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Journal articles on the topic 'Bilirubin neurotoxicity'

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Author: Grafiati
Published: 11 March 2023

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1

Painter, Michael J. "BILIRUBIN NEUROTOXICITY." Developmental Medicine & Child Neurology 14, no. 3 (November 12, 2008): 395–97. http://dx.doi.org/10.1111/j.1469-8749.1972.tb02607.x.

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2

Ahlfors, Charles. "Plasma bilirubin binding and bilirubin neurotoxicity." Developmental Medicine & Child Neurology 59, no. 3 (October 27, 2016): 242–43. http://dx.doi.org/10.1111/dmcn.13303.

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3

Ostrow, J. Donald, Lorella Pascolo, and Claudio Tiribelli. "Mechanisms of bilirubin neurotoxicity." Hepatology 35, no. 5 (May 2002): 1277–80. http://dx.doi.org/10.1053/jhep.2002.33432.

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4

Cashore, William J. "The Neurotoxicity of Bilirubin." Clinics in Perinatology 17, no. 2 (June 1990): 437–47. http://dx.doi.org/10.1016/s0095-5108(18)30577-3.

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5

Zhang, Fanhui, Lihua Chen, and Kewen Jiang. "Neuroinflammation in Bilirubin Neurotoxicity." Journal of Integrative Neuroscience 22, no. 1 (January 5, 2023): 9. http://dx.doi.org/10.31083/j.jin2201009.

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6

Stevenson, David K., Hendrik J. Vreman, and Ronald J. Wong. "Bilirubin Production and the Risk of Bilirubin Neurotoxicity." Seminars in Perinatology 35, no. 3 (June 2011): 121–26. http://dx.doi.org/10.1053/j.semperi.2011.02.005.

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7

Bortolussi, Giulia, and Andrés F. Muro. "Experimental models assessing bilirubin neurotoxicity." Pediatric Research 87, no. 1 (September 7, 2019): 17–25. http://dx.doi.org/10.1038/s41390-019-0570-x.

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8

Ahlfors, Charles E. "Predicting bilirubin neurotoxicity in jaundiced newborns." Current Opinion in Pediatrics 22, no. 2 (April 2010): 129–33. http://dx.doi.org/10.1097/mop.0b013e328336eb28.

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9

Kaplan, Michael, Ruben Bromiker, and Cathy Hammerman. "Hyperbilirubinemia, hemolysis, and increased bilirubin neurotoxicity." Seminars in Perinatology 38, no. 7 (November 2014): 429–37. http://dx.doi.org/10.1053/j.semperi.2014.08.006.

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10

Ostrow, J. Donald, Lorella Pascolo, Dora Brites, and Claudio Tiribelli. "Molecular basis of bilirubin-induced neurotoxicity." Trends in Molecular Medicine 10, no. 2 (February 2004): 65–70. http://dx.doi.org/10.1016/j.molmed.2003.12.003.

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11

Daood, M. J., A. F. McDonagh, and J. F. Watchko. "Calculated free bilirubin levels and neurotoxicity." Journal of Perinatology 29, S1 (January 28, 2009): S14—S19. http://dx.doi.org/10.1038/jp.2008.218.

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12

HANSEN, THOR WILLY RUUD. "Bilirubin and Brain Toxicity in Neonates: Dead but Won't Lie Down?" Pediatrics 91, no. 6 (June 1, 1993): 1218–19. http://dx.doi.org/10.1542/peds.91.6.1218a.

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To the Editor.— During a meeting a few years ago, while discussing the issue of bilirubin and neurotoxicity, Dr Timos Valaes, a notable expert in the bilirubin field, suggested to me that "we may be flogging a dead horse." A couple of provocative articles recently published in Pediatrics seem to argue along the same lines.1,2 However, commentaries on those same articles, as well as the continued scientific interest in bilirubin neurotoxicity, suggest that the "animal" may still be standing.
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13

VAN DE BOR, MARGOT, MARTINA ENS-DOKKUM, ANNEKE M. SCHREUDER, SYLVIA VEEN, S. PAULINE VERLOOVE-VANHORICK, and RONALD BRAND. "Questions about Bilirubin." Pediatrics 91, no. 1 (January 1, 1993): 165–66. http://dx.doi.org/10.1542/peds.91.1.165.

