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Journal articles on the topic 'The Cycling'

Author: Grafiati

Published: 28 June 2021

Last updated: 1 February 2022

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1

Buchkovich, K. J., and E. B. Ziff. "Nerve growth factor regulates the expression and activity of p33cdk2 and p34cdc2 kinases in PC12 pheochromocytoma cells." Molecular Biology of the Cell 5, no. 11 (November 1994): 1225–41. http://dx.doi.org/10.1091/mbc.5.11.1225.

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In the absence of serum, nerve growth factor (NGF) promotes the survival and differentiation of the PC12 pheochromocytoma cell line. In the presence of serum, NGF acts primarily as a differentiation factor and negative regulator of cell cycling. To investigate NGF control of cell cycling, we have analyzed the regulation of cyclin dependent kinases during PC12 cell differentiation. NGF treatment leads to a reduction in the steady-state protein levels of p33cdk2 and p34cdc2, two key regulators of cell cycle progression. The decrease in p33cdk2 and p34cdc2 coincides with a decrease in the enzymatic activity of cyclinA-p34cdc2, cyclinB-p34cdc2, cyclinE-p33cdk2, and cyclinA-p33cdk2 kinases. The decline in p33cdk2 and p34cdc2 kinase activity in response to NGF is accelerated in cells that over-express the p140trk NGF receptor, suggesting that the timing of the down- regulation is dependent on the level of p140trk and the strength of the NGF signal. The level of cyclin A, a regulatory subunit of p33cdk2 and p34cdc2, is relatively constant during PC12 differentiation. Nevertheless, the DNA binding activity of the cyclinA-associated transcription factor E2F/DP decreases. Thus, NGF down-regulates the activity of cyclin dependent kinases and cyclin-transcription factor complexes during PC12 differentiation.

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2

Holding, Cathy. "Cycling without cyclins." Genome Biology 5 (2004): spotlight—20040824–01. http://dx.doi.org/10.1186/gb-spotlight-20040824-01.

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3

Traganos, Frank. "Cycling without Cyclins." Cell Cycle 3, no. 1 (January 2004): 31–33. http://dx.doi.org/10.4161/cc.3.1.608.

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4

Yi, Xie, and Li Bing. "The Transcription Express Characteristics of Several Genes in the Process of Bombyx mori Ovarian Carcinoma." Advanced Materials Research 796 (September 2013): 39–42. http://dx.doi.org/10.4028/www.scientific.net/amr.796.39.

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Bombyx mori cell line (BmN) comes fromBombyx moriovary cell subculture. In order to study the change of several genes transcription in the process ofBombyx moriovary cells primary culture and subculture, we usedBombyx moriovary organizations and BmN cell lines as research materials, used Real Time fluorescent quantitative RT-PCR to detect cyclin gene family (CyclinA, CyclinB, CyclinB3, CyclinE, CyclinL1), p53 and Telomerase genes transcription level in the ovary and BmN cell lines, and took Actin3 gene as reference to dispose the results. The results showed that in theBombyx moriBmN cell lines the expression of CyclinA, CyclinB, CyclinB3, CyclinE, CyclinL1 and Telomerase genes were higher than those in the ovary. The expression of CyclinB in the BmN was more then 3.8 which was 76 times higher than that in the ovary; The expression of p53 gene in the BmN cell was lower than that in the ovary; The expression of Telomerase gene in the BmN cell was higher than that in the ovary. The results accumulated a reliable data for further study on the the role of cyclin gene family, p53 gene, and Telomerase gene in the process ofBombyx moriovarian carcinoma.

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5

Diehl, J. Alan. "Cycling to Cancer with Cyclin D1." Cancer Biology & Therapy 1, no. 3 (May 5, 2002): 226–31. http://dx.doi.org/10.4161/cbt.72.

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6

Ježek, Jan, Daniel G. J. Smethurst, David C. Stieg, Z. A. C. Kiss, Sara E. Hanley, Vidyaramanan Ganesan, Kai-Ti Chang, Katrina F. Cooper, and Randy Strich. "Cyclin C: The Story of a Non-Cycling Cyclin." Biology 8, no. 1 (January 4, 2019): 3. http://dx.doi.org/10.3390/biology8010003.

