bluuebunny/crossref_metadata_2025_split huggingface dataset:
Verification of Temporal Variations in Mesoscale Numerical Wind Forecasts
Authors: Rife Daran L. , Davis Christopher A. 
Published: November 2005

AbstractThe authors address a particular example of the general question of whether high-resolution forecasts provide additional deterministic skill beyond what can be achieved with a coarser-resolution model. To this end, real-time forecasts using the fifth-generation Pennsylvania State University–NCAR Mesoscale Model (MM5) with grid increments of 30 and 3.3 km are compared over a domain centered on the complex terrain region of southern New Mexico during the 1 June 2002 to 1 June 2003 period. The authors use time series of surface data to evaluate the relative ability of the two forecasts to capture significant temporal variations of wind. The authors hypothesize that the additional detail and structure provided by high resolution becomes a “liability” when the forecasts are scored by traditional verification metrics, because such metrics sharply penalize forecasts with small temporal or spatial errors of predicted features. Thus, a set of verification metrics is designed that is increasingly tolerant of timing errors for temporal changes of wind.The authors find that the barrier-normal (i.e., zonal) wind component over complex terrain reveals the greatest improvement in skill due to increased horizontal resolution for the cases considered here. In addition, the fine-grid forecasts better replicate the cessation of drainage flow or onset of upslope flow near and within complex terrain. The most surprising result is the marginal benefit of the higher resolution over valley locations not in immediate proximity to the mountain slopes, even though the valley is only about 60 km across (east–west). Overall, the gains in forecast accuracy from finer grid spacing are generally incremental, but increase with greater tolerance for timing errors, culminating in the greatest improvement for forecasts of temporal variance.
Molecular Pathogenesis of MDS
Authors: Look A. Thomas 
Published: November 2005

Abstract
Clonal disorders of hematopoiesis, such as myelodysplastic syndromes (MDS) and myeloproliferative diseases (MPD), affect both hematopoietic stem cells and progenitor cells within the erythroid, platelet and granulocytic lineages and can have devastating consequences in children and adults. The genetic features of these diseases often include clonal, nonrandom chromosomal deletions (e.g., 7q–, 5q–, 20q–, 6q–, 11q– and 13q–) that appear to inactivate tumor suppressor genes required for the normal development of myeloid cells (reviewed in Bench1 and Fenaux2). These putative tumor suppressors have proved to be much more difficult to identify than oncogenes activated by chromosomal translocations, the other major class of chromosomal lesions in MDS and MPD.3 Although MDS and MPD are almost certainly caused by mutations in stem/progenitor cells,4 the role of inactivated tumor suppressor genes in this process remains poorly understood. In a small portion of myeloid diseases, mutations have been identified in genes encoding factors known to be required for normal hematopoiesis, such as PU.1, RUNX1, CTNNA1 (α-catenin) and c/EBPα, and implicating these genes as tumor suppressors.5–7 Nonetheless, the identities of most deletion-associated tumor suppressors in these diseases remains elusive, despite complete sequencing of the human genome. The deleted regions detected by cytogenetic methods are generally very large, containing many hundreds of genes, thus making it hard to locate the critical affected gene or genes. It is also unclear whether dysfunctional myelopoiesis results from haploinsufficiency, associated with the deletion of one allele, or from homozygous inactivation due to additional point mutations or microdeletions of the retained wild-type allele. In general MDS have proved surprisingly resistant to conventional treatments. Targeted therapeutic advances in MDS will likely depend on a full comprehension of underlying molecular mechanisms, in particular the tumor suppressor genes lost through clonal, nonrandom chromosomal deletions, such as the 7q– and (del)5q.
Diffuse Large B-Cell Lymphoma: Risk Stratification and Management of Relapsed Disease
Authors: Sweetenham John W. 
Published: November 2005

