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Статті в журналах з теми "Rubicon"

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Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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1

Espinoza, Sandra, Felipe Grunenwald, Wileidy Gomez, Felipe García, Lorena Abarzúa-Catalan, Sebastián Oyarce-Pezoa, Maria Fernanda Hernandez та ін. "Neuronal Rubicon Represses Extracellular APP/Amyloid β Deposition in Alzheimer’s Disease". Cells 11, № 12 (7 червня 2022): 1860. http://dx.doi.org/10.3390/cells11121860.

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Alzheimer’s disease (AD) is the most prevalent age-associated neurodegenerative disease. A decrease in autophagy during aging contributes to brain disorders by accumulating potentially toxic substrates in neurons. Rubicon is a well-established inhibitor of autophagy in all cells. However, Rubicon participates in different pathways depending on cell type, and little information is currently available on neuronal Rubicon’s role in the AD context. Here, we investigated the cell-specific expression of Rubicon in postmortem brain samples from AD patients and 5xFAD mice and its impact on amyloid β burden in vivo and neuroblastoma cells. Further, we assessed Rubicon levels in human-induced pluripotent stem cells (hiPSCs), derived from early-to-moderate AD and in postmortem samples from severe AD patients. We found increased Rubicon levels in AD-hiPSCs and postmortem samples and a notable Rubicon localization in neurons. In AD transgenic mice lacking Rubicon, we observed intensified amyloid β burden in the hippocampus and decreased Pacer and p62 levels. In APP-expressing neuroblastoma cells, increased APP/amyloid β secretion in the medium was found when Rubicon was absent, which was not observed in cells depleted of Atg5, essential for autophagy, or Rab27a, required for exosome secretion. Our results propose an uncharacterized role of Rubicon on APP/amyloid β homeostasis, in which neuronal Rubicon is a repressor of APP/amyloid β secretion, defining a new way to target AD and other similar diseases therapeutically.
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2

Cliff, Michelle. "Rubicon." Callaloo 23, no. 1 (2000): 134–38. http://dx.doi.org/10.1353/cal.2000.0008.

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3

Matsunaga, Kohichi, Takeshi Noda, and Tamotsu Yoshimori. "Binding Rubicon to cross the Rubicon." Autophagy 5, no. 6 (August 16, 2009): 876–77. http://dx.doi.org/10.4161/auto.9098.

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4

Bhargava, Hersh K., Keisuke Tabata, Jordan M. Byck, Maho Hamasaki, Daniel P. Farrell, Ivan Anishchenko, Frank DiMaio, Young Jun Im, Tamotsu Yoshimori, and James H. Hurley. "Structural basis for autophagy inhibition by the human Rubicon–Rab7 complex." Proceedings of the National Academy of Sciences 117, no. 29 (July 6, 2020): 17003–10. http://dx.doi.org/10.1073/pnas.2008030117.

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Анотація:
Rubicon is a potent negative regulator of autophagy and a potential target for autophagy-inducing therapeutics. Rubicon-mediated inhibition of autophagy requires the interaction of the C-terminal Rubicon homology (RH) domain of Rubicon with Rab7–GTP. Here we report the 2.8-Å crystal structure of the Rubicon RH domain in complex with Rab7–GTP. Our structure reveals a fold for the RH domain built around four zinc clusters. The switch regions of Rab7 insert into pockets on the surface of the RH domain in a mode that is distinct from those of other Rab–effector complexes. Rubicon residues at the dimer interface are required for Rubicon and Rab7 to colocalize in living cells. Mutation of Rubicon RH residues in the Rab7-binding site restores efficient autophagic flux in the presence of overexpressed Rubicon, validating the Rubicon RH domain as a promising therapeutic target.
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5

Armstrong, Barry. "Platform: Rubicon." Musical Times 132, no. 1783 (September 1991): 447. http://dx.doi.org/10.2307/965647.

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6

Zambrano, Joelle N., Scott T. Eblen, Melissa Abt, J. Matthew Rhett, Robin Muise-Helmericks, and Elizabeth S. Yeh. "HUNK Phosphorylates Rubicon to Support Autophagy." International Journal of Molecular Sciences 20, no. 22 (November 19, 2019): 5813. http://dx.doi.org/10.3390/ijms20225813.

