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Journal articles on the topic 'Cell synchronization'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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1

PRESNOV, E. V. "SYNCHRONIZATION OF CELL DIVISION." Journal of Biological Systems 07, no. 02 (June 1999): 213–23. http://dx.doi.org/10.1142/s0218339099000140.

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Most living organisms display many types of biological rhythms. We describe how a growing population of cells may be distributed between age classes or cell types, and define conditions necessary to produce synchronous population development. A probabilistic model describing the changes in cell numbers during proliferation is presented. The model predicts that during cell reproduction with constant parameters any cell population approaches a stationary behavior. According to this model, synchronization of cell growth is possible if there is a uniform parameter set for cell division. This point is illustrated by a set of graphs showing snapshots of model simulations with different parameter sets for transient and stationary behaviors.

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2

Galgano, Paul J., and Carl L. Schildkraut. "Cell Synchronization Using Centrifugal Elutriation." Cold Spring Harbor Protocols 2006, no. 2 (July 2006): pdb.prot4490. http://dx.doi.org/10.1101/pdb.prot4490.

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3

Wang, Yong, Guo Qing Xiong, and Pan Fei Wu. "Performance Analysis of Synchronization Detection Algorithms in TD-LTE Cell Search." Advanced Materials Research 1049-1050 (October 2014): 1911–16. http://dx.doi.org/10.4028/www.scientific.net/amr.1049-1050.1911.

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This paper mainly studies the TD-LTE cell search synchronization process. The synchronization process is mainly divided into the Primary Synchronization and the secondary synchronization detection process synchronization process. This paper present a mixed-correlation primary synchronization detection algorithm and Non-coherent secondary synchronization detection algorithm. Mixed-related synchronization detection algorithm can reduce the impact of frequency offset and multipath effects of detection. Non-coherent detection algorithm can reduce computation complexity so that it can improve the secondary synchronous detection rate.

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4

Kumagai-Sano, Fumi, Tomomi Hayashi, Toshio Sano, and Seiichiro Hasezawa. "Cell cycle synchronization of tobacco BY-2 cells." Nature Protocols 1, no. 6 (December 2006): 2621–27. http://dx.doi.org/10.1038/nprot.2006.381.

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5

Kryukov, Yakov, Dmitriy Pokamestov, and Eugeniy Rogozhnikov. "Cell search and synchronization in 5G NR." ITM Web of Conferences 30 (2019): 04007. http://dx.doi.org/10.1051/itmconf/20193004007.

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An overview of the physical signals foreseen by the 3GPP 5G New Radio specification for frame synchronization and cell search in fifth- generation wireless broadband access systems is presented in the paper. The frame synchronization algorithm and the cell initialization procedure are demonstrated. An estimate of probability of error detection of a physical identifier by the signals of the primary and secondary synchronization is obtained. The comparison of the successful synchronization in AWGN channel for 4G LTE and 5G NR is shown.

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6

Koo, Ok Jae, Mohammad Shamim Hossein, So Gun Hong, Jose A. Martinez-Conejero, and Byeong Chun Lee. "Cell cycle synchronization of canine ear fibroblasts for somatic cell nuclear transfer." Zygote 17, no. 1 (February 2009): 37–43. http://dx.doi.org/10.1017/s096719940800498x.

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SummaryCycle synchronization of donor cells in the G0/G1 stage is a crucial step for successful somatic cell nuclear transfer. In the present report, we evaluated the effects of contact inhibition, serum starvation and the reagents – dimethyl sulphoxide (DMSO), roscovitine and cycloheximide (CHX) – on synchronization of canine fibroblasts at the G0/G1 stage. Ear fibroblast cells were collected from a beagle dog, placed into culture and used for analysis at passages three to eight. The population doubling time was 36.5 h. The proportion of G0/G1 cells was significantly increased by contact inhibition (77.1%) as compared with cycling cells (70.1%); however, extending the duration of culture did not induce further synchronization. After 24 h of serum starvation, cells were effectively synchronized at G0/G1 (77.1%). Although synchronization was further increased gradually after 24 h and even showed significant difference after 72 h (82.8%) of starvation, the proportion of dead cells also significantly increased after 24 h. The percentage of cells at the G0/G1 phase was increased (as compared with controls) after 72 h treatment with DMSO (76.1%) and after 48 h treatment with CHX (73.0%) or roscovitine (72.5%). However, the rate of cell death was increased after 24 and 72 h of treatment with DMSO and CHX, respectively. Thus, we recommend the use of roscovitine for cell cycle synchronization of canine ear fibroblasts as a preparatory step for SCNT.

