Relevant bibliographies by topics / Thalassemia

Academic literature on the topic 'Thalassemia'

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Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Thalassemia"

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Pattanapanyasat, Kovit, Kosol Yongvanitchit, Pongsri Tongtawe, Kalaya Tachavanich, Wanchai Wanachiwanawin, Suthat Fucharoen, and Douglas S. Walsh. "Impairment of Plasmodium falciparum Growth in Thalassemic Red Blood Cells: Further Evidence by Using Biotin Labeling and Flow Cytometry." Blood 93, no. 9 (May 1, 1999): 3116–19. http://dx.doi.org/10.1182/blood.v93.9.3116.

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Abstract Certain red blood cell (RBC) disorders, including thalassemia, have been associated with an innate protection against malaria infection. However, many in vitro correlative studies have been inconclusive. To better understand the relationship between human RBCs with thalassemia hemoglobinopathies and susceptibility to in vitro infection, we used an in vitro coculture system that involved biotin labeling and flow cytometry to study the ability of normal and variant RBC populations in supporting the growth of Plasmodium falciparum malaria parasites. Results showed that both normal and thalassemic RBCs were susceptible to P falciparum invasion, but the parasite multiplication rates were significantly reduced in the thalassemic RBC populations. The growth inhibition was especially marked in RBCs from -thalassemia patients (both -thalassemia1/-thalassemia2 and -thalassemia1 heterozygote). Our observations support the contention that thalassemia confers protection against malaria and may explain why it is more prevalent in malaria endemic areas.
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Pattanapanyasat, Kovit, Kosol Yongvanitchit, Pongsri Tongtawe, Kalaya Tachavanich, Wanchai Wanachiwanawin, Suthat Fucharoen, and Douglas S. Walsh. "Impairment of Plasmodium falciparum Growth in Thalassemic Red Blood Cells: Further Evidence by Using Biotin Labeling and Flow Cytometry." Blood 93, no. 9 (May 1, 1999): 3116–19. http://dx.doi.org/10.1182/blood.v93.9.3116.409a37_3116_3119.

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Certain red blood cell (RBC) disorders, including thalassemia, have been associated with an innate protection against malaria infection. However, many in vitro correlative studies have been inconclusive. To better understand the relationship between human RBCs with thalassemia hemoglobinopathies and susceptibility to in vitro infection, we used an in vitro coculture system that involved biotin labeling and flow cytometry to study the ability of normal and variant RBC populations in supporting the growth of Plasmodium falciparum malaria parasites. Results showed that both normal and thalassemic RBCs were susceptible to P falciparum invasion, but the parasite multiplication rates were significantly reduced in the thalassemic RBC populations. The growth inhibition was especially marked in RBCs from -thalassemia patients (both -thalassemia1/-thalassemia2 and -thalassemia1 heterozygote). Our observations support the contention that thalassemia confers protection against malaria and may explain why it is more prevalent in malaria endemic areas.
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Olivieri, O., L. De Franceschi, MD Capellini, D. Girelli, R. Corrocher, and C. Brugnara. "Oxidative damage and erythrocyte membrane transport abnormalities in thalassemias." Blood 84, no. 1 (July 1, 1994): 315–20. http://dx.doi.org/10.1182/blood.v84.1.315.bloodjournal841315.

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Oxidative damage induced by free globin chains has been implicated in the pathogenesis of the membrane abnormalities observed in alpha and beta thalassemia. We have evaluated transport of Na+ and K+ in erythrocytes of patients with thalassemias as well as in two experimental models that use normal human red blood cells, one for alpha thalassemia (methylhydrazine treatment, alpha thalassemia like) and one for beta thalassemia (phenylhydrazine treatment, beta thalassemia like). With the exception of the Na-K pump, similar alterations in membrane transport were observed in thalassemia and thalassemia-like erythrocytes. These were: increased K-Cl cotransport, Na-Li countertransport and reduced Na-K-Cl cotransport. The Na-K pump was reduced in thalassemia-like cells, whereas it was increased in severe alpha thalassemia and in beta thalassemia cells. The increased K- Cl cotransport activity could be observed in light and dense fractions of beta-thalassemic cells. K-Cl cotransport in thalassemic and thalassemia-like erythrocytes was partially inhibited by [(dihydro- indenyl) oxy] alkanoic acid and completely abolished by dithiothreitol. Thus, oxidative damage represents an important factor in the increased activity of the K-Cl cotransport observed in thalassemias, and of the K+ loss observed in beta-thalassemia erythrocytes.
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Olivieri, O., L. De Franceschi, MD Capellini, D. Girelli, R. Corrocher, and C. Brugnara. "Oxidative damage and erythrocyte membrane transport abnormalities in thalassemias." Blood 84, no. 1 (July 1, 1994): 315–20. http://dx.doi.org/10.1182/blood.v84.1.315.315.

