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Journal articles on the topic 'Hemoglobin F'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Olufemi, Akanni E., Oseni B. Sola, Bamisaye E. Oluwaseyi, Raji A. Ajani, Mewoyeka O. Olusoji, and Hassan R. Olubunmi. "Hemoglobin F level in different hemoglobin variants." Korean Journal of Hematology 46, no. 2 (2011): 118. http://dx.doi.org/10.5045/kjh.2011.46.2.118.

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2

Rees, D. C. "Hemoglobin F and Hemoglobin E/β-Thalassemia". Journal of Pediatric Hematology/Oncology 22, № 6 (2000): 567–72. http://dx.doi.org/10.1097/00043426-200011000-00025.

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3

Moscoso, H., C. R. Kiefer, A. Kutlar, and F. A. Garver. "Quantification of hemoglobins S, C, and F by a magnetic affinity immunoassay." Clinical Chemistry 34, no. 5 (1988): 902–5. http://dx.doi.org/10.1093/clinchem/34.5.902.

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Abstract This magnetic affinity immunoassay (MAIA) quantifies hemoglobins (Hb) S, C, and F in hemolysates from adults or newborns. Monospecific antisera to the hemoglobins are covalently conjugated to magnetic beads and reacted with the corresponding 125I-labeled hemoglobin. After centrifugation to separate the free and antibody-bound 125I-labeled hemoglobin, the amount of radioactive hemoglobin in the pellet is measured. To determine the concentration of the Hb under study, the percent inhibition of the reaction is quantified. The standard curve is established by adding known quantities of un

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4

Hirsch, R. E., M. J. Lin, and R. L. Nagel. "The inhibition of hemoglobin C crystallization by hemoglobin F." Journal of Biological Chemistry 263, no. 12 (1988): 5936–39. http://dx.doi.org/10.1016/s0021-9258(18)60656-8.

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5

Uygun, Vedat, and Gülsün Tezcan Karasu. "Hemoglobin F and Related Conditions." Van Medical Journal 23, no. 2 (2016): 229–34. http://dx.doi.org/10.5505/vtd.2016.96268.

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6

Reinhardt, D., D. Haase, C. Schoch, et al. "Hemoglobin F in myelodysplastic syndrome." Annals of Hematology 76, no. 3-4 (1998): 135–38. http://dx.doi.org/10.1007/s002770050377.

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7

Adachi, K., J. Pang, P. Konitzer, and S. Surrey. "Polymerization of recombinant hemoglobin F gamma E6V and hemoglobin F gamma E6V, gamma Q87T alone, and in mixtures with hemoglobin S." Blood 87, no. 4 (1996): 1617–24. http://dx.doi.org/10.1182/blood.v87.4.1617.bloodjournal8741617.

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To further understand determinants for Hemoglobin (Hb) S polymerization, as well as the inhibitory mechanism of Hb F on Hb S polymerization, Hb F variants containing Val-gamma 6 (Hb F gamma E6V) or Val-gamma 6, Thr-gamma 87 (Hb F gamma E6V, gamma Q87T) were expressed in yeast. The oxy form of Hb F gamma E6V was about 10-fold less stable to mechanical agitation than native oxy Hb F, which is similar to stability differences comparing oxy Hb S and oxy Hb A. Deoxy Hb F gamma E6V showed approximately 20-fold decreased solubility compared with native deoxy Hb F in high phosphate buffer and formed g

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8

Mosca, Andrea, Cristian Arsene, Renata Paleari, et al. "Standardization of hemoglobin A2 and hemoglobin F: Achievements and perspectives." Clinica Chimica Acta 567 (February 2025): 120087. https://doi.org/10.1016/j.cca.2024.120087.

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9

Gordeuk, Victor R., Andrew Campbell, Sohail Rana, et al. "Relationship of erythropoietin, fetal hemoglobin, and hydroxyurea treatment to tricuspid regurgitation velocity in children with sickle cell disease." Blood 114, no. 21 (2009): 4639–44. http://dx.doi.org/10.1182/blood-2009-04-218040.