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In Reply.— We agree with Dr Stein that there is ample discussion as to the potential neurotoxicity of bilirubin in relation to the etiology of hyperbilirubinemia. Unfortunately, no data were collected regarding the etiology of hyperbilirubinemia in our study population other than blood group incompatibility. Only two children suffered from blood group incompatibility. The maximal serum total bilirubin concentrations of these two children were between 151 to 200 µmol/L (8.8 to 11.6 mg/dL) and 201 to 250 µmol (11.7 to 14.6 mg/dL), respectively.
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14

Huang, Hongbiao, Mingxing Guo, Ningning Liu, Chong Zhao, Haoyu Chen, Xiaoli Wang, Siyan Liao, et al. "Bilirubin neurotoxicity is associated with proteasome inhibition." Cell Death & Disease 8, no. 6 (June 2017): e2877-e2877. http://dx.doi.org/10.1038/cddis.2017.274.

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15

Watchko, Jon F. "Bilirubin-Induced Neurotoxicity in the Preterm Neonate." Clinics in Perinatology 43, no. 2 (June 2016): 297–311. http://dx.doi.org/10.1016/j.clp.2016.01.007.

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16

Smith, Camille M., Galen P. Barnes, Claire A. Jacobson, and David G. Oelberg. "Auditory Brainstem Response Detects Early Bilirubin Neurotoxicity at Low Indirect Bilirubin Values." Journal of Perinatology 24, no. 11 (October 27, 2004): 730–32. http://dx.doi.org/10.1038/sj.jp.7211164.

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17

POLAND, RONALD L. "In Search of a `Gold Standard' for Bilirubin Toxicity." Pediatrics 89, no. 5 (May 1, 1992): 823–24. http://dx.doi.org/10.1542/peds.89.5.823.

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In this issue of Pediatrics, Newman and Maisels1 have given us a thorough and thoughtful review of current knowledge about the toxicity of bilirubin in term, otherwise healthy, newborn infants and have concluded that there is little evidence that bilirubin toxicity can be predicted from the concentration of bilirubin in the serum. They propose that we worry about bilirubin less in this population and treat hyperbilirubinemia only if it reaches much higher concentrations than the traditional 20 mg/dL. Their conclusions and recommendations are very reasonable given that the serum bilirubin concentration is the primary predictive measure for bilirubin neurotoxicity available to us.
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18

Bhutani, VinodK, and RonaldJ Wong. "Bilirubin neurotoxicity in preterm infants: Risk and prevention." Journal of Clinical Neonatology 2, no. 2 (2013): 61. http://dx.doi.org/10.4103/2249-4847.116402.

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19

Gupta, Ashok K., and Smer Baj S. Mann. "Is auditory brainstem response a bilirubin neurotoxicity marker?" American Journal of Otolaryngology 19, no. 4 (July 1998): 232–36. http://dx.doi.org/10.1016/s0196-0709(98)90123-5.

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20

Zhang, Benzhong, Xi Yang, and Xiaoling Gao. "Taurine protects against bilirubin-induced neurotoxicity in vitro." Brain Research 1320 (March 2010): 159–67. http://dx.doi.org/10.1016/j.brainres.2010.01.036.

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21

Hulzebos, C. V., D. E. van Imhoff, A. F. Bos, C. E. Ahlfors, H. J. Verkade, and P. H. Dijk. "Usefulness of the bilirubin/albumin ratio for predicting bilirubin-induced neurotoxicity in premature infants." Archives of Disease in Childhood - Fetal and Neonatal Edition 93, no. 5 (September 1, 2008): F384—F388. http://dx.doi.org/10.1136/adc.2007.134056.

