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Journal articles on the topic 'Colony'

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Published: 4 June 2021
Last updated: 25 May 2024

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1

Reece, Bob, Richard Davis, and George Cargeeg. "Colony to Colony." Books Ireland, no. 140 (1990): 55. http://dx.doi.org/10.2307/20626275.

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2

Liu, Y., H. Huang, B. Yuan, L. Zhuang, T. Luo, and Q. Zhang. "Lentivirus-Mediated Knockdown of NOB1 Suppresses the Proliferation of Colon Cancer Cells." Zeitschrift für Gastroenterologie 52, no. 05 (May 2014): 429–35. http://dx.doi.org/10.1055/s-0033-1356338.

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AbstractNOB1 is important for ribosome biogenesis and protein degradation. Previous studies showed that it could regulate the growth and colony-formation ability of ovarian, breast and hepatocellular carcinoma cells. However, its function in colon cancer cells is largely unknown. In this study, we found that NOB1 could express in 6 different colon cancer cell lines. Lentivirus-mediated shRNA targeted NOB1 could suppress the endogenous gene expression. NOB1 depletion significantly inhibited cell proliferation and colony formation ability, as determined by MTT and colony formation assays. Flow cytometry analysis showed NOB1 silencing arrested cell cycle in G0 / G1 phase. Moreover, the percentage of cells at sub-G1 phase dramatically increased after NOB1 knockdown. These results indicate that NOB1 may play an important role in the growth and tumorigensis of colon cancer and knockdown of NOB1 may be a potential therapeutic method for colon cancer in the future.
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3

Myrup, B., N. H. Valerius, and P. B. Mortensen. "Treatment of enteritis in chronic granulomatous disease with granulocyte colony stimulating factor." Gut 42, no. 1 (January 1, 1998): 127–30. http://dx.doi.org/10.1136/gut.42.1.127.

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Background—In several diseases there is a relation between deficiency of neutrophil granulocytes and granulomatous lesions. Recently, in glycogen storage disease type Ib, this relation has been supported by the beneficial effect of treatment of enteritis with granulocyte-macrophage colony stimulating factor.Aim—To investigate whether chronic granulomatous disease could be treated according to the same principle.Patients and methods—Inflammatory lesions were monitored in two brothers with chronic granulomatous disease demonstrated by very low superoxide production in neutrophil granulocytes. The two patients were treated with recombinant human granulocyte colony stimulating factor on three occasions when the disease was active.Results—In one patient, remission of an inflamed stenosis of the colon sigmoideum was shown by granulocyte scintigraphy after one month of treatment with granulocyte colony stimulating factor. In the other patient, remission of colon disease and later of a non-malignant tumour in the right lung hilum was shown by colonoscopy and computed tomography scans respectively.Conclusion—Remission of inflammatory lesions in two brothers with chronic granulomatous disease was induced by granulocyte colony stimulating factor on three occasions. The mechanism for this effect is not known. The result is similar to the response found in patients with leucocyte deficiency due to glycogen storage disease type Ib.
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4

Bertelsmeier, Cleo, Sébastien Ollier, Amaury Avril, Olivier Blight, Hervé Jourdan, and Franck Courchamp. "Colony–colony interactions between highly invasive ants." Basic and Applied Ecology 17, no. 2 (March 2016): 106–14. http://dx.doi.org/10.1016/j.baae.2015.09.005.

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5

Chang, Xiaotian, Zhengbin Chai, Jiaorui Zou, Hongxing Wang, Yao Wang, Yabing Zheng, Hui Wu, and Chunyan Liu. "PADI3 induces cell cycle arrest via the Sirt2/AKT/p21 pathway and acts as a tumor suppressor gene in colon cancer." Cancer Biology & Medicine 16, no. 4 (November 1, 2019): 729–42. http://dx.doi.org/10.20892/j.issn.2095-3941.2019.0065.

