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Journal articles on the topic 'Digibind'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Ocal, Idris T., and Terrence R. Green. "Serum digoxin in the presence of Digibind: determination of digoxin by the Abbott AxSYM and Baxter Stratus II immunoassays by direct analysis without pretreatment of serum samples." Clinical Chemistry 44, no. 9 (September 1, 1998): 1947–50. http://dx.doi.org/10.1093/clinchem/44.9.1947.

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Abstract We have reevaluated the feasibility of using direct immunochemical methods to track free digoxin in patients receiving Digibind®. We report here that results obtained by the Stratus II and AxSYM immunoassays on patients receiving digoxin (without Digibind), digoxin-fortified serum samples supplemented with Digibind, and a digitoxic patient treated with Digibind, show no clinically significant biases. We conclude that useful free digoxin concentrations may be obtained for Digibind-treated patients using either the AxSYM or Stratus immunoassays without subjecting samples to ultrafiltration before analysis.

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2

YAMADA, Kaoru, Atsuo GOTO, Chen HUI, Noriko YAGI, and Tsuneaki SUGIMOTO. "Effects of the Fab fragment of digoxin antibody on the natriuresis and increase in blood pressure induced by intracerebroventricular infusion of hypertonic saline solution in rats." Clinical Science 82, no. 6 (June 1, 1992): 625–30. http://dx.doi.org/10.1042/cs0820625.

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1. The effects of intravenous injection of Fab fragments of anti-digoxin IgG (Digibind) on the changes in blood pressure, urine volume and urinary sodium excretion after intracerebroventricular infusion of artificial cerebrospinal fluid with normal or high sodium concentration were examined in anaesthetized rats. 2. The biological efficacy of Digibind was confirmed by experiments in vitro and in vivo, which showed that pre-treatment with Digibind completely abolished or significantly attenuated the aortic contractile response or pressor response to digoxin in guinea-pigs. 3. Infusion of high-sodium cerebrospinal fluid, but not normal-sodium cerebrospinal fluid, into the lateral brain ventricle of rats caused marked increases in blood pressure, urine volume and urinary sodium excretion. 4. Digibind did not significantly affect the increases in blood pressure, urine volume and urinary sodium excretion caused by intracerebroventricular infusion of high-sodium cerebrospinal fluid. 5. Digoxin-like immunoreactive factor may play a minor role, if any, in central nervous system-induced natriuresis in rats.

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3

Rainey, Petrie. "Digibind and Free Digoxin." Clinical Chemistry 45, no. 5 (May 1, 1999): 719–21. http://dx.doi.org/10.1093/clinchem/45.5.719.

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4

Schakenbach, L., and P. Arft. "Digoxin toxicity treated with Digibind." Critical Care Nurse 9, no. 5 (June 1, 1989): 16–22. http://dx.doi.org/10.4037/ccn1989.9.5.16.

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5

Fazio, Anthony. "Misuse of Digibind is costly." American Journal of Health-System Pharmacy 47, no. 11 (November 1, 1990): 2460. http://dx.doi.org/10.1093/ajhp/47.11.2460.

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6

Dasgupta, Amitava, Amanda Peterson, Alice Wells, and Jeffrey K. Actor. "Effect of Indian Ayurvedic Medicine Ashwagandha on Measurement of Serum Digoxin and 11 Commonly Monitored Drugs Using Immunoassays: Study of Protein Binding and Interaction With Digibind." Archives of Pathology & Laboratory Medicine 131, no. 8 (August 1, 2007): 1298–303. http://dx.doi.org/10.5858/2007-131-1298-eoiama.