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22

Aschner, Michael. "Bilirubin and Other Brain Cells." Pediatrics 93, no. 1 (January 1, 1994): 155–56. http://dx.doi.org/10.1542/peds.93.1.155a.

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Drs Newman and Maisels1 agree that the current management of hyperbilirubinemia in the term newborn is based on assumptions searching for scientific validation. As I was reading these letters I could not help but think about another "hot" topic occupying the "Letters to the Editor" section of Pediatrics—lead. As with lead-induced neurotoxicity, children practitioners cannot wait until there are data to fully guide decision making. In their article Newman and Maisels2 indicate some areas in the treatment of newborn hyperbilirubinemia in which there are wide disparities about the preferred management approach, and they identify those aspects of treatment that require a revised consensus statement to help guide therapy.
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23

Amin, Sanjiv B. "Clinical assessment of bilirubin-induced neurotoxicity in premature infants." Seminars in Perinatology 28, no. 5 (October 2004): 340–47. http://dx.doi.org/10.1053/j.semperi.2004.09.005.

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24

Zhou, Changwei, Rong Sun, Chongyi Sun, Minghao Gu, Chuan Guo, Jiyan Zhang, Yansheng Du, Huiying Gu, and Qingpeng Liu. "Minocycline protects neurons against glial cells-mediated bilirubin neurotoxicity." Brain Research Bulletin 154 (January 2020): 102–5. http://dx.doi.org/10.1016/j.brainresbull.2019.11.005.

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25

Hansen, Thor Willy Ruud. "Letter to the Editor." Pediatrics 93, no. 1 (January 1, 1994): 156. http://dx.doi.org/10.1542/peds.93.1.156.

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Dr Aschner has some very interesting comments on the role of glial cells in bilirubin neurotoxicity. His suggestion that bilirubin researchers should focus some of their interest on this group of cells, given the increase in knowledge about their more complex role in nervous system homeostasis, is well taken. It would certainly be quite welcome if investigators with relevant research experience would include bilirubin in their future experimental designs. It seems appropriate in this context to mention the fact that bilirubin researchers in the past have given attention to glial cells, although perhaps with a more limited scope than that suggested by Dr Aschner.
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26

Berska, Joanna, Jolanta Bugajska, and Krystyna Sztefko. "Bilirubin monitoring – future prospects." Diagnostyka Laboratoryjna 56, no. 4 (July 27, 2021): 175–80. http://dx.doi.org/10.5604/01.3001.0015.0563.

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Monitoring of bilirubin concentration is essential during early neonatal life. According to the American Academy of Pediatrics Clinical Practice Guideline, the total serum bilirubin or transcutaneous bilirubin level should be measured in each infant in the first 24 hours of life. The concentration of bilirubin has been measured for 150 years. During that time the analytical methods for its determination have been significantly improved, the nomenclature of bilirubin has been also unified, but it is still unknown what concentration of bilirubin cause a life-threatening encephalopathy in the newborn. Under the current recommendations, clinical decisions to introduce phototherapy in the treatment of newborns’ hyperbilirubinemia are based on total bilirubin concentration, which is determined on biochemical analyzers and point of care testing systems. However, it is not always possible to predict encephalopathy based on the total bilirubin level. Probably in the future, as the availability of routine methods for the determination of unconjugated, free bilirubin becomes more available, measurement of “free” bilirubin will improve risk assessment for bilirubin neurotoxicity.
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27

Shapiro, Steven M., and Sean M. Riordan. "Review of bilirubin neurotoxicity II: preventing and treating acute bilirubin encephalopathy and kernicterus spectrum disorders." Pediatric Research 87, no. 2 (October 3, 2019): 332–37. http://dx.doi.org/10.1038/s41390-019-0603-5.

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28

Ostrow, J. Donald, and Claudio Tiribelli. "New concepts in bilirubin neurotoxicity and the need for studies at clinically relevant bilirubin concentrations." Journal of Hepatology 34, no. 3 (March 2001): 467–70. http://dx.doi.org/10.1016/s0168-8278(00)00051-9.