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Abstract Oxidative damage induced by free globin chains has been implicated in the pathogenesis of the membrane abnormalities observed in alpha and beta thalassemia. We have evaluated transport of Na+ and K+ in erythrocytes of patients with thalassemias as well as in two experimental models that use normal human red blood cells, one for alpha thalassemia (methylhydrazine treatment, alpha thalassemia like) and one for beta thalassemia (phenylhydrazine treatment, beta thalassemia like). With the exception of the Na-K pump, similar alterations in membrane transport were observed in thalassemia and thalassemia-like erythrocytes. These were: increased K-Cl cotransport, Na-Li countertransport and reduced Na-K-Cl cotransport. The Na-K pump was reduced in thalassemia-like cells, whereas it was increased in severe alpha thalassemia and in beta thalassemia cells. The increased K- Cl cotransport activity could be observed in light and dense fractions of beta-thalassemic cells. K-Cl cotransport in thalassemic and thalassemia-like erythrocytes was partially inhibited by [(dihydro- indenyl) oxy] alkanoic acid and completely abolished by dithiothreitol. Thus, oxidative damage represents an important factor in the increased activity of the K-Cl cotransport observed in thalassemias, and of the K+ loss observed in beta-thalassemia erythrocytes.
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Jha, R. "Distribution of hemoglobinopathies in patients presenting for electrophoresis and comparison of result with High performance liquid chromatography." Journal of Pathology of Nepal 5, no. 10 (September 14, 2015): 850–58. http://dx.doi.org/10.3126/jpn.v5i10.15642.

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Background: Nearly 226 million carriers of thalassemias and abnormal hemoglobin are present worldwide according to the World Health Organization (WHO). The laboratory plays an important role in the investigation of the thalassemias and hemoglobinopathies. Cellulose acetate electrophoresis at alkaline pH and diagnosis based mainly on visual impression of thickness of band may miss the thalassemic trait patients. The aim of this study was to find out different hemoglobinopathies and thalassemia presenting in our hospital and to compare electrophoresis results with HPLC.Materials and Methods: This study was performed in the hematopathology section of Department of Pathology of Tribhuvan University Teaching Hospital on cases sent for electrophoresis during 18 months period from October 2013 to March 2015 and included hemoglobinopathies and thalassemias identified by either electrophoresis or HPLC. 97 cases fulfilled the inclusion criteria and thus were included in the study. Electrophoresis at alkaline pH was done in all whereas HPLC was performed in 27 cases.Results: A sharp peak of hemoglobinopathies and thalassemias was seen in Tharu community though other communities are also affected. Thalassemia trait was the most common diagnosis (26.8%) followed by sickle cell anemia (21.6%). Electrophoresis was efficient in detecting some alpha thalassemia variants but missed many cases of beta thalassemia trait.Conclusion: Beta Thalassemia trait and sickle cell anemia both are common in Nepal , along with some other hemoglobinopathies A sharp peak of hemoglobinopathies and thalassemias are seen in Tharu community. These abnormal hemoglobins and thalassemias are mainly seen in Terai region. Electrophoresis fails to quantify hemoglobin percentage and thus is not appropriate test in beta thalassemia screening.
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De Sanctis, Vincenzo. "CONCISE REVIEW ON THE FREQUENCY, MAJOR RISK FACTORS AND SURVEILLANCE OF HEPATOCELLULAR CARCINOMA (HCC) IN Β-THALASSEMIAS: PAST, PRESENT AND FUTURE PERSPECTIVES." Mediterranean Journal of Hematology and Infectious Diseases 12, no. 1 (January 1, 2020): e2020006. http://dx.doi.org/10.4084/mjhid.2020.006.