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Background: Autophagy is a catabolic cellular recycling pathway that is essential for maintaining intracellular homeostasis. Autophagosome formation is achieved via the coordination of the Beclin-1 protein complex. Rubicon is a Beclin-1 associated protein that suppresses autophagy by impairing the activity of the class III PI3K, Vps34. However, very little is known about the molecular mechanisms that regulate Rubicon function. Methods: In this study, co-immunoprecipitation and kinase assays were used to investigate the ability of Hormonally Upregulated Neu-associated Kinase (HUNK) to bind to and phosphorylate Rubicon. LC3B was monitored by immunofluorescence and immunoblotting to determine whether phosphorylation of Rubicon by HUNK controls the autophagy suppressive function of Rubicon. Results: Findings from this study identify Rubicon as a novel substrate of HUNK and show that phosphorylation of Rubicon inhibits its function, promoting autophagy.
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7

Kim, Jae-Sung, Ye-Ram Kim, Sein Jang, Sang Geon Wang, Euni Cho, Seok-Jun Mun, Hye-In Jeon, Hyo-Keun Kim, Sun-Joon Min, and Chul-Su Yang. "Mito-TIPTP Increases Mitochondrial Function by Repressing the Rubicon-p22phox Interaction in Colitis-Induced Mice." Antioxidants 10, no. 12 (December 6, 2021): 1954. http://dx.doi.org/10.3390/antiox10121954.

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Анотація:
The run/cysteine-rich-domain-containing Beclin1-interacting autophagy protein (Rubicon) is essential for the regulation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase by interacting with p22phox to trigger the production of reactive oxygen species (ROS) in immune cells. In a previous study, we demonstrated that the interaction of Rubicon with p22phox increases cellular ROS levels. The correlation between Rubicon and mitochondrial ROS (mtROS) is poorly understood. Here, we report that Rubicon interacts with p22phox in the outer mitochondrial membrane in macrophages and patients with human ulcerative colitis. Upon lipopolysaccharide (LPS) activation, the binding of Rubicon to p22phox was elevated, and increased not only cellular ROS levels but also mtROS, with an impairment of mitochondrial complex III and mitochondrial biogenesis in macrophages. Furthermore, increased Rubicon decreases mitochondrial metabolic flux in macrophages. Mito-TIPTP, which is a p22phox inhibitor containing a mitochondrial translocation signal, enhances mitochondrial function by inhibiting the association between Rubicon and p22phox in LPS-primed bone-marrow-derived macrophages (BMDMs) treated with adenosine triphosphate (ATP) or dextran sulfate sodium (DSS). Remarkably, Mito-TIPTP exhibited a therapeutic effect by decreasing mtROS in DSS-induced acute or chronic colitis mouse models. Thus, our findings suggest that Mito-TIPTP is a potential therapeutic agent for colitis by inhibiting the interaction between Rubicon and p22phox to recover mitochondrial function.
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8

Yamamuro, Tadashi, Shuhei Nakamura, Yu Yamano, Tsutomu Endo, Kyosuke Yanagawa, Ayaka Tokumura, Takafumi Matsumura, et al. "Rubicon prevents autophagic degradation of GATA4 to promote Sertoli cell function." PLOS Genetics 17, no. 8 (August 5, 2021): e1009688. http://dx.doi.org/10.1371/journal.pgen.1009688.

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Анотація:
Autophagy degrades unnecessary proteins or damaged organelles to maintain cellular function. Therefore, autophagy has a preventive role against various diseases including hepatic disorders, neurodegenerative diseases, and cancer. Although autophagy in germ cells or Sertoli cells is known to be required for spermatogenesis and male fertility, it remains poorly understood how autophagy participates in spermatogenesis. We found that systemic knockout mice of Rubicon, a negative regulator of autophagy, exhibited a substantial reduction in testicular weight, spermatogenesis, and male fertility, associated with upregulation of autophagy. Rubicon-null mice also had lower levels of mRNAs of Sertoli cell–related genes in testis. Importantly, Rubicon knockout in Sertoli cells, but not in germ cells, caused a defect in spermatogenesis and germline stem cell maintenance in mice, indicating a critical role of Rubicon in Sertoli cells. In mechanistic terms, genetic loss of Rubicon promoted autophagic degradation of GATA4, a transcription factor that is essential for Sertoli cell function. Furthermore, androgen antagonists caused a significant decrease in the levels of Rubicon and GATA4 in testis, accompanied by elevated autophagy. Collectively, we propose that Rubicon promotes Sertoli cell function by preventing autophagic degradation of GATA4, and that this mechanism could be regulated by androgens.
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9

Nah, Jihoon, Daniela Zablocki, and Junichi Sadoshima. "The roles of the inhibitory autophagy regulator Rubicon in the heart: A new therapeutic target to prevent cardiac cell death." Experimental & Molecular Medicine 53, no. 4 (April 2021): 528–36. http://dx.doi.org/10.1038/s12276-021-00600-3.