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29

Scheidt, Peter C., Barry I. Graubard, Howard J. Hoffman, Dolores A. Bryla, Karin B. Nelson, Deborah G. Hirtz, and Lawrence M. Gartner. "Intelligence at Six Years in Relation to Neonatal Bilirubin Level: Follow-up of The National Institute of Child Health and Human Development Clinical Trial of Phototherapy." Pediatrics 87, no. 6 (June 1, 1991): 797–805. http://dx.doi.org/10.1542/peds.87.6.797.

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Results of the National Institute of Child Health and Human Development Randomized Controlled Trial of Phototherapy were examined for the relationship of neonatal bilirubin level to neurological and developmental outcome at 6-year follow-up. This analysis focused on 224 control children with birth weight of less than 2000 g. Bilirubin levels were maintained below previously specified levels by the use of exchange transfusion only (24%). Rates of cerebral palsy were not significantly higher for children with elevated maximum bilirubin level than for those whose level remained low. No association was evident between maximum bilirubin level and IQ (Full Scale, Verbal, or Performance) by simple correlation analysis (r = -.087, P = .2 for Full Scale) or by multiple linear regression adjusting for factors that covary with IQ (β = -.15, P = .58). IQ was not associated with mean bilirubin level, time and duration of exposure to bilirubin, or measures of bilirubin-albumin binding. Thus, over the range of bilirubin levels permitted in this clinical trial, there was no evidence of bilirubin toxicity to the central nervous system. Measures used to control the level of bilirubin in low birth weight neonates appear to prevent effectively the risk of bilirubin-induced neurotoxicity.
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30

NEWMAN, THOMAS B., and M. JEFFREY MAISELS. "Response to Commentaries Re: Evaluation and Treatment of Jaundice in the Term Newborn: A Kinder, Gentler Approach." Pediatrics 89, no. 5 (May 1, 1992): 831–33. http://dx.doi.org/10.1542/peds.89.5.831.

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We thank Dr Lucey for soliciting expert commentaries on our manuscript and for providing us the opportunity to respond to them. Although we do not have space to respond to each of the commentaries in depth, we will address the major points brought up by more than one author and selected points from the individual commentaries. Drs Poland and Wennberg emphasize that neurotoxicity due to bilirubin is a complicated process, with many determinants besides the serum bilirubin level; Dr Cashore's four example cases illustrate this point. We agree. A bilirubin level that may be toxic in one infant may not be hazardous in another.
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31

Becerir, Cem, İlknur Kılıç, Özlem Şahin, Özmert Özdemir, Onur Tokgün, Bülent Özdemir, and Hakan Akca. "The protective effect of docosahexaenoic acid on the bilirubin neurotoxicity." Journal of Enzyme Inhibition and Medicinal Chemistry 28, no. 4 (May 16, 2012): 801–7. http://dx.doi.org/10.3109/14756366.2012.684053.

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32

Penn, Anna A., Dieter R. Enzmann, Jin S. Hahn, and David K. Stevenson. "Kernicterus in a Full Term Infant." Pediatrics 93, no. 6 (June 1, 1994): 1003–6. http://dx.doi.org/10.1542/peds.93.6.1003.

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Neonatal jaundice can represent a benign physiologic process or be the harbinger of serious illness with associated severe neurotoxicity. The neurological manifestations of kernicterus, a condition resulting from the deposition of unconjugated bilirubin in the central nervous system, are rarely seen in modern neonatal care, but jaundice, which reflects elevated serum bilirubin levels, is one of the most common findings in the neonatal period.1 More than half of all term infants will develop some neonatal jaundice and at least 6% will have a serum bilirubin concentration above 12.9 mg/dL.2 The appropriate treatment of hyperbilirubinemia is currently a topic of much debate in pediatrics, particularly treatment of full term infants without risk factors for hemolytic disease.3,4
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33

Gartner, Lawrence M., Charlotte S. Catz, and Sumner J. Yaffe. "Neonatal Bilirubin Workshop." Pediatrics 94, no. 4 (October 1, 1994): 537–40. http://dx.doi.org/10.1542/peds.94.4.537.