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Objective As a member of the peptidyl arginine deiminase (PAD) family, PADI3 is weakly expressed in colon cancer tissues and highly expressed in adjacent colon cancer tissues. However, the role of PADI3 in colon cancer is unclear. In this study, we investigated the function and molecular mechanism of PADI3 in colon cancer tumorigenesis. Methods Western blot and real-time PCR were used to detect the expression levels of several genes. CCK-8, flow cytometry (FCM) and colony formation assays were used to examine cell proliferation, the cell cycle and colony formation ability. RNA-sequencing analysis was used to study the molecular mechanism of PADI3 in tumorigenesis. A truncation mutation experiment was performed to determine the key functional domain of PADI3. Results PADI3 overexpression inhibited cell proliferation and colony formation and led to G1 phase arrest in both HCT116 (originating from primary colon cancer) and LoVo (originating from metastatic tumor nodules of colon cancer) cells. PADI3-expressing HCT116 cells had a lower tumor formation rate and produced smaller tumors than control cells. PADI3 significantly decreased Sirtuin2 (Sirt2) and Snail expression and AKT phosphorylation and increased p21 expression, and Sirt2 overexpression partly reversed the effects induced by PADI3 overexpression. Immunocytochemistry showed that PADI3 is mainly localized in the cytoplasm. Truncation mutation experiments showed that the C-domain is the key domain involved in the antitumor activity of PADI3. Conclusions PADI3 suppresses Snail expression and AKT phosphorylation and promotes p21 expression by downregulating Sirt2 expression in the cytoplasm, and the C-domain is the key domain for its antitumor activity.
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6

Saeed, Mahmoud. "Lizards' Colony." World Literature Today 86, no. 6 (2012): 30–41. http://dx.doi.org/10.1353/wlt.2012.0179.

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7

Wolfle, Thomas L. "Chimpanzee Colony." Science 227, no. 4694 (March 29, 1985): 1530. http://dx.doi.org/10.1126/science.227.4694.1530.c.

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8

Mahmoud Saeed and Translated by William M. Hutchins. "Lizards' Colony." World Literature Today 86, no. 6 (2012): 30. http://dx.doi.org/10.7588/worllitetoda.86.6.0030.

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9

Clark, W. G. "Lost Colony." Perspecta 28 (1997): 114. http://dx.doi.org/10.2307/1567196.

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10

WOLFLE, T. L. "Chimpanzee Colony." Science 227, no. 4694 (March 29, 1985): 1530. http://dx.doi.org/10.1126/science.227.4694.1530-b.

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11

Dart, Anna. "Colony takeover." Nature Reviews Cancer 18, no. 12 (November 12, 2018): 725. http://dx.doi.org/10.1038/s41568-018-0080-x.

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12

Cabello, Felipe C. "ESO's colony." Nature 364, no. 6440 (August 1993): 753. http://dx.doi.org/10.1038/364753c0.

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13

Wright, Suzanne. "holding colony." Feminist Review 116, no. 1 (July 2017): 101. http://dx.doi.org/10.1057/s41305-017-0056-9.

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14

Chakravorty, Sayantan, Celso L. Mendes, Laxmikant V. Kalé, Terry Jones, Andrew Tauferner, Todd Inglett, and José Moreira. "HPC-Colony." ACM SIGOPS Operating Systems Review 40, no. 2 (April 2006): 43–49. http://dx.doi.org/10.1145/1131322.1131334.

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15

Costa, Gina L., and Michael P. Weiner. "Colony PCR." Cold Spring Harbor Protocols 2006, no. 1 (January 1, 2006): pdb.prot4141. http://dx.doi.org/10.1101/pdb.prot4141.

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16

Tofighian, Nadi. "Celluloid Colony." Visual Anthropology 35, no. 4-5 (October 20, 2022): 472–75. http://dx.doi.org/10.1080/08949468.2022.2129260.

