bluuebunny/crossref_metadata_2025_split huggingface dataset:
Functional Distinction Between Cln1p and Cln2p Cyclins in the Control of the Saccharomyces cerevisiae Mitotic Cycle
Authors: Queralt Ethel , Igual J Carlos 
Published: September 2004

Abstract
Cln1p and Cln2p are considered as equivalent cyclins on the basis of sequence homology, regulation, and functional studies. Here we describe a functional distinction between the Cln1p and Cln2p cyclins in the control of the G1/S transition. Inactivation of CLN2, but not of CLN1, leads to a larger-than-normal cell size, whereas overexpression of CLN2, but not of CLN1, results in smaller-than-normal cells. Furthermore, mild ectopic expression of CLN2, but not of CLN1, suppresses the lethality of swi4swi6 and cdc28 mutant strains. In the absence of Cln1p, the kinetics of budding, initiation of DNA replication, and activation of the Start-transcription program are not affected; by contrast, loss of Cln2p causes a delay in bud emergence. A primary role for Cln2p but not for Cln1p in budding is reinforced by the observation that only the cln2 mutation is synthetic lethal with a cdc42 mutation, and only the cln2 mutant strain is hypersensitive to latrunculin B. In addition, we found that Cln1p showed a more prominent nuclear staining than Cln2p. Finally, chimeric proteins composed of Cln1p and Cln2p revealed that Cln2p integrity is required for its functional specificity.
stall-Mediated Extrinsic Control of Ovarian Follicle Formation in Drosophila
Authors: Willard Stacey S , Ozdowski Emily F , Jones Natasha A , Cronmiller Claire 
Published: September 2004

AbstractComplex patterns of morphogenesis require intricate coordination of multiple, regulatory processes that control cellular identities, shapes, and behaviors, both locally and over vast distances in the developing organism or tissue. Studying Drosophila oogenesis as a model for tissue morphogenesis, we have discovered extraovarian regulation of follicle formation. Clonal analysis and ovary transplantation have demonstrated that long-range control of follicle individualization requires stall gene function in cells outside of the ovary. Although tissue nonautonomous regulation has been shown to govern follicle maturation and survival, this is the first report of an extraovarian pathway involved in normal follicle formation.
Interactions Between Imprinting Effects in the Mouse
Authors: Cattanach Bruce M , Beechey Colin V , Peters Josephine 
Published: September 2004

Abstract
Mice with uniparental partial or complete disomies for any one of 11 identified chromosomes show abnormal phenotypes. The abnormalities, or imprinting effects, can be attributable to an incorrect dosage of maternal or paternal copies of imprinted gene(s) located within the regions involved. Here we show that combinations of partial disomies may result in interactions between imprinting effects that seemingly independently affect fetal and/or placental growth in different ways or modify neonatal and postnatal imprinting effects. Candidate genes within the regions have been identified. The findings are generally in accord with the “conflict hypothesis” for the evolution of genomic imprinting but do not clearly demonstrate common growth axes within which imprinted genes may interact. Instead, it would seem that any gene that represses or limits embryonic/fetal growth to the advantage of the mother—by any developmental means—will have been subject to evolutionary selection for paternal allele repression. Likewise, any gene that favors embryonic/fetal development at consequent cost to the mother—by any developmental means—will have faced selection for maternal allele repression. The classical Igf2-Igf2r axis may therefore be unique. The findings involve reinterpretation of older imprinting data and consequently revision of the mouse imprinting map.
A Novel Yeast Mutation, rad52-L89F, Causes a Specific Defect in Rad51-Independent Recombination That Correlates With a Reduced Ability of Rad52-L89F to Interact With Rad59
Authors: Cortés-Ledesma Felipe , Malagón Francisco , Aguilera Andrés 
Published: September 2004

Abstract
We isolated a novel rad52 mutation, rad52-L89F, which specifically impairs recombination in rad51Δ cells. rad52-L89F displays phenotypes similar to rad59Δ and encodes a mutant protein impaired in its ability to interact with Rad59. These results support the idea that Rad59 acts in homologous recombination via physical interaction with Rad52.
Near‐fatal uterine hemorrhage during induction chemotherapy for acute myeloid leukemia: A case report of bilateral uterine artery embolization
Authors: Phelan John T. , Broder Jonathan , Kouides Peter A. 
Published: September 2004