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The class I cyclin family is a well-studied group of structurally conserved proteins that interact with their associated cyclin-dependent kinases (Cdks) to regulate different stages of cell cycle progression depending on their oscillating expression levels. However, the role of class II cyclins, which primarily act as transcription factors and whose expression remains constant throughout the cell cycle, is less well understood. As a classic example of a transcriptional cyclin, cyclin C forms a regulatory sub-complex with its partner kinase Cdk8 and two accessory subunits Med12 and Med13 called the Cdk8-dependent kinase module (CKM). The CKM reversibly associates with the multi-subunit transcriptional coactivator complex, the Mediator, to modulate RNA polymerase II-dependent transcription. Apart from its transcriptional regulatory function, recent research has revealed a novel signaling role for cyclin C at the mitochondria. Upon oxidative stress, cyclin C leaves the nucleus and directly activates the guanosine 5’-triphosphatase (GTPase) Drp1, or Dnm1 in yeast, to induce mitochondrial fragmentation. Importantly, cyclin C-induced mitochondrial fission was found to increase sensitivity of both mammalian and yeast cells to apoptosis. Here, we review and discuss the biology of cyclin C, focusing mainly on its transcriptional and non-transcriptional roles in tumor promotion or suppression.

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7

Resnitzky, D., M. Gossen, H. Bujard, and S. I. Reed. "Acceleration of the G1/S phase transition by expression of cyclins D1 and E with an inducible system." Molecular and Cellular Biology 14, no. 3 (March 1994): 1669–79. http://dx.doi.org/10.1128/mcb.14.3.1669.

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Conditional overexpression of human cyclins B1, D1, and E was accomplished by using a synthetic cDNA expression system based on the Escherichia coli tetracycline repressor. After induction of these cyclins in asynchronous Rat-1 fibroblasts, a decrease in the length of the G1 interval was observed for cyclins D1 and E, consistent with an acceleration of the G1/S phase transition. We observed, in addition, a compensatory lengthening of S phase and G2 so that the mean cell cycle length in populations constitutively expressing these cyclins was unchanged relative to those of their uninduced counterparts. We found that expression of cyclin B1 had no effect on cell cycle dynamics, despite elevated levels of cyclin B-associated histone H1 kinase activity. Induction of cyclins D1 and E also accelerated entry into S phase for synchronized cultures emerging from quiescence. However, whereas cyclin E exerted a greater effect than cyclin D1 in asynchronous cycling cells, cyclin D1 conferred a greater effect upon stimulation from quiescence, suggesting a specific role for cyclin D1 in the G0-to-G1 transition. Overexpression of cyclins did not prevent cells from entering into quiescence upon serum starvation, although a slight delay in attainment of quiescence was observed for cells expressing either cyclin D1 or cyclin E. These results suggest that cyclins D1 and E are rate-limiting activators of the G1-to-S phase transition and that cyclin D1 might play a specialized role in facilitating emergence from quiescence.

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8

Resnitzky, D., M. Gossen, H. Bujard, and S. I. Reed. "Acceleration of the G1/S phase transition by expression of cyclins D1 and E with an inducible system." Molecular and Cellular Biology 14, no. 3 (March 1994): 1669–79. http://dx.doi.org/10.1128/mcb.14.3.1669-1679.1994.

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Conditional overexpression of human cyclins B1, D1, and E was accomplished by using a synthetic cDNA expression system based on the Escherichia coli tetracycline repressor. After induction of these cyclins in asynchronous Rat-1 fibroblasts, a decrease in the length of the G1 interval was observed for cyclins D1 and E, consistent with an acceleration of the G1/S phase transition. We observed, in addition, a compensatory lengthening of S phase and G2 so that the mean cell cycle length in populations constitutively expressing these cyclins was unchanged relative to those of their uninduced counterparts. We found that expression of cyclin B1 had no effect on cell cycle dynamics, despite elevated levels of cyclin B-associated histone H1 kinase activity. Induction of cyclins D1 and E also accelerated entry into S phase for synchronized cultures emerging from quiescence. However, whereas cyclin E exerted a greater effect than cyclin D1 in asynchronous cycling cells, cyclin D1 conferred a greater effect upon stimulation from quiescence, suggesting a specific role for cyclin D1 in the G0-to-G1 transition. Overexpression of cyclins did not prevent cells from entering into quiescence upon serum starvation, although a slight delay in attainment of quiescence was observed for cells expressing either cyclin D1 or cyclin E. These results suggest that cyclins D1 and E are rate-limiting activators of the G1-to-S phase transition and that cyclin D1 might play a specialized role in facilitating emergence from quiescence.

