1,733,987 research outputs found
AGenDA: gene prediction by cross-species sequence comparison
Full text linkTaher L, Rinner O, Garg S, Sczyrba A, Morgenstern B. AGenDA: gene prediction by cross-species sequence comparison. Nucleic Acids Research. 2004;32(Web Server):W305-W308.Automatic gene prediction is one of the major challenges in computational sequence analysis. Traditional approaches to gene finding rely on statistical models derived from previously known genes. By contrast, a new class of comparative methods relies on comparing genomic sequences from evolutionary related organisms to each other. These methods are based on the concept of phylogenetic footprinting: they exploit the fact that functionally important regions in genomic sequences are usually more conserved than non-functional regions. We created a WWW-based software program for homology-based gene prediction at BiBiServ (Bielefeld Bioinformatics Server). Our tool takes pairs of evolutionary related genomic sequences as input data, e.g. from human and mouse. The server runs CHAOS and DIALIGN to create an alignment of the input sequences and subsequently searches for conserved splicing signals and start/stop codons near regions of local sequence conservation. Genes are predicted based on local homology information and splice signals. The server returns predicted genes together with a graphical representation of the underlying alignment. The program is available at http://bibiserv.TechFak.Uni-Bielefeld.DE/agenda/
Interview with Salah Taher
No full textفي هذه المقابلة، يتحدث صلاح طاهر، رائد الفن التجريدي في مصر، عن لقائه بالأديب المصري عباس محمود العقاد. أجرى المقابلة حسن شمس الدين.In this interview, Salah Taher, a pioneer of abstract art in Egypt, recounts meeting Egyptian author Abbas Mahmoud al-Akkad. The interview was conducted by Hassan Shams al-Din
Management of Non-Transfusion-Dependent Thalassemia: A Practical Guide
No full textDespite their transfusion-independence, non-transfusion-dependent thalassemia (NTDT) patients experience a variety of serious clinical complications that require prompt and comprehensive management. Transfusion therapy may still be an important part of management of this disease, in cases of acute stress, to support growth and development in childhood, or to prevent clinical morbidities stemming from ineffective erythropoiesis or hemolytic anemia. Although splenectomy is associated with improvements in hemoglobin levels, it leads to several short- and long-term adverse events, warranting caution in application of this intervention. Fetal hemoglobin induction therapy has been evaluated in non-randomized studies, with benefits extending beyond hematologic improvements to lowering morbidity risk. Effective and safe iron chelation therapy is now available for NTDT patients in whom iron overload develops, irrespective of transfusions, due to increased intestinal absorption, ultimately leading to clinically high iron burden levels and subsequent morbidity. Optimal management of NTDT patients requires a holistic approach targeting all hallmarks of the disease to ensure favorable patient outcomes.Akrawinthawong K, 2011, HEMATOLOGY, V16, P113, DOI 10.1179-102453311X12940641877768; Allen A, 2010, BLOOD, V116, P5368, DOI 10.1182-blood-2010-06-289488; Amoozgar H, 2011, EUR J HAEMATOL, V87, P61, DOI 10.1111-j.1600-0609.2011.01620.x; Angelucci E, 2000, NEW ENGL J MED, V343, P327, DOI 10.1056-NEJM200008033430503; Cappellini MD, 2012, EXPERT REV HEMATOL, V5, P505, DOI [10.1586-ehm.12.42, 10.1586-EHM.12.42]; Cappellini MD, 2012, BLOOD REV, V26, pS20, DOI 10.1016-S0268-960X(12)70007-3; Cappellini MD, 2000, BRIT J HAEMATOL, V111, P467, DOI 10.1046-j.1365-2141.2000.02376.x; Cavazzana-Calvo M, 2010, NATURE, V467, P318, DOI 10.1038-nature09328; CAZZOLA M, 1995, BRIT J HAEMATOL, V89, P473, DOI 10.1111-j.1365-2141.1995.tb08351.x; CAZZOLA M, 1987, BLOOD, V69, P296; CAZZOLA M, 1987, HAEMATOLOGICA, V72, P195; Chan JCW, 2006, BRIT J HAEMATOL, V133, P198, DOI 10.1111-j.1365-2141.2006.05984.x; 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Thrombosis in thalassemia: Why are we so concerned?