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17

Ellis, James D., Jay D. Evans, and Jeff Pettis. "Colony losses, managed colony population decline, and Colony Collapse Disorder in the United States." Journal of Apicultural Research 49, no. 1 (January 2010): 134–36. http://dx.doi.org/10.3896/ibra.1.49.1.30.

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18

MASUDA, Go, Tetsuji SAWADA, Tomohisa OKUNO, Junko SHIROTSUKI, Kuniyasu MURAHASHI, and Koichi NISHINO. "A Case of Granulocyte-colony Stimulating Factor Producing Colon Cancer." Nihon Rinsho Geka Gakkai Zasshi (Journal of Japan Surgical Association) 75, no. 4 (2014): 998–1004. http://dx.doi.org/10.3919/jjsa.75.998.

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19

Kawaida, Keisuke, Jun Kadono, Hideaki Kanda, Masahiko Osako, Naoki Ishizaki, Ken Shimizu, Junichiro Sameshima, Yutaka Imoto, and Mineo Tabata. "A Case of Granulocyte-colony Stimulating Factor Producing Colon Cancer." Japanese Journal of Gastroenterological Surgery 45, no. 5 (2012): 537–43. http://dx.doi.org/10.5833/jjgs.45.537.

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20

Shen, Sha, Qingqing Guo, and Shuiping Zhan. "MicroRNA-612 regulates the proliferation and epithelial-to-mesenchymal transition of human colon cancer cells via G protein-coupled receptor 132 (GPR132)." Tropical Journal of Pharmaceutical Research 20, no. 7 (February 9, 2022): 1345–50. http://dx.doi.org/10.4314/tjpr.v20i7.4.

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Purpose: To investigate the effect of microRNA-612 (miR-612) on human colon cancer cells, and the mechanism involved. Methods: Expressions of miR-612 and GPR132 were determined by quantitative real-time polymerase chain reaction (qRT-PCR)el , while cell viability was evaluated using cell counting kit-8 (CCK8) and colony formation assays. Dual luciferase assay was used to determine the interaction between miR-612 and GPR132, while cell migration and invasion were measured by Transwell assay. Results: The expression levels of miR-612 in colon cancer tissues and cell lines were significantly down-regulated (p < 0.05). Overexpression of miR-612 in colon cancer cells led to significant inhibition of their proliferation and colony formation. Transwell assays revealed that miR-612 overexpression markedly stopped the migration, invasion and epithelial-to-mesenchymal transition. Conclusion: These results indicate that miR-612 exerts anti-cancer effect by suppressing the expression of GPR132 at the translational level. The in vitro tumor suppressive activity of miR-612 against colon cancer reveals its potential for the management of colon cancer.
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21

&NA;. "Granulocyte colony-stimulating factor/granulocyte-macrophage colony-stimulating factor." Reactions Weekly &NA;, no. 743 (March 1999): 8. http://dx.doi.org/10.2165/00128415-199907430-00024.

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22

&NA;. "Granulocyte colony-stimulating factors/granulocyte-macrophage colony-stimulating factors." Reactions Weekly &NA;, no. 1166 (August 2007): 13. http://dx.doi.org/10.2165/00128415-200711660-00041.

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23

&NA;. "Granulocyte colony-stimulating factor/granulocyte-macrophage colony-stimulating factor." Reactions Weekly &NA;, no. 455 (June 1993): 9. http://dx.doi.org/10.2165/00128415-199304550-00035.

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24

&NA;. "Granulocyte colony-stimulating factors/granulocyte-macrophage colony-stimulating factors." Reactions Weekly &NA;, no. 523 (October 1994): 7. http://dx.doi.org/10.2165/00128415-199405230-00027.

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25

Moritz, Robin F. A. "Colony level and within colony level selection in honeybees." Behavioral Ecology and Sociobiology 25, no. 6 (December 1989): 437–44. http://dx.doi.org/10.1007/bf00300190.

