bluuebunny/crossref_metadata_2025_split huggingface dataset:
Aggressive Peripheral T-Cell Lymphomas (Specified and Unspecified Types)
Authors: Savage Kerry J. 
Published: November 2005

AbstractPeripheral T-cell lymphomas (PTCLs) are a biologically diverse and uncommon group of diseases. Compared to their B-cell counterparts, PTCLs remain largely unexplored and the optimal treatment ill-defined due to disease rarity and biological heterogeneity. For the majority of PTCL subtypes, prognosis is poor with a 5-year overall survival of approximately 30% in most series.The notable exception is ALK-positive anaplastic large-cell lymphoma (ALK-pos ALCL), which has a superior outcome. The international prognostic index can be used to some extent to define risk groups within some PTCL subtypes, including PTCL unspecified (PTCLUS). It is likely that the observed clinical heterogeneity reflects differences at the molecular level. With the more widespread availability of gene expression profiling, it may be possible in the future to further refine the classification of PTCLs and elucidate novel therapeutic targets. Future clinical trials are needed that focus specifically on PTCL to advance our understanding and define the optimal management in this disease.
Clinical Presentation and Management of Marginal Zone Lymphomas
Authors: Thieblemont Catherine 
Published: November 2005

Abstract
Marginal-zone lymphoma (MZL) includes three subtypes depending on the site of lymphoma involvement: extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT-lymphoma); splenic MZL; and nodal MZL. Beside a common cell-of-origin and similarities concerning a possible chronic antigenic stimulation by microbial pathogens and/or autoantigens, the clinical presentation is very different with symptoms related to lymphoma location. MALT and splenic MZL present with an indolent disease with good performance status, no B symptoms, and no adverse prognostic factors and are associated with long survival. Patients with nodal MZL present with a more aggressive disease and have a shorter failure-free survival. Clinical and biological prognostic factors identified in reported series are heterogeneous. The optimal treatment has yet to be defined for the three subtypes, and current strategies will be described in this review.
Acquired Disorders of Platelet Function
Authors: Hassan Amy A. , Kroll Michael H. 
Published: November 2005

Abstract
A qualitative abnormality of platelet function should be considered in patients with mucocutaneous bleeding in the absence of thrombocytopenia or von Willebrand disease. Antiplatelet drugs are the most common cause of acquired platelet disorders leading to bleeding. Uremia, hepatic cirrhosis, myeloma and related disorders, polycythemia vera, essential thrombocythemia, and cardiopulmonary bypass have long been recognized as clinical situations in which platelet dysfunction may contribute to bleeding. When an acquired platelet disorder is suspected, it is useful to examine platelet function by measuring the bleeding time, examining platelet-dependent closure time in a platelet function analyzer and performing platelet aggregometry. When a specific acquired platelet disorder is diagnosed, many treatment options are available including controlling the underlying disease, giving platelet transfusions and administering a hemostatic drug.
Genetic Risk Factors for Arterial Thrombosis and Inflammation
Authors: Ginsburg David 
Published: November 2005

AbstractArterial thrombosis is a central pathologic mechanism contributing to myocardial infarction and stroke, together the leading causes of death in developed countries. This article reviews the current state of knowledge concerning the role of inherited variation in hemostatic and inflammatory factor genes in determining the risk of arterial thrombosis/ischemic heart disease. Despite considerable progress in identifying important genetic risk factors underlying predisposition to venous thrombosis, the genetic factors contributing to the risk for arterial thrombosis remain largely unknown. However, the rapid development of powerful new genomic resources should facilitate considerably more sophisticated analyses, leading to novel insight into the molecular pathophysiology of this important set of human diseases.
The Transfusion Services Committee—Responsibilities and Response to Adverse Transfusion Events
Authors: Shulman Ira A. , Saxena Sunita 
Published: November 2005

