamento com crisotila foram observados, como morte em metáfase, divisão gerando duas ou três células filhas, fusão de células durante a telófase e retenção em metáfase. Os dados sugerem também a indução da amplificação centrossômica, que parece ocorrer inicialmente em células interfásicas, e também devido à fusão de células.<br>Asbestos is a general name given to six different fibrous silicate minerals found naturally in the earth\'s crust. These fibers are being exploited industrially since 1970, but several workers exposed to the fibers developed diseases in the respiratory tract, such as fibrosis and carcinomas. Some types of fiber were banished from the market, but the type of asbestos chrysotile can still be marketed in most countries. Studies in vivo and in vitro are trying to elucidate the asbestos effects in tissues and cells that could be related to the development of diseases, and these studies verified that asbestos exposure lead to DNA double strand breaks, oxidative stress, multinucleated and aneuploid cell formation. The present work aimed to verify the alterations in culture cells exposed to chrysotile for 48 h and recovered in fiber-free medium for 48 h, 4 days and 8 days, and also observe aberrant mitosis using time-lapse microscopy after 24 h and 48 h of chrysotile exposure. Some alterations were observed and remained in cell culture even after 8 days of recovery when chrysotile fibers were no longer observed - such as aneuploid cell formation, increased frequencies of G2/M cell, decreased frequencies of G1 cells, and increased frequencies of cells in early M phases as metaphase. The induction of micronuclei occurred only during the periods that fibers were observed in cell culture. For the analysis of multipolar mitosis formation and destinies of these cells after chrysotile treatment, DNA vectors for the expression of tubulins fused to fluorescent proteins (GFP and RFP) were constructed, and the conditions for cells transfection and image acquisition for time-lapse microscopy were established. The fate of some multipolar metaphases was observed: cell retention on metaphase, cell cycle progression generating two or three daughter cells, cell fusion during cytokinesis or during telophase after a multipolar anaphase, and cell death. The centrosome amplification was not observed during the M phase of cell cycle, and may occur in interphase, and also despite cell fusion.
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Masiá, Fandos Nuria. "Targeting mitosis in hormone-refractory prostate cancer." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670655.