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26

Zhou, Jiajun, Xifan Yao, Felix T. S. Chan, Yingzi Lin, Hong Jin, Liang Gao, and Xuping Wang. "An individual dependent multi-colony artificial bee colony algorithm." Information Sciences 485 (June 2019): 114–40. http://dx.doi.org/10.1016/j.ins.2019.02.014.

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27

Cox, Helen M. "Receptors for calcitonin gene related peptide (CGRP) in gastrointestinal epithelia." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 974–80. http://dx.doi.org/10.1139/y95-135.

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A pharmacological comparison of calcitonin gene related peptide (CGRP) receptors expressed in normal rat colon mucosa and two human adenocarcinoma cell lines has been undertaken. Using voltage-clamp techniques electrogenic ion transport was continuously monitored across either mucosal preparations or confluent epithelial monolayers grown on permeable supports. The data presented at this meeting show that CGRP receptors are preferentially located on the basolateral epithelial surface and that their stimulation by a variety of CGRP analogues results in enhanced Cl− secretion mediated via a cyclic AMP dependent mechanism. Responses to rat αCGRP in rat descending colon mucosa and in the adenocarcinoma cell line Colony-29 are insensitive to the inhibitory effects of the C-terminal fragment human CGRP(8–37); however, significant inhibition of rat αCGRP responses was observed in the parent epithelial cell line HCA-7. This together with the subtle differences seen in agonist orders of potency in the three preparations indicates that different CGRP receptor subtypes exist in the basolateral domains of HCA-7 compared with rat colon and Colony-29 epithelia.Key words: calcitonin gene related peptide, receptors, ion transport, rat colon, epithelial cell lines.
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28

Gao, Chang, Rui Sun, Ya-Rong Xie, An-Li Jiang, Mei Lin, Min Li, Zheng-Wang Chen, Ping Zhang, Honglin Jin, and Jue-Ping Feng. "The soy-derived peptide Vglycin inhibits the growth of colon cancer cells in vitro and in vivo." Experimental Biology and Medicine 242, no. 10 (March 1, 2017): 1034–43. http://dx.doi.org/10.1177/1535370217697383.

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Vglycin, a novel natural polypeptide isolated from pea seeds, possesses antidiabetic properties. Our previous studies have shown that Vglycin can induce the differentiation of human colon adenocarcinoma cells. We aimed to determine the anticancer activity of Vglycin against colon cancer cells and to elucidate related apoptosis-inducing mechanisms. Treatment with purified Vglycin significantly reduced growth, viability, and colony formation of CT-26, SW480, and NCL-H716 colon cancer cells in a dose-dependent manner while down-regulating the expression of proliferating cell nuclear antigen. Mouse xenograft studies showed a 38% inhibition of colon cancer growth in mice treated with Vglycin (20 mg/kg/day) at day 21. Furthermore, the potential mechanisms involved in Vglycin-induced cell apoptosis were examined using cell cycle studies, ultrastructural examination, as well as apoptosis-associated pathway analysis. The results showed that Vglycin significantly promoted apoptosis and G1/S phase cell cycle arrest. As revealed by Western blot, the expression of CDK2 and Cyclin D1 was down-regulated in all three Vglycin-treated colon cancer cells, indicating that the CDK2/Cyclin D1 cell cycle pathway involved in the initiation and progression of colon cancer. Moreover, the inhibition of Vglycin-induced cell proliferation in colon cancer cells was accompanied by alteration of the expression levels of the apoptosis-related proteins Bax, Bcl-2 and Mcl-1, and an increase of caspase-3 activity. Together, our results suggest that Vglycin may be another plant-derived peptide that suppresses colon cancer, supporting the continued investigation of Vglycin as therapeutic agent for colon cancer. Impact statement The antidiabetic properties and the capability of inducing differentiation of human colon adenocarcinoma cells of Vglycin have been reported in our previous studies. However, the anticancer potential of Vglycin on colon cancer cells and its possible related mechanisms were still unknown. In this study, we found that Vglycin could reduce growth, viability, and colony formation or colony size of CT-26, SW480, and NCL-H716 colon cancer cells. Moreover, Vglycin decreased tumor volume by 38% in xenograft mice transplanted with CT-26 cells. The mechanisms of these phenomena may be due to the down-regulated CDK2 and Cyclin D1, G1/S phase cell cycle arrest, and the dysregulated expression of Bax, Bcl-2, and Mcl-1. The findings highlight the anticancer potential of Vglycin against colon cancer cells, and suggest Vglycin may be another colon cancer potential suppressive component of plant-derived peptides.
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29