No full textAlthough life expectancy of thalassemia patients has markedly improved over the last few decades, patients still suffer from many complications of this congenital disease. The presence of a high incidence of thromboembolic events (TEE), mainly in β-thalassemia intermedia (β-TI), has led to the identification of a hypercoagulable state in these patients. In this review, the molecular and cellular mechanisms leading to hypercoagulability in thalassemia are highlighted, with a special focus on thalassemia intermedia being the group with the highest incidence of thrombotic events as compared to other types of thalassemia. Clinical experience and available clues on optimal management are also discussed. © 2011 Informa Healthcare USA, Inc.Atichartakarn V, 2002, BRIT J HAEMATOL, V118, P893, DOI 10.1046-j.1365-2141.2002.03711.x; Atichartakarn V, 2003, INT J HEMATOL, V77, P299, DOI 10.1007-BF02983790; Yashar Vered Borenstain-Ben, 1993, American Journal of Hematology, V44, P63, DOI 10.1002-ajh.2830440114; Pignatti CB, 1998, ACTA HAEMATOL-BASEL, V99, P76; Borgna-Pignatti C, 2004, HAEMATOLOGICA, V89, P1187; BUTTHEP P, 1995, THROMB HAEMOSTASIS, V74, P1045; Butthep P, 1997, SE ASIAN J TROP M S3, V28, P141; Cadili A, 2008, AM J MED, V121, P371, DOI 10.1016-j.amjmed.2008.02.014; Cappellini MD, 2010, ANN N Y ACAD SCI, V1202, P231; Cappellini MD, 2000, BRIT J HAEMATOL, V111, P467, DOI 10.1046-j.1365-2141.2000.02376.x; Cappellini MD, 2005, ANN N Y ACAD SCI, V1054, P317; Crary SE, 2009, BLOOD, V114, P2861, DOI 10.1182-blood-2009-04-210112; DELPRINCIPE D, 1993, BRIT J HAEMATOL, V84, P111; ELDOR A, 1991, BLOOD, V77, P1749; ELDOR A, 1989, AM J HEMATOL, V32, P94, DOI 10.1002-ajh.2830320204; Habib A, 2008, HAEMATOL-HEMATOL J, V93, P941, DOI 10.3324-haematol.12460; Helley D, 1996, THROMB HAEMOSTASIS, V76, P322; HERSHKO C, 1978, BRIT J HAEMATOL, V40, P255, DOI 10.1111-j.1365-2141.1978.tb03662.x; Hovav T, 1999, BRIT J HAEMATOL, V106, P178; Iolascon A, 2001, HAEMATOLOGICA, V86, P1112; Karimi M, 2010, THROMB HAEMOSTASIS, V103, P989, DOI 10.1160-TH09-09-0661; Kuypers FA, 2004, CELL MOL BIOL, V50, P147; Manfre L, 1999, AM J ROENTGENOL, V173, P1477; Ruf A, 1997, BRIT J HAEMATOL, V98, P51, DOI 10.1046-j.1365-2141.1997.1502965.x; Rund D, 2005, NEW ENGL J MED, V353, P1135, DOI 10.1056-NEJMra050436; Steinberg MH, 2009, DISORDERS OF HEMOGLOBIN: GENETICS, PATHOPHYSIOLOGY, AND CLINICAL MANAGEMENT, 2ND EDITION, P1, DOI 10.1017-CBO9780511596582; Sumiyoshi A, 1992, SE ASIAN J TROP M S2, V23, P29; Taher A, 2006, THROMB HAEMOSTASIS, V96, P488, DOI 10.1160-TH06-05-0267; Taher A, 2009, BRIT J HAEMATOL, V147, P634, DOI 10.1111-j.1365-2141.2009.07848.x; Taher AT, 2008, BLOOD REV, V22, P283, DOI 10.1016-j.blre.2008.04.001; Taher AT, 2010, BRIT J HAEMATOL, V150, P486, DOI 10.1111-j.1365-2141.2010.08220.x; Taher AT, 2011, BRIT J HAEMATOL, V152, P512, DOI 