AbstractHealthcare institutions in the United States must review blood transfusion practices and adverse outcomes in order to receive payments from the Centers for Medicare/Medicaid program, but it is not required for a specific committee to be assigned to oversee the review process. Regardless of the group or individuals responsible, the review process must include a program of quality assessment and performance improvement that is ongoing, hospital-wide, and data-driven, reflects the complexity of the hospital’s organization and services, and involves all hospital departments and services (including those contracted). To be most effective, the performance improvement activity should be prioritized around high-risk, high-volume activities and/or in problem-prone areas. Even if a hospital elects not to receive payments from Medicare, it must still comply with applicable sections of the Code of Federal Regulations pertaining to transfusion services such as the follow up of adverse outcomes of transfusion.
Cardiopulmonary Complications of Sickle Cell Disease: Role of Nitric Oxide and Hemolytic Anemia
Authors: Gladwin Mark T. , Kato Gregory J. 
Published: November 2005

Abstract
Medical advances in the management of patients with sickle cell disease, thalassemia, and other hemolytic anemias have led to significant increases in life expectancy. Improved public health, neonatal screening, parental and patient education, advances in red cell transfusion medicine, iron chelation therapy, penicillin prophylaxis for children, pneumococcal immunization, and hydroxyurea therapy have all likely contributed to this effect on longevity.1,2 Importantly, as a generation of patients with sickle cell disease and thalassemia ages, new chronic complications of these hemoglobinopathies develop. In this context, pulmonary hypertension is emerging as one of the leading causes of morbidity and mortality in adult sickle cell and thalassemia patients, and likely in patients with other hemolytic anemias. A common feature of both sickle cell disease and thalassemia is intravascular hemolysis and chronic anemia. Recent data suggest that chronic intravascular hemolysis is associated with a state of endothelial dysfunction characterized by reduced nitric oxide (NO) bioavailability, pro-oxidant and pro-inflammatory stress and coagulopathy, leading to vasomotor instability and ultimately producing a proliferative vasculopathy, a hallmark of which is the development of pulmonary hypertension in adulthood.3–5 In conclusion, pulmonary hypertension is common in patients with hereditary hemolytic anemias and is associated with a high risk of death in patients with sickle cell disease. New therapies targeting this vasculopathy and aimed at normalizing the vasodilator:vasoconstrictor balance are discussed.
Hematology Grants K08 and K23
Authors: Bodine David M. 
Published: November 2005

Abstract
The first National Institutes of Health (NIH) grant awarded to physician scientists is often a K08 or K23 award. This chapter is designed for the Hematology Fellow who is preparing for an independent faculty position in 3–5 years. The topics covered include deciding which award to apply for, advice about planning and writing the application, as well as a description of the review process and how candidates can make their application stand out.
Role of platelet surface PF4 antigenic complexes in heparin-induced thrombocytopenia pathogenesis: diagnostic and therapeutic implications
Authors: Rauova Lubica , Zhai Li , Kowalska M. Anna , Arepally Gowthami M. , Cines Douglas B. , Poncz Mortimer 
Published: November 2005

AbstractHeparin-induced thrombocytopenia (HIT) antibodies recognize complexes between heparin and platelet factor 4 (PF4). Heparin and PF4 bind HIT antibodies only over a narrow molar ratio. We explored the involvement of platelet surface–bound PF4 as an antigen in the pathogenesis of experimental HIT. We show that cell-surface PF4 complexes are also antigenic only over a restricted concentration range of PF4. Heparin is not required for HIT antibody binding but shifts the concentration of PF4 needed for optimal surface antigenicity to higher levels. These data are supported by in vitro studies involving both human and murine platelets with exogenous recombinant human (h) PF4 and either an anti–PF4-heparin monoclonal antibody (KKO) or HIT immunoglobulin. Injection of KKO into transgenic mice expressing different levels of hPF4 demonstrates a correlation between the severity of the thrombocytopenia and platelet hPF4 expression. Therapeutic interventions in this model using high-dose heparin or protamine sulfate support the pathogenic role of surface PF4 antigenic complexes in the etiology of HIT. We believe that this focus on surface PF4 advances our understanding of the pathogenesis of HIT, suggests ways to identify patients at high risk to develop HIT upon heparin exposure, and offers new therapeutic strategies.
Chemokine and chemokine receptor expression during colony stimulating factor-1–induced osteoclast differentiation in the toothless osteopetrotic rat: a key role for CCL9 (MIP-1γ) in osteoclastogenesis in vivo and in vitro
Authors: Yang Meiheng , Mailhot Geneviève , MacKay Carole A. , Mason-Savas April , Aubin Justin , Odgren Paul R. 
Published: November 2005