AbstractThe clinical factors described by the International Prognostic Index (IPI) provide a model for risk stratification in diffuse large B-cell lymphomas (DLBCLs). However, there is variability in outcome within IPI risk groups, indicating the biological and clinical heterogeneity of these diseases. Studies of gene expression profiling (GEP) in DLBCL are uncovering biological heterogeneity with prognostic significance. Various gene expression signatures with predictive value independent of the IPI are now recognized. Immunophenotypic features of DLBCL have also been shown to have prognostic value. The use of fluorodeoxyglucose–positron emission tomography (FDG-PET) scanning may provide additional predictive information when used at diagnosis or soon after initiation of treatment. Future prognostic models in DLBCL are likely to incorporate functional imaging, immunophenotype and GEPs as well as clinical data in risk stratification and choice of treatment.Treatment of relapsed DLBCL remains a major problem. High-dose therapy (HDT) and stem cell transplantation (SCT) has been shown to produce superior overall survival (OS) compared with conventional dose salvage therapy in patients with relapsed, chemosensitive DLBCL. However, only 20% to 30% of patients are cured by this approach, and the effectiveness of HDT and SCT in patients treated with rituximab-based combinations as first-line therapy is unknown. Although new transplant techniques including non-myeloablative allogeneic SCT are being investigated, their role is unclear. New treatment strategies are needed for these patients. The use of molecular techniques such as GEP is identifying many potential new therapeutic targets in DLBCL including histone deacetylase, HLA-DR, bcl-2, bcl-6, mTOR and TRAIL.
CLL Biology and Prognosis
Authors: Dighiero Guillaume 
Published: November 2005

AbstractChronic lymphocytic leukemia (CLL) follows an extremely variable course with survival ranging from months to decades. Recently, there has been major progress in the identification of molecular and cellular markers that may predict the tendency for disease progression in CLL patients. In particular, the mutational profile of Ig genes and some cytogenetic abnormalities have been found to be important predictors of prognosis in CLL. However, this progress has raised new questions about the biology and prognosis of the disease, some of which are addressed here. Such questions include: 1) What is the role of the B-cell receptor (BCR) in CLL pathogenesis? 2) Is CLL one disease? 3) Is CLL an accumulative disease? 4) What is the normal counterpart of the CLL B lymphocyte? 5) Have the Rai and Binet staging systems become obsolete? 6) Which is the best surrogate for Ig mutational profiles?
Targeting CD20 in Follicular NHL: Novel Anti-CD20 Therapies, Antibody Engineering, and the Use of Radioimmunoconjugates
Authors: Leonard John P. 
Published: November 2005

AbstractRituximab (chimeric anti-CD20 monoclonal antibody) is widely employed in the treatment of patients with B cell non-Hodgkin lymphoma (NHL). This agent has activity in both indolent and aggressive disease, alone and in combination with chemotherapy. Unfortunately, however, many patients develop resistant disease. Ongoing efforts to improve outcomes include changes in dose and schedule, as well as the use of other biologic agents or antibodies that may enhance activity when administered together with rituximab. A relatively new focus is the development of engineered anti-CD20 antibodies that are optimized for their capability to mediate antibody-mediated cellular cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC). Human or humanized structures have also been employed to potentially improve these attributes, as well as to improve on pharmacokinetics and immunogenicity. Other studies in NHL have clearly demonstrated that radiolabeled anti-CD20 antibodies (such as I-131 tositumomab and Y-90 ibritumomab tiuxetan) may be useful in relapsed and refractory disease, and have potential utility as part of initial treatment as well. Further studies of these modified anti-CD20 antibodies are ongoing in order to optimize their use for maximal clinical benefit.
Cryoglobulinemia
Authors: Morra Enrica 
Published: November 2005

Abstract
Mixed cryoglobulinemia (MC) type II is a disorder characterized by circulating cold-precipitable immune complexes composed of polyclonal immunoglobulin IgG and monoclonal IgM rheumatoid factor (RF). The systemic vasculitis which characterizes the disease is caused by the deposition of immune complexes on the walls of small vessels, and by the subsequent activation of the complement cascade. MC may be asymptomatic or lead to clinical manifestations characterized by a typical triad—purpura, arthralgia, and weakness—and in some cases by a more serious vasculitis with neurologic and renal involvement. In the vast majority (more than 90%) of patients, MC is associated with hepatitis C virus (HCV) infection, which is considered the triggering factor of the disease. The association between cryoglobulinemia and HCV infection, and the possible evolution to B-cell lymphomas usually after long-term follow-up, suggest the role of HCV infection both in the pathogenesis of MC and in lymphomagenesis. In fact, the virus chronically stimulates the polyclonal proliferation of B cells from which a monoclonal population may emerge. This paper also reviews the treatment strategies for MC syndrome, emphasizing the issue of the eradication of HCV, and the clinical and biological activity of ritux-imab for selective B-cell control.
Thrombosis and the Antiphospholipid Syndrome
Authors: Ortel Thomas L. 
Published: November 2005