10.1111-j.1365-2141.2010.08486.x; Taher AT, 2010, J THROMB HAEMOST, V8, P2152, DOI 10.1111-j.1538-7836.2010.03940.x; Taher AT, 2010, J THROMB HAEMOST, V8, P54, DOI 10.1111-j.1538-7836.2009.03651.x; Taher AT, 2010, BLOOD, V115, P1886, DOI 10.1182-blood-2009-09-243154; Tavazzi D, 2001, BRIT J HAEMATOL, V112, P48, DOI 10.1046-j.1365-2141.2001.02482.x; Tripodi A, 2009, HAEMATOL-HEMATOL J, V94, P1520, DOI 10.3324-haematol.2009.010546; WINICHAGOON P, 1981, Southeast Asian Journal of Tropical Medicine and Public Health, V12, P556; Zalloua PA, 2003, THROMB HAEMOSTASIS, V89, P767; ZURLO MG, 1989, LANCET, V2, P2716191
Stroke in thalassemia: A dilemma
No full text[No abstract available]KARIMI M, 2007, AM J HEMATOL 0815; Taher A, 2006, THROMB HAEMOSTASIS, V96, P488, DOI 10.1160-TH06-05-026796
Riau berdarah (kisah perjalanan hidupku)
No full textBagiku yang hidup di rantau ini, di samping segala kegembiraan yang kupereloh, hatiku juga terenyuh dan menangis. Aku ingat teman-teman sekolah, teman-teman sependeritaan dalam tahanan, teman-teman yang diambil dari tahanan dan dibunuh ORBA tanpa diketahui di mana kuburnya, sanak saudara dan handai taulan yang terpaksa kutinggalkan demi menyelamtkan hidup ini, satu-satunya pemberian Tuhan yang paling berharga. Buku ini merupakan biografi Yoseph Tugio Taher
Iron overload in β-thalassemia intermedia: An emerging concern
No full textPurpose of Review: The aim is to overview recent evidence on consequences, assessment, and management of iron overload in transfusion-independent patients with β-thalassemia intermedia. Recent Findings: Despite their transfusion-independence, β-thalassemia intermedia patients can still accumulate iron due to increased intestinal absorption. Recent observational studies show that iron burden in this group of patients can ultimately reach considerably high thresholds, and leads to a variety of serious morbidities involving the liver, endocrine glands, and arguably the vascular system. The diagnosis of iron overload in this patient population can follow established guidelines from β-thalassemia major patients, although with careful interpretation of spot serum ferritin levels. Data from a recent randomized clinical trial demonstrated the efficacy and safety of iron chelation therapy in decreasing liver iron concentration in this group of patients, which may ultimately help in reducing morbidity risk. Summary: Iron overload in transfusion-independent patients with β-thalassemia intermedia deserves careful attention, and prompt diagnosis and management are recommended. © 2013 Wolters Kluwer Health | Lippincott Williams and Wilkins.Casanovas G, 2013, HAEMATOLOGICA, V98, P444, DOI 10.3324-haematol.2012.069807; Gardenghi S, 2010, J CLIN INVEST, V120, P4466, DOI 10.1172-JCI41717; Ginzburg Y, 2011, BLOOD, V118, P4321, DOI 10.1182-blood-2011-03-283614; Karimi M, 2011, EUR J INTERN MED, V22, P607, DOI 