AbstractOsteoclasts differentiate from hematopoietic precursors under systemic and local controls. Chemokines and receptors direct leukocyte traffic throughout the body and may help regulate site-specific bone resorption. We investigated bone gene expression in vivo during rapid osteoclast differentiation induced by colony-stimulating factor 1 (CSF-1) in Csf1-null toothless (tl/tl) rats. Long-bone RNA from CSF-1–treated tl/tl rats was analyzed by high-density microarray over a time course. TRAP (tartrate-resistant acid phosphatase)–positive osteoclasts appeared on day 2, peaked on day 4, and decreased slightly on day 6, as marrow space was expanding. TRAP and cathepsin K mRNA paralleled the cell counts. We examined all chemokine and receptor mRNAs on the arrays. CCL9 was strongly induced and peaked on day 2, as did its receptor, CCR1, and regulatory receptors c-Fms (CSF-1 receptor) and RANK (receptor activator of nuclear factor κB). Other chemokines and receptors showed little or no significant changes. In situ hybridization and immunohistochemistry revealed CCL9 in small, immature osteoclasts on day 2 and in mature cells at later times. Anti-CCL9 antibody inhibited osteoclast differentiation in culture and significantly suppressed the osteoclast response in CSF-1–treated tl/tl rats. While various chemokines have been implicated in osteoclastogenesis in vitro, this first systematic analysis of chemokines and receptors during osteoclast differentiation in vivo highlights the key role of CCL9 in this process.
Epigenetic processes play a major role in B-cell-specific gene silencing in classical Hodgkin lymphoma
Authors: Ushmorov Alexey , Leithäuser Frank , Sakk Olena , Weinhaüsel Andreas , Popov Sergey W. , Möller Peter , Wirth Thomas 
Published: November 2005

AbstractMany B-lineage-specific genes are down-regulated in Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL). We investigated the involvement of epigenetic modifications in gene silencing in cHL cell lines and in microdissected primary HRS cells. We assessed the expression and methylation status of CD19, CD20, CD79B, SYK, PU.1, BOB.1/OBF.1, BCMA, and LCK, all of which are typically down-regulated in cHL. We could reactivate gene expression in cHL cell lines with the DNA demethylating agent 5-aza-deoxycytidine (5-aza-dC). Using methylation-specific polymerase chain reaction (MSP), bisulfite genomic sequencing, and digestion with methylation-sensitive endonuclease followed by polymerase chain reaction (PCR), we determined the methylation status of promoter regions of PU.1, BOB.1/OBF.1, CD19, SYK, and CD79B. Down-regulation of transcription typically correlated with hypermethylation. Using bisulfite genomic sequencing we found that in microdissected HRS cells of primary cHL SYK, BOB.1/OBF.1, and CD79B promoters were also hypermethylated. Ectopic expression of both Oct2 and PU.1 in a cHL cell line potentiated endogenous PU.1 and SYK expression after 5-aza-dC treatment. These observations indicate that silencing of the B-cell-specific genes in cHL may be the consequence of a compromised regulatory network where down-regulation of a few master transcription factors results in silencing of numerous genes. (Blood. 2006;107:2493-2500)
Expression and genomic organization of zonadhesin-like genes in three species of fish give insight into the evolutionary history of a mosaic protein
Authors: Hunt Peter ND , Wilson Michael D , von Schalburg Kristian R , Davidson William S , Koop Ben F 
Published: November 2005

