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Artículos de revistas sobre el tema "Potentiateurs"

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Autor: Grafiati

Publicado: 20 de abril de 2024

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1

S, Hanumitha, Mahalakshmi V y 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 (31 de agosto de 2018): 1796–802. http://dx.doi.org/10.31142/ijtsrd17137.

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2

&NA;. "Ecadotril potentiates captopril". Inpharma Weekly &NA;, n.º 1005 (septiembre de 1995): 10. http://dx.doi.org/10.2165/00128413-199510050-00021.

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3

Zahl, K., J. B. Eisenkraft, I. H. Sampson y R. Miller. "LIDOCAINE POTENTIATES VECURONIUM". Anesthesiology 71, Supplement (septiembre de 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 y Roger D. Kornberg. "Chromatin potentiates transcription". Proceedings of the National Academy of Sciences 114, n.º 7 (30 de enero de 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 y M. A. Lazzari. "Amiodarone potentiates acenocoumarin". Thrombosis Research 53, n.º 2 (enero de 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, n.º 6 (18 de mayo de 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 y Akio Inui. "Hesperidin Potentiates Ghrelin Signaling". Recent Patents on Food, Nutrition & Agriculture 6, n.º 1 (10 de diciembre de 2014): 60–63. http://dx.doi.org/10.2174/2212798406666140825120623.

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8

&NA;. "Paracetamol potentiates warfarin anticoagulation". Reactions Weekly &NA;, n.º 692 (marzo de 1998): 4. http://dx.doi.org/10.2165/00128415-199806920-00006.

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9

&NA;. "Paracetamol potentiates warfarin anticoagulation". Inpharma Weekly &NA;, n.º 1128 (marzo de 1998): 20. http://dx.doi.org/10.2165/00128413-199811280-00039.

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10

&NA;. "Dipyridamole potentiates nucleoside antivirals". Inpharma Weekly &NA;, n.º 957 (octubre de 1994): 19. http://dx.doi.org/10.2165/00128413-199409570-00050.

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11

Kim, Karissa Y. y Michael A. Mancano. "Fenofibrate Potentiates Warfarin Effects". Annals of Pharmacotherapy 37 (febrero de 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 y P. D. Adams. "Wnt signaling potentiates nevogenesis". Proceedings of the National Academy of Sciences 110, n.º 40 (16 de septiembre de 2013): 16009–14. http://dx.doi.org/10.1073/pnas.1303491110.

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13

Narkiewicz, Krzysztof, Ryan L. Cooley y Virend K. Somers. "Alcohol Potentiates Orthostatic Hypotension". Circulation 101, n.º 4 (febrero de 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 y M. J. BRODIE. "Verapamil Potentiates Carbamazepine Neurotoxicity". Survey of Anesthesiology 31, n.º 1 (febrero de 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, n.º 3 (julio de 2007): 259–78. http://dx.doi.org/10.1177/1076029607302404.

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16

Kim, Karissa Y. y Michael A. Mancano. "Fenofibrate Potentiates Warfarin Effects". Annals of Pharmacotherapy 37, n.º 2 (febrero de 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 y Jean-Louis Montastruc. "Apomorphine potentiates vagal bradycardia". European Journal of Pharmacology 166, n.º 3 (agosto de 1989): 511–14. http://dx.doi.org/10.1016/0014-2999(89)90365-8.

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18

Valeria Vergoni, Anna, Arcangela Scarano y A. Bertolini. "Pinacidil potentiates morphine analgesia". Life Sciences 50, n.º 16 (enero de 1992): PL135—PL138. http://dx.doi.org/10.1016/0024-3205(92)90467-4.

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19

Saha, Suchandrima, Monisankar Ghosh y Samir Kumar Dutta. "The dual-hit metabolic modulator LDCA synergistically potentiates doxorubicin to selectively combat cancer-associated hallmarks". RSC Advances 7, n.º 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 y 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, n.º 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, n.º 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 y Zhi-Jie Liu. "Ligand identification of the adenosine A2Areceptor in self-assembled nanodiscs by affinity mass spectrometry". Anal. Methods 9, n.º 40 (2017): 5851–58. http://dx.doi.org/10.1039/c7ay01891f.

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23

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

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24

&NA;. "Moclobemide potentiates effect of ephedrine". Reactions Weekly &NA;, n.º 635 (enero de 1997): 5. http://dx.doi.org/10.2165/00128415-199706350-00010.

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25

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

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26

Parry, David E. y Robert F. Lemanske. "AIRWAY EDEMA POTENTIATES AIRWAY REACTIVITY". Pediatrics 98, n.º 2 (1 de agosto de 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 y David Baltimore. "MicroRNA-125b Potentiates Macrophage Activation". Journal of Immunology 187, n.º 10 (14 de octubre de 2011): 5062–68. http://dx.doi.org/10.4049/jimmunol.1102001.