AbstractSevere transfusion‐dependent uterine hemorrhage is a relatively uncommon complication of induction chemotherapy for acute myeloid leukemia (AML). Even less common is the failure of systemic conjugated estrogens in this setting. We report a case of life‐threatening uterine hemorrhage in a 38‐year‐old woman in the setting of transfusion‐refractory thrombocytopenia after completing induction chemotherapy for AML. She experienced dramatic breakthrough uterine hemorrhage despite multiple platelet transfusions, conjugated estrogens, recombinant factor VIIa, ϵ‐aminocaproic acid, and intracavitary thrombin‐soaked gauze tamponade. At the point of near‐exsanguination in the setting of hypotension, hematocrit of 14%, and a platelet count of 3,000/μL, she underwent bilateral uterine artery embolization which proved immediately successful. We review the literature and indications for this procedure in the oncologic patient care setting. Am. J. Hematol. 77:151–155, 2004. © 2004 Wiley‐Liss Inc. © 2004 Wiley‐Liss, Inc.
Second case of CML with aberrant BCR‐ABL fusion transcript (e8/a2) with insertion of an inverted ABL intron 1b sequence
Authors: Sugimoto Takeshi , Ijima Kentaro , Hisatomi Hisashi , Murayama Tohru , Mizuno Ishikazu , Hato Akio , Imoto Shion , Nishimura Ryuichiro , Koizumi Tamio 
Published: September 2004

AbstractWe found a case of Ph‐positive chronic myelogenous leukemia (CML) patient with an atypical BCR‐ABL transcript that was undetectable by a routine reverse transcription polymerase chain reaction (RT‐PCR) for major BCR‐ABL. Additional RT‐PCR and sequence analyses have demonstrated that the aberrant transcript consists of a fusion of BCR exon 8 (e8) and ABL exon 2 (a2) with an insertion of a 55‐bp inverted sequence of intron 1b between them. The nucleotide sequences of the aberrant transcript were identical to those of a previously reported CML patient. These are the only two CML cases in the literature with identical aberrant BCR‐ABL transcripts. Am. J. Hematol. 77:164–166, 2004. © 2004 Wiley‐Liss, Inc.
Dysplastic changes in the peripheral blood of children with microdeletion 22q11.2
Authors: Özbek Namık , Derbent Murat , Olcay Lale , Yılmaz Zerrin , Tokel Kürşat 
Published: September 2004

AbstractMyelodysplasia refers to abnormal morphology of the bone marrow and/or peripheral blood. This condition is frequently due to myelodysplastic syndrome; however, myelodysplasia is caused by a variety of factors and is not always a sign of pre‐malignant disease. We observed myelodysplastic changes in peripheral blood smears and bone marrow specimens from a patient who had chromosomal microdeletion 22q11.2 (del22q11.2). We then investigated such changes in several other patients who were newly diagnosed with del22q11.2 (n = 5 total, including the index case) and compared the findings to those in four sets of controls without this chromosomal abnormality. Specifically, the controls were children with conotruncal heart defects (n = 3); otherwise healthy children with bacterial (n = 4) or viral infection (n = 4); and healthy children (n = 4). The myelodysplasia scores in the myeloid cells and eosinophils of the children with del22q11 were higher than those in all four of the control groups. Myelodysplastic changes in the peripheral blood of children with del22q11.2 have not been reported previously. We believe that certain gene(s) in the deleted region may be responsible for the myelodysplastic changes that we observed in our patients with this chromosomal abnormality. Am. J. Hematol. 77:126–131, 2004. © 2004 Wiley‐Liss, Inc.
Microvascular blood flow and stasis in transgenic sickle mice: Utility of a dorsal skin fold chamber for intravital microscopy
Authors: Kalambur Venkatasubramaniam S. , Mahaseth Hemchandra , Bischof John C. , Kielbik Miroslaw C. , Welch Thomas E. , Vilbäck Åsa , Swanlund David J. , Hebbel Robert P. , Belcher John D. , Vercellotti Gregory M. 
Published: September 2004