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Abstract Context.—Ashwagandha, a popular Ayurvedic medicine, is now available in the United States. Alkaloids found in this herb have structural similarity with digoxin. Objective.—To study potential interference of Ashwagandha with serum digoxin measurement by immunoassays. Potential interference was also investigated with immunoassays for 11 other commonly monitored drugs. In addition, interaction of components of Ashwagandha with the Fab fragment of antidigoxin antibody (Digibind) was investigated. Design.—Two different brands of liquid extract and 1 dry powdered form of Ashwagandha were used for this investigation. Aliquots of drug-free serum were supplemented with various concentrations of Ashwagandha and apparent digoxin concentrations were measured by 3 digoxin immunoassays. Mice were fed with Ashwagandha and apparent digoxin concentrations were measured 1 and 3 hours after feeding. Potential interference of Ashwagandha with immunoassays of 11 other drugs was also investigated. Interaction of components of Ashwagandha with Digibind was studied in vitro. Results.—Significant apparent digoxin concentrations were observed both in vitro and in vivo using the fluorescence polarization immunoassay of digoxin, whereas the Beckman and the microparticle enzyme immunoassay digoxin assay demonstrated minimal interference. Immunoassays of 11 other drugs tested were unaffected. When Ashwagandha extract was added to a serum pool containing digoxin, falsely elevated digoxin value was observed with fluorescence polarization immunoassay, but values were falsely lowered when measured by the microparticle enzyme immunoassay. Digibind neutralized digoxin-like immunoreactive components of Ashwagandha in vitro. Conclusions.—Components of Ashwagandha interfered with serum digoxin measurements using immunoassays. Digibind neutralized free digoxin-like immunoreactive components of Ashwagandha.

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7

Wang, Y., D. F. Lewis, C. D. Adair, Y. Gu, L. Mason, and J. H. Kipikasa. "Digibind attenuates cytokine TNFα-induced endothelial inflammatory response: potential benefit role of Digibind in preeclampsia." Journal of Perinatology 29, no. 3 (January 15, 2009): 195–200. http://dx.doi.org/10.1038/jp.2008.222.

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8

Greenberg, Michael I. "Digibind, an Important Antidote, if Used Properly." Emergency Medicine News 24, no. 2 (February 2002): 18. http://dx.doi.org/10.1097/00132981-200202000-00015.

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9

Ip, D., H. Syed, and M. Cohen. "Digoxin specific antibody fragments (Digibind) in digoxin toxicity." BMJ 339, sep03 1 (September 3, 2009): b2884. http://dx.doi.org/10.1136/bmj.b2884.

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10

Miles, M. V., R. E. Dupuis, J. R. Miranda-Massari, and M. Soucie. "Digibind Interference with FPIA and ELIA Digoxin Methods." Therapeutic Drug Monitoring 15, no. 2 (April 1993): 172. http://dx.doi.org/10.1097/00007691-199304000-00149.

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11

Hill, Daniell B. "DRUG INTERACTION BETWEEN DIGOXIN IMMUNE FAB (DIGIBIND) AND WARFARIN." Southern Medical Journal 83, Supplement (September 1990): 2S—31. http://dx.doi.org/10.1097/00007611-199009001-00117.

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12

Fedorova, O., V. Reznik, N. Tapilskaya, V. Kashkin, E. V. Frolova, E. Nikitina, and A. Bagrov. "Immunoneutralization of endogenousNa/K-ATPase inhibitors in preeclampsia." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 14, no. 1 (February 28, 2008): 44–48. http://dx.doi.org/10.18705/1607-419x-2008-14-1-44-48.

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Although preeclampsia (PE) is a major cause of maternal and fetal mortality, its pathogenesis is not fully understood. Endogenous digitalis-like cardiotonic steroids (CTS) are implicated in the pathophysiology of PE, as illustrated by clinical observations that Digibind, a digoxin antibody which binds CTS, lowers blood pressure in patients with PE. Recently we reported that plasma levels of marinobufagenin (MBG), a bufadienolide vasoconstrictor CTS, are increased four-fold in patients with severe PE. In the present study, we compared levels of MBG in normal and preeclamptic placentae, and tested whether antibodies against MBG, and against ouabain for their interaction with the material purified from preeclamptic placentae via high-performance liquid chromatography (HPLC). Levels of MBG, but not that of endogenous ouabain, exhibited a four-fold elevation in preeclamptic placentae. The elution time of endogenous placental MBG-like immunoreactive material from reverse-phase HPLC column was identical to that of authentic MBG. Immunoassay based on Digibind did not detect cross-reactivity with HPLC containing ouabain-like immunoreactive material, but cross-reacted with HPLC fractions having retention time similar to that of MBG and other bufadienolides. Our results demonstrate that levels of MBG are significantly elevated in preeclamptic placentae, and suggest that MBG is a potential target for immunoneutralization in patients with preeclampsia.