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AbstractHydroxyurea and higher hemoglobin F improve the clinical course and survival in sickle cell disease, but their roles in protecting from pulmonary hypertension are not clear. We studied 399 children and adolescents with sickle cell disease at steady state; 38% were being treated with hydroxyurea. Patients on hydroxyurea had higher hemoglobin concentration and lower values for a hemolytic component derived from 4 markers of hemolysis (P ≤ .002) but no difference in tricuspid regurgitation velocity compared with those not receiving hydroxyurea; they also had higher hemoglobin F (P < .0

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10

Whitham, Megan, Jayson Pagaduan, Steven L. Clark, et al. "Validation of the Siggaard–Andersen Acid–Base Nomogram for Hemoglobin F: Implications for Fetal Cord Blood Gas Analysis." American Journal of Perinatology 36, no. 14 (2019): 1481–84. http://dx.doi.org/10.1055/s-0039-1677800.

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Objective The calculation of HCO3 and base excess in current blood gas analysis is based on the Siggaard–Andersen equation. One of the constants in this equation is dependent on the known buffering capacity of hemoglobin A. We sought to investigate differences in buffering capacity between adult hemoglobin A and fetal hemoglobin F as a potential explanation for the observed poor correlation between calculated base excess in umbilical cord blood and newborn outcomes. Such differences would influence a key constant in the Van Slyke/Siggaard–Andersen equation used to calculate HCO3 and base exces

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11

Yee, Marianne E. M., Maa-Ohui Quarmyne, Catherine Segbefia, Andrew N. Young, Lina Zhuang, and Ferdane Kutlar. "Hemoglobin F Only Syndrome at Birth." Journal of Pediatric Hematology/Oncology 38, no. 1 (2016): e32-e34. http://dx.doi.org/10.1097/mph.0000000000000477.

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12

Menzel, Stephan, and Swee Lay Thein. "Genetic architecture of hemoglobin F control." Current Opinion in Hematology 16, no. 3 (2009): 179–86. http://dx.doi.org/10.1097/moh.0b013e328329d07a.

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13

Perrine, Susan P. "Hemoglobin F: new targets, new path." Blood 108, no. 3 (2006): 783–84. http://dx.doi.org/10.1182/blood-2006-05-022582.

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14

Lazarchick, J. "Kleihauer-Betke Hemoglobin F Acid Resistance." ASH Image Bank 2004, no. 0125 (2004): 100983. http://dx.doi.org/10.1182/ashimagebank-2004-100983.

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15

Desimone, Joseph, Paul Heller, Robert E. Molokie, Lemuel Hall, and David Zwiers. "Tetrahydrouridine, cytidine analogues, and hemoglobin F." American Journal of Hematology 18, no. 3 (1985): 283–88. http://dx.doi.org/10.1002/ajh.2830180310.

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16

Ogbonna, Ogbodo Sylvester, Chukwurah Ejike Felix, Eze Chukwuka Wencelaus, Eze Richard Ikechukwu, and Udengwu Nonyerem Lilian. "Fetal Hemoglobin Levels as Indicator of Frequency and Duration of Blood Donation." International Journal of Scientific Research and Management 9, no. 06 (2021): 389–94. http://dx.doi.org/10.18535/ijsrm/v9i06.mp03.

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Hemoglobin F is normal hemoglobin seen in minute amount in adults. Increase in its level in adults is an indication of erythropoietic stress, which in most cases is linked to hemoglobinopathy. This study was undertaken to assess if physiological erythropoietic stress as seen in commercial blood donation, can increase it and thus be used as an indicator of frequency and duration of blood donation. The study involved 152 subjects including 88 commercial blood donors and 64 controls. Hemoglobin F was expressed as percentage concentration of the total hemoglobin. Results showed that hemoglobin F s

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17

Olufemi-Aworinde, Kehinde, Tolulase Olutogun, Ademola Abolarin, Yetunde Olasinde, and Daniel Gbadero. "Markers of Disease Severity Amongst Homozygous Sickle Cell Anaemia Attending Outpatient At Bowen University Teaching Hospital Ogbomoso, Nigeria." International Journal of Medical Science and Clinical invention 7, no. 02 (2020): 4746–50. http://dx.doi.org/10.18535/ijmsci/v7i02.03.