Abstract
The antiphospholipid syndrome is an antibody-mediated hypercoagulable state characterized by recurrent venous and arterial thromboembolic events. Several studies have determined that the frequency of antiphospholipid syndrome in patients presenting with a venous thromboembolic event is between 4% and 14%. Because of the high risk for recurrent thromboembolism in these patients, current recommendations suggest a longer, potentially lifelong, course of antithrombotic therapy following an initial event. Although most authorities agree on an extended course of therapy, considerable controversy surrounds the optimal target therapeutic INR for patients with antiphospholipid syndrome. For an initial venous thromboembolic event, a target INR of 2.0 to 3.0 is supported by two prospective, randomized clinical trials. In contrast, relatively limited data exist for an initial arterial thromboembolic event in patients who have the antiphospholipid syndrome, and therapeutic recommendations range from aspirin to warfarin with a high target INR. Recurrent thromboembolic events can be extremely difficult to treat, and some patients may benefit from the addition of immunosuppressive therapies. Importantly, as many as 50% of the initial thromboembolic events sustained by patients with antiphospholipid antibodies occur in the setting of additional, coincident prothrombotic risk factors, indicating the importance of addressing any additional risk factors, such as hypercholesterolemia, in these patients. Prospective studies are needed to address the role of thromboprophylactic strategies in asymptomatic individuals with antiphospholipid antibodies in the absence of additional risk factors.
Practical and Ethical Issues with Genetic Screening
Authors: Wagner John E. 
Published: November 2005

Abstract
Clinical hematologists are faced with a growing list of new genetic-based tools for identifying a patient’s risk of disease. While many of the disease-specific tests are readily available, validation studies are required. Furthermore, genetic-based tests are being pushed to their technical limits, such as testing a single cell prior to embryo selection and transfer for couples at risk of genetic disease. As a result, misdiagnosis or misinterpretation of the data may result. As new genetic testing opportunities proliferate, the hematologist needs to be aware of the medical and legal issues surrounding their use. Furthermore, the hematologist needs to consider the psychological, ethical and social implications of this new field of genomic-based medicine.
Medical Errors
Authors: Holder Angela Roddey 
Published: November 2005

AbstractFollowing the 2000 report of the Institute of Medicine, To Err Is Human, which documented that as many as 98,000 people in this country die of medical errors every year, medical, hospital, and governmental agencies began to consider changes in hospital systems. The report had found that errors were much more likely to result from systemic problems than from inept health care providers. Progress in reinventing hospital systems has been very slow, although some institutions have made great gains.“Medical errors” may be of several types. Some lead to malpractice claims, many do not. Many people who have been severely injured by errors never file claims. Making a medical mistake is not necessarily “malpractice.”There are six elements a patient must prove in order to win a malpractice case: a physician-patient relationship must exist, the care provider must owe the patient a duty of care, evidence (usually expert testimony) must be presented that there was a failure in some part of the duty of care, there must proof that the lack of care was the proximate cause of harm, and proof of evidence that harm occurred. The patient must also prove his or her assessment of damages.Solutions to the problem of patient injuries are suggested.
Hereditary Periodic Fever Syndromes
Authors: Kastner Daniel L. 
Published: November 2005