AbstractVascular inflammation, secondary to ischemia–reperfusion injury, may play an essential role in vaso‐occlusion in sickle cell disease (SCD). To investigate this hypothesis, dorsal skin fold chambers (DSFCs) were implanted on normal and transgenic sickle mice expressing human α and βs/βs‐Antilles globin chains. Microvessels in the DSFC were visualized by intravital microscopy at baseline in ambient air and after exposure to hypoxia–reoxygenation. The mean venule diameter decreased 9% (P < 0.01) in sickle mice after hypoxia–reoxygenation but remained constant in normal mice. The mean RBC velocity and wall shear rate decreased 55% (P < 0.001) in sickle but not normal mice after hypoxia–reoxygenation. None of the venules in normal mice became static at any time during hypoxia–reoxygenation; however, after 1 hr of hypoxia and 1 hr of reoxygenation, 11.9% of the venules in sickle mice became static (P < 0.001). After 1 hr of hypoxia and 4 hr of reoxygenation, most of the stasis had resolved; only 3.6% of the subcutaneous venules in sickle mice remained static (P = 0.01). All of the venules were flowing again after 24 hr of reoxygenation. Vascular stasis could not be induced in the subcutaneous venules of sickle mice by tumor necrosis factor alpha (TNF‐α). Leukocyte rolling flux and firm adhesion, manifestations of vascular inflammation, were significantly higher at baseline in sickle mice compared to normal (P < 0.01) and increased 3‐fold in sickle (P < 0.01), but not in normal mice, after hypoxia–reoxygenation. Plugs of adherent leukocytes were seen at bifurcations at the beginning of static venules. Misshapen RBCs were also seen in subcutaneous venules. Am. J. Hematol. 77:117–125, 2004. © 2004 Wiley‐Liss, Inc.
Evaluation of kidney damage in patients with acute lymphoblastic leukemia in long‐term follow‐up: Value of renal scan
Authors: Yetgin Sevgi , Olgar Şeref , Aras Tülin , Çetin Mualla , Düzova Ali , Beylergil Volkan , Akhan Okan , Oĝuz Oĝuzhan , Saraçbaşı Osman 
Published: September 2004

AbstractIn order to evaluate potential long‐term kidney damage of childhood leukemia and risk factors affecting renal damage, we studied 116 children treated for acute lymphoblastic leukemia (ALL) using the St. Jude Total XI and XIII protocols in 1991–1998. The median follow‐up period after the completion of treatment was 35 months. The following parameters were examined: urinalysis, urinary creatinine (Cr), calcium (Ca), phosphorus, β2‐microglobulin, glomerular filtration rate (GFR), tubular phosphorus reabsorption (TPR), and renal function tests. Radiological evaluation included renal ultrasonography (US), and renal scans with DMSA or MAG‐3 were performed. Blood chemistry and renal US patients were normal in all patients except two. GFR, TPR, urinary Ca/Cr, β2‐microglobulin, and renal scan were abnormal in 19.0%, 16.4%, 13.8%, 6.0%, and 40.5% of patients, respectively. The abnormality rate in GFR was significantly higher in patients <2 years of age. TPR abnormality was found to be significantly higher in patients who did not have G‐CSF. An abnormal renal scan was associated with Hb < 10 g/dL, kidney infiltration, or hypertension at presentation and also occurred patients who underwent methotrexate treatment with frequent intervals during the follow‐up period. Patients should be followed‐up after cessation of therapy with the conventional tests mentioned above. In case of any abnormality, further detailed tests should be performed; renal scan seems to be more predictive for renal damage. Am. J. Hematol. 77:132–139, 2004. © 2004 Wiley‐Liss, Inc.
Genetic variability of platelet glycoprotein Ibα gene
Authors: Ozelo Margareth C. , Costa Devanira S.P. , Siqueira Lucia H. , Machado Tania M.F. , Castro Vagner , Gonçalves Marilda S. , Menezes Raimundo C. , Soares Manoel , Annichino‐Bizzacchi Joyce M. , Costa Fernando F. , Arruda Valder R. 
Published: September 2004

AbstractPlatelet membrane glycoprotein (GP) Ibα is a critical component of platelet adhesion complex to subendothelium structures following tissue injury or pathological surfaces, such as atherosclerotic plaques. Polymorphisms of the GPIbα gene have been associated with a high risk for occlusive vascular disease, and its distribution varies considerably among distinct populations. These polymorphisms comprise the human platelet antigen (HPA)‐2 system, the −5C/T dimorphism of the Kozak sequence, and the variable number of tandem 39‐bp repeats (VNTR). Here we report the prevalence of the GPIbα gene polymorphisms among Brazilians, a highly ethnically diverse population. We analyzed 492 subjects of European, African, or Indigenous origin. It was possible to determine ten distinct haplotypes. The most common (∽40%) haplotype was the Kozak‐TT/HPA‐2aa/VNTR‐CC for both Caucasian and African descent. However, among Indigenous, Kozak‐TT/HPA‐2aa/VNTR‐CC and Kozak‐TC/HPA‐2aa/VNTR‐CC were equally present. Although a strong linkage disequilibrium between VNTR and HPA‐2 polymorphism had also been observed, here we determined incomplete linkage disequilibrium in 10% of subjects from all ethnic groups. VNTR‐E, a rare variant lacking the 39‐bp repeat, was identified in two unrelated subjects, and functional platelet studies revealed no abnormalities. The VNTR‐A allele, the largest variant containing four copies of the repeats, was not identified in this population. However, homozygosity for the VNTR‐A allele (Kozak‐TT/HPA‐2aa/VNTR‐AA) was determined in two distinct species of nonhuman primates. These results suggest a greater complex evolutionary mechanism in the macroglycoprotein region of the GPIbα gene and may be useful in the design of gene–disease association studies for vascular disease. Am. J. Hematol. 77:107–116, 2004. © 2004 Wiley‐Liss, Inc.
Monoclonal gammopathy in extranodal marginal zone lymphoma (ENMZL) correlates with advanced disease and bone marrow involvement
Authors: Asatiani Ekatherine , Cohen Philip , Ozdemirli Metin , Kessler Craig M. , Mavromatis Blanche , Cheson Bruce D. 
Published: September 2004