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9

Soniat, Katherine. "Cycling." Women's Review of Books 21, no. 2 (November 2003): 16. http://dx.doi.org/10.2307/4024300.

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10

Cox, Peter. "Cycling." Transfers 2, no. 1 (March 1, 2012): 159–64. http://dx.doi.org/10.3167/trans.2012.020113.

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The mechanized mobility practices that came to dominate road use in the twentieth century—using cars, motorbikes, and bicycles—have been notable for the concurrent development of accompanying print literatures in the form of magazines and newspapers. The developmental history of each mode can be told through a number of distinct lenses, each revealing a part of the story of the mobility technology in use. In the context of a renaissance in cycling, there is an emergence of a new style of bicycle magazine that breaks the mould of previous journals.

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11

Reiser, Raoul, Jon Watt, and Michael Peterson. "Cycling." Sports Biomechanics 2, no. 2 (July 2003): 237–49. http://dx.doi.org/10.1080/14763140308522821.

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12

Dixon, Warren, and Matthew Bellman. "Cycling." Mechanical Engineering 138, no. 09 (September 1, 2016): S3—S7. http://dx.doi.org/10.1115/1.2016-sep-4.

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This article presents an overview of a control systems perspective. An electric field when applied to yield functional tasks is called as functional electrical stimulation (FES). FES is commonly prescribed as a treatment for various neurological disorders. Given the existence of regions in the crank cycle where it is inefficient to produce torque, a motor can be included as another torque source. FES control of the muscles yields cadence tracking in torque efficient regions, while the motor yields cadence tracking when it is efficient for the limbs to produce torque. The inclusion of a motor enables switching between stable systems and eliminates the need for the development of sufficient dwell-time conditions. Hence, the development of adaptive switched controllers for motorized FES-cycling systems may have a closer horizon. The inclusion of a motor also expands the possible control objectives that can be pursued.

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13

&NA;. "Cycling." Back Letter 5, no. 3 (1991): 4. http://dx.doi.org/10.1097/00130561-199105030-00005.

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14

Welberg, Leonie. "Cycling vesicles for a cycling SCN." Nature Reviews Neuroscience 11, no. 1 (December 9, 2009): 5. http://dx.doi.org/10.1038/nrn2799.

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15

Ehrhardt, Harald, Catarina Castro Alves, Franziska Wachter, and Irmela Jeremias. "TRAIL Preferentially Affects Cell Cycle-Arrested Tumor Cells Including Stem- and Progenitor Cells From Patients with Acute Lymphoblastic Leukemia." Blood 120, no. 21 (November 16, 2012): 1879. http://dx.doi.org/10.1182/blood.v120.21.1879.1879.