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Due to the recent alarming increase in the incidence of hepatocellular carcinoma (HCC) in thalassemias, the aim of the present report is to review briefly the frequency, the major risk factors and the surveillance of HCC in β-thalassemias. Over the past 33 years, 153 cases of HCC were reported in patients with thalassemia, mainly in Italy, and Greece. Among HCV-infected patients additional factors promoting development of HCC, included: advanced age, male sex, chronic hepatitis B (CHB) coinfection, and iron overload. For early diagnosis of HCC sequential ultrasound screening is recommended especially for thalassemia patients with chronic hepatitis C (CHC), that coincide with (one or more) additional risk factors for HCC. Here we report also the preliminary data of thalassemic patients, above the age of 30 years, followed in 13 different centers. The total number of enrolled patients was 1,313 (males: 612 and 701 females). The prevalence of HCC in thalassemia major patients [characterized by transfusion-dependency (TDT)] and thalassemia intermedia [characterized by nontransfusion dependency (NTDT)] was 1.68 % and 1.98 % ,respectively The lowest age at diagnosis was 36 years in TDT and 47 years in NTDT patients.We hope that our review can be used to develop more refined and prospective analyses of HCC magnitude and risk in patients with thalassemia, and to define specific international guidelines to support clinicians for an early diagnosis and treatment of HCC in thalassemic patients.
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Sunarto, Sunarto. "Prenatal Diagnosis of Thalassemia." Paediatrica Indonesiana 33, no. 7-8 (January 24, 2019): 191–9. http://dx.doi.org/10.14238/pi33.7-8.1993.191-9.

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Thalassemia is an individual as well as a community health problem in some countries. It causes a lifelong suffering for the affected individuals. There is no treatment other than supportive, i.e. regular transfusions and removal of iron overload from the body. Only by such continuous and expensive treatment thalassemic patients can-generally achieve nearly normal health, but the health burden of such therapy for a large number of thalassemic patients is unaffordable by the affected communities. Prevention of the births of thalassemic babies is the choice for controlling the thalassemia and has been successful in many countries. For this purpose reliable and time accurate prenatal diagnosis is a conditio sine qua non. Blood fetal sampling is safe and can be done after 16 weeks gestation, amniocentesis after 14 weeks, and even chorionic villi sampling as early as 8 weeks gestation. In vitro globin synthesis analysis applied to the fetal blood sample is very reliable to measure the rate of synthesis of the globin chains that make up the hemoglobin. The-DNA analysis of the fibroblasts obtained by amniocentesis or of the chorionic villus sample is very sensitive and specific for the diagnosis of the genetic disorder in thalassemias. By involving the prenatal diagnosis, the birth of B-homozygous thalassemia has decreased by up to 90%.
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Advani, R., S. Sorenson, E. Shinar, W. Lande, E. Rachmilewitz, and SL Schrier. "Characterization and comparison of the red blood cell membrane damage in severe human alpha- and beta-thalassemia." Blood 79, no. 4 (February 15, 1992): 1058–63. http://dx.doi.org/10.1182/blood.v79.4.1058.1058.

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Abstract The aim of the present work was to understand the pathophysiology of the severe human thalassemias as represented by beta-thalassemia intermedia and hemoglobin (Hb) H (alpha-thalassemia) disease. We have previously shown that the material properties of the red blood cell (RBC) and its membrane differ in severe alpha- and beta-thalassemia, and we now show that this difference is probably caused by accumulation of alpha-globin chains at the cytoskeleton in beta-thalassemia, whereas beta-globin chains are associated with the cytoskeleton in alpha- thalassemia. In both alpha- and beta-thalassemia, some of these globin chains have become oxidized as evidenced by loss of the free thiols. Furthermore, there is similar evidence of oxidation of protein 4.1 in beta-thalassemia, whereas beta-spectrin appears to be subject to oxidation in alpha-thalassemia. These observations support the idea that the association of partly oxidized globin chains with the cytoskeleton results in oxidation of adjacent skeletal proteins. The abnormality of protein 4.1 in beta-thalassemia is consistent with a prior observation, and is also in accord with the known importance of protein 4.1 in maintenance of membrane stability, a property that is abnormal in beta-thalassemic membranes.
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Advani, R., S. Sorenson, E. Shinar, W. Lande, E. Rachmilewitz, and SL Schrier. "Characterization and comparison of the red blood cell membrane damage in severe human alpha- and beta-thalassemia." Blood 79, no. 4 (February 15, 1992): 1058–63. http://dx.doi.org/10.1182/blood.v79.4.1058.bloodjournal7941058.