AbstractMonoclonal gammopathy is a well‐recognized occurrence in splenic marginal zone lymphoma (MZL); however, its prevalence has never been reported in extranodal MZL (ENMZL). We present results of a retrospective analysis of 26 patients with newly diagnosed as well as previously treated ENMZL. Monoclonal gammopathy was detected in 7 out of 26 (27%) patients. All patients with a monoclonal gammopathy had stage IV disease, and most of them had involvement of lymph nodes and/or bone marrow (n = 6). Only 1 out of 7 patients with a monoclonal spike had stage IV disease diagnosed based on multifocal mucosal involvement. There was also a strong correlation between the involvement of bone marrow and the presence of a monoclonal spike (Fisher's exact test, P = 0.0007). Prevalence of monoclonal gammopathy is higher than previously recognized and indicates advanced disease. However, the prognostic significance of the presence of monoclonal gammopathy in this population is unknown. Am. J. Hematol. 77:144–146, 2004. © 2004 Wiley‐Liss, Inc.
Presentation and pattern of symptoms in 382 patients with Glanzmann thrombasthenia in Iran
Authors: Toogeh G. , Sharifian R. , Lak M. , Safaee R. , Artoni A. , Peyvandi F. 
Published: September 2004

AbstractGlanzmann thrombasthenia (GT) is a rare autosomal recessive disease characterized by prolonged bleeding time with normal platelet count and morphology. It is caused by the quantitative or qualitative deficiency of the platelet glycoprotein IIb–IIIa. In 382 Iranian patients with GT diagnosed at a single center during the period 1969–2001, consanguinity between parents was 86.6%, in accord with the high frequency of intrafamilial marriages in Iran. Almost all patients had had abnormal mucocutaneous bleeding (epistaxis and gum bleeding); at follow‐up, 4/5 of the patients had been transfused at least once to control hemorrhagic episodes. As expected, almost all the patients had a normal platelet count while the leukocyte count was increased in 19.3%. Among women, an unexpected low rate of pregnancies was observed. Am. J. Hematol. 77:198–199, 2004. © 2004 Wiley‐Liss, Inc.
Squamous cell carcinoma of the tongue complicating chronic oral mucosal graft‐versus‐host disease after allogeneic hematopoietic stem cell transplantation
Authors: Szeto Ching H. , Shek Tony W.H. , Lie Albert K.W. , Au Wing Y. , Yuen Anthony P.W. , Kwong Yok L. 
Published: September 2004

AbstractTwo patients underwent allogeneic hematopoietic stem cell transplantation (HSCT) for acute myeloid leukemia. Chronic graft‐versus‐host disease (GVHD) developed, with persistent symptomatic oral lesions. At 2 and 6 years post‐HSCT, both patients developed squamous cell carcinoma (SCC) of the tongue in areas previously involved by chronic GVHD. None had any known risk factor for SCC. Histologically, moderate to severe dysplasia was present in noncancerous oral mucosa. Oral SCC is rarely described after HSCT, and a review of the reported cases showed chronic GVHD to be a common risk, suggesting that the chronic inflammation associated with GVHD might be of pathogenetic significance. Am. J. Hematol. 77:200–202, 2004. © 2004 Wiley‐Liss, Inc.
Home prothrombin time monitoring: A literature analysis
Authors: Yang David T. , Robetorye Ryan S. , Rodgers George M. 
Published: September 2004