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Zhang, De Min, Xiang Zhu, Zhi Hui Qiu, and Chao Bo Duan. "Design and Implementation of Cell Search Time Synchronization in LTE System Based on FPGA." Applied Mechanics and Materials 380-384 (August 2013): 4076–79. http://dx.doi.org/10.4028/www.scientific.net/amm.380-384.4076.

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LTE is accepted worldwide as the Long Term Evolution Perspective for todays 3G and 4G networks. Cell search time synchronization is an important physical layer procedure by which a user equipment (UE) acquires synchronization with a cell and detects the physical layer cell ID of that cell. Timing synchronization is consisted of the symbol timing synchronization and frame synchronization. This paper supplies the introduction of synchronization signals, presents the detection method, and analyzes the design based on FPGA platform and finally simulated on the Modelsim 6.5 and implemented in Xilinx Virtex-6 kit.

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8

Hyun, Hyuk, Seung-Eun Lee, Yeo-Jin Son, Min-Young Shin, Yun-Gwi Park, Eun-Young Kim, and Se-Pill Park. "Cell Synchronization by Rapamycin Improves the Developmental Competence of Porcine SCNT Embryos." Cellular Reprogramming 18, no. 3 (June 2016): 195–205. http://dx.doi.org/10.1089/cell.2015.0090.

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9

Biberstein, M., Y. Harel, and A. Heilper. "Clock synchronization in Cell/B.E. traces." Concurrency and Computation: Practice and Experience 21, no. 14 (September 25, 2009): 1760–74. http://dx.doi.org/10.1002/cpe.1436.

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10

Tian, Yuan, Chunxiong Luo, Yuheng Lu, Chao Tang, and Qi Ouyang. "Cell cycle synchronization by nutrient modulation." Integrative Biology 4, no. 3 (2012): 328. http://dx.doi.org/10.1039/c2ib00083k.

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11

Cooper, S. "Rethinking synchronization of mammalian cells for cell cycle analysis." Cellular and Molecular Life Sciences 60, no. 6 (June 2003): 1099–106. http://dx.doi.org/10.1007/s00018-003-2253-2.

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12

Davis, Penny K., Alan Ho, and Steven F. Dowdy. "Biological Methods for Cell-Cycle Synchronization of Mammalian Cells." BioTechniques 30, no. 6 (June 2001): 1322–31. http://dx.doi.org/10.2144/01306rv01.

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13

Cao, Guanghui, Li-Ming Liu, and Stephen F. Cleary. "Modified method of mammalian cell synchronization improves yield and degree of synchronization." Experimental Cell Research 193, no. 2 (April 1991): 405–10. http://dx.doi.org/10.1016/0014-4827(91)90113-9.

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14

Perillo-Adamer, F., M. Kosinski, Y. M. Dupertuis, D. Viertl, A. Bischof Delaloye, and F. Buchegger. "Fluorodeoxyuridine mediated cell cycle synchronization in S-phase increases the Auger radiation cell killing with 125I-iododeoxyuridine." Nuklearmedizin 48, no. 06 (2009): 233–42. http://dx.doi.org/10.3413/nukmed-0247.

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Summary Aim: 125I-iododeoxyuridine is a potential Auger radiation therapy agent. Its incorporation in DNA of proliferating cells is enhanced by fluorodeoxyuridine. Here, we evaluated therapeutic activities of 125I-iododeoxyuridine in an optimized fluorodeoxyuridine pre-treatment inducing S-phase synchronization. Methods: After S-phase synchronization by fluorodeoxyuridine, cells were treated with 125I-iododeoxyuridine. Apoptosis analysis and S-phase synchronization were studied by flow cytometry. Cell survival was determined by colony-forming assay. Based on measured growth parameters, the number of decays per cell that induced killing was extrapolated. Results: Treatment experiments showed that 72 to 91% of synchronized cells were killed after 0.8 and 8 kBq/ml 125I-iododeoxyuridine incubation, respectively. In controls, only 8 to 38% of cells were killed by corresponding 125I-iododeoxyuridine activities alone and even increasing the activity to 80 kBq/ml gave only 42 % killing. Duplicated treatment cycles or repeated fluorodeoxyuridine pre-treatment allowed enhancing cell killing to >95 % at 8 kBq/ml 125I-iododeoxyuridine. About 50 and 160 decays per S-phase cells in controls and S-phase synchronization, respectively, were responsible for the observed cell killing at 0.8 kBq/ml radio-iododeoxyuridine. Conclusion: These data show the successful application of fluorodeoxyuridine that provided increased 125I-iododeoxyuridine Auger radiation cell killing efficacy through S-phase synchronization and high DNA incorporation of radio-iododeoxyuridine.