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AbstractAutophagy contributes to the maintenance of cardiac homeostasis. The level of autophagy is dynamically altered in heart disease. Although autophagy is a promising therapeutic target, only a few selective autophagy activator candidates have been reported thus far. Rubicon is one of the few endogenous negative regulators of autophagy and a potential target for autophagy-inducing therapeutics. Rubicon was initially identified as a component of the Class III PI3K complex, and it has multiple functions, not only in canonical autophagy but also in endosomal trafficking and inflammatory responses. This review summarizes the molecular action of Rubicon in canonical and noncanonical autophagy. We discuss the roles of Rubicon in cardiac stress and the therapeutic potential of Rubicon in cardiac diseases through its modulation of autophagy.
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10

Etzioni, Amitai. "Crossing the Rubicon." Challenge 57, no. 2 (March 2014): 65–79. http://dx.doi.org/10.2753/0577-5132570205.

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11

Laulan, Anne-Marie. "Franchir le Rubicon ?" Hermès 63, no. 2 (2012): 87. http://dx.doi.org/10.4267/2042/48324.

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12

Gary-Bobo. "Crossing the Rubicon." Annals of Economics and Statistics, no. 93/94 (2009): 5. http://dx.doi.org/10.2307/27917380.

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13

Aleksei Linnik. "DONETSK BASIN RUBICON." Current Digest of the Post-Soviet Press, The 69, no. 010 (March 6, 2017): 11–12. http://dx.doi.org/10.21557/dsp.48548398.

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14

Frank. "CHASING THE RUBICON?" American Journal of Psychology 129, no. 1 (2016): 99. http://dx.doi.org/10.5406/amerjpsyc.129.1.0099.

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15

Lowenstein, Pedro R. "Crossing the Rubicon." Nature Biotechnology 27, no. 1 (January 2009): 42–44. http://dx.doi.org/10.1038/nbt0109-42.

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16

Vy Sharpe, Celeste Tuòng. "The Eugenic Rubicon." Journal of American History 106, no. 3 (December 1, 2019): 856–57. http://dx.doi.org/10.1093/jahist/jaz669.

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17

Ehrhardt, C. T. H. R. "Crossing the Rubicon." Antichthon 29 (1995): 30–41. http://dx.doi.org/10.1017/s0066477400000927.

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Everyone knows that Caesar crossed the Rubicon because his political enemies at Rome had manoeuvred him into a position where he would soon be forced to leave his province, give up his imperium, and return to Rome as a private citizen, there to be put on trial, found guilty and have his political career ended. Yet over thirty years ago, Shackleton Bailey, in less than two pages of his introduction to Cicero's Letters to Atticus, destroyed the basis for this belief, and in the three decades since, no one has been able to rebuild it. Everyone also knows that Caesar, when he crossed the Rubicon, was grossly outnumbered and conquered Italy only through his own rapidity and his enemies' sluggishness and incompetence; yet this belief was irreparably shattered by H.-M. Ottmer in 1979, in a book which professional scholars have practically ignored. The justification for this article is that it may bring to others' attention the real state of researches on the circumstances of Caesar's invasion of Italy, and perhaps even inhibit further restatements of exploded beliefs.
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18

Hamilton, G. J. A. "Over de Rubicon." Tijdschrift voor Gezondheidsrecht 29, no. 7 (July 2005): 468. http://dx.doi.org/10.1007/bf03056178.

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19

Hastings-Tolsma, Marie. "Crossing the Rubicon." Biological Research For Nursing 7, no. 3 (January 2006): 161–62. http://dx.doi.org/10.1177/1099800405283630.

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20

Langmore, John P. "Rubicon Genomics, Inc." Pharmacogenomics 3, no. 4 (July 2002): 557–60. http://dx.doi.org/10.1517/14622416.3.4.557.

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21

Wilkinson, James, and John Boehrer. "Crossing the Rubicon." Change: The Magazine of Higher Learning 25, no. 6 (December 1993): 52–58. http://dx.doi.org/10.1080/00091383.1993.9938479.