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The aim of the present work was to understand the pathophysiology of the severe human thalassemias as represented by beta-thalassemia intermedia and hemoglobin (Hb) H (alpha-thalassemia) disease. We have previously shown that the material properties of the red blood cell (RBC) and its membrane differ in severe alpha- and beta-thalassemia, and we now show that this difference is probably caused by accumulation of alpha-globin chains at the cytoskeleton in beta-thalassemia, whereas beta-globin chains are associated with the cytoskeleton in alpha- thalassemia. In both alpha- and beta-thalassemia, some of these globin chains have become oxidized as evidenced by loss of the free thiols. Furthermore, there is similar evidence of oxidation of protein 4.1 in beta-thalassemia, whereas beta-spectrin appears to be subject to oxidation in alpha-thalassemia. These observations support the idea that the association of partly oxidized globin chains with the cytoskeleton results in oxidation of adjacent skeletal proteins. The abnormality of protein 4.1 in beta-thalassemia is consistent with a prior observation, and is also in accord with the known importance of protein 4.1 in maintenance of membrane stability, a property that is abnormal in beta-thalassemic membranes.
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Santos, Daniel Garcia, Marc Mikhael, Stefano Rivella, Monika Horvathova, and Prem Ponka. "Heme Oxygenase 1 Plays a Role In The Pathophysiology Of β-Thalassemia." Blood 122, no. 21 (November 15, 2013): 3449. http://dx.doi.org/10.1182/blood.v122.21.3449.3449.

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Abstract Thalassemias are a heterogeneous group of red blood cell disorders ranging from a clinically severe phenotype requiring life-saving transfusions (thalassemia major) to a relatively moderate symptomatic disorder, sometimes requiring transfusions (thalassemia intermedia). Thalassemia minor, the least severe form of the disorder, is characterized by minimal to mild symptoms. While thalassemia minor and intermedia are vastly more prevalent than thalassemia major, the latter is often fatal when not treated. Though considered a major cause of morbidity and mortality worldwide, there is still no universally available cure for this severe form of thalassemia. A reason for this is at least in part due to the lack of full understanding of pathophsyiology of thalassemia. The underlying cause of pathology in thalassemia is the premature apoptotic destruction of erythroblasts causing ineffective erythropoeisis. Normally, the assembly of adult hemoglobin (consisting of a tetramer of two α- and two β-globin chains) features a very tight coordination of α- and β-globin chain synthesis. However, in β-thalassemia, β-globin synthesis is decelerated causing α-globin accumulation; while in α-thalassemia the opposite scenario occurs. Unpaired globin chains that accumulate in thalassemic erythroblasts are bound to heme. In addition, in β-thalassemia an erythroid specific protease destroys excess α-globin chains, likely leading to the generation of a pool of “free” heme in erythroblasts. “Free” heme is toxic, but this toxicity will likely be augmented, if heme oxygenase 1 (HO-1) can release iron from heme. To date, virtually no information about the expression of HO-1 in erythroblasts has been produced; however, we have recently provided unequivocal evidence that this enzyme is present in several model erythroid cells1. Based on this novel and important finding, we hypothesize that in β-thalassemic erythroblasts HO-1 mediated release of iron from heme is the major culprit responsible for cellular damage. To test this hypothesis we exploited the mouse model of β-thalassemia, th3/+. Thus far, our data indicates that HO-1 expression is increased in liver, spleen and kidney of β-thalassemic mice compared to wild type mice. Importantly, we observed that Epo-mediated erythroid differentiation of fetal liver (FL) cells isolated from β-thalassemic fetuses, display increased levels of HO-1 as well as decreased phosphorylated eiF2-α. These results indicate that β-thalassemic erythroblasts have inappropriately high levels of unbound heme that is continuously degraded by HO-1. Further research is needed to determine whether HO-1 liberated iron is responsible for the damage of β-thalassemic erythroblasts. 1Garcia Santos D, Schranzhofer M, Bogo Chies JA, Ponka P. Heme Oxygenase 1 plays an unexpected role during erythroid differentiation. Blood (ASH Annual Meeting Abstracts) 118: 344, 2011. Disclosures: No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Thalassemia"

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Kwong, Yen-hwa Colinette. "Quality of life and psychosocial high risk factors in adolescents with Cooleys Anaemia /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B40163842.

