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70 results

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Quoted phrase not found in phrase index: "Persistence of hemoglobin F"
Page 1
Iron deficiency in pregnancy.
Georgieff MK. Georgieff MK. Am J Obstet Gynecol. 2020 Oct;223(4):516-524. doi: 10.1016/j.ajog.2020.03.006. Epub 2020 Mar 14. Am J Obstet Gynecol. 2020. PMID: 32184147 Free PMC article. Review.
Newborns with iron deficiency have compromised recognition memory, slower speed of processing, and poorer bonding that persist despite postnatal iron repletion. Preclinical models of fetal iron deficiency confirm that expected iron-dependent processes such as monoam …
Newborns with iron deficiency have compromised recognition memory, slower speed of processing, and poorer bonding that persist despit …
Hydroxyurea Decouples Persistent F-Cell Elevation and Induction of gamma-Globin.
Walker AL, Crosby D, Miller V, Weidert F, Ofori-Acquah S. Walker AL, et al. Exp Hematol. 2022 Aug-Sep;112-113:15-23.e1. doi: 10.1016/j.exphem.2022.07.005. Epub 2022 Jul 15. Exp Hematol. 2022. PMID: 35843392 Free article.
Mechanisms that control the fetal-to-adult hemoglobin switch are attractive therapeutic targets in sickle cell disease. In this study, we investigated developmental gamma-globin silencing in the Townes humanized knock-in mouse model, which harbors a construct contai …
Mechanisms that control the fetal-to-adult hemoglobin switch are attractive therapeutic targets in sickle cell disease. In thi …
Wake-up Sleepy Gene: Reactivating Fetal Globin for beta-Hemoglobinopathies.
Wienert B, Martyn GE, Funnell APW, Quinlan KGR, Crossley M. Wienert B, et al. Trends Genet. 2018 Dec;34(12):927-940. doi: 10.1016/j.tig.2018.09.004. Epub 2018 Oct 1. Trends Genet. 2018. PMID: 30287096 Review.
Disorders in hemoglobin (hemoglobinopathies) were the first monogenic diseases to be characterized and remain among the most common and best understood genetic conditions. ...Over 50 years ago it was recognized that mutations that cause lifelong persistence of fe …
Disorders in hemoglobin (hemoglobinopathies) were the first monogenic diseases to be characterized and remain among the most common a …
Small molecule therapeutics to treat the β-globinopathies.
Yu L, Myers G, Engel JD. Yu L, et al. Curr Opin Hematol. 2020 May;27(3):129-140. doi: 10.1097/MOH.0000000000000579. Curr Opin Hematol. 2020. PMID: 32167945 Free PMC article. Review.
SUMMARY: We summarize current information regarding the binding of transcription factors that appear to be impeded or augmented by different hereditary persistence of fetal hemoglobin (HPFH) mutations. As transcription factors have historically proven to be d …
SUMMARY: We summarize current information regarding the binding of transcription factors that appear to be impeded or augmented by different …
The Genetic and Clinical Significance of Fetal Hemoglobin Expression in Sickle Cell Disease.
Adekile A. Adekile A. Med Princ Pract. 2021;30(3):201-211. doi: 10.1159/000511342. Epub 2020 Sep 4. Med Princ Pract. 2021. PMID: 32892201 Free PMC article. Review.
Sickle cell disease (SCD) is phenotypically heterogeneous. One major genetic modifying factor is the patient's fetal hemoglobin (HbF) level. The latter is determined by the patient's beta-globin gene cluster haplotype and cis- and trans-acting single nucleotide poly …
Sickle cell disease (SCD) is phenotypically heterogeneous. One major genetic modifying factor is the patient's fetal hemoglobin …
Oxygen targeting in preterm infants: a physiological interpretation.
Lakshminrusimha S, Manja V, Mathew B, Suresh GK. Lakshminrusimha S, et al. J Perinatol. 2015 Jan;35(1):8-15. doi: 10.1038/jp.2014.199. Epub 2014 Oct 30. J Perinatol. 2015. PMID: 25357098 Free PMC article. Review.
Randomized controlled trials evaluating low-target oxygen saturation (SpO2:85% to 89%) vs high-target SpO2 (91% to 95%) have shown variable results regarding mortality and morbidity in extremely preterm infants. Because of the variation inherent to the accuracy of pulse ox …
Randomized controlled trials evaluating low-target oxygen saturation (SpO2:85% to 89%) vs high-target SpO2 (91% to 95%) have shown va …
Congenital hypoplastic anemia.
Diamond LK, Wang WC, Alter BP. Diamond LK, et al. Adv Pediatr. 1976;22:349-78. Adv Pediatr. 1976. PMID: 773132 Review.
Thereafter, this therapy may need to be continued, often at an extremely low dosage level, sometimes intermittently, for many years before the hemoglobin value maintains itself without medication. Spontaneous remission has occurred in a few cases after years of transfusion …
Thereafter, this therapy may need to be continued, often at an extremely low dosage level, sometimes intermittently, for many years before t …
Genome editing strategies for fetal hemoglobin induction in beta-hemoglobinopathies.
Demirci S, Leonard A, Tisdale JF. Demirci S, et al. Hum Mol Genet. 2020 Sep 30;29(R1):R100-R106. doi: 10.1093/hmg/ddaa088. Hum Mol Genet. 2020. PMID: 32406490 Free PMC article. Review.
Approaches to genetically engineer high HbF include de novo generation of naturally occurring hereditary persistence of fetal hemoglobin (HPFH) mutations, editing of transcriptional HbF repressors or their binding sites and/or regulating epigenetic intermedia …
Approaches to genetically engineer high HbF include de novo generation of naturally occurring hereditary persistence of fetal …
Targeting fetal hemoglobin expression to treat beta hemoglobinopathies.
Steinberg MH. Steinberg MH. Expert Opin Ther Targets. 2022 Apr;26(4):347-359. doi: 10.1080/14728222.2022.2066519. Epub 2022 Apr 26. Expert Opin Ther Targets. 2022. PMID: 35418266
Fetal hemoglobin (HbF) prevents sickle hemoglobin polymerization; in beta thalassemia HbF compensates for the deficit of normal hemoglobin. ...If HbF is the only hemoglobin present, much higher levels are needed to 'cure' beta thalassemia. ...
Fetal hemoglobin (HbF) prevents sickle hemoglobin polymerization; in beta thalassemia HbF compensates for the deficit o …
Natural history and determinants of clinical severity of sickle cell disease.
Serjeant GR. Serjeant GR. Curr Opin Hematol. 1995 Mar;2(2):103-8. doi: 10.1097/00062752-199502020-00001. Curr Opin Hematol. 1995. PMID: 9371979 Review.
Some of the factors determining the extremely variable clinical course of homozygous sickle cell disease are being identified. Genetic factors include alpha-thalassemia, beta-globin gene haplotypes, heterocellular hereditary persistence of fetal hemoglobin …
Some of the factors determining the extremely variable clinical course of homozygous sickle cell disease are being identified. Geneti …
70 results