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A neonatal bilirubin workshop took place at The Rockefeller University on June 20 through 22, 1993 to consider controversial issues in the field of neonatal jaundice and bilirubin neurotoxicity, particularly as they relate to management. The conference was sponsored by the National Institute of Child Health and Human Development (Pregnancy and Perinatology Branch, Center for Mothers and Children), The Rockefeller University, and the Consiglio Nazionale delle Richerche (Italy). tk;4Presentations and discussion emphasized diagnosis, biochemistry, and mechanisms of bilirubin toxicity, the definition and consequences of kernicterus, and the appropriateness and safety of the various therapies currently in use. Identification of future research needs was an important agenda item. The conferees agreed that conventional management of jaundice in the newborn with phototherapy and exchange transfusion, as well as with phenobarbital in certain situations, had significantly reduced the occurrence of "traditional" kernicterus. However, the conferees acknowledged that the classical definition of kernicterus was in need of re-examination in view of the potential of bilirubin as a CNS toxin. Early discharge of newborns from the hospital has significantly altered diagnostic and therapeutic management of neonatal jaundice, transforming it into an outpatient problem. This transformation raises new questions regarding the best time to ascertain the cause(s) of jaundice and to identify risk factors to insure optimal management of the infant. Review of the current state of knowledge of bilirubin metabolism focused on new methods for measurement of unconjugated and conjugated bilirubin, measurement of bilirubin synthesis rates, the molecular biology of bilirubin conjugation and the developmental role of the family of enzymes known as glucuronyl transferase(s), and the role of genetic and other host factors in determining the safety or toxicity of bilirubin in the newborn.
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34

Ahlfors, Charles E., Richard P. Wennberg, J. Donald Ostrow, and Claudio Tiribelli. "Unbound (Free) Bilirubin: Improving the Paradigm for Evaluating Neonatal Jaundice." Clinical Chemistry 55, no. 7 (July 1, 2009): 1288–99. http://dx.doi.org/10.1373/clinchem.2008.121269.

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Abstract Background: The serum or plasma total bilirubin concentration (BT) has long been the standard clinical laboratory test for evaluating neonatal jaundice, despite studies showing that BT correlates poorly with acute bilirubin encephalopathy (ABE) and its sequelae including death, classical kernicterus, or bilirubin-induced neurological dysfunction (BIND). The poor correlation between BT and ABE is commonly attributed to the confounding effects of comorbidities such as hemolytic diseases, prematurity, asphyxia, or infection. Mounting evidence suggests, however, that BT inherently performs poorly because it is the plasma non–protein-bound (unbound or free) bilirubin concentration (Bf), rather than BT, that is more closely associated with central nervous system bilirubin concentrations and therefore ABE and its sequelae. Content: This article reviews (a) the complex relationship between serum or plasma bilirubin measurements and ABE, (b) the history underlying the limited use of Bf in the clinical setting, (c) the peroxidase method for measuring Bf and technical and other issues involved in adapting the measurement to routine clinical use, (d) clinical experience using Bf in the management of newborn jaundice, and (e) the value of Bf measurements in research investigating bilirubin pathochemistry. Summary: Increasing evidence from clinical studies, clinical experience, and basic research investigating bilirubin neurotoxicity supports efforts to incorporate Bf expeditiously into the routine evaluation of newborn jaundice. .
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35

Chang, Pearl, Thomas Newman, and M. Maisels. "Update on Predicting Severe Hyperbilirubinemia and Bilirubin Neurotoxicity Risks in Neonates." Current Pediatric Reviews 13, no. 999 (January 23, 2017): 1. http://dx.doi.org/10.2174/1573396313666170123151408.

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36

Berns, M., M. Toennessen, B. Gerstner, U. Felderhoff-Mueser, and M. Obladen. "36 Combined Neurotoxicity of Bilirubin and Hyperoxia in Cortical Neuronal Culture." Pediatric Research 58, no. 2 (August 2005): 360. http://dx.doi.org/10.1203/00006450-200508000-00065.

