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Journal articles on the topic 'Potentiateurs'

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Author: Grafiati

Published: 20 April 2024

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1

S, Hanumitha, Mahalakshmi V, and Abirami S. "Biosynthesis of Zinc Oxide Nanoparticles Using Bacillus Species Potentiates Anticancer and Antimicrobial Activity." International Journal of Trend in Scientific Research and Development Volume-2, Issue-5 (August 31, 2018): 1796–802. http://dx.doi.org/10.31142/ijtsrd17137.

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2

&NA;. "Ecadotril potentiates captopril." Inpharma Weekly &NA;, no. 1005 (September 1995): 10. http://dx.doi.org/10.2165/00128413-199510050-00021.

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3

Zahl, K., J. B. Eisenkraft, I. H. Sampson, and R. Miller. "LIDOCAINE POTENTIATES VECURONIUM." Anesthesiology 71, Supplement (September 1989): A789. http://dx.doi.org/10.1097/00000542-198909001-00789.

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4

Nagai, Shigeki, Ralph E. Davis, Pierre Jean Mattei, Kyle Patrick Eagen, and Roger D. Kornberg. "Chromatin potentiates transcription." Proceedings of the National Academy of Sciences 114, no. 7 (January 30, 2017): 1536–41. http://dx.doi.org/10.1073/pnas.1620312114.

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Chromatin isolated from the chromosomal locus of the PHO5 gene of yeast in a transcriptionally repressed state was transcribed with 12 pure proteins (80 polypeptides): RNA polymerase II, six general transcription factors, TFIIS, the Pho4 gene activator protein, and the SAGA, SWI/SNF, and Mediator complexes. Contrary to expectation, a nucleosome occluding the TATA box and transcription start sites did not impede transcription but rather, enhanced it: the level of chromatin transcription was at least sevenfold greater than that of naked DNA, and chromatin gave patterns of transcription start sites closely similar to those occurring in vivo, whereas naked DNA gave many aberrant transcripts. Both histone acetylation and trimethylation of H3K4 (H3K4me3) were important for chromatin transcription. The nucleosome, long known to serve as a general gene repressor, thus also performs an important positive role in transcription.

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5

Fondevila, C., S. Meschengieser, and M. A. Lazzari. "Amiodarone potentiates acenocoumarin." Thrombosis Research 53, no. 2 (January 1989): 203–8. http://dx.doi.org/10.1016/0049-3848(89)90381-2.

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6

Visan, Ioana. "Mn potentiates cGAS." Nature Immunology 19, no. 6 (May 18, 2018): 511. http://dx.doi.org/10.1038/s41590-018-0126-y.

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7

Suzuki, Hajime, Akihiro Asakawa, Namiko Kawamura, Takakazu Yagi, and Akio Inui. "Hesperidin Potentiates Ghrelin Signaling." Recent Patents on Food, Nutrition & Agriculture 6, no. 1 (December 10, 2014): 60–63. http://dx.doi.org/10.2174/2212798406666140825120623.

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8

&NA;. "Paracetamol potentiates warfarin anticoagulation." Reactions Weekly &NA;, no. 692 (March 1998): 4. http://dx.doi.org/10.2165/00128415-199806920-00006.

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9

&NA;. "Paracetamol potentiates warfarin anticoagulation." Inpharma Weekly &NA;, no. 1128 (March 1998): 20. http://dx.doi.org/10.2165/00128413-199811280-00039.

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10

&NA;. "Dipyridamole potentiates nucleoside antivirals." Inpharma Weekly &NA;, no. 957 (October 1994): 19. http://dx.doi.org/10.2165/00128413-199409570-00050.

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11

Kim, Karissa Y., and Michael A. Mancano. "Fenofibrate Potentiates Warfarin Effects." Annals of Pharmacotherapy 37 (February 2003): 212–15. http://dx.doi.org/10.1345/aph.1c257.

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12

Pawlikowski, J. S., T. McBryan, J. van Tuyn, M. E. Drotar, R. N. Hewitt, A. B. Maier, A. King, K. Blyth, H. Wu, and P. D. Adams. "Wnt signaling potentiates nevogenesis." Proceedings of the National Academy of Sciences 110, no. 40 (September 16, 2013): 16009–14. http://dx.doi.org/10.1073/pnas.1303491110.

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13

Narkiewicz, Krzysztof, Ryan L. Cooley, and Virend K. Somers. "Alcohol Potentiates Orthostatic Hypotension." Circulation 101, no. 4 (February 2000): 398–402. http://dx.doi.org/10.1161/01.cir.101.4.398.