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El CaP és la segona neoplàsia maligna invasiva diagnosticada amb major freqüència i la taxa de supervivència a 5 anys dels homes amb malaltia metastàtica cau per sota del 30%. Els andrògens, a través del receptor d'andrògens, són crucials per a l'inici i la progressió del CaP i, per tant, la ADT ha estat el principal tractament del CaP localment avançat, metastàtic i recurrent. Les teràpies de deprivació androgènica són capaces d'aconseguir inicialment una resposta bioquímica en la majoria dels pacients; no obstant això, les remissions són temporals i la malaltia acaba progressant a un estat independent d'andrògens, també denominat CRPC. Després de la progressió a CRPC, la supervivència mitjana d'aquests pacients és de menys de 2 anys i la malaltia acaba sent pràcticament intractable. Els mecanismes moleculars que causen aquesta transició continuen sent en gran part desconeguts. La creixent evidència en els últims anys suggereix que les cèl·lules de CaP insensibles als andrògens han estat reprogramades genèticament per a regular de manera selectiva l'expressió de gens de la fase M del cicle cel·lular. Els taxans, dirigits als microtúbuls, ja s'estan utilitzant en la pràctica clínica per a pacients amb CaP avançat, però la supervivència continua sent modesta i els pacients acaben desenvolupant resistència a la teràpia. Pel fet que la progressió mitòtica és un procés altament regulat, la nostra hipòtesi és que les proteïnes de fase M expressades de manera aberrant poden conferir a les cèl·lules CaP un avantatge per al creixement en condicions de depleció d'andrògens i, en conseqüència, representen possibles dianes terapèutiques per a la intervenció molecular de pacients amb CRPC. Encara que diversos inhibidors del cicle cel·lular no han aconseguit demostrar benefici en l'entorn clínic del CRPC, continua havent-hi un gran interès en aquest enfocament i encara hi ha desafiaments importants per a intentar tractar a aquests pacients amb teràpies dirigides que siguin eficaces. En aquest context, l'objectiu principal d'aquesta tesi és obtenir nous coneixements moleculars sobre la progressió del CaP, amb especial èmfasi en la participació dels reguladors mitòtics en l'adquisició de la independència a andrògens dels tumors de pròstata.<br>El CaP es la segunda neoplasia maligna invasiva diagnosticada con mayor frecuencia y la tasa de supervivencia a 5 años de los hombres con enfermedad metastásica cae por debajo del 30%. Los andrógenos, a través del receptor de andrógenos, son cruciales para el inicio y la progresión del CaP y, por tanto, la ADT ha sido el principal tratamiento del CaP localmente avanzado, metastásico y recurrente. Las terapias de deprivación androgénica son capaces de conseguir inicialmente una respuesta bioquímica en la mayoría de los pacientes; sin embargo, las remisiones son temporales y la enfermedad acaba progresando a un estado independiente de andrógenos, también denominado CRPC. Tras la progresión a CRPC, la supervivencia media de estos pacientes es de menos de 2 años y la enfermedad acaba siendo prácticamente intratable. Los mecanismos moleculares que causan esta transición siguen siendo en gran parte desconocidos. La creciente evidencia en los últimos años sugiere que las células de CaP insensibles a andrógenos han sido reprogramadas genéticamente para regular de forma selectiva la expresión de genes de la fase M del ciclo celular. Los taxanos, dirigidos a los microtúbulos, ya se están utilizando en la práctica clínica para pacientes con CaP avanzado, pero la supervivencia sigue siendo modesta y los pacientes acaban desarrollando resistencia a la terapia. Debido a que la progresión mitótica es un proceso altamente regulado, nuestra hipótesis es que las proteínas de fase M expresadas de manera aberrante pueden conferir a las células CaP una ventaja para el crecimiento en condiciones de depleción de andrógenos y, en consecuencia, representan posibles dianas terapéuticas para la intervención molecular de pacientes con CRPC. Aunque varios inhibidores del ciclo celular no han logrado demostrar beneficio en el entorno clínico del CRPC, sigue habiendo un gran interés en este enfoque y todavía hay desafíos importantes para intentar tratar a estos pacientes con terapias dirigidas que sean eficaces. En este contexto, el objetivo principal de esta tesis es obtener nuevos conocimientos moleculares sobre la progresión del CaP, con especial énfasis en la participación de los reguladores mitóticos en la adquisición de la independencia a andrógenos de los tumores de próstata.<br>PCa is the second most frequently diagnosed invasive malignancy and the 5-year survival rate of men with metastatic disease drops below 30%. Androgens, through the AR, are crucial for the initiation and progression of PCa and thus, ADT has been the mainstay of treatment for locally advanced, metastatic and recurring PCa. Androgen-ablation therapies can initially achieve a biochemical response in the majority of patients; however, remissions are temporary and the disease invariably progresses to an androgen-independent state, also termed CRPC. Upon progression to CRPC, the median survival for those patients is less than 2 years, and the disease is essentially untreatable. The molecular mechanisms that cause this transition remain largely unknown. Increasing evidence in recent years suggest that androgen insensitive PCa cells have undergone a genetic reprogramming to selectively upregulate the expression of M-phase cell cycle genes. Microtubule-targeting taxanes are already being used in the clinical practice for patients with advanced PCa, but survival remains modest and resistance inevitably develops. Because mitotic progression is a highly regulated process, we hypothesized that aberrantly expressed M-phase proteins may confer PCa cells an advantage to growth in androgen-depleted conditions and consequently represent potential therapeutic targets for the molecular intervention of CRPC patients. Although several small molecule inhibitors of the cell cycle have failed to demonstrate benefit in the clinical setting of CRPC, there remains a keen interest in this approach and significant challenges persist to match patients with effective targeted therapies. In this context, the main goal of this thesis is to gain novel molecular insights into the progression of PCa, with special emphasis on the involvement of mitotic regulators in the acquisition of prostate tumors androgen independence.<br>Universitat Autònoma de Barcelona. Programa de Doctorat en Bioquímica, Biologia Molecular i Biomedicina
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Books on the topic "Mitosis"

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Hinchcliffe, Edward H., ed. Mitosis. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1904-9.

