WordNet
- an abnormal accumulation of bile pigment in the brain and other nerve tissue; causes yellow staining and tissue damage
- of or relating to or constituting the nucleus of an atom; "nuclear physics"; "nuclear fission"; "nuclear forces"
- (weapons) deriving destructive energy from the release of atomic energy; "nuclear war"; "nuclear weapons"; "atomic bombs" (同)atomic
- constituting or like a nucleus; "annexation of the suburban fringe by the nuclear metropolis"; "the nuclear core of the congregation"
- of or relating to or constituting the nucleus of a cell; "nuclear membrane"; "nuclear division"
- distort adversely; "Jealousy had jaundiced his judgment"
- yellowing of the skin and the whites of the eyes caused by an accumulation of bile pigment (bilirubin) in the blood; can be a symptom of gallstones or liver infection or anemia (同)icterus
- affect with, or as if with, jaundice
- showing or affected by prejudice or envy or distaste; "looked with a jaundiced eye on the growth of regimentation"; "takes a jaundiced view of societies and clubs"
- affected by jaundice which causes yellowing of skin etc (同)icteric, yellow
PrepTutorEJDIC
- 『核の』,細胞核の / [『原子』]『核の』
- 黄疸(おうだん) / ひがみ,ねたみ,偏見 / 〈人〉‘に'偏見をもたせる;〈見解など〉‘を'ゆがめる
- 黄疸にかかった / ひがんだ
UpToDate Contents
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- 1. 黄疸または無症候性高ビリルビン血症成人患者に対する診断的アプローチ diagnostic approach to the adult with jaundice or asymptomatic hyperbilirubinemia
- 2. 術後黄疸患者に対するアプローチ approach to the patient with postoperative jaundice
- 3. 小児における非抱合型高ビリルビン血症による黄疸の評価 evaluation of jaundice caused by unconjugated hyperbilirubinemia in children
- 4. 早産児（妊娠35週未満）における高ビリルビン血症 hyperbilirubinemia in the premature infant less than 35 weeks gestation
- 5. 正期産児および後期早産児における非抱合型高ビリルビン血症の治療 treatment of unconjugated hyperbilirubinemia in term and late preterm infants
English Journal
- PCR-Based Allelic Discrimination for Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency in Ugandan Umbilical Cord Blood.
- Hsu J, Fink D, Langer E, Carter ML, Bengo D, Ndidde S, Slusher T, Ross JA, Lund TC.Author information Mayo Medical School , Rochester, Minnesota , USA.AbstractGlucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common X-linked disorder in the world. G6PD deficiency puts children at risk for hyperbilirubinemia and kernicterus during the newborn period and an increased risk of severe hemolysis after exposure to many antimalarial medications. A laboratory diagnosis of G6PD deficiency is rare in the developing world due to limited resources. We developed a TaqMan-based allele-specific assay to rapidly determine rates of G6PD deficiency contributing alleles (G202A and A376G) in East Africa. We tested umbilical cord blood from 100 Ugandan newborns and found that the overall allele frequency of G202A was .13 and A376G was .32. The overall incidence of G6PD A- (G202A/A376G) was 6%; all A- variants were males. There was no correlation between G6PD deficiency and umbilical cord blood hemoglobin, white blood count, platelet count, or other hematologic parameters. Allele-specific PCR can serve as a rapid method to determine specific G6PD deficiency allele frequencies in a given population and as a diagnostic tool in a hospital setting in which laboratory resources are present.
- Pediatric hematology and oncology.Pediatr Hematol Oncol.2013 Dec 5. [Epub ahead of print]
- Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common X-linked disorder in the world. G6PD deficiency puts children at risk for hyperbilirubinemia and kernicterus during the newborn period and an increased risk of severe hemolysis after exposure to many antimalarial medications. A l
- PMID 24308819
- Bilirubin mediated oxidative stress involves antioxidant response activation via Nrf2 pathway.