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37

Shapiro, Steven M., Sompong Sombati, Angela Geiger, and Ann C. Rice. "NMDA Channel Antagonist MK-801 Does Not Protect against Bilirubin Neurotoxicity." Neonatology 92, no. 4 (2007): 248–57. http://dx.doi.org/10.1159/000103743.

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38

Riordan, Sean M., and Steven M. Shapiro. "Review of bilirubin neurotoxicity I: molecular biology and neuropathology of disease." Pediatric Research 87, no. 2 (October 10, 2019): 327–31. http://dx.doi.org/10.1038/s41390-019-0608-0.

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39

Shapiro, Steven M. "Brainstem Auditory Evoked Potentials in an Experimental Model of Bilirubin Neurotoxicity." Clinical Pediatrics 33, no. 8 (August 1994): 460–67. http://dx.doi.org/10.1177/000992289403300803.

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40

Kuter, Nazli, Nese Aysit-Altuncu, Gurkan Ozturk, and Eren Ozek. "The Neuroprotective Effects of Hypothermia on Bilirubin-Induced Neurotoxicity in vitro." Neonatology 113, no. 4 (2018): 360–65. http://dx.doi.org/10.1159/000487221.

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41

Lai, Ke, Xing-Lei Song, Hao-Song Shi, Xin Qi, Chun-Yan Li, Jia Fang, Fan Wang, et al. "Bilirubin enhances the activity of ASIC channels to exacerbate neurotoxicity in neonatal hyperbilirubinemia in mice." Science Translational Medicine 12, no. 530 (February 12, 2020): eaax1337. http://dx.doi.org/10.1126/scitranslmed.aax1337.

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Neonatal hyperbilirubinemia is a common clinical condition that can lead to brain encephalopathy, particularly when concurrent with acidosis due to infection, ischemia, and hypoxia. The prevailing view is that acidosis increases the permeability of the blood-brain barrier to bilirubin and exacerbates its neurotoxicity. In this study, we found that the concentration of the cell death marker, lactate dehydrogenase (LDH) in cerebrospinal fluid (CSF), is elevated in infants with both hyperbilirubinemia and acidosis and showed stronger correlation with the severity of acidosis rather than increased bilirubin concentration. In mouse neonatal neurons, bilirubin exhibits limited toxicity but robustly potentiates the activity of acid-sensing ion channels (ASICs), resulting in increases in intracellular Ca2+ concentration, spike firings, and cell death. Furthermore, neonatal conditioning with concurrent hyperbilirubinemia and hypoxia-induced acidosis promoted long-term impairments in learning and memory and complex sensorimotor functions in vivo, which are largely attenuated in ASIC1a null mice. These findings suggest that targeting acidosis and ASICs may attenuate neonatal hyperbilirubinemia complications.
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42

Hansen, Thor W. R., Ronald J. Wong, and David K. Stevenson. "Molecular Physiology and Pathophysiology of Bilirubin Handling by the Blood, Liver, Intestine, and Brain in the Newborn." Physiological Reviews 100, no. 3 (July 1, 2020): 1291–346. http://dx.doi.org/10.1152/physrev.00004.2019.

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Bilirubin is the end product of heme catabolism formed during a process that involves oxidation-reduction reactions and conserves iron body stores. Unconjugated hyperbilirubinemia is common in newborn infants, but rare later in life. The basic physiology of bilirubin metabolism, such as production, transport, and excretion, has been well described. However, in the neonate, numerous variables related to nutrition, ethnicity, and genetic variants at several metabolic steps may be superimposed on the normal physiological hyperbilirubinemia that occurs in the first week of life and results in bilirubin levels that may be toxic to the brain. Bilirubin exists in several isomeric forms that differ in their polarities and is considered a physiologically important antioxidant. Here we review the chemistry of the bilirubin molecule and its metabolism in the body with a particular focus on the processes that impact the newborn infant, and how differences relative to older children and adults contribute to the risk of developing both acute and long-term neurological sequelae in the newborn infant. The final section deals with the interplay between the brain and bilirubin and its entry, clearance, and accumulation. We conclude with a discussion of the current state of knowledge regarding the mechanism(s) of bilirubin neurotoxicity.
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43