Sawaya, Katia, Sonia Abou Najem, Ghada Khawaja, and Mahmoud Khalil. "Proapoptotic and Antiproliferative Effects of the Desert Truffle Terfezia boudieri on Colon Cancer Cell Lines." Evidence-Based Complementary and Alternative Medicine 2023 (April 7, 2023): 1–13. http://dx.doi.org/10.1155/2023/1693332.

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Background. Colon cancer is the second leading cause of cancer-related mortality, and ranks third among cancers in terms of prevalence. Despite advances in early detection and treatment with chemotherapy and surgery, colon cancer continues to be associated with high recurrence rates, thereby resulting in a heavy disease burden. Moreover, the effectiveness of currently available treatment modalities is limited by the occurrence of toxic side effects. Hence, there is an urgent need to develop alternative treatments. Extracts from the black desert truffle Terfezia boudieri (T. boudieri) have shown promising anticancer properties. However, the cellular mechanisms underlying this activity remain poorly understood. Methods. In this study, the colon cancer cell lines HCT-116 and Caco-2 were treated with either water or ethanolic extract of T. boudieri. Cell viability and the half-maximal inhibitory concentration were determined using MTT assays. Then, the activity of the more potent water extract was further verified using crystal violet assays, and its role in inhibiting colony formation and wound healing was investigated. Protein levels of p53, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X (Bax), cyclin D1 (CCND1), and c-Myc were measured in cells treated with different doses of the water extract. Results. Treatment with the water extract of T. boudieri reduced the capacity of cells for wound healing and colony formation in a dose-dependent manner. The Bax/Bcl-2 ratio and p53 expression were elevated in both cell lines. In contrast, the levels of cyclin D1 and c-Myc were suppressed. Conclusion. T. boudieri water extract exerted a cytotoxic effect on colon cancer cells, and blocked colony formation and wound healing potentially through inhibition of proliferation. Mechanistically, these effects are attributed to influence the mitochondrial pathway of apoptosis, proteins involved in cellular proliferation, and the cell cycle.
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30

Weathers, Winston. "Artists Colony, 1954." Antioch Review 62, no. 2 (2004): 331. http://dx.doi.org/10.2307/4614656.

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31

Moore-Gilbert, Bart. "Cosmos and Colony." New Formations 74, no. 74 (December 19, 2011): 138–43. http://dx.doi.org/10.3898/newf.74.rev04.2011.

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32

Ericksen, Bryan. "Virtual colony count." WikiJournal of Science 3, no. 1 (2020): 3. http://dx.doi.org/10.15347/wjs/2020.003.

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33

Saul, Norman E., and Frederick S. Starr. "Russia's American Colony." Russian Review 48, no. 1 (January 1989): 86. http://dx.doi.org/10.2307/130259.

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34

Klumpp, Andrew. "Colony before Party." Annals of Iowa 79, no. 1 (January 2020): 1–34. http://dx.doi.org/10.17077/0003-4827.12636.

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35

Fox, R. M. "Colony-Stimulating Factors." PharmacoEconomics 6, Supplement 2 (1994): 1–8. http://dx.doi.org/10.2165/00019053-199400062-00003.