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Introduction: Genetic, cellular and molecular modifiers are responsible for the notoriously variable sickle cell phenotype. Haemoglobin F is a principal modulator of the SCD phenotype. Haemoglobin F inhibits the polymerization of Haemoglobin S and ameliorates the secondary effects of sickling. We measured the Haemoglobin F(HbF) in our population and compared it with other markers associated with clinical severity and clinical status of the patients. Methods: we randomly selected 40 Hemoglobin S(HbS) patients who have never taken hydroxyurea. We measured hemoglobin F levels, packed cell v

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18

Dover, GJ, and SH Boyer. "Fetal hemoglobin-containing cells have the same mean corpuscular hemoglobin as cells without fetal hemoglobin: a reciprocal relationship between gamma- and beta-globin gene expression in normal subjects and in those with high fetal hemoglobin production." Blood 69, no. 4 (1987): 1109–13. http://dx.doi.org/10.1182/blood.v69.4.1109.1109.

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Abstract We have developed methodology that allows comparison of the mean corpuscular hemoglobin (MCH) of fetal hemoglobin (HbF)-containing red cells (F cells) with the MCH of non-F cells from the same individual. To do this, suspensions of peripheral blood erythrocytes and their internal contents are fixed with an imidodiester, dimethyl-3,3′- dithiobispropionimidate dihydrochloride (DTBP). Thereafter fixed cells are made permeable to antisera by treatment with Triton X-100 and isopropanol, reacted with a mouse monoclonal antibody (MoAb) against HbF, and then with fluorescein-conjugated antimo

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19

Dover, GJ, and SH Boyer. "Fetal hemoglobin-containing cells have the same mean corpuscular hemoglobin as cells without fetal hemoglobin: a reciprocal relationship between gamma- and beta-globin gene expression in normal subjects and in those with high fetal hemoglobin production." Blood 69, no. 4 (1987): 1109–13. http://dx.doi.org/10.1182/blood.v69.4.1109.bloodjournal6941109.

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We have developed methodology that allows comparison of the mean corpuscular hemoglobin (MCH) of fetal hemoglobin (HbF)-containing red cells (F cells) with the MCH of non-F cells from the same individual. To do this, suspensions of peripheral blood erythrocytes and their internal contents are fixed with an imidodiester, dimethyl-3,3′- dithiobispropionimidate dihydrochloride (DTBP). Thereafter fixed cells are made permeable to antisera by treatment with Triton X-100 and isopropanol, reacted with a mouse monoclonal antibody (MoAb) against HbF, and then with fluorescein-conjugated antimouse IgG.

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20

Opeyemi Olufeyisola, Adesina, Ekwe Sonia, and Adesina Oluwafemi Adewale. "Evaluation of Haemoglobin F and Haemoglobin A2 among Sickle Cell Patients in Steady State at Selected Hospital in Ogun State, Nigeria." Archives of Hematology Case Reports and Reviews 9, no. 1 (2024): 019–25. http://dx.doi.org/10.17352/ahcrr.000046.

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Background: Sickle cell anemia (SCA) is a genetic disorder characterized by abnormal hemoglobin variants, including hemoglobin F (Hb F) and hemoglobin A2 (Hb A2). Evaluating the levels of these hemoglobin variants in steady-state sickle cell patients can provide insights into disease prognosis and management. This study aimed to assess Hb F and Hb A2 levels among sickle cell patients in steady state at a selected hospital in Ogun State, Nigeria. Objective: To evaluate the levels of hemoglobin F (Hb F) and hemoglobin A2 (Hb A2) in sickle cell anemia patients and determine their associations wit

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21

Ryan, C. Anthony, Keith J. Barrington, Diane Vaughan, and Neil N. Finer. "MEASUREMENT OF HEMOGLOBIN F BY CO-OXIMETRY." Critical Care Medicine 14, no. 4 (1986): 425. http://dx.doi.org/10.1097/00003246-198604000-00226.

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22

Ayesha, Shahid, and Peerzada Fawad ullah Jan. "Correlation of fetal hemoglobin in different cancer patients and sickle cell anaemia: A review." World Journal of Advanced Research and Reviews 12, no. 1 (2021): 396–400. https://doi.org/10.5281/zenodo.5651442.