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Abstract Abstract 1879 Leukemic stem- and progenitor cells exhibit low cycling activity which might represent a major cause for their increased treatment resistance. TRAIL (TNF-related apoptosis inducing ligand) is a novel putative anticancer drug currently in phase I and II clinical testing. We recently showed that TRAIL is able to address stem- and progenitor cells from patients with acute lymphoblastic leukemia (ALL) in xenotransplantation assays (Alves et al., Blood 2012,119,4224). As stem- and progenitor cells are often non-cycling, we asked here, whether TRAIL is able to address resting leukemia cells. We used cell lines and primary tumor cells from children with ALL which were amplified in severely immuno-compromised mice (NSG mice). Cell cycle arrest was induced (i) by addition of conventional cytotoxic drugs which are known to act as cytostatic drugs such as doxorubicine; (ii) by biochemical inhibitors known to induce cell cycle arrest at different defined points of the cell cycle such as mimosine; (iii) by molecular approaches and knockdown of cyclinB arresting cell cycle in G2 or knockdown of cyclinE arresting cell cycle in G1. Unexpectedly, TRAIL-induced apoptosis was enhanced, whenever cell cycle was arrested. Cell cycle arrest sensitized towards TRAIL-induced apoptosis independently from the point or phase of cell cycle which was arrested (G0, G1 or G2) and independently from the agent used to arrest the cell cycle. Similarly, knockdown of cyclinB or cyclinE both clearly sensitized cell line cells towards TRAIL-induced apoptosis. Cytotoxic drugs and cell cycle inhibitors might arrest the cell cycle by activation of p53. Accordingly, when caffeine was added which inhibited p53 activity and drug-induced cell cycle arrest, sensitization towards TRAIL-induced apoptosis was blocked. We have recently established a novel method which enables performing knockdown experiments in tumor cells derived from ALL patients (Höfig et al., Cell Comm. Signal. 2012,10,8). Using this method and most important for clinical translation, we could show that knockdown of either cyclinB or cyclinE clearly sensitized patient-derived ALL cells towards TRAIL-induced apoptosis. Taken together and in contrast to most conventional cytotoxic drugs, TRAIL exerts anti-tumor activity preferentially against tumor cells in cell cycle arrest and less against actively cycling tumor cells. This special feature of TRAIL might explain its anti-tumor activity against stem- and progenitor cells in patients with ALL. Thus, TRAIL might represent an interesting drug to treat disease stages with accumulation of stem- and progenitor cells and static tumor disease, e.g., during minimal residual disease. Disclosures: No relevant conflicts of interest to declare.

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16

Cogswell, J. P., M. M. Godlevski, M. Bonham, J. Bisi, and L. Babiss. "Upstream stimulatory factor regulates expression of the cell cycle-dependent cyclin B1 gene promoter." Molecular and Cellular Biology 15, no. 5 (May 1995): 2782–90. http://dx.doi.org/10.1128/mcb.15.5.2782.

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Progression through the somatic cell cycle requires the temporal regulation of cyclin gene expression and cyclin protein turnover. One of the best-characterized examples of this regulation is seen for the B-type cyclins. These cyclins and their catalytic component, cdc2, have been shown to mediate both the entry into and maintenance of mitosis. The cyclin B1 gene has been shown to be expressed between the late S and G2 phases of the cell cycle, while the protein is degraded specifically at interphase via ubiquitination. To understand the molecular basis for transcriptional regulation of the cyclin B1 gene, we cloned the human cyclin B1 gene promoter region. Using a chloramphenicol acetyltransferase reporter system and both stable and transient assays, we have shown that the cyclin B1 gene promoter (extending to -3800 bp relative to the cap site) can confer G2-enhanced promoter activity. Further analysis revealed that an upstream stimulatory factor (USF)-binding site and its cognate transcription factor(s) are critical for expression from the cyclin B1 promoter in cycling HeLa cells. Interestingly, USF DNA-binding activity appears to be regulated in a G2-specific fashion, supporting the idea that USF may play some role in cyclin B1 gene activation. These studies suggest an important link between USF and the cyclin B1 gene, which in part explains how maturation promoting factor complex formation is regulated.

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17

Bouftas, Nora, and Katja Wassmann. "Cycling through mammalian meiosis: B-type cyclins in oocytes." Cell Cycle 18, no. 14 (June 23, 2019): 1537–48. http://dx.doi.org/10.1080/15384101.2019.1632139.

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18

Wang, Jia-Hao, Yan Li, Shou-Long Deng, Yi-Xun Liu, Zheng-Xing Lian, and Kun Yu. "Recent Research Advances in Mitosis during Mammalian Gametogenesis." Cells 8, no. 6 (June 10, 2019): 567. http://dx.doi.org/10.3390/cells8060567.

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Mitosis is a highly sophisticated and well-regulated process during the development and differentiation of mammalian gametogenesis. The regulation of mitosis plays an essential role in keeping the formulation in oogenesis and gametogenesis. In the past few years, substantial research progress has been made by showing that cyclins/cyclin-dependent kinase (CDK) have roles in the regulation of meiosis. In addition, more functional signaling molecules have been discovered in mitosis. Growing evidence has also indicated that miRNAs influence cell cycling. In this review, we focus on specific genes, cyclins/Cdk, signaling pathways/molecules, and miRNAs to discuss the latest achievements in understanding their roles in mitosis during gametogenesis. Further elucidation of mitosis during gametogenesis may facilitate delineating all processes of mammalian reproduction and the development of disease treatments.