- Qaisiya M1, Coda Zabetta CD2, Bellarosa C3, Tiribelli C4.Author information 1Fondazione Italiana Fegato ONLUS, Italian Liver Foundation ONLUS, Bldg Q AREA Science Park - Basovizza Campus, 34149 Trieste, Italy. Electronic address: m.qaisiya@csf.units.it.2Fondazione Italiana Fegato ONLUS, Italian Liver Foundation ONLUS, Bldg Q AREA Science Park - Basovizza Campus, 34149 Trieste, Italy. Electronic address: carlos.zabetta@csf.units.it.3Fondazione Italiana Fegato ONLUS, Italian Liver Foundation ONLUS, Bldg Q AREA Science Park - Basovizza Campus, 34149 Trieste, Italy. Electronic address: cristina.bellarosa@csf.units.it.4Fondazione Italiana Fegato ONLUS, Italian Liver Foundation ONLUS, Bldg Q AREA Science Park - Basovizza Campus, 34149 Trieste, Italy; Department of Medical Sciences, University of Trieste, 34100 Trieste, Italy. Electronic address: ctliver@csf.units.it.AbstractUnconjugated bilirubin (UCB) is responsible for neonatal jaundice and high level of free bilirubin (Bf) can lead to kernicterus. Previous studies suggest that oxidative stress is a critical component of UCB-induced neurotoxicity. The Nrf2 pathway is a powerful sensor for cellular redox state and is activated directly by oxidative stress and/or indirectly by stress response protein kinases. Activated Nrf2 translocates to nucleus, binds to Antioxidant Response Element (ARE), and enhances the up-regulation of cytoprotective genes that mediate cell survival. The aim of the present study was to investigate the role of Nrf2 pathway in cell response to bilirubin mediated oxidative stress in the neuroblastoma SH-SY5Y cell line. Cells exposed to a toxic concentration of UCB (140nM Bf) showed an increased intracellular ROS levels and enhanced nuclear accumulation of Nrf2 protein. UCB stimulated transcriptional induction of ARE-GFP reporter gene and induced mRNA expression of multiple antioxidant response genes as: xCT, Gly1, γGCL-m, γGCL-c, HO-1, NQO1, FTH, ME1, and ATF3. Nrf2 siRNA decreased UCB induced mRNA expression of HO1 (75%), NQO1 (54%), and FTH (40%). The Nrf2-related HO-1 induction was reduced to 60% in cells pre-treated with antioxidant (NAC) or specific signaling pathway inhibitors for PKC, P38α and MEK1/2 (80, 40 and 25%, respectively). In conclusion, we demonstrated that SH-SY5Y cells undergo an adaptive response against UCB-mediated oxidative stress by activation of multiple antioxidant response, in part through Nrf2 pathway.
- Cellular signalling.Cell Signal.2013 Dec 2;26(3):512-520. doi: 10.1016/j.cellsig.2013.11.029. [Epub ahead of print]
- Unconjugated bilirubin (UCB) is responsible for neonatal jaundice and high level of free bilirubin (Bf) can lead to kernicterus. Previous studies suggest that oxidative stress is a critical component of UCB-induced neurotoxicity. The Nrf2 pathway is a powerful sensor for cellular redox state and is
- PMID 24308969
- Jaundice and kernicterus in the moderately preterm infant.
- Wallenstein MB, Bhutani VK.Author information Division of Neonatal-Developmental Medicine, Department of Pediatrics, Lucile Packard Children's Hospital, Stanford University School of Medicine, 750 Welch Road #315, Stanford, CA 94304, USA.AbstractModerate preterm infants remain at increased risk for adverse outcomes, including acute bilirubin encephalopathy (ABE). Evidence-based guidelines for management of hyperbilirubinemia in preterm infants less than 35 weeks' gestational age are not yet optimized. High concentrations of unconjugated bilirubin can cause permanent posticteric neurologic sequelae (kernicterus). Clinical manifestations of ABE in preterm infants are similar to, but often more subtle than, those of term infants. This review outlines clinical strategies to operationalize management of hyperbilirubinemia in moderately preterm infants to meet recently published consensus-based recommendations.