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15

Cooper, Stephen. "The synchronization manifesto: a critique of whole‐culture synchronization." FEBS Journal 286, no. 23 (September 11, 2019): 4650–56. http://dx.doi.org/10.1111/febs.15050.

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Vittadello, Sean T., Scott W. McCue, Gency Gunasingh, Nikolas K. Haass, and Matthew J. Simpson. "Mathematical models incorporating a multi-stage cell cycle replicate normally-hidden inherent synchronization in cell proliferation." Journal of The Royal Society Interface 16, no. 157 (August 2019): 20190382. http://dx.doi.org/10.1098/rsif.2019.0382.

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We present a suite of experimental data showing that cell proliferation assays, prepared using standard methods thought to produce asynchronous cell populations, persistently exhibit inherent synchronization. Our experiments use fluorescent cell cycle indicators to reveal the normally hidden cell synchronization, by highlighting oscillatory subpopulations within the total cell population. These oscillatory subpopulations would never be observed without these cell cycle indicators. On the other hand, our experimental data show that the total cell population appears to grow exponentially, as in an asynchronous population. We reconcile these seemingly inconsistent observations by employing a multi-stage mathematical model of cell proliferation that can replicate the oscillatory subpopulations. Our study has important implications for understanding and improving experimental reproducibility. In particular, inherent synchronization may affect the experimental reproducibility of studies aiming to investigate cell cycle-dependent mechanisms, including changes in migration and drug response.

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17

BATTOGTOKH, DORJSUREN. "FORCED SYNCHRONIZATION OF EUKARYOTIC CELLS." Modern Physics Letters B 21, no. 30 (December 30, 2007): 2033–53. http://dx.doi.org/10.1142/s0217984907014395.

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A comprehensive mathematical model of the budding yeast cell cycle, accounting for several dozen published experiments, has thirty five variables and one hundred and forty parameters.5 Detailed models describing cell cycle regulation in other organisms have also a large number of variables and parameters. Complexity rises further upon integrating the cell cycle network to other pathways in the cell. For some practical and theoretical issues, abundant complexity in realistic models can be tackled by studying first a functional subset of a model to understand the mechanism of a concerned process, and then by revealing the conditions of its occurrence in a detailed model. Here we review this approach applied to the problem of cell synchronization. Using analytic results obtained from a minimal model, we simulate cell synchronization in comprehensive mathematical models for budding and fission yeast cell cycles. Our results demonstrate that an experimental method based on periodic forcing of the synthesis of cell cycle regulators can be a powerful tool for cell synchronization.

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18

Eckhorn, R., H. J. Reitboeck, M. Arndt, and P. Dicke. "Feature Linking via Synchronization among Distributed Assemblies: Simulations of Results from Cat Visual Cortex." Neural Computation 2, no. 3 (September 1990): 293–307. http://dx.doi.org/10.1162/neco.1990.2.3.293.

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We recently discovered stimulus-specific interactions between cell assemblies in cat primary visual cortex that could constitute a global linking principle for feature associations in sensory and motor systems: stimulus-induced oscillatory activities (35-80 Hz) in remote cell assemblies of the same and of different visual cortex areas mutually synchronize, if common stimulus features drive the assemblies simultaneously. Based on our neurophysiological findings we simulated feature linking via synchronizations in networks of model neurons. The networks consisted of two one-dimensional layers of neurons, coupled in a forward direction via feeding connections and in lateral and backward directions via modulatory linking connections. The models' performance is demonstrated in examples of region linking with spatiotemporally varying inputs, where the rhythmic activities in response to an input, that initially are uncorrelated, become phase locked. We propose that synchronization is a general principle for the coding of associations in and among sensory systems and that at least two distinct types of synchronization do exist: stimulus-forced (event-locked) synchronizations support “crude instantaneous” associations and stimulus-induced (oscillatory) synchronizations support more complex iterative association processes. In order to bring neural linking mechanisms into correspondence with perceptual feature linking, we introduce the concept of the linking field (association field) of a local assembly of visual neurons. The linking field extends the concept of the invariant receptive field (RF) of single neurons to the flexible association of RFs in neural assemblies.

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19

Shin, Soon-Lim, and Erik De Schutter. "Dynamic Synchronization of Purkinje Cell Simple Spikes." Journal of Neurophysiology 96, no. 6 (December 2006): 3485–91. http://dx.doi.org/10.1152/jn.00570.2006.