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14

MACPHEE, G. J. A., G. G. THOMSON, G. T. McINNES, and M. J. BRODIE. "Verapamil Potentiates Carbamazepine Neurotoxicity." Survey of Anesthesiology 31, no. 1 (February 1987): 13. http://dx.doi.org/10.1097/00132586-198702000-00013.

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15

Stief, Thomas W. "Singlet Oxygen Potentiates Thrombolysis." Clinical and Applied Thrombosis/Hemostasis 13, no. 3 (July 2007): 259–78. http://dx.doi.org/10.1177/1076029607302404.

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16

Kim, Karissa Y., and Michael A. Mancano. "Fenofibrate Potentiates Warfarin Effects." Annals of Pharmacotherapy 37, no. 2 (February 2003): 212–15. http://dx.doi.org/10.1177/106002800303700210.

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OBJECTIVE: To describe 2 patients in whom the initiation of fenofibrate potentiated warfarin's anticoagulant effects. CASE SUMMARY: A 71-year-old white woman and an 80-year-old white woman with multiple medical conditions were both stabilized on long-term warfarin therapy. During the course of anticoagulation, both patients were prescribed fenofibrate and experienced threefold and twofold increases in international normalized ratio (INR), respectively, requiring total weekly warfarin dosage reductions of 30–40%. Before starting fenofibrate therapy, both patients' coagulation values were within the therapeutic range. When interviewed, patients and caregivers denied bleeding, bruising, changes in diet, alcohol ingestion, nonadherence with therapy, or changes in drug regimen except for the addition of fenofibrate. Upon chart review, evaluation of potentially contributory parameters, such as other changes in drug therapy, thyroid function, liver function, and drug–disease interactions, showed that these parameters remained stable and were ruled noncontributory. DISCUSSION: The addition of fenofibrate in 2 patients on stable and therapeutic doses of warfarin increased the anticoagulant response to warfarin. A clear temporal relationship with the addition of fenofibrate and the appearance of the interaction was seen. Fenofibrate is highly protein bound, with the potential to displace warfarin from its binding protein, leading to an enhanced hypoprothrombinemic effect. Fenofibrate is also a mild to moderate inhibitor of CYP2C9, the enzyme responsible for warfarin metabolism. The combination of these effects — displacement of warfarin by fenofibrate coupled with decreased metabolism of warfarin — may increase the anticoagulant response to warfarin. Using the Naranjo probability scale, these interactions were designated as probable. CONCLUSIONS: We suggest serial monitoring of INR and consider an empiric 20% reduction in warfarin dosage when fenofibrate is initiated, with the possibility for a greater warfarin dosage reduction based on INR results.

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17

Montastruc, Paul, Christine Damase-Michel, and Jean-Louis Montastruc. "Apomorphine potentiates vagal bradycardia." European Journal of Pharmacology 166, no. 3 (August 1989): 511–14. http://dx.doi.org/10.1016/0014-2999(89)90365-8.

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18

Valeria Vergoni, Anna, Arcangela Scarano, and A. Bertolini. "Pinacidil potentiates morphine analgesia." Life Sciences 50, no. 16 (January 1992): PL135—PL138. http://dx.doi.org/10.1016/0024-3205(92)90467-4.

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19

Saha, Suchandrima, Monisankar Ghosh, and Samir Kumar Dutta. "The dual-hit metabolic modulator LDCA synergistically potentiates doxorubicin to selectively combat cancer-associated hallmarks." RSC Advances 7, no. 84 (2017): 53322–33. http://dx.doi.org/10.1039/c7ra08625c.

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20

Harvestine, Jenna N., Hakan Orbay, Jonathan Y. Chen, David E. Sahar, and J. Kent Leach. "Cell-secreted extracellular matrix, independent of cell source, promotes the osteogenic differentiation of human stromal vascular fraction." Journal of Materials Chemistry B 6, no. 24 (2018): 4104–15. http://dx.doi.org/10.1039/c7tb02787g.

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21

Ieranò, Caterina, Luigi Portella, Sara Lusa, Giuseppina Salzano, Crescenzo D'Alterio, Maria Napolitano, Maria Buoncervello, et al. "CXCR4-antagonist Peptide R-liposomes for combined therapy against lung metastasis." Nanoscale 8, no. 14 (2016): 7562–71. http://dx.doi.org/10.1039/c5nr06335c.