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22

Tabata, Keisuke, Kohichi Matsunaga, Ayuko Sakane, Takuya Sasaki, Takeshi Noda, and Tamotsu Yoshimori. "Rubicon and PLEKHM1 Negatively Regulate the Endocytic/Autophagic Pathway via a Novel Rab7-binding Domain." Molecular Biology of the Cell 21, no. 23 (December 2010): 4162–72. http://dx.doi.org/10.1091/mbc.e10-06-0495.

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The endocytic and autophagic pathways are involved in the membrane trafficking of exogenous and endogenous materials to lysosomes. However, the mechanisms that regulate these pathways are largely unknown. We previously reported that Rubicon, a Beclin 1–binding protein, negatively regulates both the autophagic and endocytic pathways by unidentified mechanisms. In this study, we performed database searches to identify potential Rubicon homologues that share the common C-terminal domain, termed the RH domain. One of them, PLEKHM1, the causative gene of osteopetrosis, also suppresses endocytic transport but not autophagosome maturation. Rubicon and PLEKHM1 specifically and directly interact with Rab7 via their RH domain, and this interaction is critical for their function. Furthermore, we show that Rubicon but not PLEKHM1 uniquely regulates membrane trafficking via simultaneously binding both Rab7 and PI3-kinase.
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23

Catlaw, Thomas J. "Crossing the Relational-Rubicon." Administration & Society 42, no. 4 (July 2010): 466–73. http://dx.doi.org/10.1177/0095399710375402.

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24

Ebright, Michael I. "Commentary: Crossing the Rubicon." Journal of Thoracic and Cardiovascular Surgery 159, no. 5 (May 2020): 2069–70. http://dx.doi.org/10.1016/j.jtcvs.2019.11.058.

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25

Reardon, Michael J., and Vinod H. Thourani. "Racing to the Rubicon." Journal of Thoracic and Cardiovascular Surgery 155, no. 4 (April 2018): 1457–58. http://dx.doi.org/10.1016/j.jtcvs.2017.07.055.

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26

Wolf, Stewart. "Medicine at the Rubicon." Integrative Physiological and Behavioral Science 33, no. 4 (October 1998): 312–14. http://dx.doi.org/10.1007/bf02688698.

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27

Rommelfanger, Karen S., and Paul F. Boshears. "The Rubicon Already Crossed." AJOB Neuroscience 8, no. 4 (October 2, 2017): 197–99. http://dx.doi.org/10.1080/21507740.2017.1392384.

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28

Andersson, Jonas. "INCOSE Crosses the Rubicon." INSIGHT 15, no. 3 (September 2012): 33. http://dx.doi.org/10.1002/inst.201215333.

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29

Bakøy, Eva, and Vilde Schanke Sundet. "‘Remember, it’s just television’." VIEW Journal of European Television History and Culture 6, no. 11 (September 22, 2017): 53. http://dx.doi.org/10.18146/2213-0969.2017.jethc123.

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This article discusses the corporate strategy of one of the most successful television production companies in Norway: Rubicon TV. Based on a historical analysis from the company’s establishment in the early 1990s until today, the article illuminates how Rubicon TV has navigated in and contributed to the changing Norwegian television landscape. Rubicon TV has gone from a supplier of popular and provocative programmes to a small group of Norwegian broadcasters to a truly digital and global industrial force which produces linear ‘flow’ programmes as well as web-TV and streaming series for both national and international players.
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30

Asare, Patrick F., Hai B. Tran, Plinio R. Hurtado, Griffith B. Perkins, Phan Nguyen, Hubertus Jersmann, Eugene Roscioli, and Sandra Hodge. "Inhibition of LC3-associated phagocytosis in COPD and in response to cigarette smoke." Therapeutic Advances in Respiratory Disease 15 (January 2021): 175346662110397. http://dx.doi.org/10.1177/17534666211039769.