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13

Fedorova, Olga V., Natalia I. Tapilskaya, Anton M. Bzhelyansky, Elena V. Frolova, Elena R. Nikitina, Vitaly A. Reznik, Vladimir A. Kashkin, and Alexei Y. Bagrov. "Interaction of Digibind with endogenous cardiotonic steroids from preeclamptic placentae." Journal of Hypertension 28, no. 2 (February 2010): 361–66. http://dx.doi.org/10.1097/hjh.0b013e328333226c.

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14

Schneider, Philip J., Patrick L. McCollam, and John J. Osborn. "Possible Dissociation of the Digibind-Digoxin Complex in Renal Failure." DICP 25, no. 11 (November 1991): 1269. http://dx.doi.org/10.1177/106002809102501119.

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15

McMillin, Gwendolyn A., William E. Owen, Thomas L. Lambert, Barun K. De, Elizabeth L. Frank, Phillip R. Bach, Thomas M. Annesley, and William L. Roberts. "Comparable Effects of DIGIBIND and DigiFab in Thirteen Digoxin Immunoassays." Clinical Chemistry 48, no. 9 (September 1, 2002): 1580–84. http://dx.doi.org/10.1093/clinchem/48.9.1580.

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16

Agunanne, Enoch, Darijana Horvat, Mohammad Uddin, and Jules Puschett. "The Treatment of Preeclampsia in a Rat Model Employing Digibind®." American Journal of Perinatology 27, no. 04 (October 12, 2009): 299–305. http://dx.doi.org/10.1055/s-0029-1241739.

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17

Ward, Suzanne B., Lena Sjostrom, and Michael R. Ujhelyi. "Comparison of the Pharmacokinetics and In Vivo Bioaffinity of DigiTAb Versus Digibind." Therapeutic Drug Monitoring 22, no. 5 (October 2000): 599–607. http://dx.doi.org/10.1097/00007691-200010000-00016.

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18

Jortani, Saeed A., Asli Pinar, Nancy A. Johnson, and Roland Valdes. "Validity of unbound digoxin measurements by immunoassays in presence of antidote (Digibind®)." Clinica Chimica Acta 283, no. 1-2 (May 1999): 159–69. http://dx.doi.org/10.1016/s0009-8981(99)00043-1.

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19

Ujhelyi, Michael R., Suzanne Brody Ward, Lena Sjostrom, and R. Stephen Porter. "IN VIVO BIOAFFINITY OF TWO DIGOXIN IMMUNE FAB PRODUCTS: DIGITAB® VERSUS DIGIBIND®." Critical Care Medicine 27, Supplement (December 1999): A92. http://dx.doi.org/10.1097/00003246-199912001-00240.

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20

Allen, Geoffrey. "The Affinity of Binding of Digoxin to Ovine Anti-digoxin Fab (DIGIBIND™)* Preparations." Biologicals 24, no. 1 (March 1996): 19–24. http://dx.doi.org/10.1006/biol.1996.0002.

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21

Datta, P. "95 A BLOCKER REAGENT TO REDUCE DIGIBIND INTERFERENCE IN A NON-PRETREATMENT DIGOXIN ASSAY." Therapeutic Drug Monitoring 17, no. 4 (August 1995): 407. http://dx.doi.org/10.1097/00007691-199508000-00107.

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22

Brubacher, J. R., D. Lachmanen, P. R. Ravikumar, and R. S. Hoffman. "Efficacy of digoxin specific Fab fragments (Digibind®) in the treatment of toad venom poisoning." Toxicon 37, no. 6 (June 1999): 931–42. http://dx.doi.org/10.1016/s0041-0101(98)00224-4.

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23

Li, M. "Hemodynamic Effects of the Fab Fragment of Digoxin Antibody (Digibind) in Corticotropin (ACTH)-Induced Hypertension." American Journal of Hypertension 10, no. 3 (March 1997): 332–36. http://dx.doi.org/10.1016/s0895-7061(96)00318-4.

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24

Henning Krep, H. "Reversal of sodium pump inhibitor induced vascular smooth muscle contraction with digibind Stoichiometry and its implications." American Journal of Hypertension 9, no. 1 (January 1996): 39–46. http://dx.doi.org/10.1016/0895-7061(95)00260-x.