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Fetal hemoglobin is the main hemoglobin during gestation period. But this globin chain is replaced and is taken over by adult hemoglobin. Sometimes this switch from fetal to adult fails to occur leading to production of fetal hemoglobin as in case of sickle cell anemia. It is also observed that fetal hemoglobin expression is also seen under malignant condition. In malignancy the spleen, liver as well as gut acquire its ability to produce fetal hemoglobin. Certain HbF cells inducing factor such as stem cell growth factor and interleukin -3 also promote HbF erythropoiesis. HbF cells are indicate

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23

Kutlar, Ferdane, Richard Shell, Joan Atkin та ін. "Neonatal Cyanosis Due to a Novel Fetal M-Hemoglobin: Hemoglobin F-M Circleville (Gγ63 His→Leu)." Blood 106, № 11 (2005): 3806. http://dx.doi.org/10.1182/blood.v106.11.3806.3806.

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Abstract Neonatal cyanosis can result from a multitude of acquired and inherited causes. Cyanosis resulting from fetal M-Hemoglobin variants is a rare cause of this condition. In fact, to date, only two Gγ variants causing methemoglobinemia and cyanosis in the newborn have been reported. These are Hb F-M Osaka (Gγ63 His→Tyr) and Hb F-M Fort Ripley (Gγ92 His→Tyr). We report a novel fetal M-hemoglobin presenting with neonatal cyanosis. The propositus was a 1-day old Caucasian male admitted to the hospital because of cyanotic episodes. The patient had an O2 saturation of 85% on room air and requi

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24

KOELLER, DAVID M. "Fetal Hemoglobin in Neonatal Anemia." Pediatrics 87, no. 2 (1991): 269–70. http://dx.doi.org/10.1542/peds.87.2.269b.

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To the Editor.— A recent paper in Pediatrics by Bard and Prosmanne1 described an elevation of fetal hemoglobin (Hb-F) production in infants with bronchopulmonary dysplasia (BPD) and oxygen dependency. The authors described a novel approach to the evaluation of occult hypoxemia in infants, with potential application in a wide range of disorders. However, in their paper the etiology of the elevation of Hb-F production in BPD patients may have been due to factors other than pulmonary disease.

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25

Lamba, S. S., B. A. Bricker, K. Y. Buch, and H. Lewis, Ill. "Use of Commercially Available Hemoglobin Standards to Quantitatively Calibrate a High Performance Liquid Chromatography Method." Current Medicinal Chemistry 5, no. 1 (1998): 63–72. http://dx.doi.org/10.2174/0929867305666220314195610.

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High performance liquid chromatography (HPLC) has proven to be an extremely useful analytical technique to separate and identify different types of hemoglobins, particularly A, C, F and S in blood samples, and compute their relative percentages. Such data provide useful information in the diagnosis of hemoglobinopathies including sickle cell anemia, β -thalassemia, hemoglobin C disease,etc. In the present investigation, we have explored the determination of absolute concentrations of individual hemoglobins in g/dal nd recommend it as an additional parameter which could be included .as part of

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26

Allen, Angela, Christopher Fisher, Anuja Premawardhena та ін. "Adaptation to anemia in hemoglobin E-β thalassemia". Blood 116, № 24 (2010): 5368–70. http://dx.doi.org/10.1182/blood-2010-06-289488.

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Abstract Hemoglobin E β thalassemia is the commonest form of severe thalassemia in many Asian countries. Its remarkably variable clinical phenotype presents a major challenge to determining its most appropriate management. In particular, it is not clear why some patients with this condition can develop and function well at very low hemoglobin levels. Here, we demonstrate that patients with hemoglobin Eβ thalassemia have a significant decrease in the oxygen affinity of their hemoglobin, that is an increased P50 value, in response to anemia. This may in part reflect the lower level of hemoglobin

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27

Laks, Kane M., Cara Hirner, Barbara Gruner, Jared Coberly, Katsiaryna Laziuk та Bindu Kanathezhath Sathi. "EF Bart’s Disease with Coinheritance of Gγ-XmnI and Aγ-Globin Polymorphisms: A Case of Nontransfusion-Dependant Thalassemia". Case Reports in Hematology 2020 (30 жовтня 2020): 1–5. http://dx.doi.org/10.1155/2020/8869335.