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Introduction/Rationale: In chronic obstructive pulmonary disease (COPD), defective macrophage phagocytic clearance of cells undergoing apoptosis by efferocytosis may lead to secondary necrosis of the uncleared cells and contribute to airway inflammation. The precise mechanisms for this phenomenon remain unknown. LC3-associated phagocytosis (LAP) is indispensable for effective efferocytosis. We hypothesized that cigarette smoke inhibits the regulators of LAP pathway, potentially contributing to the chronic airways inflammation associated with COPD. Methods: Bronchoalveolar (BAL)-derived alveolar macrophages, lung tissue macrophages obtained from lung resection surgery, and monocyte-derived macrophages (MDM) were prepared from COPD patients and control participants. Lung/airway samples from mice chronically exposed to cigarette smoke were also investigated. Differentiated THP-1 cells were exposed to cigarette smoke extract (CSE). The LAP pathway including Rubicon, as an essential regulator of LAP, efferocytosis and inflammation was examined using western blot, ELISA, flow cytometry, and/or immunofluorescence. Results: Rubicon was significantly depleted in COPD alveolar macrophages compared with non-COPD control macrophages. Rubicon protein in alveolar macrophages of cigarette smoke-exposed mice and cigarette smoke-exposed MDM and THP-1 was decreased with a concomitant impairment of efferocytosis. We also noted increased expression of LC3 which is critical for LAP pathway in COPD and THP-1 macrophages. Furthermore, THP-1 macrophages exposed to cigarette smoke extract exhibited higher levels of other key components of LAP pathway including Atg5 and TIM-4. There was a strong positive correlation between Rubicon protein expression and efferocytosis. Conclusion: LAP is a requisite for effective efferocytosis and an appropriate inflammatory response, which is impaired by Rubicon deficiency. Our findings suggest dysregulated LAP due to reduced Rubicon as a result of CSE exposure. This phenomenon could lead to a failure of macrophages to effectively process phagosomes containing apoptotic cells during efferocytosis. Restoring Rubicon protein expression has unrecognized therapeutic potential in the context of disease-related modifications caused by exposure to cigarette smoke.
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31

Barber, James. "South Africa: crossing the Rubicon." International Affairs 68, no. 4 (October 1992): 779–80. http://dx.doi.org/10.2307/2622819.

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32

Tkachenko, Stanislav L. "Wikileaks as Rubicon and Zeitgeist." Russia in Global Affairs 17, no. 2 (2019): 131–33. http://dx.doi.org/10.31278/1810-6374-2019-17-2-131-133.

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33

Romanelli, Frank, Denise H. Rhoney, Esther P. Black, Jeannine Conway, and Daniel R. Kennedy. "Pharmacy Education Crosses the Rubicon." American Journal of Pharmaceutical Education 84, no. 6 (June 2020): ajpe8131. http://dx.doi.org/10.5688/ajpe8131.

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34

Earnshaw, Owen. "E. Falque, Crossing the Rubicon." Phenomenological Reviews 2 (2016): 74. http://dx.doi.org/10.19079/pr.2016.11.ear.

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35

LAM, Peng Er. "Japan's Politics: Crossing the Rubicon." East Asian Policy 08, no. 01 (January 2016): 71–78. http://dx.doi.org/10.1142/s1793930516000064.

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In 2015, an unprecedented set of security bills was passed in Japanese parliament, permitting Tokyo to engage in collective security by aiding allies against third parties and to loosen the tight restrictions on the Self-Defence Force in United Nations Peace Keeping Operations, its rules of engagement and other multilateral deployment abroad. With these bills, Japan has crossed the Rubicon and evolved into a “normal” state in international affairs.
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36

Boyle, Keith B., and Felix Randow. "Rubicon swaps autophagy for LAP." Nature Cell Biology 17, no. 7 (June 30, 2015): 843–45. http://dx.doi.org/10.1038/ncb3197.

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37

Ellard, J. "Euthanasia: over the Rubicon already?" Australian and New Zealand Journal of Medicine 28, no. 1 (February 1998): 57. http://dx.doi.org/10.1111/j.1445-5994.1998.tb04460.x.

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38

Ruiz, M. Pilar Nunez. "Vers le franchissement du Rubicon?" ERA Forum 5, no. 2 (June 2004): 154–57. http://dx.doi.org/10.1007/s12027-004-0001-1.

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39

Millis, J. Michael. "Liver transplantation and the Rubicon." Liver Transplantation 21, no. 6 (May 26, 2015): 716–17. http://dx.doi.org/10.1002/lt.24130.

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40

Rondholz, Anke. "Crossing the Rubicon. A Historiographical Study." Mnemosyne 62, no. 3 (2009): 432–50. http://dx.doi.org/10.1163/156852509x384220.