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25

Wagener, Osvaldo E., Salim K. Mujais, Francesco Del Greco, and Antonio P. Quintanilla. "Stimulation of Erythrocyte and Renal Na+, K+-Adenosine Triphosphatase Activity by Antidigoxin Antibody in Normal Rats." Clinical Science 77, no. 6 (December 1, 1989): 617–21. http://dx.doi.org/10.1042/cs0770617.

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1. A circulating ouabain-like factor which inhibits the Na+, K+-pump has been implicated in volume-expanded states. To assess the role of this putative factor in normovolaemic rats, we measured erythrocyte and renal Na+, K+-adenosine triphosphatase activity after the infusion of a mixture of high-affinity digoxin-binding Fab fragments (Digibind) capable of removing digoxin from pump sites. 2. Compared with either saline (vehicle) or sheep immunoglobin G, infusion of the antidigoxin antibody caused a moderate increase of Na+, K+-adenosine triphosphatase activity in the erythrocyte (saline 348 ± 12; immunoglobulin G 339 ± 16; antidigoxin antibody 432 ± 22 nmol h−1 mg−1; P < 0.005 by analysis of variance) and a larger increase in the renal cortex (saline 9.7 ± 0.9; immunoglobulin G 9 ± 1.4; antidigoxin antibody 24.3 ± 1.8 μmol h−1 mg−1; P < 0.0005 by analysis of variance) without a change in blood pressure 3. These results are consistent with the presence of a digoxin-like inhibitor of the Na+, K+ -pump in normal rats.

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26

Dasgupta, Amitava, and Lyska Emerson. "Neutralization of cardiac toxins oleandrin, oleandrigenin, bufalin, and cinobufotalin by digibind: Monitoring the effect by measuring free digitoxin concentrations." Life Sciences 63, no. 9 (July 1998): 781–88. http://dx.doi.org/10.1016/s0024-3205(98)00333-6.

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27

Yamada, Kaoru, Atsuo Goto, Chen Hui, Hiroshi Nagoshi, and Masao Omata. "Effects of Intracerebroventricular Infusion of Fab Fragments of Digoxin Antibody(Digibind) on Development of Reduced Renal Mass-Saline Hypertension in Rats." Hypertension Research 18, no. 2 (1995): 145–50. http://dx.doi.org/10.1291/hypres.18.145.

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28

Hopoate-Sitake, Moana L., C. David Adair, Lorrie A. Mason, Carlos Torres, Joseph Kipikasa, and Steven W. Graves. "Digibind Reverses Inhibition of Cellular Rb+ Uptake Caused by Endogenous Sodium Pump Inhibitors Present in Serum and Placenta of Women with Preeclampsia." Reproductive Sciences 18, no. 2 (October 19, 2010): 190–99. http://dx.doi.org/10.1177/1933719110385133.

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29

Huang, B. S., and F. H. Leenen. "Sympathoexcitatory and pressor responses to increased brain sodium and ouabain are mediated via brain ANG II." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 1 (January 1, 1996): H275—H280. http://dx.doi.org/10.1152/ajpheart.1996.270.1.h275.

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Intracerebroventricular administration of hypertonic saline, ouabain, brain ouabainlike activity (OLA), or angiotensin II (ANG II) causes sympathoexcitatory and pressor effects in rats. To clarify the possible interaction between increased brain sodium, brain OLA, and the brain renin-angiotensin system (RAS), increases in mean arterial pressure, heart rate (HR), and renal sympathetic nerve activity (RSNA) in response to intracerebroventricular 0.3 M NaCl, ouabain, and ANG II were recorded in conscious Wistar rats before and after intracerebroventricular pretreatment with the angiotensin-receptor (AT1) blocker losartan, antibody Fab fragments (Digibind), or, as control, gamma-globulins. These Fab fragments bind ouabain and brain OLA with high affinity. The arginine vasopressin (AVP) antagonist [d(CH2)5Tyr(Me)]AVP (30 micrograms/ kg) was injected intravenously before each intracerebroventricular injection. Intracerebroventricularly administered 0.3 M NaCl (3.8 mul/min for 10 min), ouabain (0.3 and 0.6 microgram), and ANG II (10 and 30 ng) caused similar pressor responses. However, the extent of HR and RSNA responses to ANG II was smaller than those to 0.3 M NaCl and ouabain. Intracerebroventricular losartan (10 and 20 micrograms) blocked responses to ANG II and 0.3 M NaCl and significantly attenuated the responses to ouabain (pressor response by 50-70%; RSNA and HR by 60-80%). In contrast, intracerebroventricular Fab fragments (66 micrograms) blocked only the responses to 0.3 M NaCl and ouabain and did not affect the responses to ANG II. These results suggest that an acute rise in brain sodium concentration increases brain OLA and the latter exerts its sympathoexcitatory and pressor effects at least partly via activation of the brain RAS.