10.1016-j.ejim.2011.05.013; Li HH, 2010, NAT MED, V16, P177, DOI 10.1038-nm.2073; Maakaron JE, 2013, ANN HEPATOL, V12, P142; Musallam KM, 2012, ANN HEMATOL, V91, P235, DOI 10.1007-s00277-011-1291-3; Musallam KM, 2011, HEMOGLOBIN, V35, P503, DOI 10.3109-03630269.2011.605499; Musallam KM, 2012, BLOOD CELL MOL DIS, V49, P136, DOI 10.1016-j.bcmd.2012.06.001; Musallam KM, 2011, HAEMATOL-HEMATOL J, V96, P1605, DOI 10.3324-haematol.2011.047852; Musallam KM, 2012, CSH PERSPECT MED, V2, DOI 10.1101-cshperspect.a013482; Musallam KM, 2012, BLOOD, V120; Musallam KM, 2012, BLOOD, V120; Musallam KM, 2012, BLOOD REV, V26, pS16, DOI 10.1016-S0268-960X(12)70006-1; Musallam KM, 2011, EUR J HAEMATOL, V87, P539, DOI 10.1111-j.1600-0609.2011.01706.x; Musallam KM, 2012, THROMB RES, V130, P695, DOI 10.1016-j.thromres.2012.07.013; Nai A, 2012, BLOOD, V119, P5021, DOI 10.1182-blood-2012-01-401885; Origa R, 2007, HAEMATOL-HEMATOL J, V92, P583, DOI 10.3324-haematol.10842; Pakbaz Z, 2007, PEDIATR BLOOD CANCER, V49, P329, DOI 10.1002-pbc.21275; Parrow NL, 2012, BLOOD, V119, P3187, DOI 10.1182-blood-2012-01-405563; Rivella S, 2012, BLOOD REV, V26, pS12, DOI 10.1016-S0268-960X(12)70005-X; Taher A, 2008, HAEMATOL-HEMATOL J, V93, P1584, DOI 10.3324-haematol.13098; Taher A, 2009, BRIT J HAEMATOL, V146, P569, DOI 10.1111-j.1365-2141.2009.07810.x; Taher A, 2012, HAEMATOLOGICA, V96, P0924; Taher A., 2012, HAEMATOLOGICA, V96; Taher AT, 2010, AM J HEMATOL, V85, P288, DOI 10.1002-ajh.21626; Taher AT, 2010, BRIT J HAEMATOL, V150, P486, DOI 10.1111-j.1365-2141.2010.08220.x; Taher AT, 2012, BLOOD, V120, P970, DOI 10.1182-blood-2012-02-412692; Taher AT, 2011, BRIT J HAEMATOL, V152, P512, DOI 10.1111-j.1365-2141.2010.08486.x; Taher AT, 2012, BLOOD, V120, P3258; Taher AT, 2010, BLOOD, V115, P1886, DOI 10.1182-blood-2009-09-243154; Wood John C, 2011, Hematology Am Soc Hematol Educ Program, V2011, P443, DOI 10.1182-asheducation-2011.1.443; Ziyadeh FN, 2012, NEPHRON CLIN PRACT, V121, pC136, DOI 10.1159-00033978789
Covert brain ischaemia in splenectomised adults with thalassemia intermedia: An emerging entity
No full text[No abstract available]Chen SQ, 1996, AM J PHYSIOL-HEART C, V270, pH1951; Goldschmidt N, 2008, THROMB HAEMOSTASIS, V100, P864, DOI 10.1160-TH08-03-0157; Karimi M, 2010, THROMB HAEMOSTASIS, V103, P989, DOI 10.1160-TH09-09-0661; LONGSTRETH WT JR, 2005, STROKE, V36, P56; Pantoni L, 2007, CURR OPIN NEUROL, V20, P390, DOI 10.1097-WCO.0b013e328172d661; Taher A, 2006, THROMB HAEMOSTASIS, V96, P488, DOI 10.1160-TH06-05-0267; Taher AT, 2008, BLOOD REV, V22, P283, DOI 10.1016-j.blre.2008.04.001; Taher AT, 2010, J THROMB HAEMOST, V8, P54, DOI 10.1111-j.1538-7836.2009.03651.x21
Update on the use of deferasirox in the management of iron overload