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36

Stroud, Louise. "The idiot colony." Mental Health Practice 12, no. 3 (November 13, 2008): 22–23. http://dx.doi.org/10.7748/mhp.12.3.22.s23.

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37

Jensen, Ronald J., and S. Frederick Starr. "Russia's American Colony." American Historical Review 94, no. 1 (February 1989): 184. http://dx.doi.org/10.2307/1862193.

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38

Gordon, Michael S., and Janice L. Gabrilove. "Colony-stimulating factors." Current Opinion in ONCOLOGY 2, no. 6 (December 1990): 1152–58. http://dx.doi.org/10.1097/00001622-199012000-00021.

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39

&NA;. "Colony-stimulating factors." Reactions Weekly &NA;, no. 532 (December 1994): 7. http://dx.doi.org/10.2165/00128415-199405320-00022.

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40

Fox, John Matthew. "The Children Colony." Cream City Review 37, no. 1 (2013): 16–27. http://dx.doi.org/10.1353/ccr.2013.0012.

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41

Bennett, Tony. "MUSEUM, FIELD, COLONY." Journal of Cultural Economy 2, no. 1-2 (July 2009): 99–116. http://dx.doi.org/10.1080/17530350903064097.

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42

Dorigo, Marco, Mauro Birattari, and Thomas Stutzle. "Ant colony optimization." IEEE Computational Intelligence Magazine 1, no. 4 (November 2006): 28–39. http://dx.doi.org/10.1109/mci.2006.329691.

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43

Linder, Evan. "The New Colony." Theatre Topics 26, no. 2 (2016): E—19—E—22. http://dx.doi.org/10.1353/tt.2016.0045.

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44

Niu, Ben, and Hong Wang. "Bacterial Colony Optimization." Discrete Dynamics in Nature and Society 2012 (2012): 1–28. http://dx.doi.org/10.1155/2012/698057.

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This paper investigates the behaviors at different developmental stages inEscherichia coli(E. coli) lifecycle and developing a new biologically inspired optimization algorithm named bacterial colony optimization (BCO). BCO is based on a lifecycle model that simulates some typical behaviors ofE. colibacteria during their whole lifecycle, including chemotaxis, communication, elimination, reproduction, and migration. A newly created chemotaxis strategy combined with communication mechanism is developed to simplify the bacterial optimization, which is spread over the whole optimization process. However, the other behaviors such as elimination, reproduction, and migration are implemented only when the given conditions are satisfied. Two types of interactive communication schemas: individuals exchange schema and group exchange schema are designed to improve the optimization efficiency. In the simulation studies, a set of 12 benchmark functions belonging to three classes (unimodal, multimodal, and rotated problems) are performed, and the performances of the proposed algorithms are compared with five recent evolutionary algorithms to demonstrate the superiority of BCO.
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45

Kintisch, Eli. "The lost colony." Science 367, no. 6484 (March 19, 2020): 1318–20. http://dx.doi.org/10.1126/science.367.6484.1318.

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46

Vignieri, Sacha. "Protecting the colony." Science 362, no. 6417 (November 22, 2018): 905.6–906. http://dx.doi.org/10.1126/science.362.6417.905-f.

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47

Sen, Satadru. "The orphaned colony." Indian Economic & Social History Review 44, no. 4 (December 2007): 463–88. http://dx.doi.org/10.1177/001946460704400403.

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48

Armstrong, Hannah Rae. "Africa’s Last Colony." World Policy Journal 31, no. 4 (2014): 77–84. http://dx.doi.org/10.1177/0740277514564950.

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49

Adams, Alex. "Empire, colony, postcolony." Interventions 19, no. 5 (May 8, 2017): 738–40. http://dx.doi.org/10.1080/1369801x.2017.1281399.

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50

Lawyer, P. "Sandfly Colony Database." Trends in Parasitology 17, no. 6 (June 2001): 272. http://dx.doi.org/10.1016/s1471-4922(01)01980-8.

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