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30

Kaide, J. "Effects of digoxin-specific antibody Fab fragment (Digibind) on blood pressure and renal water–sodium metabolism in 5/6 reduced renal mass hypertensive rats." American Journal of Hypertension 12, no. 6 (June 1999): 611–19. http://dx.doi.org/10.1016/s0895-7061(99)00029-1.

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31

Dasgupta, Amitava, and Kathleen A. Szelei-Stevens. "Neutralization of Free Digoxin-like Immunoreactive Components of Oriental Medicines Dan Shen and Lu-Shen-Wan by the Fab Fragment of Antidigoxin Antibody (Digibind)." American Journal of Clinical Pathology 121, no. 2 (February 2004): 276–81. http://dx.doi.org/10.1309/93uf4yelemg9v548.

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32

Dasgupta, Amitava, Ana E. Lopez, Alice Wells, Margaret Olsen, and Jeffery Actor. "The Fab fragment of anti-digoxin antibody (digibind) binds digitoxin-like immunoreactive components of Chinese medicine Chan Su: monitoring the effect by measuring free digitoxin." Clinica Chimica Acta 309, no. 1 (July 2001): 91–95. http://dx.doi.org/10.1016/s0009-8981(01)00499-5.

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33

Cada, Dennis J. "Questions and Answers from the F.I.X./• Digibind in Chronic Digoxin Dosing /• Fosphenytoin (Cerebyx) Use in Dialysis Patients/ • MMR vs MR/ • Insulin Drip Protocol/ • Tobramycin Powder Alternatives." Hospital Pharmacy 36, no. 1 (January 2001): 41–49. http://dx.doi.org/10.1177/001857870103600106.

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34

Wansapura, Arshani N., Valerie M. Lasko, Jerry B. Lingrel, and John N. Lorenz. "Mice expressing ouabain-sensitive α1-Na,K-ATPase have increased susceptibility to pressure overload-induced cardiac hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 1 (January 2011): H347—H355. http://dx.doi.org/10.1152/ajpheart.00625.2010.

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The Na,K-ATPase is a ubiquitous transmembrane pump and a specific receptor for cardiac glycosides such as ouabain and digoxin, which are used in the management of congestive heart failure (CHF). A potential role for these so-called endogenous cardiotonic steroids (CS) has been explored, and it has become apparent that such compounds are elevated and may play an important role in a variety of physiological and pathophysiological conditions such as hypertension and CHF. Recent evidence suggests that the Na,K-ATPase may act as a signal transducer upon CS binding and induce nonproliferative cardiac growth, implicating a role for endogenous CS in the development of cardiac hypertrophy and progressive failure of the heart. In the present study, we tested whether hypertrophic responses to pressure overload would be altered in mutant mice that specifically express ouabain-sensitive or ouabain-resistant α1- and α2-Na,K-ATPase subunits, as follows: α1-resistant, α2-resistant (α1R/Rα2R/R); α1-sensitive, α2-resistant (α1S/Sα2R/R); and α1-resistant, α2-sensitive (α1R/Rα2S/S, wild-type). In α1S/Sα2R/R mice, pressure overload by transverse aortic coarctation induced severe left ventricular (LV) hypertrophy with extensive perivascular and replacement fibrosis at only 4 wk. Responses in α1R/Rα2S/S and α1R/Rα2R/R mice were comparatively mild. Mutant α1S/Sα2R/R mice also had LV dilatation and depressed LV systolic contractile function by 4 wk of pressure overload. In separate experiments, chronic Digibind treatment prevented the rapid progression of cardiac hypertrophy and fibrosis in α1S/Sα2R/R mice. These data demonstrate that mice with a ouabain-sensitive α1-Na,K-ATPase subunit have a dramatic susceptibility to the development of cardiac hypertrophy, and failure from LV pressure overload and provide evidence for the involvement of endogenous CS in this process.