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EF Bart’s disease is a rare form of nontransfusion-dependant thalassemia (NTDT) due to the coinheritance of homozygous hemoglobin E (βE/βE) genotype with hemoglobin H disease. These individuals are routinely found to have thalassemia intermedia with moderate anemia, increased hemoglobin Bart’s and hemoglobin F on electrophoresis. The contribution of hemoglobin F-inducing polymorphisms in this disease has not been described previously. Here, we describe the hematological profile in a young child with coinheritance of Gγ-XmnI and Aγ-globin gene polymorphisms in EF Bart’s disease. Interestingly,

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28

Sae-ung, Nattaya, Hataichanok Srivorakun, Goonnapa Fucharoen, Supawadee Yamsri, Kanokwan Sanchaisuriya, and Supan Fucharoen. "Phenotypic expression of hemoglobins A2, E and F in various hemoglobin E related disorders." Blood Cells, Molecules, and Diseases 48, no. 1 (2012): 11–16. http://dx.doi.org/10.1016/j.bcmd.2011.09.008.

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29

Knapp, Esther E., Deepa Manwani, Abdullah Kutlar, Hillel W. Cohen, and Richard G. Ghalie. "Intra-Patient Variability in Fetal Hemoglobin Measurements over Time in Sickle Cell Disease Patients Not on Fetal Hemoglobin Inducing Agents." Blood 124, no. 21 (2014): 4096. http://dx.doi.org/10.1182/blood.v124.21.4096.4096.

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Abstract Introduction: We previously reported results of the placebo-controlled phase II study of the short-chain fatty acid derivative 2,2-dimethylbutyrate in inducing fetal hemoglobin (Hb F) in 76 patients with sickle cell disease (SCD). The primary endpoint was a comparison of Hb F levels in the treatment versus the placebo arms. Week 24 interim analyses revealed no statistically significant difference in change in Hb F levels between the 2 groups. We examined the placebo arm in order to assess untreated, intra-patient variability of Hb F%. Methods: Only Hb F values performed by HPLC at the

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30

Puukka, R., and M. Puukka. "Effect of hemoglobin F on measurements of hemoglobin A1c with physicians' office analyzers." Clinical Chemistry 40, no. 2 (1994): 342–43. http://dx.doi.org/10.1093/clinchem/40.2.342.

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31

Pakdee, Naruwat, Supawadee Yamsri, Goonnapa Fucharoen, Kanokwan Sanchaisuriya, Serge Pissard, and Supan Fucharoen. "Variability of hemoglobin F expression in hemoglobin EE disease: Hematological and molecular analysis." Blood Cells, Molecules, and Diseases 53, no. 1-2 (2014): 11–15. http://dx.doi.org/10.1016/j.bcmd.2014.02.005.

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32

Hò, Gia-Gia T., Wiebke Hiemisch, Andreas Pich, Georg M. N. Behrens, Rainer Blasczyk, and Christina Bade-Doeding. "The Loss of HLA-F/KIR3DS1 Ligation Is Mediated by Hemoglobin Peptides." International Journal of Molecular Sciences 21, no. 21 (2020): 8012. http://dx.doi.org/10.3390/ijms21218012.

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The human leukocyte antigen (HLA)-Ib molecule, HLA-F, is known as a CD4+ T-cell protein and mediator of HIV progression. While HLA-Ia molecules do not have the chance to select and present viral peptides for immune recognition due to protein downregulation, HLA-F is upregulated. Post HIV infection, HLA-F loses the affinity to its activating receptor KIR3DS1 on NK cells leading to progression of the HIV infection. Several studies aimed to solve the question of the biophysical interface between HLA ligands and their cognate receptors. It became clear that even an invariant HLA molecule can be st

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33

Chen, S. L. S. "Fecal Hemoglobin Concentrations and Personalized Screening for Colorectal Cancer." Journal of Global Oncology 4, Supplement 2 (2018): 212s. http://dx.doi.org/10.1200/jgo.18.85600.