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22

Ma, Jun, Yan Lu, Dong Wu, Yao Peng, Wendy Loa-Kum-Cheung, Chao Peng, Ronald J. Quinn, Wenqing Shui, and Zhi-Jie Liu. "Ligand identification of the adenosine A2Areceptor in self-assembled nanodiscs by affinity mass spectrometry." Anal. Methods 9, no. 40 (2017): 5851–58. http://dx.doi.org/10.1039/c7ay01891f.

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23

Fanburg, Barry L., and Susan M. Deneke. "Protein Deficiency Potentiates Oxygen Toxicity." Experimental Lung Research 14, sup1 (January 1988): 911–19. http://dx.doi.org/10.3109/01902148809064183.

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24

&NA;. "Moclobemide potentiates effect of ephedrine." Reactions Weekly &NA;, no. 635 (January 1997): 5. http://dx.doi.org/10.2165/00128415-199706350-00010.

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25

Li, J., Z. Sun, Z. Lv, and D. Shi. "Microtubule stabilization potentiates cartilage regeneration." Osteoarthritis and Cartilage 29 (April 2021): S196. http://dx.doi.org/10.1016/j.joca.2021.02.265.

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26

Parry, David E., and Robert F. Lemanske. "AIRWAY EDEMA POTENTIATES AIRWAY REACTIVITY." Pediatrics 98, no. 2 (August 1, 1996): 336. http://dx.doi.org/10.1542/peds.98.2.336.

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Acute volume loading with saline causes an increase in airway wall thickness and a decrease in airway area and a subsequent enhanced constrictor response to aerosolized histamine. Although this study examines effects of acute edema, to the extent that chronic inflammation (such as in asthma) leads to increased vascular permeability, airway edema and increased responsiveness, acute or chronic edema should have similar effects on airway responsiveness.

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27

Chaudhuri, Aadel A., Alex Yick-Lun So, Nikita Sinha, William S. J. Gibson, Konstantin D. Taganov, Ryan M. O’Connell, and David Baltimore. "MicroRNA-125b Potentiates Macrophage Activation." Journal of Immunology 187, no. 10 (October 14, 2011): 5062–68. http://dx.doi.org/10.4049/jimmunol.1102001.

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28

Nguyen, Hieu D., and Loi H. Do. "Taming glutathione potentiates metallodrug action." Current Opinion in Chemical Biology 71 (December 2022): 102213. http://dx.doi.org/10.1016/j.cbpa.2022.102213.

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29

BACH, V., P. CARL, O. RAVLO, M. CRAWFORD, and L. KRUSE. "EXTRADURAL DROPERIDOL POTENTIATES EXTRADURAL OPIOIDS." British Journal of Anaesthesia 57, no. 2 (February 1985): 238–39. http://dx.doi.org/10.1093/bja/57.2.238-a.

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30

Brown, R. H., E. A. Zerhouni, and W. Mitzner. "Airway edema potentiates airway reactivity." Journal of Applied Physiology 79, no. 4 (October 1, 1995): 1242–48. http://dx.doi.org/10.1152/jappl.1995.79.4.1242.

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Thickening of the airway wall has been hypothesized to be one of the mechanisms contributing to airway hyperresponsiveness in asthma. If such thickening of the wall is internal to the airway smooth muscle or otherwise causes a decrease in baseline airway caliber, it should also cause exaggerated airway responsiveness. In the present study, we used high-resolution computed tomography to directly measure the changes in the caliber and wall thickness of conducting airways after aerosol histamine challenge before and after normal saline volume loading. On separate days, five anesthetized dogs received either a baseline aerosol challenge of 3 mg/ml of histamine for five breaths or the same aerosol challenge immediately after a 100 ml/kg bolus of normal saline infused over a 10-min period. Baseline aerosol histamine challenge decreased airway area to 71 +/- 2% (SE) of the control value (P < 0.05). Intravenous administration of 100 ml/kg of normal saline increased wall area by decreasing airway luminal area to 78 +/- 3% of the control value (P < 0.01), with no change in outer airway area. Aerosol histamine challenge superimposed on this engorgement with normal saline challenge further decreased airway luminal area to 54 +/- 3% of the control value (P < 0.01). Quantitative modeling indicated that the edema in the airway wall was mostly outside the smooth muscle and that the smooth muscle shortening with histamine was similar with and without edema. We conclude that a moderate degree of acute airway wall thickening can lead to a potentiated constrictor response to histamine.