AbstractBackgroundThe mosaic sperm protein zonadhesin (ZAN) has been characterized in mammals and is implicated in species-specific egg-sperm binding interactions. The genomic structure and testes-specific expression of zonadhesin is known for many mammalian species. All zonadhesin genes characterized to date consist of meprin A5 antigen receptor tyrosine phosphatase mu (MAM) domains, mucin tandem repeats, and von Willebrand (VWD) adhesion domains. Here we investigate the genomic structure and expression of zonadhesin-like genes in three species of fish.ResultsThe cDNA and corresponding genomic locus of a zonadhesin-like gene (zlg) in Atlantic salmon (Salmo salar) were sequenced. Zlg is similar in adhesion domain content to mammalian zonadhesin; however, the domain order is altered. Analysis of puffer fish (Takifugu rubripes) and zebrafish (Danio rerio) sequence data identified zonadhesin (zan) genes that share the same domain order, content, and a conserved syntenic relationship with mammalian zonadhesin. A zonadhesin-like gene inD. reriowas also identified. Unlike mammalian zonadhesin,D. rerio zanandS. salar zlgwere expressed in the gut and not in the testes.ConclusionWe characterized likely orthologs of zonadhesin in bothT. rubripesandD. rerioand uncovered zonadhesin-like genes inS. salarandD. rerio. Each of these genes contains MAM, mucin, and VWD domains. While these domains are associated with several proteins that show prominent gut expression, their combination is unique to zonadhesin and zonadhesin-like genes in vertebrates. The expression patterns of fish zonadhesin and zonadhesin-like genes suggest that the reproductive role of zonadhesin evolved later in the mammalian lineage.
Review of the temporal and geographical distribution of measles virus genotypes in the prevaccine and postvaccine eras
Authors: Riddell Michaela A , Rota Jennifer S , Rota Paul A 
Published: November 2005

Abstract
Molecular epidemiological investigation of measles outbreaks can document the interruption of endemic measles transmission and is useful for establishing and clarifying epidemiological links between cases in geographically distinct clusters. To determine the distribution of measles virus genotypes in the prevaccine and postvaccine eras, a literature search of biomedical databases, measles surveillance websites and other electronic sources was conducted for English language reports of measles outbreaks or genetic characterization of measles virus isolates. Genotype assignments based on classification systems other than the currently accepted WHO nomenclature were reassigned using the current criteria. This review gives a comprehensive overview of the distribution of MV genotypes in the prevaccine and postvaccine eras and describes the geographically diverse distribution of some measles virus genotypes and the localized distributions of other genotypes.
The Effect of Microbial Fe(III) Reduction on Smectite Flocculation
Authors: Kim Jin-Wook , Furukawa Yoko , Dong Hailiang , Newell Steven W. 
Published: November 2005

AbstractThis study was undertaken to investigate the changes in flocculation properties of Fe-rich smectite (nontronite, NAu-1) suspensions, including settling velocity, aggregate size and floc architecture associated with microbial Fe(III)-reduction in the smectite structure. The dissimilatory Fe-reducing bacterium Shewanella oneidensis MR-1 was incubated with lactate as the electron donor and structural Fe(III) as the sole electron acceptor for 3, 12, 24 and 48 h in an anaerobic chamber. Two controls were prepared; the first was identical to the experimental treatments except that heat-killed cells were used (non-reduced control), and the second control was the same as the first except that the incubation was carried out in an aerobic environment. The extent of Fe(III) reduction for the 48 h incubation was observed to reach up to 18%. Neither the non-reduced control nor the aerobically inoculated sample showed Fe(III) reduction. Compared with the non-reduced control, there was a 2.7 μm increase in mean aggregate size and a 30-fold increase in average settling velocity in the bioreduced smectite suspensions as measured using a Micromeritics Sedigraph®. The aerobically inoculated smectite showed a similar aggregate-size distribution to that of the non-reduced control. Significant changes in physical properties of smectite suspensions induced by microbial Fe(III) reduction were measured directly using transmission electron microscopy. The floc architecture of bioreduced smectite revealed less open structures compared to those of a non-reduced control. The aspect ratio (thickness/length) of individual smectite particle increased from 0.11 for the non-reduced control to 0.18 on average for the bioreduced smectite suspensions. The effects of pH on the clay flocculation were minimal in this study because the value of pH remained nearly constant at pH = 7.0–7.3 before and after the experiments. We therefore suggest that the increase in net negative charge caused by microbial Fe(III) reduction significantly promoted clay flocculation by increasing the electrochemical attraction in the smectite suspensions.
Fe-Cycle Bacteria from Industrial Clays Mined in Georgia, USA
Authors: Shelobolina Evgenya S. , Pickering Sam M. , Lovley Derek R. 
Published: November 2005