AbstractThe anticoagulant activity of warfarin sodium is monitored by the prothrombin time (PT) using the international normalized ratio (INR). Standard oral anticoagulant therapy monitoring requires frequent patient visits to physicians' offices and/or laboratories to optimize warfarin dosage. Home PT monitoring by patients can increase testing frequency and may thus decrease complications associated with oral anticoagulant therapy. Clinical studies suggest that home PT monitoring is more effective than uncoordinated management and is as effective as care through specialized anticoagulation clinics for keeping INRs within a therapeutic range. There are accurate and reliable instruments available, but paramount to the success of home PT monitoring is sound patient selection, appropriate patient training, and consistent quality control. Am. J. Hematol. 77:177–186, 2004. © 2004 Wiley‐Liss, Inc.
Prevention of bleeds in hemophilia patients with inhibitors: Emerging data and clinical direction
Authors: Leissinger Cindy A. 
Published: September 2004

AbstractIn patients with hemophilia, the development of high‐responding inhibitors to factor VIII prevents adequate replacement therapy and results in increased risk of serious bleeding episodes, poor control of joint bleeding, and progressive, debilitating joint disease. Immune tolerance therapy can eradicate inhibitors, but it is not uniformly successful. Emerging data suggest that prophylaxis using activated prothrombin complex concentrates may be effective and safe in reducing the incidence of joint bleeding during immune tolerance therapy and for patients in whom immune tolerance induction fails. However, only controlled clinical trials will ultimately demonstrate whether prophylaxis can prevent joint bleeding and damage, and improve quality of life in patients with inhibitors. Am. J. Hematol. 77:187–193, 2004. © 2004 Wiley‐Liss, Inc.
Acute lymphoblastic leukemia with the phenotype of a putative B‐cell/T‐cell bipotential precursor
Authors: Lau Lee Gong , Tan Lip Kun , Koay Evelyn S.C. , Ee Melvin H.L. , Tan Suat Hoon , Liu Te Chih 
Published: September 2004

AbstractBiphenotypic acute leukemias (BALs) are uncommon. Most are of myeloid‐B‐cell or myeloid‐T‐cell lineage. We report herein a 70‐year‐old man with an unusual acute leukemia where the blasts expressed both B‐ and T‐lymphoid markers. He presented to us with an enlarging cutaneous tumor. The presenting peripheral blood and bone marrow aspirate showed 40% and 90% blasts, respectively, which were negative for the usual cytochemical stains. The flow cytometric analysis revealed that the blasts were positive for CD19, CD20, CD22, cytoplasmic (Cyt) CD79a, CD10, Cyt CD3, CD5, CD7, CD4, HLA‐DR, TdT, and were negative for myeloid markers. According to the scoring system from the European Group for the Immunological Characterization of Acute Leukaemias (EGIL), this case was an unequivocal B‐cell/T‐cell BAL. Conventional cytogenetic analysis revealed 46XY [t(4;11)(q31;q13), add(8)(q24), der(9)del(9)(p21)del(9)(q32q34), −13, +mar] in all 25 metaphases analyzed. Fluorescence in situ hybridization (FISH) and polymerase chain reaction (PCR) for 11q23 rearrangements as well as t(9;22) were negative. PCR for both TCR‐γ and IgH gene analyses revealed polyclonal rearrangements. We postulate that this case of BAL might have arisen from the putative common lymphoid progenitor cell. Am. J. Hematol. 77:156–160, 2004. © 2004 Wiley‐Liss, Inc.
Case of chronic‐phase chronic myelogenous leukemia with an abdominal hematopoietic tumor of leukemic clone origin
Authors: Sakakura Miho , Ohishi Kohshi , Nomura Kenichi , Katayama Naoyuki , Nishii Kazuhiro , Masuya Masahiro , Nakase Kazunori , Shiku Hiroshi 
Published: September 2004

AbstractWe report a 59‐year‐old man with chronic myelogenous leukemia (CML) in chronic phase who presented with a large abdominal tumor. Biopsy revealed proliferation of granulocytic‐, erythroid‐, and megakaryocytic‐lineage cells in a retroperitoneal lymph node. The BCR/ABL fusion gene was detected on a paraffin‐embedded tissue section of the lymph node by double‐color fluorescence in situ hybridization, indicating an extramedullary hematopoietic tumor of CML origin. This patient has achieved a complete cytogenetic response for 19 months with imatinib mesylate (STI571; Gleevec), in association with the regression of the tumor. However, the development of an extramedullary tumor in chronic‐phase CML generally indicates a poor prognosis, because it commonly consists of blast proliferation and is followed by blast crisis in the marrow within a few months. This case, therefore, points to the importance of histological examination of extramedullary tumors in CML for evaluation of disease status and for therapeutic decisions. Am. J. Hematol. 77:167–170, 2004. © 2004 Wiley‐Liss, Inc.