LABRUNE, P. H., M. ODIÈVRE, A. MYARA, F. TRIVIN, and J. FRANCOUAL. "Cerebellar Symptoms as the Presenting Manifestations of Bilirubin Encephalopathy in Children with Crigler-Najjar Type I Disease." Pediatrics 89, no. 4 (April 1, 1992): 768–70. http://dx.doi.org/10.1542/peds.89.4.768.

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Crigler-Najjar (CN) disease is a rare metabolic disorder characterized by a permanent deficiency in hepatic bilirubin UDPglucuronate β-d-glucuronosyl-transferase (UDPG-T, EC 2.1.4.17) activity. Since 1969, patients affected by this disease have been classified in two groups: in the first group (CN type I), the serum bilirubin concentration does not decrease under treatment with phenobarbital although it does so dramatically in the second group (CN type II).1,2 Despite the use of phototherapy and cholestyramine to avoid bilirubin neurotoxicity, patients affected by CN type I disease are at permanent risk of developing kernicterus with severe neurologic sequelae. The classic symptoms of kernicterus in the neonate, with or without CN disease, do not comprise prominent cerebellar manifestations, and, in most cases, the infants die or develop choreoathetosis, hearing loss, and severe mental retardation.3,4
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44

Dobrovanov, O., and K. Kralinsky. "Unbound bilirubin as a predictor of neurotoxicity — the question of the future?" PERINATOLOGIYA I PEDIATRIYA, no. 4(76) (December 28, 2018): 67–73. http://dx.doi.org/10.15574/pp.2018.76.67.

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45

Bortolussi, Giulia, Xiaoxia Shi, Lysbeth ten Bloemendaal, Bhaswati Banerjee, Dirk R. De Waart, Gabriele Baj, Weiyu Chen, et al. "Long-Term Effects of Biliverdin Reductase a Deficiency in Ugt1−/− Mice: Impact on Redox Status and Metabolism." Antioxidants 10, no. 12 (December 20, 2021): 2029. http://dx.doi.org/10.3390/antiox10122029.

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Accumulation of neurotoxic bilirubin due to a transient neonatal or persistent inherited deficiency of bilirubin glucuronidation activity can cause irreversible brain damage and death. Strategies to inhibit bilirubin production and prevent neurotoxicity in neonatal and adult settings seem promising. We evaluated the impact of Bvra deficiency in neonatal and aged mice, in a background of unconjugated hyperbilirubinemia, by abolishing bilirubin production. We also investigated the disposal of biliverdin during fetal development. In Ugt1−/− mice, Bvra deficiency appeared sufficient to prevent lethality and to normalize bilirubin level in adults. Although biliverdin accumulated in Bvra-deficient fetuses, both Bvra−/− and Bvra−/−Ugt1−/− pups were healthy and reached adulthood having normal liver, brain, and spleen histology, albeit with increased iron levels in the latter. During aging, both Bvra−/− and Bvra−/−Ugt1−/− mice presented normal levels of relevant hematological and metabolic parameters. Interestingly, the oxidative status in erythrocytes from 9-months-old Bvra−/− and Bvra−/−Ugt1−/− mice was significantly reduced. In addition, triglycerides levels in these 9-months-old Bvra−/− mice were significantly higher than WT controls, while Bvra−/−Ugt1−/− tested normal. The normal parameters observed in Bvra−/−Ugt1−/− mice fed chow diet indicate that Bvra inhibition to treat unconjugated hyperbilirubinemia seems safe and effective.
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46

Pranty, Abida Islam, Sara Shumka, and James Adjaye. "Bilirubin-Induced Neurological Damage: Current and Emerging iPSC-Derived Brain Organoid Models." Cells 11, no. 17 (August 25, 2022): 2647. http://dx.doi.org/10.3390/cells11172647.