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Purkinje cells (PCs) integrate all computations performed in the cerebellar cortex to inhibit neurons in the deep cerebellar nuclei (DCN). Simple spikes recorded in vivo from pairs of PCs separated by <100 μm are known to be synchronized with a sharp peak riding on a broad peak, but the significance of this finding is unclear. We show that the sharp peak consists exclusively of simple spikes associated with pauses in firing. The broader, less precise peak was caused by firing-rate co-modulation of faster firing spikes. About 13% of all pauses were synchronized, and these pauses had a median duration of 20 ms. As in vitro studies have reported that synchronous pauses can reliably trigger spikes in DCN neurons, we suggest that the subgroup of spikes causing the sharp peak is important for precise temporal coding in the cerebellum.

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20

Shaw, Josephine, Kristofor Payer, Sungmin Son, William H. Grover, and Scott R. Manalis. "A microfluidic “baby machine” for cell synchronization." Lab on a Chip 12, no. 15 (2012): 2656. http://dx.doi.org/10.1039/c2lc40277g.

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21

JavanMoghadam-Kamrani, Sonia, and Khandan Keyomarsi. "Synchronization of the cell cycle using Lovastatin." Cell Cycle 7, no. 15 (August 2008): 2434–40. http://dx.doi.org/10.4161/cc.6364.

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22

Dano, S., M. F. Madsen, and P. G. Sorensen. "Quantitative characterization of cell synchronization in yeast." Proceedings of the National Academy of Sciences 104, no. 31 (July 25, 2007): 12732–36. http://dx.doi.org/10.1073/pnas.0702560104.

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23

Zou, Kingsley Jun, and Kristo Wenjie Yang. "Network synchronization for dense small cell networks." IEEE Wireless Communications 22, no. 2 (April 2015): 108–17. http://dx.doi.org/10.1109/mwc.2015.7096293.

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24

Tsakraklides, Vasiliki, Elena Brevnova, Gregory Stephanopoulos, and A. Joe Shaw. "Improved Gene Targeting through Cell Cycle Synchronization." PLOS ONE 10, no. 7 (July 20, 2015): e0133434. http://dx.doi.org/10.1371/journal.pone.0133434.

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25

Kuritz, Karsten, Dirke Imig, Michael Dyck, and Frank Allgöwer. "Ensemble control for cell cycle synchronization of heterogeneous cell populations." IFAC-PapersOnLine 51, no. 19 (2018): 44–47. http://dx.doi.org/10.1016/j.ifacol.2018.09.034.

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26

VM, krovskii, Nechepurenko AA, Tarasov DG, Korotkov KG, and Abushkevich VG. "Sinoatrial node pacemaker cell pool dynamics upon synchronization with vagus nerve rhythm." Journal of Applied Biotechnology & Bioengineering 6, no. 3 (May 2, 2019): 114–16. http://dx.doi.org/10.15406/jabb.2019.06.00182.

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Aim: To reveal the dynamics of sinoatrial node pacemaker cell pools upon synchronization with vagus nerve rhythm through the model of vagal-cardiac synchronization. Materials and methods: Observations were carried out on 10 narcotized cats. The animals were tracheostomized and pump-ventilated, and the pericardium accessed via an open-chest transsternal incision. A device (KELSY scanner manufactured by Elsys, St. Petersburg, Russia) accompanied by a microscope and a video-camera, to visualize the luminescence of excitation processes in the sinoatrial node in a high-frequency electromagnetic field (1024 Hz) was placed in the sinoatrial area of a working heart. Luminescent focus in the sinoatrial node was registered as a peripherally cut end of the vagus nerve was stimulated with bursts of electrical impulses (5 impulses, 2 ms, 20 Hz) from an electrostimulator. Results: Luminescence localized at the entrance of the cranial vena cava was visualized in a high-frequency electrical field in narcotized cats. The luminescent focal area was not homogenous and looked like a number of luminescent pools. Upon vagal-cardiac synchronization caused by the stimulation of a peripherally cut end of the vagus nerve with bursts of electrical impulses, the focus was wide and solid. Conclusion: Here, pacemaker cell dynamics were studied in the feline heart. When vagal- cardiac synchronization was activated, synchronization of the heart with vagus nerve rhythm was accompanied by an increase in the early depolarization area in the sinoatrial area of the feline heart. The mechanisms underlying heart rate synchronization are not clearly defined. Rhythm is achieved through actions of the SA node and the vagus nerve. Our data confirm the vagal- cardiac synchronization model.