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Анотація:
This paper contains a typological comparison of the extant accounts of Caesar's crossing of the Rubicon (Velleius Paterculus, Lucan, Plutarch, Suetonius, Appian, Orosius) and highlights interrelationships among the various accounts as well as patterns and topoi in the Rubicon myth. This episode has been dramatized by five of the authors as a point of transition from peace to war, although Caesar has set himself at fault much earlier by maneuvering to resign his command. Common motifs are the speed with which Caesar proceeds, his hesitation and pondering the consequences, and the connection of the crossing with a supernatural element. Caesar's nocturnal wanderings in Suetonius can be explained as a misinterpretation of Plutarch's account; the scene about the apparition with the reed pipe plays with generic markers to express the beginning of war. Finally, a conclusion can be drawn about Asinius Pollio as the common source. As a child of the Late Republic he might have been interested in mitigating his representation of the Rubicon scene by having Caesar hesitate, ponder the consequences, be under divine influence and act in self-defense, features that were exploited by his successors and turned into topoi of the Rubicon myth.
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41

Davids, Karel. "Aan de oever van de Rubicon." Tijdschrift voor Sociale en Economische Geschiedenis/ The Low Countries Journal of Social and Economic History 1, no. 1 (March 15, 2004): 120. http://dx.doi.org/10.18352/tseg.797.

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42

Kozintsev, Alexander. "Communication, semiotics, and the language Rubicon." Russian Journal of Communication 10, no. 1 (January 2, 2018): 1–20. http://dx.doi.org/10.1080/19409419.2017.1421095.

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43

Carlile, Alex. "Legislation to Law: Rubicon or Styx?" International Journal of Mental Health and Capacity Law 1, no. 13 (September 5, 2014): 107. http://dx.doi.org/10.19164/ijmhcl.v1i13.173.

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<p>I wrote this article as a reflection on the activities of the Joint Scrutiny Committee on the Draft Mental Health Bill 2004. My credentials for authorship are that I acted as the Chair of the Committee, elected by the Committee at the beginning of its proceedings.</p>
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44

Anderson, Maija. "The Eugenic Rubicon: California's Sterilization Stories." American Archivist 82, no. 1 (March 2019): 225–29. http://dx.doi.org/10.17723/0360-9081-82.1.225.

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45

Trippett, David. "An Uncrossable Rubicon: Liszt's Sardanapalo Revisited." Journal of the Royal Musical Association 143, no. 2 (2018): 361–432. http://dx.doi.org/10.1080/02690403.2018.1507120.

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Анотація:
AbstractIn 1850, after five years of planning, Liszt began composing music for his Italian opera, Sardanapalo, after Byron. It was central to his ambition to attain status as a European composer, but he abandoned the project halfway through. La Mara (1911), Humphrey Searle (1954) and others declared the manuscript fragmentary and partially illegible, but in 2016 this verdict was categorically overturned when work began on an edition of what Liszt notated: almost the entirety of Act 1. This article draws on an array of sources – published and unpublished – significantly to update our knowledge of the circumstances surrounding Liszt's composition and abandonment of Sardanapalo. In light of his inconsistently Italianate music and idiosyncratic treatment of the libretto, it also reinterprets Liszt's mid-century aesthetic orientation, as a confidant of Wagner and would-be pillar of Franz Brendel's future neudeutsche Schule. By contextualizing key aspects of the uncovered musical score and libretto within Liszt's mid-century writings on aesthetics, it posits character, declamatory melody and the visuality of the stage as (initially) critical criteria in the communication of a literary narrative, and suggests that Liszt's impulse towards symphonic poetry may first have been kindled within the aesthetic potential of opera.
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46

DeBlois, Bruce M., Richard L. Garwin, R. Scott Kemp, and Jeremy C. Marwell. "Space Weapons: Crossing the U.S. Rubicon." International Security 29, no. 2 (October 2004): 50–84. http://dx.doi.org/10.1162/0162288042879922.

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47

H. R. H. "Some Defining Moments: Crossing the Rubicon." Nationalities Papers 23, no. 4 (December 1995): 671–72. http://dx.doi.org/10.1080/00905999508408408.

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48

Visioli, Francesco. "Pharma and nutrition: Crossing the Rubicon." PharmaNutrition 1, no. 1 (January 2013): 9. http://dx.doi.org/10.1016/j.phanu.2012.10.002.

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49

Trewavas, Anthony J. "Rubicon The fifth dimension of biology." Cell Calcium 18, no. 1 (July 1995): 86–87. http://dx.doi.org/10.1016/0143-4160(95)90048-9.

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50

Savage-Rumbaugh, Sue. "Multi-tasking: the Pan-human rubicon." Seminars in Neuroscience 3, no. 5 (October 1991): 417–22. http://dx.doi.org/10.1016/1044-5765(91)90032-j.

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