No full textAli Taher,1 Maria Domenica Cappellini21American University of Beirut, Beirut, Lebanon; 2Universitá di Milano, Policlinico Foundation IRCCS, Milan, ItalyAbstract: Regular blood transfusions as supportive care for patients with chronic anemia inevitably lead to iron overload as humans cannot actively remove excess iron. The cumulative effects of iron overload cause significant morbidity and mortality if not effectively treated with chelation therapy. Based on a comprehensive clinical development program, the once-daily, oral iron chelator deferasirox (Exjade®) is approved for the treatment of transfusional iron overload in adult and pediatric patients with various transfusion-dependent anemias, including β-thalassemia and the myelodysplastic syndromes. Deferasirox dose should be titrated for each individual patient based on transfusional iron intake, current iron burden and whether the goal is to decrease or maintain body iron levels. Doses of >30 mg/kg/day have been shown to be effective with a safety profile consistent with that observed at doses <30 mg/kg/day. Recent data have highlighted the ability of deferasirox to decrease cardiac iron levels and to prevent the accumulation of iron in the heart. The long-term efficacy and safety of deferasirox for up to 5 years of treatment have now been established. The availability of this effective and generally well tolerated oral therapy represents a significant advance in the management of transfusional iron overload. Keywords: deferasirox, Exjade, oral, iron chelation, iron overload, cardiac iron&nbsp
Contemporary approaches to treatment of beta-thalassemia intermedia
No full textBeta-thalassemia intermedia (TI) is associated with a variety of serious clinical complications that require proactive and comprehensive management. These include skeletal deformities and osteopenia, compensatory extramedullary hematopoiesis and tumor formation, progressive splenomegaly, a hypercoagulable state resulting in thromboembolic events and pulmonary hypertension, and increased gastrointestinal iron absorption that often results in nontransfusional iron overload and liver damage. Although TI is generally considered a non-transfusion-dependent thalassemia, transfusion therapy may be an important part of the comprehensive management of this disease. This review describes the current state of the art for medical management of TI, with particular focus on the roles of splenectomy, transfusion, and iron chelation therapy. © 2012 Elsevier Ltd.Aessopos A, 2005, ANN NY ACAD SCI, V1054, P342, DOI 10.1196-annals.1345.041; Aessopos A, 2007, HAEMATOL-HEMATOL J, V92, P658, DOI 10.3324-haematol.10915; Aessopos A, 2001, BLOOD, V97, P3411, DOI 10.1182-blood.V97.11.3411; Amoozgar H, 2011, EUR J HAEMATOL, V87, P61, DOI 10.1111-j.1600-0609.2011.01620.x; [Anonymous], FERR SUMM PROD CHAR; [Anonymous], 2010, EXJADE PACK INS; [Anonymous], EXJADE SUMM PROD CHA; Ataga KI, 2007, BRIT J HAEMATOL, V139, P3, DOI 