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Background: Although cancer screening programs have been established in some Asian countries, resources are still insufficient to maintain high participation rates. The aim of this study was to assess whether any observed relationship persisted after adjusting for the pathologic stage of CRC to assess whether the increasing fecal hemoglobin (f-Hb) concentration on the risk of CRC death is partially explained by its intermediate influence on the pathologic stage of CRC and to propose the risk stratification by using f-Hb concentration for developing individual-tailored CRC screening. Methods: O

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34

Ekwattanakit, Supachai, Yuwarat Monteerarat, Suchada Riolueang, Kalaya Tachavanich, and Vip Viprakasit. "Association ofXmnI Polymorphism and Hemoglobin E Haplotypes on Postnatal Gamma Globin Gene Expression in Homozygous Hemoglobin E." Advances in Hematology 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/528075.

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Background and Objectives. To explore the role ofcis-regulatory sequences within theβglobin gene cluster at chromosome 11 on humanγglobin gene expression related to Hb E allele, we analyze baseline hematological data and Hb F values together withβglobin haplotypes in homozygous Hb E.Patients and Methods. 80 individuals with molecularly confirmed homozygous Hb E were analyzed for theβglobin haplotypes andXmnI polymorphism using PCR-RFLPs. 74 individuals with complete laboratory data were further studied for association analyses.Results. Eight differentβglobin haplotypes were found linked to Hb

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35

Poillon, W. N., B. C. Kim, G. P. Rodgers, C. T. Noguchi, and A. N. Schechter. "Sparing effect of hemoglobin F and hemoglobin A2 on the polymerization of hemoglobin S at physiologic ligand saturations." Proceedings of the National Academy of Sciences 90, no. 11 (1993): 5039–43. http://dx.doi.org/10.1073/pnas.90.11.5039.

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36

Awasthi, Vikky, Debprasad Chattopadhyay, and Jyoti Das. "Potential Hemoglobin A/F role in clinical Malaria." Bioinformation 13, no. 08 (2017): 269–73. http://dx.doi.org/10.6026/97320630013269.

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37

Mendek-Czajkowska, E., M. Słomkowski, E. Zdebska, et al. "Hemoglobin F in primary myelofibrosis and in myelodysplasia." Clinical & Laboratory Haematology 25, no. 5 (2003): 289–92. http://dx.doi.org/10.1046/j.1365-2257.2003.00537.x.

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38

Hoyer, James D., Connie S. Penz, Virgil F. Fairbanks, Curtis A. Hanson, and Jerry A. Katzmann. "Flow Cytometric Measurement of Hemoglobin F in RBCs." American Journal of Clinical Pathology 117, no. 6 (2002): 857–63. http://dx.doi.org/10.1309/a63x-hg9t-vyg2-x6tx.

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39

Bunn, HF. "Subunit assembly of hemoglobin: an important determinant of hematologic phenotype." Blood 69, no. 1 (1987): 1–6. http://dx.doi.org/10.1182/blood.v69.1.1.1.

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Abstract Hemoglobin's physiologic properties depend on the orderly assembly of its subunits in erythropoietic cells. The biosynthesis of alpha- and beta-globin polypeptide chains is normally balanced. Heme rapidly binds to the globin subunit, either during translation or shortly thereafter. The formation of the alpha beta-dimer is facilitated by electrostatic attraction of a positively charged alpha-subunit to a negatively charged beta-subunit. The alpha beta-dimer dissociates extremely slowly. The difference between the rate of dissociation of alpha beta- and alpha gamma-dimers with increasin

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40

Bunn, HF. "Subunit assembly of hemoglobin: an important determinant of hematologic phenotype." Blood 69, no. 1 (1987): 1–6. http://dx.doi.org/10.1182/blood.v69.1.1.bloodjournal6911.