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35

Huang, Bing S., Sara Ahmadi, Monir Ahmad, Roselyn A. White, and Frans H. H. Leenen. "Central neuronal activation and pressor responses induced by circulating ANG II: role of the brain aldosterone-“ouabain” pathway." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 2 (August 2010): H422—H430. http://dx.doi.org/10.1152/ajpheart.00256.2010.

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An increase in plasma ANG II causes neuronal activation in hypothalamic nuclei and a slow pressor response, presumably by increasing sympathetic drive. We evaluated whether the activation of a neuromodulatory pathway, involving aldosterone and “ouabain,” is involved in these responses. In Wistar rats, the subcutaneous infusion of ANG II at 150 and 500 ng·kg−1·min−1 gradually increased blood pressure up to 60 mmHg at the highest dose. ANG II at 500 ng·kg−1·min−1 increased plasma ANG II by 4-fold, plasma aldosterone by 25-fold, and hypothalamic aldosterone by 3-fold. The intracerebroventricular infusion of an aldosterone synthase (AS) inhibitor prevented the ANG II-induced increase in hypothalamic aldosterone without affecting the increase in plasma aldosterone. Neuronal activity, as assessed by Fra-like immunoreactivity, increased transiently in the subfornical organ (SFO) but progressively in the paraventricular nucleus (PVN) and supraoptic nucleus (SON). The central infusion of the AS inhibitor or a mineralocorticoid receptor blocker markedly attenuated the ANG II-induced neuronal activation in the PVN but not in the SON. Pressor responses to ANG II at 150 ng·kg−1·min−1 were abolished by an intracerebroventricular infusion of the AS inhibitor. Pressor responses to ANG II at 500 ng·kg−1·min−1 were attenuated by the central infusion of the AS inhibitor or the mineralocorticoid receptor blocker by 70–80% and by Digibind (to bind “ouabain”) by 50%. These results suggest a novel central nervous system mechanism for the ANG II-induced slow pressor response, i.e., circulating ANG II activates the SFO, leading to the direct activation of the PVN and SON, and, in addition, via aldosterone-dependent amplifying mechanisms, causes sustained activation of the PVN and thereby hypertension.

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36

Fedorova, Olga, Valentina Ishkaraeva, Yulia Grigorova, Vitaly Reznik, Nikolai Kolodkin, Irina Zazerskaya, Valentina Zernetkina, et al. "Antibody to Marinobufagenin Reverses Placenta-Induced Fibrosis of Umbilical Arteries in Preeclampsia." International Journal of Molecular Sciences 19, no. 8 (August 13, 2018): 2377. http://dx.doi.org/10.3390/ijms19082377.

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Background: Previous studies implicated cardiotonic steroids, including Na/K-ATPase inhibitor marinobufagenin (MBG), in the pathogenesis of preeclampsia (PE). Immunoneutralization of heightened MBG by Digibind, a digoxin antibody, reduces blood pressure (BP) in patients with PE, and anti-MBG monoclonal antibody lessens BP in a rat model of PE. Recently, we demonstrated that MBG induces fibrosis in cardiovascular tissues via a mechanism involving inhibition of Fli-1, a nuclear transcription factor and a negative regulator of collagen-1 synthesis. Objectives and Methods: We hypothesized that in PE, elevated placental MBG levels are associated with development of fibrosis in umbilical arteries. Eleven patients with PE (mean BP 124 ± 4 mmHg; age 29 ± 2 years; 39 weeks gest. age) and 10 gestational age-matched normal pregnant subjects (mean BP 92 ± 2 mmHg; controls) were enrolled in the clinical study. Results: PE was associated with a higher placental (0.04 ± 0.01 vs. 0.49 ± 0.11 pmol/g; p < 0.01) and plasma MBG (0.5 ± 0.1 vs. 1.6 ± 0.5 nmol/L; p < 0.01), lower Na/K-ATPase activity in erythrocytes (2.7 ± 0.2 vs. 1.5 ± 0.2 µmol Pi/mL/hr; p < 0.01), 9-fold decrease of Fli-1 level and 2.5-fold increase of collagen-1 in placentae (p < 0.01) vs. control. Incubation of umbilical arteries from control patients with 1 nmol/L MBG was associated with four-fold decrease in Fli-1 level and two-fold increase in collagen-1 level vs. those incubated with placebo (p < 0.01), i.e., physiological concentration of MBG mimicked effect of PE in vitro. Collagen-1 abundance in umbilical arteries from PE patients was 4-fold higher than in control arteries, and this PE-associated fibrosis was reversed by monoclonal anti-MBG antibody ex vivo. Conclusion: These results demonstrate that elevated placental MBG level is implicated in the development of fibrosis of the placenta and umbilical arteries in PE.