- Clinics in perinatology.Clin Perinatol.2013 Dec;40(4):679-88. doi: 10.1016/j.clp.2013.07.007. Epub 2013 Sep 20.
- Moderate preterm infants remain at increased risk for adverse outcomes, including acute bilirubin encephalopathy (ABE). Evidence-based guidelines for management of hyperbilirubinemia in preterm infants less than 35 weeks' gestational age are not yet optimized. High concentrations of unconjugated bi
- PMID 24182955
Japanese Journal
- 黄疸の成因と病態
- 足立 幸彦,諸岡 留美
- 胆道 = Journal of Japan Biliary Association 23(2), 174-180, 2009-05-31
- NAID 10025363921
- 2)先天代謝スクリーニング,血清ビリルビン検査(21.新生児検査,C.産婦人科検査法,研修コーナー)
- 宮崎 亮一郎
- 日本産科婦人科學會雜誌 59(11), "N-650"-"N-655", 2007-11-01
- NAID 110006958183
- 大細胞神経内分泌癌成分を伴う下部胆管原発腺内分泌細胞癌の1例
- 佐藤 勝明,上見 嘉子,河村 常作,谷本 一夫,岡崎 恵子,上田 善道,勝田 省吾
- 日本臨床細胞学会雑誌 44(5), 314-318, 2005-09-22
- NAID 110001868260
Related Links
- jaundice /jaun·dice/ (jawn´dis) icterus; yellowness of the skin, scleras, mucous membranes, and excretions due to hyperbilirubinemia and deposition of bile pigments. acholuric jaundice jaundice without bilirubinemia, associated with elevated ...
- 7 May 2013 ... Nuclear jaundice symptoms, causes, diagnosis, and treatment information for Nuclear jaundice (Kernicterus) with alternative diagnoses, full-text book chapters, misdiagnosis, research treatments, prevention, and prognosis.
Related Pictures
★リンクテーブル★
| リンク元 | 「核黄疸」「nuclear icterus」 |
| 関連記事 | 「nuclear」「jaundiced」「jaundice」 |
「核黄疸」
小児科学第2版 p.423-
概念
- 新生児において高度の高間接ビリルビン血症(5mg/dL異常)の持続により、血管脳肝門を通過したビリルビンが脳に蓄積して生じる。生後3-7日で症状が出現する。
症状
- ビリルビン脳症の症状である
- 急性ビリルビン脳症(核黄疸)
- 1期(発病約2-3日)
- 嗜眠、筋緊張低下、吸啜反射減弱
- 2期(発病約3-1週)
- 発熱、筋緊張、後弓反射。落陽現象
- 3期(発病約1週以降)
- 筋緊張亢進症状消失
- 慢性ビリルビン脳症(核黄疸後遺症)
- 過渡的症状(約1年以内)
- ほ乳不良、甲高い鳴き声、筋緊張低下(深部反射亢進)、運動発達千円
- 核黄疸後遺症(約1.5年以降)
- アテトーゼ型脳性麻痺
- 難聴
- 上方凝視麻痺
- 知的障害
核黄疸の臨床所見(Praaghの分類)
治療
出生体重 光線療法 交換療法 ＜1,500g 0.3μg/dl 0.8μg/dl ≧1,500g 0.6μg/dl 1.0μg/dl
- 光線療法
- 光によりビリルビンが光学異性体となり、血流に入る
予後
- 第1期症状(Moro反射が消失し元気がなくなる)で治療を行えば、障害は防ぐことができる。
- 後弓反張や落陽現象、痙攣など神経学的所見が明らかになった症例では、アテトーゼを伴う脳性小児麻痺、高温域の感音性難聴の後遺症を残すリスクが高い。
「nuclear icterus」
「nuclear」
- adj.
- 核の、(生物)細胞核の、(物理)原子核の
「jaundiced」
- 黄疸性の
- 関
- icteric
「jaundice」