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Rodríguez-Martínez, Marta, Stephanie A. Hills, John F. X. Diffley, and Jesper Q. Svejstrup. "Multiplex Cell Fate Tracking by Flow Cytometry." Methods and Protocols 3, no. 3 (July 17, 2020): 50. http://dx.doi.org/10.3390/mps3030050.

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Measuring differences in cell cycle progression is often essential to understand cell behavior under different conditions, treatments and environmental changes. Cell synchronization is widely used for this purpose, but unfortunately, there are many cases where synchronization is not an option. Many cell lines, patient samples or primary cells cannot be synchronized, and most synchronization methods involve exposing the cells to stress, which makes the method incompatible with the study of stress responses such as DNA damage. The use of dual-pulse labelling using EdU and BrdU can potentially overcome these problems, but the need for individual sample processing may introduce a great variability in the results and their interpretation. Here, we describe a method to analyze cell proliferation and cell cycle progression by double staining with thymidine analogues in combination with fluorescent cell barcoding, which allows one to multiplex the study and reduces the variability due to individual sample staining, reducing also the cost of the experiment.

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Yaghoubi, Zahra, and Hassan Zarabadipour. "Phase and Antiphase Synchronization between 3-Cell CNN and Volta Fractional-Order Chaotic Systems via Active Control." Mathematical Problems in Engineering 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/121323.

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Synchronization of fractional-order chaotic dynamical systems is receiving increasing attention owing to its interesting applications in secure communications of analog and digital signals and cryptographic systems. In this paper, a drive-response synchronization method is studied for “phase and antiphase synchronization” of a class of fractional-order chaotic systems via active control method, using the 3-cell and Volta systems as an example. These examples are used to illustrate the effectiveness of the synchronization method.

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Rosas Almeida, David I., and Laura O. Orea Leon. "Robust-Output-Controlled Synchronization Strategy for Arrays of Pancreatic β-Cells." Complexity 2018 (November 5, 2018): 1–10. http://dx.doi.org/10.1155/2018/5174981.

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This paper presents a synchronization strategy based on second-order sliding mode control, to obtain robust controlled synchronization in an array of uncertain pancreatic β-cells. This strategy considers a synchronization scheme with a reference cell, which incorporates the desired dynamics, and an array of cells, which does not demonstrate adequate synchronization. The array may be formed by active and inactive cells having different strengths in gap junctions. For an array with three cells, we design the coupling signal considering that only the output of an active cell of the array is available. The coupling signal is the signum of the difference between the output of the reference cell and the output of an active cell in the array; this ensures exact synchronization in finite time between both cells. Then, this coupling signal is applied to the other cells in the array, and we establish the conditions required to be satisfied to obtain approximate synchronization between the reference cell and all other cells in the array. The performance of this technique is demonstrated by the results of numerical simulations performed for several cases of connections for an array with three cells and the reference cell. Finally, we show through a numerical simulation that this technique can be applied to arrays with many β-cells.

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Gibbons, John, and Leigh Anne Busbee. "Ovulation Synchronization in Sheep." Biology of Reproduction 81, Suppl_1 (July 1, 2009): 586. http://dx.doi.org/10.1093/biolreprod/81.s1.586.

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31

Reddy, G. Prem Veer, Cheryl Y. Tiarks, Lizhen Pang, Joanne Wuu, Chung-Cheng Hsieh, and Peter J. Quesenberry. "Cell Cycle Analysis and Synchronization of Pluripotent Hematopoietic Progenitor Stem Cells." Blood 90, no. 6 (September 15, 1997): 2293–99. http://dx.doi.org/10.1182/blood.v90.6.2293.