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37

Dasgupta, Amitava, and Meredith A. Reyes. "Effect of Brazilian, Indian, Siberian, Asian, and North American Ginseng on Serum Digoxin Measurement by Immunoassays and Binding of Digoxin-like Immunoreactive Components of Ginseng With Fab Fragment of Antidigoxin Antibody (Digibind)." American Journal of Clinical Pathology 124, no. 2 (August 2005): 229–36. http://dx.doi.org/10.1309/utftk2lh1rmhcbd7.

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38

Pantho, AF, SH Afroze, DC Zawieja, JM Wages, JW Larrick, TJ Kuehl, and MN Uddin. "ID: 69: MARINOBUFAGENIN-INDUCED ANTI-ANGIOGENIC MILIEU IN CYTOTROPHOBLASTS IS ATTENUATED BY NOVEL ANTI-MBG ANTIBODIES." Journal of Investigative Medicine 64, no. 4 (March 22, 2016): 914–15. http://dx.doi.org/10.1136/jim-2016-000120.7.

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Preeclampsia (PreE) is a hypertensive pregnancy disorder, which occurs in approximately 10% of all gestations. Recently, a digitalis-like factor, marinobufagenin (MBG) has been implicated as a causative factor in preE. We demonstrated that MBG inhibits the proliferation, migration, and invasion of cytotrophoblast (CTB) cells. We have identified a novel human monoclonal antibody with higher specificity than Digibind for MBG. We assessed the attenuation of MBG-induced CTBs dysfunction by three anti-MBG antibodies: 206–208, H1L2, and 3e9.MethodsA panel of anti-MBG antibodies with potential as human therapeutic agents was developed by Panorama Research, Inc.; Sunnyvale, CA (206–208, H1L2). H1L2 was a humanized version of previously described anti-MBG murine antibody 3e9. 206–208 was identified in a human phage antibody library. Human CTBs were treated with DMSO (vehicle) or 0.1, 1, 10 or 100 nM of MBG for 48 h. Some cells were pretreated with 206–208, H1L2, or 3e9 for 2h, while others were co-treated with these antibodies prior to MBG treatment. Culture media were collected for analysis of pro-angiogenic and anti-angiogenic factors. Cell viability was measured using a CellTiter Assay kit. Cell lysates were utilized to evaluate the expression of proliferating cell nuclear antigen (PCNA) and p38 MAPK phosphorylation by western blot. Levels of vascular endothelial growth factor (VEGF), placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), and soluble endoglin (sEng) were measured in culture media using ELISA kits. Statistical comparisons were performed using analysis of variance with Duncan's post hoc test.ResultsMBG down-regulated PCNA and up-regulated p38 phosphorylation in CTBs treated with ≥1 nM MBG compared to basal (DMSO treatment) (*p<0.05 for each). Secretion of sFlt-1 and sEng were increased, while VEGF and PIGF were decreased in CTBs treated with ≥1.0 nM MBG (*p<0.05 for each). Both anti-MBG antibodies pretreatment and co-treatment significantly up-regulated PCNA and down-regulated p38 phosphorylation, and corrected the angiogenic profile of CTBs (p<0.05 for each). The anti-proliferative and anti-angiogenic effects of MBG were not due to a cytotoxic effect, as evaluated by a cell viability assay. MBG at 0.1 nM had no effect.ConclusionsWe found that all 3 anti-MBG antibodies attenuate MBG-induced anti-proliferative and anti-angiogenic milieu in cultured CTBs. Here we describe for the first time two fully human anti-MBG antibodies, which can be targeted as therapeutic agents for the development of innovative treatment strategies for preE and potentially other disorders involving aberrant MBG signaling.

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Sengar, Harsh. "Solving the Mystery of Crypto’s Bubble." Ushus Journal of Business Management 19, no. 3 (August 26, 2020): 25–39. http://dx.doi.org/10.12725/ujbm.52.2.