AbstractDark Fe oxides and sulfides are major discoloring impurities in mined commercial white kaolin clay. In order to evaluate the potential influence of Fe-cycle bacteria on Fe cycling during post-depositional clay-weathering alteration, Fe(III)-reducing and/or Fe(II)-oxidizing microorganisms were examined in open-pit, subsurface mine samples from kaolin lenses and smectite formations collected from sites in central Georgia. Samples of varying age were examined, including late Eocene smectite overburden, hard kaolin of Middle Eocene age, soft gray kaolin from the late Paleocene, and soft tan kaolin of late Cretaceous age. These clays contained 0.06–5.33% organic carbon, which included various potential organic electron donors for bacterial metabolism: formate (1.1–30.6 mmol/kg), acetate (0–40.5 mmol/kg), lactate (0–12.1 mmol/kg), pyruvate (0.4–78 mmol/kg), oxalate (0–141.7 mmol/kg), and citrate (0–1.4 mmol/kg). All clay samples studied had small concentrations of ‘bio-available’ Fe(III) (0.5 M HCl-extractable Fe, 0.5–2.8 mmol/kg) compared to total Fe (HF-extractable, 25–171.9 mmol/kg). The highest Fe(III)/[Fe(II)+Fe(III)] ratio and the lowest organic carbon content were in kaolin samples in which Fe(III) reduction was determined to be the dominant terminal electron accepting process by hydrogen analysis. All clay samples showed greater numbers of Fe(II)-oxidizing bacteria (22–22,000 cells/g) than Fe(III)-reducing bacteria (3–410 cells/g) as determined by MPN analysis. The Fe(III)-reducing activity in clays could be stimulated with the addition of 1 mM of the Fe(III) chelator, nitrilotriacetic acid. The addition of nitrate stimulated anaerobic Fe(II) oxidation. These results suggest that anaerobic bacteria involved in both oxidation and reduction of Fe exist in these subsurface clay formations, and might have had an influence on post-depositional weathering reactions.
Oxidation of 1-Naphthol Coupled to Reduction of Structural Fe3+ in Smectite
Authors: Jacqueline Arroyo L. , Li Hui , Teppen Brian J. , Johnston Cliff T. , Boyd Stephen A. 
Published: November 2005

AbstractSorption and transformation of 1-naphthol by a K-smectite (K-SWy-2) were studied using batch sorption isotherms, Fourier-transform infrared spectroscopy (FTIR), and X-ray diffraction (XRD). The sorbents included three preparations of the reference smectite clay (SWy-2): (1) whole clay containing naturally occurring carbonate impurities, (2) SWy-2 with the removal of carbonate impurities, and (3) the carbonate-free SWy-2 fraction amended with calcite. For the whole clay and carbonate-free clay amended with calcite, >80% of added 1-naphthol disappeared from aqueous solution within 24 h, corresponding to a sorbed concentration of ≥2 mg/g of clay. In contrast, only 35% of the added 1-naphthol disappeared from solution in the carbonate-free clay after 24 h of exposure. For the clays from the three preparations in this study, <1% of sorbed 1-naphthol could be recovered by methanol extraction from the clays. The XRD data suggested that 1-naphthol was intercalated in the smectite, but was not conclusive because the 1-naphthol sorption range (1.5–2.8 mg/g of clay) in this study had relatively minor effects on the XRD patterns. The FTIR spectra of sorbed 1-naphthol-clay complexes demonstrated structural Fe3+ reduction. The spectra also showed evidence of the transformation of 1-naphthol. It suggests that reduction of structural Fe3+ may be coupled to oxidation/polymerization of 1-naphthol. Further transformation of oxidized 1-naphthol, such as by oxidative coupling reactions, is implicated by formation of a dark gray color on the clay and the inability to extract sorbed 1-naphthol.