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Hemoglobin's physiologic properties depend on the orderly assembly of its subunits in erythropoietic cells. The biosynthesis of alpha- and beta-globin polypeptide chains is normally balanced. Heme rapidly binds to the globin subunit, either during translation or shortly thereafter. The formation of the alpha beta-dimer is facilitated by electrostatic attraction of a positively charged alpha-subunit to a negatively charged beta-subunit. The alpha beta-dimer dissociates extremely slowly. The difference between the rate of dissociation of alpha beta- and alpha gamma-dimers with increasing pH expl

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41

Cox, Tina, P. Patrick Hess, Gerald D. Thompson, and Stanley S. Levinson. "Interference with Glycated Hemoglobin by Hemoglobin F May Be Greater Than Is Generally Assumed." American Journal of Clinical Pathology 99, no. 2 (1993): 137–41. http://dx.doi.org/10.1093/ajcp/99.2.137.

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42

Vichinsky, Elliott. "Hemoglobin E Syndromes." Hematology 2007, no. 1 (2007): 79–83. http://dx.doi.org/10.1182/asheducation-2007.1.79.

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Abstract Hemoglobin (Hb) E is one of the world’s most common and important mutations. It results in a heterogeneous group of disorders whose phenotype range from asymptomatic to severe. Hb E trait and Hb EE are mild disorders. The combination of Hb E and Hb S (Hb SE) results in a sickle cell disease syndrome similar to sickle β+ thalassemia. It is important to distinguish Hb E disorders diagnostically because of this marked difference in clinical course among different genotypes. Screening tests, including hemoglobin electrophoresis and high-pressure liquid chromatography (HPLC), may suggest o

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43

Blau, CA, P. Constantoulakis, A. al-Khatti, et al. "Fetal hemoglobin in acute and chronic states of erythroid expansion." Blood 81, no. 1 (1993): 227–33. http://dx.doi.org/10.1182/blood.v81.1.227.227.

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Abstract Physiologic principles underlying the differences in fetal hemoglobin (HbF) induction between acute and chronic states of erythroid expansion are poorly understood. Whereas abrupt erythroid expansion is characterized by a high proportion of reticulocytes coexpressing adult and fetal globin (F reticulocytes), HbF levels wane with chronic erythropoietic stimulation. To investigate this phenomenon, we used various schedules of erythropoietin (epo) administration in primates. Acute intravenous epo administration promoted a 2- to 10-fold preferential induction of F reticulocytes compared w

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44

Blau, CA, P. Constantoulakis, A. al-Khatti, et al. "Fetal hemoglobin in acute and chronic states of erythroid expansion." Blood 81, no. 1 (1993): 227–33. http://dx.doi.org/10.1182/blood.v81.1.227.bloodjournal811227.

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Physiologic principles underlying the differences in fetal hemoglobin (HbF) induction between acute and chronic states of erythroid expansion are poorly understood. Whereas abrupt erythroid expansion is characterized by a high proportion of reticulocytes coexpressing adult and fetal globin (F reticulocytes), HbF levels wane with chronic erythropoietic stimulation. To investigate this phenomenon, we used various schedules of erythropoietin (epo) administration in primates. Acute intravenous epo administration promoted a 2- to 10-fold preferential induction of F reticulocytes compared with total

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45

Nakazawa, M., MT Mitjavila, N. Debili, et al. "KU 812: a pluripotent human cell line with spontaneous erythroid terminal maturation." Blood 73, no. 7 (1989): 2003–13. http://dx.doi.org/10.1182/blood.v73.7.2003.2003.

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Abstract A human leukemic cell line KU 812 was recently established and described as a basophilic cell line. In the present study we show that KU 812 and two of its clones are at least bipotent: in addition to a minor component of basophils, the majority of KU 812 cells belongs to the erythroid cell lineage with a significant percentage (about 15%) of mature hemoglobinized erythroblasts. This terminal differentiation is associated with the synchronized synthesis of the main erythroid proteins, including glycophorins, spectrin beta chain, band 3, and hemoglobin. The predominant hemoglobins are

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Nakazawa, M., MT Mitjavila, N. Debili, et al. "KU 812: a pluripotent human cell line with spontaneous erythroid terminal maturation." Blood 73, no. 7 (1989): 2003–13. http://dx.doi.org/10.1182/blood.v73.7.2003.bloodjournal7372003.