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Abstract Hematopoietic stem cells purified from mouse bone marrow are quiescent with less than 2% of Lin− Hoechstlow/Rhodaminelow (Lin− Holow/Rholow) and 10% to 15% of Lin−/Sca+ cells in S phase. These cells enter proliferative cycle and progress through G1 and into S phase in the presence of cytokines and 5% heat-inactivated fetal calf serum (HI-FCS). Cytokine-stimulated Lin− Holow/Rholow cells took 36 to 40 hours to complete first division and only 12 hours to complete each of 5 subsequent divisions. These cells require 16 to 18 hours to transit through G0 /G1 period and 28 to 30 hours to enter into mid-S phase during the first cycle. Up to 56% of Lin− Rholow/Holow cells are high-proliferative potential (7 factor-responsive) colony-forming cells (HPP-CFC). At isolation, HPP-CFC are quiescent, but after 28 to 30 hours of culture, greater than 60% are in S phase. Isoleucine-deprivation of Lin−Holow/Rholow cells in S phase of first cycle reversibly blocked them from entering into second cycle. After the release from isoleucine-block, these cells exhibited a G1 period of less than 2 hours and entered into mid-S phase by 12 hours. Thus, the duration of G1 phase of the cells in second cycle is 4 to 5 times shorter than that observed in their first cycle. Similar cell cycle kinetics are observed with Lin−/Sca+ population of bone marrow cells. Stem cell factor (SCF ) alone, in the presence of HI-FCS, is as effective as a cocktail of 2 to 7 cytokines in inducing quiescent Lin−/Sca+ cells to enter into proliferative cycle. Aphidicolin treatment reversibly blocked cytokine-stimulated Lin−/Sca+ cells at G1 /S boundary, allowing their tight synchrony as they progress through first S phase and enter into second G1 . For these cells also, SCF alone is sufficient for their progression through S phase. These studies indicate a very short G1 phase for stem cells induced to proliferate and offer experimental approaches to synchronize murine hematopoietic stem cells.

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Reddy, G. Prem Veer, Cheryl Y. Tiarks, Lizhen Pang, Joanne Wuu, Chung-Cheng Hsieh, and Peter J. Quesenberry. "Cell Cycle Analysis and Synchronization of Pluripotent Hematopoietic Progenitor Stem Cells." Blood 90, no. 6 (September 15, 1997): 2293–99. http://dx.doi.org/10.1182/blood.v90.6.2293.2293_2293_2299.

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Hematopoietic stem cells purified from mouse bone marrow are quiescent with less than 2% of Lin− Hoechstlow/Rhodaminelow (Lin− Holow/Rholow) and 10% to 15% of Lin−/Sca+ cells in S phase. These cells enter proliferative cycle and progress through G1 and into S phase in the presence of cytokines and 5% heat-inactivated fetal calf serum (HI-FCS). Cytokine-stimulated Lin− Holow/Rholow cells took 36 to 40 hours to complete first division and only 12 hours to complete each of 5 subsequent divisions. These cells require 16 to 18 hours to transit through G0 /G1 period and 28 to 30 hours to enter into mid-S phase during the first cycle. Up to 56% of Lin− Rholow/Holow cells are high-proliferative potential (7 factor-responsive) colony-forming cells (HPP-CFC). At isolation, HPP-CFC are quiescent, but after 28 to 30 hours of culture, greater than 60% are in S phase. Isoleucine-deprivation of Lin−Holow/Rholow cells in S phase of first cycle reversibly blocked them from entering into second cycle. After the release from isoleucine-block, these cells exhibited a G1 period of less than 2 hours and entered into mid-S phase by 12 hours. Thus, the duration of G1 phase of the cells in second cycle is 4 to 5 times shorter than that observed in their first cycle. Similar cell cycle kinetics are observed with Lin−/Sca+ population of bone marrow cells. Stem cell factor (SCF ) alone, in the presence of HI-FCS, is as effective as a cocktail of 2 to 7 cytokines in inducing quiescent Lin−/Sca+ cells to enter into proliferative cycle. Aphidicolin treatment reversibly blocked cytokine-stimulated Lin−/Sca+ cells at G1 /S boundary, allowing their tight synchrony as they progress through first S phase and enter into second G1 . For these cells also, SCF alone is sufficient for their progression through S phase. These studies indicate a very short G1 phase for stem cells induced to proliferate and offer experimental approaches to synchronize murine hematopoietic stem cells.

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33

Banfalvi, Gaspar. "Cell cycle synchronization of animal cells and nuclei by centrifugal elutriation." Nature Protocols 3, no. 4 (March 27, 2008): 663–73. http://dx.doi.org/10.1038/nprot.2008.34.

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34

Chen, Mengfei, Jingjing Huang, Xuejiao Yang, Bingqian Liu, Weizhong Zhang, Li Huang, Fei Deng, et al. "Serum Starvation Induced Cell Cycle Synchronization Facilitates Human Somatic Cells Reprogramming." PLoS ONE 7, no. 4 (April 18, 2012): e28203. http://dx.doi.org/10.1371/journal.pone.0028203.

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35

Qiu, Nasha, Xiangrui Liu, Meihua Sui, Jianbin Tang, and Youqing Shen. "Paclitaxel improved gene transfection efficiency through cell synchronization in SW480 cells." Journal of Controlled Release 213 (September 2015): e83. http://dx.doi.org/10.1016/j.jconrel.2015.05.138.