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19

Abrieu, A., T. Brassac, S. Galas, D. Fisher, J. C. Labbe, and M. Doree. "The Polo-like kinase Plx1 is a component of the MPF amplification loop at the G2/M-phase transition of the cell cycle in Xenopus eggs." Journal of Cell Science 111, no. 12 (June 15, 1998): 1751–57. http://dx.doi.org/10.1242/jcs.111.12.1751.

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We have investigated whether Plx1, a kinase recently shown to phosphorylate cdc25c in vitro, is required for activation of cdc25c at the G2/M-phase transition of the cell cycle in Xenopus. Using immunodepletion or the mere addition of an antibody against the C terminus of Plx1, which suppressed its activation (not its activity) at G2/M, we show that Plx1 activity is required for activation of cyclin B-cdc2 kinase in both interphase egg extracts receiving recombinant cyclin B, and cycling extracts that spontaneously oscillate between interphase and mitosis. Furthermore, a positive feedback loop allows cyclin B-cdc2 kinase to activate Plx1 at the G2/M-phase transition. In contrast, activation of cyclin A-cdc2 kinase does not require Plx1 activity, and cyclin A-cdc2 kinase fails to activate Plx1 and its consequence, cdc25c activation in cycling extracts.

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20

Arkesteijn, Marco, Simon Jobson, James Hopker, and Louis Passfield. "The Effect of Cycling Intensity on Cycling Economy During Seated and Standing Cycling." International Journal of Sports Physiology and Performance 11, no. 7 (October 2016): 907–12. http://dx.doi.org/10.1123/ijspp.2015-0441.

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Background:Previous research has shown that cycling in a standing position reduces cycling economy compared with seated cycling. It is unknown whether the cycling intensity moderates the reduction in cycling economy while standing.Purpose:The aim was to determine whether the negative effect of standing on cycling economy would be decreased at a higher intensity.Methods:Ten cyclists cycled in 8 different conditions. Each condition was either at an intensity of 50% or 70% of maximal aerobic power at a gradient of 4% or 8% and in the seated or standing cycling position. Cycling economy and muscle activation level of 8 leg muscles were recorded.Results:There was an interaction between cycling intensity and position for cycling economy (P = .03), the overall activation of the leg muscles (P = .02), and the activation of the lower leg muscles (P = .05). The interaction showed decreased cycling economy when standing compared with seated cycling, but the difference was reduced at higher intensity. The overall activation of the leg muscles and the lower leg muscles, respectively, increased and decreased, but the differences between standing and seated cycling were reduced at higher intensity.Conclusions:Cycling economy was lower during standing cycling than seated cycling, but the difference in economy diminishes when cycling intensity increases. Activation of the lower leg muscles did not explain the lower cycling economy while standing. The increased overall activation, therefore, suggests that increased activation of the upper leg muscles explains part of the lower cycling economy while standing.

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21

Vogetseder, Alexander, Thomas Palan, Desa Bacic, Brigitte Kaissling, and Michel Le Hir. "Proximal tubular epithelial cells are generated by division of differentiated cells in the healthy kidney." American Journal of Physiology-Cell Physiology 292, no. 2 (February 2007): C807—C813. http://dx.doi.org/10.1152/ajpcell.00301.2006.

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We searched for evidence for a contribution of stem cells in growth of the proximal S3 segments of healthy rats. According to the stem cell model, stem cells are undifferentiated and slow cycling; the bulk of cycling cells are transit amplifying, rapidly cycling cells. We show the following. 1) By continuous application of a thymidine analog (ThA) for 7 days, S3 proximal epithelial cells in healthy kidneys display a high-cycling rate. 2) Slow-cycling cells, identified by lack of ThA uptake during 14 days of continuous ThA application up to death and by expression of the cell cycle protein Ki67 at death, have the same degree of differentiation as quiescent cells. 3) To detect rapidly cycling cells, rats were killed at various time points after injection of a ThA. Double immunofluorescence for ThA and a cell cycle marker was performed, with colocalization indicating successive divisions. During one week after division, daughter cells display a very low proliferation rate, indicating the absence of rapidly cycling cells. 4) Labeling with cyclin D1 showed that this low proliferation rate is due to cycle arrest. 5) More than 50% of the S3 cells entered the cell cycle 36 h after a potent proliferative stimulus (lead acetate injection). We conclude that generation of new cells in the proximal tubule relies on division of differentiated, normally slow-cycling cells. These may rapidly enter the cycle under an adequate stimulus.