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31

White, Michael J. V., Melissa Glenn, and Richard H. Gomer. "Trypsin Potentiates Human Fibrocyte Differentiation." PLoS ONE 8, no. 8 (August 7, 2013): e70795. http://dx.doi.org/10.1371/journal.pone.0070795.

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32

Vinke, Louis N., and Sam Ling. "Luminance potentiates human visuocortical responses." Journal of Neurophysiology 123, no. 2 (February 1, 2020): 473–83. http://dx.doi.org/10.1152/jn.00589.2019.

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Our visual system is tasked with transforming variations in light within our environment into a coherent percept, typically described using properties such as luminance and contrast. Models of vision often downplay the importance of luminance in shaping cortical responses, instead prioritizing representations that do not covary with overall luminance (i.e., contrast), and yet visuocortical response properties that may reflect luminance encoding remain poorly understood. In this study, we examined whether well-established visuocortical response properties may also reflect luminance encoding, challenging the idea that luminance information itself plays no significant role in supporting visual perception. To do so, we measured functional activity in human visual cortex when presenting stimuli varying in contrast and mean luminance, and found that luminance response functions are strongly contrast dependent between 50 and 250 cd/m2, confirmed with a subsequent experiment. High-contrast stimuli produced linearly increasing responses as luminance increased logarithmically for all early visual areas, whereas low-contrast stimuli produced either flat (V1) or assorted positive linear (V2 and V3) response profiles. These results reveal that the mean luminance information of a visual signal persists within visuocortical representations, potentially reflecting an inherent imbalance of excitatory and inhibitory components that can be either contrast dependent (V1 and V2) or contrast invariant (V3). The role of luminance should be considered when the aim is to drive potent visually evoked responses and when activity is compared across studies. More broadly, overall luminance should be weighed heavily as a core feature of the visual system and should play a significant role in cortical models of vision. NEW & NOTEWORTHY This neuroimaging study investigates the influence of overall luminance on population activity in human visual cortex. We discovered that the response to a particular stimulus contrast level is reliant, in part, on the mean luminance of a signal, revealing that the mean luminance information of our environment is represented within the visual cortex. The results challenge a long-standing misconception about the role of luminance information in the processing of visual information at the cortical level.

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33

Ferrarelli, L. K. "MAPK Methylation Potentiates RAS Signaling." Science Signaling 7, no. 330 (June 17, 2014): ec162-ec162. http://dx.doi.org/10.1126/scisignal.2005593.

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34

Flajs, D., M. Mladinic, D. Zeljezic, and M. Peraica. "Citrinin potentiates ochratoxin A toxicity." Toxicology Letters 205 (August 2011): S220—S221. http://dx.doi.org/10.1016/j.toxlet.2011.05.756.

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35

Mei, Changlin, and Feng Zheng. "Chronic Inflammation Potentiates Kidney Aging." Seminars in Nephrology 29, no. 6 (November 2009): 555–68. http://dx.doi.org/10.1016/j.semnephrol.2009.07.002.

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36

Clark, Elizabeth T., and Bruce L. Gewertz. "Glucagon potentiates intestinal reperfusion injury." Journal of Vascular Surgery 11, no. 2 (February 1990): 270–79. http://dx.doi.org/10.1067/mva.1990.16786.

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37

Carrasco, M., A. M. Giordano, and C. Looser. "Transient attention potentiates perceptual learning." Journal of Vision 7, no. 9 (March 30, 2010): 88. http://dx.doi.org/10.1167/7.9.88.

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38

Mountford, Joanne C., Christopher M. Bunce, Susan V. Hughes, Mark T. Drayson, David Webb, Geoffery Brown, and Martin Hewison. "Estrone potentiates myeloid cell differentiation." Experimental Hematology 27, no. 3 (March 1999): 451–60. http://dx.doi.org/10.1016/s0301-472x(98)00078-2.

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39

van Kempen, Léon C. L., and Lisa M. Coussens. "MMP9 potentiates pulmonary metastasis formation." Cancer Cell 2, no. 4 (October 2002): 251–52. http://dx.doi.org/10.1016/s1535-6108(02)00157-5.

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40

Badets, Arnaud, Michael Andres, Samuel Di Luca, and Mauro Pesenti. "Number magnitude potentiates action judgements." Experimental Brain Research 180, no. 3 (February 6, 2007): 525–34. http://dx.doi.org/10.1007/s00221-007-0870-y.

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41

Clark, Elizabeth T., and Bruce L. Gewertz. "Glucagon potentiates intestinal reperfusion injury." Journal of Vascular Surgery 11, no. 2 (February 1990): 270–79. http://dx.doi.org/10.1016/0741-5214(90)90270-k.