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36

Bastounis, Effie, Begoña Álvarez-González, Juan C. del Álamo, Juan C. Lasheras, and Richard A. Firtel. "Cooperative cell motility during tandem locomotion of amoeboid cells." Molecular Biology of the Cell 27, no. 8 (April 15, 2016): 1262–71. http://dx.doi.org/10.1091/mbc.e15-12-0836.

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Streams of migratory cells are initiated by the formation of tandem pairs of cells connected head to tail to which other cells subsequently adhere. The mechanisms regulating the transition from single to streaming cell migration remain elusive, although several molecules have been suggested to be involved. In this work, we investigate the mechanics of the locomotion of Dictyostelium tandem pairs by analyzing the spatiotemporal evolution of their traction adhesions (TAs). We find that in migrating wild-type tandem pairs, each cell exerts traction forces on stationary sites (∼80% of the time), and the trailing cell reuses the location of the TAs of the leading cell. Both leading and trailing cells form contractile dipoles and synchronize the formation of new frontal TAs with ∼54-s time delay. Cells not expressing the lectin discoidin I or moving on discoidin I–coated substrata form fewer tandems, but the trailing cell still reuses the locations of the TAs of the leading cell, suggesting that discoidin I is not responsible for a possible chemically driven synchronization process. The migration dynamics of the tandems indicate that their TAs’ reuse results from the mechanical synchronization of the leading and trailing cells’ protrusions and retractions (motility cycles) aided by the cell–cell adhesions.

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Sun, Guoyun, Yao Teng, Zixuan Zhao, Lih Feng Cheow, Hanry Yu, and Chia-Hung Chen. "Functional Stem Cell Sorting via Integrative Droplet Synchronization." Analytical Chemistry 92, no. 11 (May 7, 2020): 7915–23. http://dx.doi.org/10.1021/acs.analchem.0c01312.

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Hermans, F., and E. Tsiporkova. "Merging microarray cell synchronization experiments through curve alignment." Bioinformatics 23, no. 2 (January 15, 2007): e64-e70. http://dx.doi.org/10.1093/bioinformatics/btl320.

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Gordon Steel, G. "Cell synchronization unfortunately may not benefit cancer therapy." Radiotherapy and Oncology 32, no. 2 (August 1994): 95–97. http://dx.doi.org/10.1016/0167-8140(94)90094-9.

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40

Brodskii, V. Ya. "Ultradian rhythms in cell population. Problem of synchronization." Bulletin of Experimental Biology and Medicine 124, no. 6 (December 1997): 1159–63. http://dx.doi.org/10.1007/bf02445107.

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Sharma, Arun Kumar. "Synchronization in mammalian system: An introduction." Methods in Cell Science 18, no. 2 (June 1996): 75–81. http://dx.doi.org/10.1007/bf00122157.

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Keyomarsi, Khandan. "Synchronization of mammalian cells by Lovastatin." Methods in Cell Science 18, no. 2 (June 1996): 109–14. http://dx.doi.org/10.1007/bf00122161.

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Abe, Hideki, Kim L. Keen, and Ei Terasawa. "Rapid Action of Estrogens on Intracellular Calcium Oscillations in Primate Luteinizing Hormone-Releasing Hormone-1 Neurons." Endocrinology 149, no. 3 (December 13, 2007): 1155–62. http://dx.doi.org/10.1210/en.2007-0942.

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Feedback controls of estrogen in LHRH-1 neurons play a pivotal role in reproductive function. However, the mechanism of estrogen action in LHRH-1 neurons is still unclear. In the present study, the effect of estrogens on intracellular calcium ([Ca2+]i) oscillations in primate LHRH-1 neurons was examined. Application of 17β-estradiol (E2, 1 nm) for 10 min increased the frequency of [Ca2+]i oscillations within a few minutes. E2 also increased the frequency of [Ca2+]i synchronization among LHRH-1 neurons. Similar E2 effects on the frequency of [Ca2+]i oscillations were observed under the presence of tetrodotoxin, indicating that estrogen appears to cause direct action on LHRH-1 neurons. Moreover, application of a nuclear membrane-impermeable estrogen dendrimer conjugate, not control dendrimer, resulted in a robust increase in the frequencies of [Ca2+]i oscillations and synchronizations, indicating that effects estrogens on [Ca2+]i oscillations and their synchronizations do not require their entry into the cell nucleus. Exposure of cells to E2 in the presence of the estrogen receptor antagonist ICI 182,780 did not change the E2-induced increase in the frequency of [Ca2+]i oscillations or the E2-induced increase in the synchronization frequency. Collectively, estrogens induce rapid, direct stimulatory actions through receptors located in the cell membrane/cytoplasm of primate LHRH-1 neurons, and this action of estrogens is mediated by an ICI 182,780-insensitive mechanism yet to be identified.