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22

Burn, Bob. "Cycling Digits." Mathematical Gazette 75, no. 472 (June 1991): 154. http://dx.doi.org/10.2307/3620242.

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23

Nehoda, Hermann, Katherine Hourmont, and Boris W. Hochleitner. "Safe cycling." Lancet 353, no. 9159 (April 1999): 1192. http://dx.doi.org/10.1016/s0140-6736(05)74422-6.

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24

Stoffers, Manuel. "Cycling Cultures." Transfers 1, no. 1 (March 1, 2011): 147–54. http://dx.doi.org/10.3167/trans.2011.010111.

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Dave Horton, Paul Rosen, and Peter Cox (ed.), Cycling and Society (Aldershot: Ashgate, 2007), xvi + 205 pp., €77.00.A.A. Albert de la Bruhèze and F.C.A. Veraart, Fietsverkeer in praktijk en beleid in de twintigste eeuw: overeenkomsten en verschillen in fietsgebruik in Amsterdam, Eindhoven, Enschede, Zuidoost-Limburg, Antwerpen, Manchester, Kopenhagen, Hannover en Basel (Den Haag: Ministerie van Verkeer en Waterstaat/Stichting Historie der Techniek, 1999), 240 pp.Anne-Katrin Ebert, Radelnde Nationen: Die Geschichte des Fahrrads in Deutschland und den Niederlanden bis 1940 (Frankfurt a.M.: Campus Verlag, 2010), 495 pp., €49.90.

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25

Musio, Antonio, and Giuseppe Rainaldi. "Cycling-PRINS." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 390, no. 1-2 (April 1997): 1–4. http://dx.doi.org/10.1016/s0165-1218(96)00132-2.

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26

Dozza, Marco, Mont Hubbard, and Arend L. Schwab. "Cycling safety." Journal of Safety Research 67 (December 2018): 125. http://dx.doi.org/10.1016/j.jsr.2018.10.002.

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27

Passfield, Louis. "Cycling Science." Journal of Sports Sciences 35, no. 14 (April 10, 2017): 1327. http://dx.doi.org/10.1080/02640414.2017.1313625.

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28

Burgess, Darren J. "Lethal cycling." Nature Reviews Cancer 10, no. 9 (August 19, 2010): 599. http://dx.doi.org/10.1038/nrc2926.

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29

Heinrichs, Arianne. "Endless cycling." Nature Reviews Cancer 3, no. 1 (January 2003): 6. http://dx.doi.org/10.1038/nrc975.

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30

Brown, Robert W., and Corbin E. Covault. "Re-Cycling." Physics Teacher 53, no. 8 (November 2015): 466–68. http://dx.doi.org/10.1119/1.4933146.

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31

Burgess, Darren J. "Lethal cycling." Nature Reviews Drug Discovery 9, no. 9 (September 2010): 682. http://dx.doi.org/10.1038/nrd3260.

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32

Dellnitz, M., M. Field, M. Golubitsky, A. Hohmann, and Jun Ma. "Cycling chaos." IEEE Transactions on Circuits and Systems I: Fundamental Theory and Applications 42, no. 10 (1995): 821–23. http://dx.doi.org/10.1109/81.473592.

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33

Rybicki, Edward. "Cycling essays." Nature 337, no. 6205 (January 1989): 316. http://dx.doi.org/10.1038/337316b0.

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34

Monsen, Rita Black. "Children cycling." Journal of Pediatric Nursing 17, no. 6 (December 2002): 439–40. http://dx.doi.org/10.1053/jpdn.2002.128952.