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42

Piper, Samantha L., and Hubert T. Kim. "Thermal Stress Potentiates Bupivacaine Chondrotoxicity." Arthroscopy: The Journal of Arthroscopic & Related Surgery 28, no. 9 (September 2012): 1246–54. http://dx.doi.org/10.1016/j.arthro.2012.02.012.

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43

&NA;. "Alteplase potentiates NMDA-induced neurotoxicity." Inpharma Weekly &NA;, no. 1273 (February 2001): 20. http://dx.doi.org/10.2165/00128413-200112730-00050.

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44

Wei, Jun, Adam Wu, Ling-Yuan Kong, Yongtao Wang, Gregory Fuller, Isabella Fokt, Giovanni Melillo, Waldemar Priebe, and Amy B. Heimberger. "Hypoxia Potentiates Glioma-Mediated Immunosuppression." PLoS ONE 6, no. 1 (January 20, 2011): e16195. http://dx.doi.org/10.1371/journal.pone.0016195.

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45

Cox, Nehemiah, Darrell Pilling, and Richard H. Gomer. "NaCl Potentiates Human Fibrocyte Differentiation." PLoS ONE 7, no. 9 (September 18, 2012): e45674. http://dx.doi.org/10.1371/journal.pone.0045674.

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46

Sahenk, Zarife, Jegatheesan Seharaseyon, and Jerry R. Mendell. "CNTF potentiates peripheral nerve regeneration." Brain Research 655, no. 1-2 (August 1994): 246–50. http://dx.doi.org/10.1016/0006-8993(94)91621-7.

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47

Delius, Ralph E., and Daniel B. Hinshaw. "Metabolic inhibition potentiates oxidant injury." Journal of Surgical Research 50, no. 4 (April 1991): 314–22. http://dx.doi.org/10.1016/0022-4804(91)90197-t.

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48

Ozcan, Mualla, Zhen Guo, Carla Valenzuela Ripoll, Aarti Asnani, Kenneth Margulies, Carmen Bergom, Abhinav Diwan, and Ali Javaheri. "Intermittent Fasting Potentiates Anthracycline Cardiotoxicity." Journal of Cardiac Failure 29, no. 4 (April 2023): 568. http://dx.doi.org/10.1016/j.cardfail.2022.10.057.

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49

Abeysekera, Walimuni Kanchana Subhashini Mendis, Chatura Tissa Dayendra Ratnasooriya, Wanigasekara Daya Ratnasooriya, and Sirimal Premakumara Galbada Arachchige. "Sri Lankan black tea (Camellia sinensis L.) inhibits the methylglyoxal mediated protein glycation and potentiates its reversing activity in vitro." Journal of Coastal Life Medicine 4, no. 2 (February 2016): 148–53. http://dx.doi.org/10.12980/jclm.4.2016j5-219.

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50

Halpert, Matthew M., R. Glenn King, and Louis B. Justement. "TLT2 Ligation Potentiates Neutrophil Migration and the Respiratory Burst Response (135.62)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 135.62. http://dx.doi.org/10.4049/jimmunol.182.supp.135.62.

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Abstract TREM-like Transcript 2 (TLT2) is a transmembrane receptor expressed on B cells, macrophages and neutrophils in the mouse and human. As of yet, an endogenous ligand has not been identified and the function of TLT2 remains to be elucidated. Because neutrophils are a primary mediator of the host innate immune response to bacterial infection, the analysis of factors that control neutrophil function is of great interest. Preliminary evidence suggests that TLT2 potentiates multiple neutrophil functions, including the respiratory burst and chemotaxis. Using a chemiluminescence system, it was shown that TLT2 ligation increases the primary phase of the respiratory burst by 20-25% in response to the bacterial peptide FMLP, although there is a slight inhibitory delay during the initial phase of the response. Transwell assays have been used to determine the effect that α-TLT2 mAb has on murine neutrophil chemotaxis. In vitro data demonstrate that TLT2 ligation increases migration 1.5-2.5 times in response to different chemotactic stimuli, such as FMLP, IL-8, and MIP-2. Importantly, α-TLT2 mAb treatment potentiates chemotaxis in response to agonists that signal via G-protein coupled receptors, but not in response to agonists that signal via tyrosine kinase-dependent pathways (e.g. G-CSF). These data suggest that TLT2 ligation effectively potentiates multiple neutrophil functional responses.

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