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Chan, Yuk-yin. "Haematological and molecular studies of Thalassaemias in Hong Kong Chinese /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19657882.

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Popovich, Bradley W. (Bradley Wayne). "Molecular characterization of an atypical B-thalassemia." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=72818.

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Leung, Kwok-yin, and 梁國賢. "Prenatal ultrasound prediction of homozygous α⁰-thalassemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47454039.

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Homozygous α0-thalassemia is a serious autosomal recessive disorder with poor fetal outcome and severe maternal complications. Conventionally, prenatal diagnosis is performed by an invasive test. A non-invasive approach using serial ultrasonography can effectively reduce the need for invasive tests in unaffected pregnancies. For two-dimensional ultrasound prediction, a total of 777 at-risk fetuses were studied from 12 to 20 weeks between 1995 and 2006. At 12–15 weeks’ gestation, the highest sensitivity (98.3%) was achieved by the combination of fetal cardiothoracic ratio (CTR) and/or middle cerebral artery peak systolic velocity (MCA-PSV) at a false-positive rate of 15.8%. At 16–20 weeks’ gestation, the sensitivity of CTR was 100.0%, but the false-positive rate was 5.2%. In contrast, the false-positive rate of MCA-PSV alone was 1.4% and that of the combination of CTR and MCA-PSV was 0%, although their sensitivities were less than 65%. In a cross-sectional retrospective study of 546 samples at-risk and control (268 fetal and 278 neonatal cord blood), the degree of anemia was only mild in 27.5% of the affected fetuses (see chapter 3 for definition of mild anemia). Because MCA-PSV is not very predictive of mild anemia, this may be one of the reasons why MCA-PSV is not very sensitive in predicting an affected pregnancy. A total of 832 at-risk pregnancies were studied using same noninvasive approach at Maternal and Neonatal Hospital of Guangzhou (MNH) and Tsan Yuk Hospital (TYH). The overall sensitivity and specificity of the noninvasive approach was 100% and 95.6% respectively. At MNH, the need for an invasive test was reduced by 78.6%, and all the affected pregnancies were diagnosed before 24 weeks’ gestation. After adequate training and monitoring the quality of the subsequent ultrasound examinations, the results achieved at MNH were comparable to TYH, with at-risk pregnancies including the affected ones being seen at a more advanced gestation at MNH. In a retrospective review of 361 women at risk of carrying an affected fetus, 311 (86.2%) opted for the non-invasive approach using CTR and/or placenta. The cost saving of this non-invasive approach was relatively small (HK$ 2,651) in comparison to the cost of the whole prenatal screening program. On the other hand, the non-invasive approach was more expensive than the direct invasive approach for low MCV couples, as well as couples discordant for α-thalassemia and β-thalassemia. ages. These results support the adoption of non-invasive approach in which routine invasive test or karyotyping is no longer performed. A total of 106 at-risk pregnancies and normal controls were prospectively studied using three-dimensional ultrasonography. Placental volume (PV) at 11-14 weeks, and PV/CRL quotient at 9-14 weeks’ gestation of affected pregnancies were significantly greater than unaffected pregnancies (P<0.05). Using a cut-off point of 1.2ml/mm for PV/CRL quotient to predict an affected pregnancy, the sensitivity, and specificity was 96.2%, and 100.0% respectively.
published_or_final_version
Obstetrics and Gynaecology
Master
Doctor of Medicine
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Li, Ming-cheng Anita. "?thalassaemia in Hong Kong children." Click to view the E-thesis via HKUTO, 1998. http://sunzi.lib.hku.hk/hkuto/record/B43893879.

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Chan, Pui-wah Vicky. "Molecular genetics of Hb H disease in Hong Kong Chinese." Click to view the E-thesis via HKUTO, 2003. http://sunzi.lib.hku.hk/hkuto/record/B31970904.

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Ma, Victor. "Laboratory diagnosis of ( --SEA) alpha-thalassaemia deletion." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2337312x.

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Yang, Dongya. "DNA diagnosis of thalassemia from ancient Italian skeletons." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0005/NQ42773.pdf.

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Yang, Dongya. "DNA diagnosis of thalassemia from ancient Italian skeletons /." *McMaster only, 1997.

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Efremov, Dimitar Georgi. "Correlation of genotype and phenotype in [beta]-thalassemia." [Maastricht : Maastricht : Rijksuniversiteit Limburg] ; University Library, Maastricht University [Host], 1994. http://arno.unimaas.nl/show.cgi?fid=6614.