10.1111-j.1365-2141.2007.06740.x; Atichartakarn V, 2003, INT J HEMATOL, V78, P139, DOI 10.1007-BF02983382; Bisharat N, 2001, J INFECTION, V43, P182, DOI 10.1053-jinf.2001.0904; Borgna-Pignatti C, 2010, ANN NY ACAD SCI, V1202, P214, DOI 10.1111-j.1749-6632.2010.05550.x; Borgna-Pignatti C, 2007, BRIT J HAEMATOL, V138, P291, DOI 10.1111-j.1365-2141.2007.06654.x; Cappellini MD, 2005, SEMIN HEMATOL, V42, pS19, DOI 10.1053-j.seminhematol.2005.01.001; Cappellini MD, 2000, BRIT J HAEMATOL, V111, P467, DOI 10.1046-j.1365-2141.2000.02376.x; COSSU P, 1981, EUR J PEDIATR, V137, P267, DOI 10.1007-BF00443255; Davies JM, 2011, BRIT J HAEMATOL, V155, P308, DOI 10.1111-j.1365-2141.2011.08843.x; Eder AF, 2007, ARCH PATHOL LAB MED, V131, P708; Gardenghi S, 2010, J CLIN INVEST, V120, P4466, DOI 10.1172-JCI41717; Haidar R, 2010, EUR SPINE J, V19, P871, DOI 10.1007-s00586-010-1357-2; Karimi M, 2010, EUR J HAEMATOL, V84, P52, DOI 10.1111-j.1600-0609.2009.01356.x; Karimi M, 2011, EUR J INTERN MED, V22, P607, DOI 10.1016-j.ejim.2011.05.013; Karimi M, 2010, PEDIATR HEMAT ONCOL, V27, P205, DOI 10.3109-08880011003639952; Kontoghiorghes GJ, 2010, HEMOGLOBIN, V34, P251, DOI 10.3109-03630269.2010.486335; Ladis V, 2010, BRIT J HAEMATOL, V151, P504, DOI 10.1111-j.1365-2141.2010.08346.x; Li HH, 2010, NAT MED, V16, P177, DOI 10.1038-nm.2073; Musallam KM, 2011, EUR J HAEMATOL, V87, P73, DOI 10.1111-j.1600-0609.2011.01623.x; Musallam KM, 2011, HAEMATOL-HEMATOL J, V96, P1605, DOI 10.3324-haematol.2011.047852; Novartis Pharmaceutical Corporation, 2010, DESF PACK INS; Porter J, 2011, 16 C EUR HEM ASS JUN; Porter JB, 2001, SEMIN HEMATOL, V38, P63, DOI 10.1053-shem.2001.20145; Rigano P, 2010, BRIT J HAEMATOL, V151, P509, DOI 10.1111-j.1365-2141.2010.08397.x; Sankaran VG, 2010, NEW ENGL J MED, V363, P2258, DOI 10.1056-NEJMcibr1010767; STURGEON P, 1955, BRIT J HAEMATOL, V1, P264, DOI 10.1111-j.1365-2141.1955.tb05509.x; Taher A, 2008, HAEMATOL-HEMATOL J, V93, P1584, DOI 10.3324-haematol.13098; Taher A, 2006, THROMB HAEMOSTASIS, V96, P488, DOI 10.1160-TH06-05-0267; Taher A, 2006, BLOOD CELL MOL DIS, V37, P12, DOI 10.1016-j.bcmd.2006.04.005; Taher A, 2009, BRIT J HAEMATOL, V147, P634, DOI 10.1111-j.1365-2141.2009.07848.x; Taher A, 2002, HEMOGLOBIN, V26, P107, DOI 10.1081-HEM-120005447; Taher AT, 2008, BLOOD REV, V22, P283, DOI 10.1016-j.blre.2008.04.001; Taher AT, 2010, BRIT J HAEMATOL, V150, P486, DOI 10.1111-j.1365-2141.2010.08220.x; Taher AT, 2011, BRIT J HAEMATOL, V152, P512, DOI 10.1111-j.1365-2141.2010.08486.x; Taher AT, 2010, J THROMB HAEMOST, V8, P54, DOI 10.1111-j.1538-7836.2009.03651.x; Taher AT, 2010, BLOOD, V115, P1886, DOI 10.1182-blood-2009-09-243154; Taher ATPJ, 2011, 53 AM SOC HEM ANN M; Treadwell MJ, 2001, SEMIN HEMATOL S1, V38, P77; Voskaridou E, 2010, BRIT J HAEMATOL, V148, P332, DOI 10.1111-j.1365-2141.2009.07930.x9151
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