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35

Adamo, Gregory. "City Cycling." Journal of Urban Technology 21, no. 3 (July 3, 2014): 103–5. http://dx.doi.org/10.1080/10630732.2014.954410.

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36

Tuma, Rabiya S. "Ribosome cycling." Journal of Cell Biology 170, no. 3 (July 25, 2005): 335. http://dx.doi.org/10.1083/jcb1703iti3.

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37

Locke, S. "Road cycling." British Journal of Sports Medicine 40, no. 11 (September 15, 2006): 950. http://dx.doi.org/10.1136/bjsm.2006.028688.

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38

John, Joseph F. "Antibiotic Cycling." Infection Control & Hospital Epidemiology 21, S1 (January 2000): S3. http://dx.doi.org/10.1017/s0195941700044660.

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39

Lambridis, Taso. "Road Cycling." Physiotherapy 86, no. 7 (July 2000): 385. http://dx.doi.org/10.1016/s0031-9406(05)60653-0.

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40

Lawton, Graham. "Pee-cycling." New Scientist 192, no. 2583-2584 (December 2006): 45–47. http://dx.doi.org/10.1016/s0262-4079(06)61458-9.

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41

Brownell, Kelly D. "Weight cycling." American Journal of Clinical Nutrition 49, no. 5 (May 1, 1989): 937. http://dx.doi.org/10.1093/ajcn/49.5.937.

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42

Marks, Julian M. "Theoretical cycling." Physics World 20, no. 1 (January 2007): 16. http://dx.doi.org/10.1088/2058-7058/20/1/26.

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43

Ringrose, Leonie, and Renato Paro. "Cycling silence." Nature 412, no. 6846 (August 2001): 493–94. http://dx.doi.org/10.1038/35087692.

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44

Berkelmans, Rik. "Fes cycling." Journal of Automatic Control 18, no. 2 (2008): 73–76. http://dx.doi.org/10.2298/jac0802073b.

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Many research with functional electrical stimulation (FES) has been done to regain mobility and for health benefits. Better results have been reported for FES-cycling than for FES-walking. The majority of the subjects during such research are people with a spinal cord injury (SCI), cause they often lost skin sensation. Besides using surface stimulation also implanted stimulators can be used. This solves the skin sensation problem, but needs a surgery. Many physiological effects of FES-cycling has been reported, e.g., increase of muscles, better blood flow, reduction of pressure ulcers, improved self-image and some reduction of bone mineral density (BMD) loss. Also people with an incomplete SCI benefit by FES-cycling, e.g. cycling time without FES, muscle strength and also the walking abilities increased. Hybrid exercise gives an even better cardiovascular training. Presently 4 companies are involved in FES-cycling. They all have a stationary mobility trainer. Two of them also use an outdoor tricycle. One combined with voluntary arm cranking. By optimizing the stimulation parameters the power output and fatigue resistance will increase, but will still be less compared to voluntary cycling.

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Gann, Joshua J., Grant M. Tinsley, and Paul M. La Bounty. "Weight Cycling." Strength and Conditioning Journal 37, no. 5 (October 2015): 105–11. http://dx.doi.org/10.1519/ssc.0000000000000168.

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Vuori, Ilkka. "Promoting Cycling." Clinical Journal of Sport Medicine 21, no. 6 (November 2011): 542–44. http://dx.doi.org/10.1097/01.jsm.0000407931.13102.0b.

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Burns, C. Conner. "Serious Cycling." Medicine &amp Science in Sports &amp Exercise 28, no. 4 (April 1996): 537. http://dx.doi.org/10.1097/00005768-199604000-00023.

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Miller, Camden. "City cycling." Community Development 49, no. 5 (October 10, 2018): 604–5. http://dx.doi.org/10.1080/15575330.2018.1529017.

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Blackburn, George L. "Weight Cycling." JAMA: The Journal of the American Medical Association 273, no. 13 (April 5, 1995): 998. http://dx.doi.org/10.1001/jama.1995.03520370038026.

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Ernsberger, Paul. "Weight Cycling." JAMA: The Journal of the American Medical Association 273, no. 13 (April 5, 1995): 998. http://dx.doi.org/10.1001/jama.1995.03520370038027.

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