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Bilirubin-induced neurological damage (BIND) has been a subject of studies for decades, yet the molecular mechanisms at the core of this damage remain largely unknown. Throughout the years, many in vivo chronic bilirubin encephalopathy models, such as the Gunn rat and transgenic mice, have further elucidated the molecular basis of bilirubin neurotoxicity as well as the correlations between high levels of unconjugated bilirubin (UCB) and brain damage. Regardless of being invaluable, these models cannot accurately recapitulate the human brain and liver system; therefore, establishing a physiologically recapitulating in vitro model has become a prerequisite to unveil the breadth of complexities that accompany the detrimental effects of UCB on the liver and developing human brain. Stem-cell-derived 3D brain organoid models offer a promising platform as they bear more resemblance to the human brain system compared to existing models. This review provides an explicit picture of the current state of the art, advancements, and challenges faced by the various models as well as the possibilities of using stem-cell-derived 3D organoids as an efficient tool to be included in research, drug screening, and therapeutic strategies for future clinical applications.
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47

Gazzin, Silvia, Matteo Dal Ben, Michele Montrone, Sri Jayanti, Andrea Lorenzon, Alessandra Bramante, Cristina Bottin, Rita Moretti, and Claudio Tiribelli. "Curcumin Prevents Cerebellar Hypoplasia and Restores the Behavior in Hyperbilirubinemic Gunn Rat by a Pleiotropic Effect on the Molecular Effectors of Brain Damage." International Journal of Molecular Sciences 22, no. 1 (December 30, 2020): 299. http://dx.doi.org/10.3390/ijms22010299.

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Bilirubin toxicity to the central nervous system (CNS) is responsible for severe and permanent neurologic damage, resulting in hearing loss, cognitive, and movement impairment. Timely and effective management of severe neonatal hyperbilirubinemia by phototherapy or exchange transfusion is crucial for avoiding permanent neurological consequences, but these therapies are not always possible, particularly in low-income countries. To explore alternative options, we investigated a pharmaceutical approach focused on protecting the CNS from pigment toxicity, independently from serum bilirubin level. To this goal, we tested the ability of curcumin, a nutraceutical already used with relevant results in animal models as well as in clinics in other diseases, in the Gunn rat, the spontaneous model of neonatal hyperbilirubinemia. Curcumin treatment fully abolished the landmark cerebellar hypoplasia of Gunn rat, restoring the histological features, and reverting the behavioral abnormalities present in the hyperbilirubinemic rat. The protection was mediated by a multi-target action on the main bilirubin-induced pathological mechanism ongoing CNS damage (inflammation, redox imbalance, and glutamate neurotoxicity). If confirmed by independent studies, the result suggests the potential of curcumin as an alternative/complementary approach to bilirubin-induced brain damage in the clinical scenario.
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48

Bortolussi, G., G. Baj, S. Vodret, G. Viviani, T. Bittolo, and A. F. Muro. "Age-dependent pattern of cerebellar susceptibility to bilirubin neurotoxicity in vivo in mice." Disease Models & Mechanisms 7, no. 9 (July 25, 2014): 1057–68. http://dx.doi.org/10.1242/dmm.016535.

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Dani, Carlo, Simone Pratesi, Alice Ilari, Daniele Lana, Maria Grazia Giovannini, Daniele Nosi, Daniele Buonvicino, et al. "Neurotoxicity of Unconjugated Bilirubin in Mature and Immature Rat Organotypic Hippocampal Slice Cultures." Neonatology 115, no. 3 (2019): 217–25. http://dx.doi.org/10.1159/000494101.

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Ye, Hai-Bo, Jian Wang, Wei-Tian Zhang, Hai-Bo Shi, and Shan-Kai Yin. "Taurine attenuates bilirubin-induced neurotoxicity in the auditory system in neonatal guinea pigs." International Journal of Pediatric Otorhinolaryngology 77, no. 5 (May 2013): 647–54. http://dx.doi.org/10.1016/j.ijporl.2012.11.037.

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