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Books on the topic "Thalassemia"

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P, Vichinsky Elliott, and New York Academy of Sciences., eds. Cooley's anemia: Eighth symposium. New York, N.Y: New York Academy of Sciences, 2005.

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2

Papavasiliou, Constantin, Theophanis Cambouris, and Phaedon Fessas, eds. Radiology of Thalassemia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-72587-6.

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1926-, Papavasiliou C., Cambouris Th 1930-, and Fessas Ph, eds. Radiology of thalassemia. Berlin: Springer-Verlag, 1989.

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Andò, Sebastiano, and Carlo Brancati, eds. Endocrine Disorders in Thalassemia. Milano: Springer Milan, 1995. http://dx.doi.org/10.1007/978-88-470-2183-9.

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Fucharoen, Suthat, Mahāwitthayālai Mahidon. Khrōngkān Sūn Thālatsīmīa., Society of Hematology of Thailand., March of Dimes Birth Defects Foundation., and International Conference on Thalassemia (1985 : Bangkok, Thailand), eds. Thalassemia: Pathophysiology and management. New York: A.R. Liss, 1988.

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T, Chirban John, ed. Thalassemia: An interdisciplinary approach. Lanham: University Press of America, 1986.

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Bank, Arthur. Turning blood red: The fight for life in Cooley's anemia. Hackensack, NJ: World Scientific, 2009.

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Vullo, Rino. What is thalassaemia? 2nd ed. Nicosia: Thalassaemia International Federation, 1995.

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Cooley's Anemia Symposium (9th 2009 New York Academy of Sciences). Cooley's anemia: Ninth symposium. Edited by Neufeld Ellis Jacob and Vichinsky Elliott P. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2010.

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Canali, Stefano. Talassemie: Storia medica e scientifica. Pisa: ETS, 2012.

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Book chapters on the topic "Thalassemia"

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Richard, Nameeta P., Kristina M. Haley, and Michael Recht. "Thalassemia." In Textbook of Clinical Pediatrics, 3029–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_326.

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Zheng, Xiwen, and Suzanne K. W. Mankowitz. "Thalassemia." In Consults in Obstetric Anesthesiology, 589–92. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-59680-8_158.

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Chen, Harold. "Thalassemia." In Atlas of Genetic Diagnosis and Counseling, 1–14. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6430-3_227-2.

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Shamoun, Mark, and Michael Callaghan. "Thalassemia." In Benign Hematologic Disorders in Children, 91–98. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-49980-8_6.

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Kulozik, A. E., and A. Deters. "Thalassemia." In Practical Algorithms in Pediatric Hematology and Oncology, 24–25. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000069584.

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Chen, Harold. "Thalassemia." In Atlas of Genetic Diagnosis and Counseling, 2739–52. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-2401-1_227.

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Pritchard, Colin C., and Jonathan F. Tait. "Alpha Thalassemia." In Diagnostic Molecular Pathology in Practice, 17–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-19677-5_3.

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Qidwai, Tabish. "Alpha-Thalassemia." In Exploration of Host Genetic Factors associated with Malaria, 29–42. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4761-8_3.

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Qidwai, Tabish. "Beta-Thalassemia." In Exploration of Host Genetic Factors associated with Malaria, 43–53. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4761-8_4.

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Raj, Satish R., S. R. Wayne Chen, Robert S. Sheldon, Arti N. Shah, Bharat K. Kantharia, Ulrich Salzer, Bodo Grimbacher, et al. "Thalassemia Syndromes." In Encyclopedia of Molecular Mechanisms of Disease, 2041–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1731.

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Conference papers on the topic "Thalassemia"

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SHARBA, Intisar Razzaq, and Arshad Noori AL-DUJAILI. "ASSESSMENT OF SERUM SCLEROSTIN LEVEL AS A BIOMARKER ASSOCIATED WITH BONE DISORDERS IN Β-THALASSEMIA PATIENTS IN AL- NAJAF CITY, IRAQ." In SOUTHERN BRAZILIAN JOURNAL OF CHEMISTRY 2021 INTERNATIONAL VIRTUAL CONFERENCE. DR. D. SCIENTIFIC CONSULTING, 2022. http://dx.doi.org/10.48141/sbjchem.21scon.05_abstract_sharba.pdf.