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McAinsh, Andrew D., ed. Mitosis. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-993-2.

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Sharp, David J., ed. Mitosis. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0329-0.

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L, Rieder Conly, ed. Mitosis and meiosis. Academic Press, 1999.

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Sarosh, Minal. Mitosis & other poems. Writers Workshop, 1992.

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Sarosh, Minal. Mitosis & other poems. Writers Workshop, 1992.

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Bowen, I. D. Mitosis and apoptosis: Matters of life and death. Chapman & Hall, 1998.

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Gagliardi, L. John. Electrostatic considerations in mitosis: Integrating physics and cell biology in mitosis. Iuniverse Inc, 2009.

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Cregan, Elizabeth R. All about mitosis and meiosis. Compass Point Books, 2010.

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Cregan, Elizabeth R. All about mitosis and meiosis. Compass Point Books, 2010.

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Book chapters on the topic "Mitosis"

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Preston, Terence M., Conrad A. King, and Jeremy S. Hyams. "Mitosis." In The Cytoskeleton and Cell Motility. Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0393-7_4.

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Ciliberto, Andrea, and Rosella Visintin. "Mitosis." In Encyclopedia of Systems Biology. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_13.

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Hangay, George, Susan V. Gruner, F. W. Howard, et al. "Mitosis." In Encyclopedia of Entomology. Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_4649.

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Preston, Terence M., Conrad A. King, and Jeremy S. Hyams. "Mitosis." In The Cytoskeleton and Cell Motility. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-8010-2_4.

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Stauffer, Sarah, Aaron Gardner, Dewi Ayu Kencana Ungu, Ainara López-Córdoba, and Matthias Heim. "Mitosis." In Labster Virtual Lab Experiments: Basic Biology. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-57996-1_2.

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Gooch, Jan W. "Mitosis." In Encyclopedic Dictionary of Polymers. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14241.

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Santra, Sangita. "Mitosis." In Encyclopedia of Animal Cognition and Behavior. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-47829-6_507-1.

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Santra, Sangita. "Mitosis." In Encyclopedia of Animal Cognition and Behavior. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-55065-7_507.

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Quinn, C. M., and N. A. Wright. "Mitosis Counting." In Assessment of Cell Proliferation in Clinical Practice. Springer Japan, 1992. http://dx.doi.org/10.1007/978-4-431-68287-5_5.

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Quinn, C. M., and N. A. Wright. "Mitosis Counting." In Assessment of Cell Proliferation in Clinical Practice. Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-3190-8_5.

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Conference papers on the topic "Mitosis"

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Ding, Ruiwen, James Hall, Neil Tenenholtz, and Kristen Severson. "Improving Mitosis Detection on Histopathology Images Using Large Vision-Language Models." In 2024 IEEE International Symposium on Biomedical Imaging (ISBI). IEEE, 2024. http://dx.doi.org/10.1109/isbi56570.2024.10635613.

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Gu, Hongyan, Zihan Yan, Ayesha Alvi, et al. "Supporting Mitosis Detection AI Training with Inter-Observer Eye-Gaze Consistencies." In 2024 IEEE 12th International Conference on Healthcare Informatics (ICHI). IEEE, 2024. http://dx.doi.org/10.1109/ichi61247.2024.00013.

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Yancey, Robin. "Parallel YOLO-based Model for Real-time Mitosis Counting." In WSCG'2022 - 30. International Conference in Central Europe on Computer Graphics, Visualization and Computer Vision'2022. Západočeská univerzita, 2022. http://dx.doi.org/10.24132/csrn.3201.32.