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28

Nguyen, Hieu D. y Loi H. Do. "Taming glutathione potentiates metallodrug action". Current Opinion in Chemical Biology 71 (diciembre de 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 y L. KRUSE. "EXTRADURAL DROPERIDOL POTENTIATES EXTRADURAL OPIOIDS". British Journal of Anaesthesia 57, n.º 2 (febrero de 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 y W. Mitzner. "Airway edema potentiates airway reactivity". Journal of Applied Physiology 79, n.º 4 (1 de octubre de 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 y Richard H. Gomer. "Trypsin Potentiates Human Fibrocyte Differentiation". PLoS ONE 8, n.º 8 (7 de agosto de 2013): e70795. http://dx.doi.org/10.1371/journal.pone.0070795.

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32

Vinke, Louis N. y Sam Ling. "Luminance potentiates human visuocortical responses". Journal of Neurophysiology 123, n.º 2 (1 de febrero de 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, n.º 330 (17 de junio de 2014): ec162-ec162. http://dx.doi.org/10.1126/scisignal.2005593.

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34

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

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35

Mei, Changlin y Feng Zheng. "Chronic Inflammation Potentiates Kidney Aging". Seminars in Nephrology 29, n.º 6 (noviembre de 2009): 555–68. http://dx.doi.org/10.1016/j.semnephrol.2009.07.002.

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36

Clark, Elizabeth T. y Bruce L. Gewertz. "Glucagon potentiates intestinal reperfusion injury". Journal of Vascular Surgery 11, n.º 2 (febrero de 1990): 270–79. http://dx.doi.org/10.1067/mva.1990.16786.

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37

Carrasco, M., A. M. Giordano y C. Looser. "Transient attention potentiates perceptual learning". Journal of Vision 7, n.º 9 (30 de marzo de 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 y Martin Hewison. "Estrone potentiates myeloid cell differentiation". Experimental Hematology 27, n.º 3 (marzo de 1999): 451–60. http://dx.doi.org/10.1016/s0301-472x(98)00078-2.

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39

van Kempen, Léon C. L. y Lisa M. Coussens. "MMP9 potentiates pulmonary metastasis formation". Cancer Cell 2, n.º 4 (octubre de 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 y Mauro Pesenti. "Number magnitude potentiates action judgements". Experimental Brain Research 180, n.º 3 (6 de febrero de 2007): 525–34. http://dx.doi.org/10.1007/s00221-007-0870-y.

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41

Clark, Elizabeth T. y Bruce L. Gewertz. "Glucagon potentiates intestinal reperfusion injury". Journal of Vascular Surgery 11, n.º 2 (febrero de 1990): 270–79. http://dx.doi.org/10.1016/0741-5214(90)90270-k.

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42

Piper, Samantha L. y Hubert T. Kim. "Thermal Stress Potentiates Bupivacaine Chondrotoxicity". Arthroscopy: The Journal of Arthroscopic & Related Surgery 28, n.º 9 (septiembre de 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;, n.º 1273 (febrero de 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 y Amy B. Heimberger. "Hypoxia Potentiates Glioma-Mediated Immunosuppression". PLoS ONE 6, n.º 1 (20 de enero de 2011): e16195. http://dx.doi.org/10.1371/journal.pone.0016195.

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45

Cox, Nehemiah, Darrell Pilling y Richard H. Gomer. "NaCl Potentiates Human Fibrocyte Differentiation". PLoS ONE 7, n.º 9 (18 de septiembre de 2012): e45674. http://dx.doi.org/10.1371/journal.pone.0045674.

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46

Sahenk, Zarife, Jegatheesan Seharaseyon y Jerry R. Mendell. "CNTF potentiates peripheral nerve regeneration". Brain Research 655, n.º 1-2 (agosto de 1994): 246–50. http://dx.doi.org/10.1016/0006-8993(94)91621-7.

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47

Delius, Ralph E. y Daniel B. Hinshaw. "Metabolic inhibition potentiates oxidant injury". Journal of Surgical Research 50, n.º 4 (abril de 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 y Ali Javaheri. "Intermittent Fasting Potentiates Anthracycline Cardiotoxicity". Journal of Cardiac Failure 29, n.º 4 (abril de 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 y 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, n.º 2 (febrero de 2016): 148–53. http://dx.doi.org/10.12980/jclm.4.2016j5-219.

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50

Halpert, Matthew M., R. Glenn King y Louis B. Justement. "TLT2 Ligation Potentiates Neutrophil Migration and the Respiratory Burst Response (135.62)". Journal of Immunology 182, n.º 1_Supplement (1 de abril de 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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