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Blockchain is the vehicle on which cryptocurrencies run, and it can’t be regulated by any legal entity during its operation.The huge growth in various cryptocurrency segments in 10 years has created the controversy of an inevitable bubble. A bubble can be generated either by queer herd behaviour or logical secular movement. Traces of evident bubbles have been a certainty and they take the perceived valuation of crypto to figures far away from its true value. This sudden diversion can be lethal due to the illogical, irrational propensity of regular market participants. This study observes ten cryptos under surveillance from September 2014 to August 2019. The selected ten (Monero, Bitcoin, XRP Ripple, Litecoin, Dogecoin, Monacoin, Ethereum, Bytecoin, Digibite, Potcoin) cryptocurrencies were studied for the last five years using Right Tailed ADF Test. Prominent traces of the rational bubble in all the underlying cryptocurrencies were found and have been considered for the study.

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Cambridge, D., C. R. Morgan, and G. Allen. "Digoxin and digoxin derivative induced arrhythmias: in vitro binding and in vivo abolition of arrhythmias by digoxin immune Fab (DIGIBAND)." Cardiovascular Research 26, no. 9 (September 1, 1992): 906–11. http://dx.doi.org/10.1093/cvr/26.9.906.

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Pamnani, Motilal B., James F. Schooley, and Howard J. Bryant. "Effect of digibind (DIG) on cardiovascular hemodynamics in rats with insulin dependent diabetes mellitus (IDDM) hypertension (HT)." FASEB Journal 21, no. 6 (January 2007). http://dx.doi.org/10.1096/fasebj.21.6.a898-c.

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Baron, Christine. "DigiBib IntrOX." Bibliotheksdienst 49, no. 1 (January 1, 2015). http://dx.doi.org/10.1515/bd-2015-0003.

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Zusammenfassung:Relevante Literatur in unterschiedlichsten bibliothekarischen Katalogen und Datenbanken zu finden, scheint vielen Anwendern heute zu kompliziert. Ein wesentlicher Grund, weshalb heute Discovery-Services und Begriffe wie One-Stop-Shop im Bibliothekswesen in aller Munde geführt werden. Diese neuen Angebote vereinfachen den Einstieg in die wissenschaftliche Recherche. Dies mit dem Ziel, den Benutzer an seine Bibliothek zu binden bzw. ihn von den großen Suchmaschinen als primären Informationsbrokern zurückzugewinnen. Das Bibliotheksportal DigiBib verfolgt das Ziel, dem Benutzer alle Angebote der Bibliothek unter einer einheitlichen Oberfläche in einem Dienstleistungsbündel anzubieten, schon seit vielen Jahren. Deshalb war es nur konsequent, die neuen Technologien zu nutzen, um die DigiBib zu einem Discovery-Service mit den gewohnten OPAC-Funktionalitäten auszubauen. Dieser Artikel beschreibt und berichtet über Teilmodule des Systems und die Umsetzung des Ausgangsprojekts zu DigiBib IntrOX.

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Hardeck, Erwin, Tatjana Mrowka, Anette Seiler, and Heiko Jansen. "Bits, Bytes, and User Comfort – The Digital Library (DigiBib)." Libri 53, no. 1 (January 2003). http://dx.doi.org/10.1515/libr.2003.11.

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Bernabéu Albert, Salvador. "José Andrés-Gallego (coord.), Nuevas aportaciones a la Historia Jurídica de Iberoamérica (I), Proyectos Históricos Tavera, Madrid, Fundación Histórica Tavera-Digibis-Fundación Hernando de Larramendi, CD-ROM, 2000." Nuevo mundo mundos nuevos, February 4, 2005. http://dx.doi.org/10.4000/nuevomundo.245.

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Langue, Frédérique. "Textos Clásicos sobre la Historia de Venezuela, Pedro Grases e Ildefonso Méndez (comp.), Madrid, Mapfre-Biblioteca Nacional de España-Fundación Histórica Tavera-Digibis, 2001, CD rom Colección Clásicos Tavera, Serie I, vol. 7 de Iberoa." Nuevo mundo mundos nuevos, February 7, 2005. http://dx.doi.org/10.4000/nuevomundo.346.

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