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It is estimated that breast cancer incidences will increase by more than 50% by 2030 from 2011. Mitosis counting is one of the most commonly used methods of assessing the level of progression, and is a routine task for every patient diagnosed with invasive cancer. Although mitotic count is the strongest prognostic value, it is a tedious and subjective task with poor reproducibility, especially for non-experts. Object detection networks such as Faster RCNN have recently been adapted to medical applications to automatically localize regions of interest better than a CNN alone. However, the speed and accuracy of newer state-of-the-art models such as YOLO are now leaders in object detection, which had yet be applied to mitosis counting. Moreover, combining results of multiple YOLO versions run in parallel and increasing the size of the data in a way that is appropriate for the specific task are some of the other methods can be used to further improve the score overall. Using these techniques the highest F-scores of 0.95 and 0.96 on the MITOS-ATYPIA 2014 challenge and MITOS-ATYPIA 2012 challenge mitosis counting datasets are achieved, respectively.
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Quiñones, Carlos García, Carlos Madriles, Jesús Sánchez, Pedro Marcuello, Antonio González, and Dean M. Tullsen. "Mitosis compiler." In the 2005 ACM SIGPLAN conference. ACM Press, 2005. http://dx.doi.org/10.1145/1065010.1065043.

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Garcia, Lluvia. "Mitosis Mystery!" In RGV STEM Ed Conference. The University of Texas Rio Grande Valley, 2024. http://dx.doi.org/10.51734/ajfm9784.

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Mitchison, Timothy J. "Abstract SY28-01: Is mitosis the target of “anti-mitotic” cancer drugs." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-sy28-01.

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Marson, Giorgia Azzurra, Sebastien Andreina, Lorenzo Alluminio, Konstantin Munichev, and Ghassan Karame. "Mitosis: Practically Scaling Permissioned Blockchains." In ACSAC '21: Annual Computer Security Applications Conference. ACM, 2021. http://dx.doi.org/10.1145/3485832.3485915.

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Rangarajan, Parthasarathy, Prabhu Ramamoorthy, Satish Ramalingam, et al. "Abstract B32: Gedunin induces autophagy during mitosis, a novel form of mitotic catastrophe." In Abstracts: Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; Oct 27-30, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1940-6215.prev-13-b32.

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Boufraqech, Myriem, Darmood Wei, Urbain Weyemi, et al. "Abstract 2727: LOX is a novel mitotic spindle-associated protein essential for mitosis." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2727.

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Paul, Angshuman, and Dipti Prasad Mukherjee. "Enhanced Random Forest for Mitosis Detection." In the 2014 Indian Conference. ACM Press, 2014. http://dx.doi.org/10.1145/2683483.2683569.

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Reports on the topic "Mitosis"

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Joukov, Vladimir. The Role of BRCA1/BARD1 Heterodimers in the Mitosis-Interphase Transition. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada471801.

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Chang, Long-Sheng. The Role of Drosophila Merlin in the Control of Mitosis Exit and Development. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada488249.

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Chang, Long-Sheng. The Role of Drosophila Merlin in the Control of Mitosis Exit and Development. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada460492.

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Keck, Jamie M., and Steve I. Reed. The Effects of Deregulated Cyclin Expression in Mitosis. A Role in Breast Tumorigenesis. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada469549.

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Keck, Jamie M., and Steven I. Reed. The Effects of Deregulated Cyclin E Expression in Mitosis: A Role in Breast Tumorigenesis. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada443699.

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Keck, Jamie M. The Effects of Deregulated Cyclin E Expression in Mitosis: A Role in Breast Tumorigenesis. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada425602.

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Miller, Stephanie. Mitosis-Specific Negative Regulation of EGF-Receptor in Breast Cancer: Molecular Mechanisms, Biological Significance and Therapeutic Application. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada398100.

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Lin, Shiaw-Yih. Mitosis-Specific Negative Regulation of EGF-Receptor in Breast Cancer: Molecular Mechanisms, Biological Significance and Therapeutic Application. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada390715.

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Miller, Stephanie. Mitosis-Specific Negative Regulation of EGF-receptor in Breast Cancer: Molecular Mechanisms, Biological Significance and Therapeutic Application. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada392131.

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Cui, Zheng. Blocking Internalization of Phosphatidylethanolamine at Cleavage Furrow of Mitosis as a Novel Mechanism of Anti-Breast-Cancer Strategy. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada417523.

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