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Wang, Xueqing, Lingya Pan, Ning Mao, Lifang Sun, Xiangjuan Qin, and Jie Yin. "Cell-cycle synchronization reverses Taxol resistance of human ovarian cancer cell lines." Cancer Cell International 13, no. 1 (2013): 77. http://dx.doi.org/10.1186/1475-2867-13-77.

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Vacková, I., M. Engelová, I. Marinov, and M. Tománek. "Cell cycle synchronization of porcine granulosa cells in G1 stage with mimosine." Animal Reproduction Science 77, no. 3-4 (July 2003): 235–45. http://dx.doi.org/10.1016/s0378-4320(03)00034-4.

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Hagan, Iain M., Agnes Grallert, and Viesturs Simanis. "Cell Cycle Synchronization of Schizosaccharomyces pombe by Centrifugal Elutriation of Small Cells." Cold Spring Harbor Protocols 2016, no. 6 (June 2016): pdb.prot091231. http://dx.doi.org/10.1101/pdb.prot091231.

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Bartha, Attila, and D. Dumitrescu. "Perturbation in Population of Pulse-Coupled Oscillators Leads to Emergence of Structure." International Journal of Computers Communications & Control 6, no. 2 (January 6, 2011): 222. http://dx.doi.org/10.15837/ijccc.2011.2.2169.

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A new synchronization model based on pulse-coupled oscillators is proposed. A population of coupled oscillators is represented as a cellular automaton. Each cell periodically enters a firing state. Firing of a cell is sensed by other cells in a neighborhood of radius R. As a result the sensing cell may change its firing rate. The interaction strength between a firing and a sensing cell decreases with the squared distance between the two cells. For most starting conditions waves of synchronized firing cells emerge. Simulations indicate that for certain parameter values the emergence of synchronization waves occurs only if there is dispersion in the intrinsic firing frequencies of the cells. Emergence of synchronization waves is an important feature of the model.

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Gekeler, Volker, and Hans Probst. "Synchronization of replicons in Ehrlich ascites cells." Experimental Cell Research 175, no. 1 (March 1988): 97–108. http://dx.doi.org/10.1016/0014-4827(88)90258-3.

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Kwon, Dae-Jin, In-Sul Hwang, Tae-Uk Kwak, Hyeon Yang, Mi-Ryung Park, Sun-A. Ock, Keon Bong Oh, Jae-Seok Woo, Gi-Sun Im, and Seongsoo Hwang. "Effects of Cell Cycle Regulators on the Cell Cycle Synchronization of Porcine induced Pluripotent Stem Cells." Development & Reproduction 21, no. 1 (March 2017): 47–54. http://dx.doi.org/10.12717/dr.2017.21.1.047.

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Trotter, Eleanor Wendy, and Iain Michael Hagan. "Release from cell cycle arrest with Cdk4/6 inhibitors generates highly synchronized cell cycle progression in human cell culture." Open Biology 10, no. 10 (October 2020): 200200. http://dx.doi.org/10.1098/rsob.200200.

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Each approach used to synchronize cell cycle progression of human cell lines presents a unique set of challenges. Induction synchrony with agents that transiently block progression through key cell cycle stages are popular, but change stoichiometries of cell cycle regulators, invoke compensatory changes in growth rate and, for DNA replication inhibitors, damage DNA. The production, replacement or manipulation of a target molecule must be exceptionally rapid if the interpretation of phenotypes in the cycle under study is to remain independent of impacts upon progression through the preceding cycle. We show how these challenges are avoided by exploiting the ability of the Cdk4/6 inhibitors, palbociclib, ribociclib and abemaciclib to arrest cell cycle progression at the natural control point for cell cycle commitment: the restriction point. After previous work found no change in the coupling of growth and division during recovery from CDK4/6 inhibition, we find high degrees of synchrony in cell cycle progression. Although we validate CDK4/6 induction synchronization with hTERT-RPE-1, A549, THP1 and H1299, it is effective in other lines and avoids the DNA damage that accompanies synchronization by thymidine block/release. Competence to return to cycle after 72 h arrest enables out of cycle target induction/manipulation, without impacting upon preceding cycles.

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