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Abstract:
Aim of the study: To assess serum sclerostin in female patients with beta-thalassemia and compare with the healthy controls and to predict its complication associated with the bone pathophysiology, for designed improvement the lifestyle goodliness for these patients. Material and methods: Sixty-nine female beta-thalassemia (βT) patients (54 βT major and 15 βT Intermedia), aged 8-40 years who dependent on transfused blood, and 20 healthy controls were evaluated serum sclerostin, and was examined the relationship with hematological parameters RBC, Hb, PCV, WBC, PLT, BMI, splenic status, iron, and ferritin levels. The information of beta-thalassemia patients was collected and recorded by the questioner. Results: A significantly increased serum sclerostin level (mean 26.80±0.91) pg/ml was shown in βT patients compared with the healthy controls (10.03±0.68, p < 0.001) pg/ml. Furthermore, a significant decrease (p<0.05) of the sclerostin level was observed in β-thalassemia major compared to intermedia β-thalassemia patients. Serum sclerostin level revealed a significant increase in progress age; it is highest in the age group (30-40) year as compared with age group (8-18) and (19-29) year respectively. Sclerostin showed no associations with the RBC, Hb, PCV, and significantly positively correlated (p<0.05) with serum iron, ferritin levels, WBC, and PLT count. Significantly higher sclerostin levels in splenectomized and underweight groups were observed compared to unsplenectomized and normal-weight groups (p<0.05) of βT patients. Conclusion: Sclerostin plays an important role in beta-thalassemia patients and can serve as a biomarker associated with the bone pathophysiology and indicator to prevent the continuation of such serious diseases caused by iron overload in these patients.
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"PSYCHOSOCIAL PRESSURES OF HAVING BETA-THALASSEMIA." In International Psychological Applications Conference and Trends. inScience Press, 2023. http://dx.doi.org/10.36315/2023inpact097.

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Devanath, Ananyna, Shahnaz Akter, Pushpita Karmaker, and Abdus Sattar. "Thalassemia Prediction using Machine Learning Approaches." In 2022 6th International Conference on Computing Methodologies and Communication (ICCMC). IEEE, 2022. http://dx.doi.org/10.1109/iccmc53470.2022.9753833.

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El-Sebakhy, E. A., and M. A. Elshafei. "Thalassemia Screening using Unconstrained Functional Networks Classifier." In 2007 IEEE International Conference on Signal Processing and Communications. IEEE, 2007. http://dx.doi.org/10.1109/icspc.2007.4728497.

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Bal, Parveen, Shahir Shamsir, Nabil Warid, Azli Yahya, Jasmy Yunus, Eko Supriyanto, and Chin Fang Ngim. "MHealth application: Mobile thalassemia patient management application." In 2014 IEEE Conference on Biomedical Engineering and Sciences (IECBES). IEEE, 2014. http://dx.doi.org/10.1109/iecbes.2014.7047618.

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Blay, C., A. Siddiqui, C. Butler, and R. Reddy. "Pulmonary Hypertension Secondary to Beta-Thalassemia Major." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3605.

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Sa'id, Alva Andhika, Zuherman Rustam, Fevi Novkaniza, Qisthina Syifa Setiawan, Faisa Maulidina, and Velery Virgina Putri Wibowo. "Twin Support Vector Machines for Thalassemia Classification." In 2021 International Conference on Innovation and Intelligence for Informatics, Computing, and Technologies (3ICT). IEEE, 2021. http://dx.doi.org/10.1109/3ict53449.2021.9581956.

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Xu, Wenlin, Yaolian Song, and Tuanbiao Zou. "Prediction of Thalassemia Based on SAELM Hybrid Algorithm." In 2019 3rd International Conference on Data Science and Business Analytics (ICDSBA). IEEE, 2019. http://dx.doi.org/10.1109/icdsba48748.2019.00054.

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Tancredi, M., and J. Gagermeier. "Beta-Thalassemia Minor Presenting as Atraumatic Splenic Rupture." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1748.

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Warid, Muhammad Nabil Mohd, Eko Supriyanto, Azli Yahya, Mohd Nizam Mat Bah, and Ngim Chin Fang. "Online framework for thalassemia medical record management system." In SECOND INTERNATIONAL CONFERENCE OF MATHEMATICS (SICME2019). Author(s), 2019. http://dx.doi.org/10.1063/1.5096740.

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