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Abstract:

A human leukemic cell line KU 812 was recently established and described as a basophilic cell line. In the present study we show that KU 812 and two of its clones are at least bipotent: in addition to a minor component of basophils, the majority of KU 812 cells belongs to the erythroid cell lineage with a significant percentage (about 15%) of mature hemoglobinized erythroblasts. This terminal differentiation is associated with the synchronized synthesis of the main erythroid proteins, including glycophorins, spectrin beta chain, band 3, and hemoglobin. The predominant hemoglobins are adult, fe

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Cuellar, Carmen. "Hemoglobin and Cholesterol Affect Apparent Tacrolimus Clearance in Pediatric Transplant Recipients – a Retrospective Cohort Study." Pharmaceutics and Pharmacology Research 4, no. 2 (2021): 01–07. http://dx.doi.org/10.31579/2693-7247/015.

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Introduction: Tacrolimus has a narrow therapeutic index with substantial inter- and intra-patient variability. Factors beyond genetic and developmental factors are poorly understood. Recent adult studies suggest that hemoglobin affects the apparent clearance (CL/F), whereas this and other potential factors in children are understudied. Methods: After ethics approval, we performed a single center retrospective cohort study of pediatric renal transplant recipients, who were followed between January 1st, 2004, and June 30th, 2018. Patients without tacrolimus therapy or concomitant sirolimus were

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Zainuddin, Viviyanti, Agus Alim Abdullah, and Mansyur Arif. "TALASEMIA BETA HEMOGLOBIN E (Hemoglobin E Beta Thalassemia)." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 21, no. 3 (2018): 309. http://dx.doi.org/10.24293/ijcpml.v21i3.1286.

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Thalassemia is a quantitative abnormality of the hemoglobin marked by inadequate hemoglobin synthesis due to the lack orabsence of synthesis of one or more globin polypeptide chains. Hemoglobin variant is a qualitative abnormality due to the presence ofthe abnormal amino acid sequence of one or more globin polypeptide chains. HbE β thalassemia is a disorder of hemoglobin that resultsfrom the fusion between the gene β-thalassemia allele from one parent with a gene HbE allele from another parent. In this case, HbEβ-Thalassemia patient was a 4.8 year girl diagnosed with hemoglobin E-beta thalasse

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Piel, Frédéric B., Thomas V. Adamkiewicz, Djesika Amendah, Thomas N. Williams, Sunetra Gupta, and Scott D. Grosse. "Observed and expected frequencies of structural hemoglobin variants in newborn screening surveys in Africa and the Middle East: deviations from Hardy-Weinberg equilibrium." Genetics in Medicine 18, no. 3 (2015): 265–74. http://dx.doi.org/10.1038/gim.2015.143.

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Abstract Purpose: Our objective was to compare observed and expected genotype proportions from newborn screening surveys of structural hemoglobin variants. Methods: We conducted a systematic review of newborn screening surveys of hemoglobins S and C in Africa and the Middle East. We compared observed frequencies to those expected assuming Hardy-Weinberg equilibrium (HWE). Significant deviations were identified by an exact test. The fixation index F IS was calculated to assess excess homozygosity. We compared newborn estimates corrected and uncorrected for HWE deviations using demographic data.

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Saylor, Philip J., Chris Bornhauser, and William Read. "Cancer Treatment with Gemcitabine Does Not Increase Fetal Hemoglobin Levels." Blood 114, no. 22 (2009): 5112. http://dx.doi.org/10.1182/blood.v114.22.5112.5112.

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Abstract Abstract 5112 Background Pharmacological induction of fetal hemoglobin (Hb F) can benefit patients with beta-hemoglobinopathies. Hydroxyurea (HU) is the drug most commonly used to induce Hb F. HU is converted to a free radical scavenger in vivo and inhibits the R2 subunit of ribonucleotide reductase. When used in the treatment of myeloproliferative syndromes, HU has been described to increase Hb F in people without hemoglobinopathies (Alter et al, Blood 66(2) 373-5). Gemcitabine is a nucleoside analog chemotherapeutic that inhibits the large R1 subunit of ribonucleotide reductase. We

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