Abstract
The hereditary periodic fevers are a group of Mendelian disorders characterized by seemingly unprovoked fever and localized inflammation. Recent data indicate that these illnesses represent inborn errors in the regulation of innate immunity. Pyrin, the protein mutated in familial Mediterranean fever, defines an N-terminal domain found in a large family of proteins involved in inflammation and apoptosis. Through this domain pyrin may play a role in the regulation of interleukin (IL)-1β, nuclear factor (NF)-κB, and leukocyte apoptosis. Cryopyrin/NALP3, another protein in this family, is mutated in three other hereditary febrile syndromes and participates in the inflammasome, a newly recognized macromolecular complex crucial to IL-1β activation. Somewhat unexpectedly, mutations in the 55 kDa receptor for tumor necrosis factor also give rise to a dominantly inherited periodic fever syndrome, rather than immunodeficiency, a finding that has stimulated important investigations into both pathogenesis and treatment. Finally, the discovery of the genetic basis of the hyperimmunoglobulinemia D with periodic fever syndrome suggests an as yet incompletely understood connection between the mevalonate pathway and the regulation of cytokine production. These insights extend our understanding of the regulation of innate immunity in man, while providing the conceptual basis for the rational design of targeted therapies, both for the hereditary periodic fevers themselves and other inflammatory disorders as well.
c-FLIP confers resistance to FAS-mediated apoptosis in anaplastic large-cell lymphoma
Authors: Oyarzo Mauricio P. , Medeiros L. Jeffrey , Atwell Coralyn , Feretzaki Marianna , Leventaki Vasiliki , Drakos Elias , Amin Hesham M. , Rassidakis George Z. 
Published: November 2005

AbstractWe hypothesized that inhibition of the FAS-mediated apoptosis pathway by FLICE-like inhibitory protein (c-FLIP) may contribute to oncogenesis in ALK+ anaplastic large-cell lymphoma (ALCL). Treatment with increasing concentrations of CH-11 (CD95/FAS agonistic antibody) had no effect on cell viability of 2 ALK+ ALCL cell lines, Karpas 299 and SU-DHL1, each expressing high levels of c-FLIP. However, inhibition of endogenous c-FLIP expression by specific c-FLIP siRNA in Karpas 299 and SU-DHL1 cells treated with CH-11 resulted in FAS-mediated cell death associated with increased annexin V binding, apoptotic morphology, and cleavage of caspase-8. In 26 ALK+ ALCL tumors, assessed for expression of DISC-associated proteins, CD95/FAS and c-FLIP were commonly expressed, in 23 (92%) of 25 and 21 (91%) of 23 tumors, respectively. By contrast, CD95L/FASL was expressed in only 3 (12%) of 26 ALCL tumors, although it was strongly expressed by surrounding small reactive lymphocytes. Our findings suggest that overexpression of c-FLIP protects ALK+ ALCL cells from death-receptor-induced apoptosis and may contribute to ALCL pathogenesis. (Blood. 2006;107:2544-2547)
Essential role of PI3Kδ and PI3Kγ in thymocyte survival
Authors: Swat Wojciech , Montgrain Vivianne , Doggett Teresa A. , Douangpanya Jason , Puri Kamal , Vermi William , Diacovo Thomas G. 
Published: November 2005

AbstractClass 1 phosphoinositide 3-kinases (PI3Ks), consisting of PI3Kα, β, γ, and δ, are a family of intracellular signaling molecules that play important roles in cell-mediated immune responses. In thymocytes, however, their role is less clear, although PI3Kγ is postulated to partially contribute to pre-TCR-dependent differentiation. We now report that PI3Kδ, in conjunction with PI3Kγ, is required for thymocyte survival and ultimately for T-cell production. Surprisingly, genetic deletion of the p110δ and p110γ catalytic subunits resulted in a dramatic reduction in thymus size, cellularity, and lack of corticomedullary differentiation. Total thymocyte counts in these animals were 27-fold lower than in wild-type (WT) controls because of a diminished number of CD4+CD8+ double-positive (DP) cells and were associated with T-cell depletion in blood and in secondary lymphoid organs. Moreover, this alteration in the DP population was intrinsic to thymocytes, because the reconstitution of p110γδ-/- animals with WT fetal liver cells restored the proportions of all thymocyte populations to those in WT controls. The observed defects were related to massive apoptosis in the DP population; TCRB expression, pre-TCR selection, and generation of DP cells appeared relatively unperturbed. Thus, class 1 PI3Ks work in concert to protect developing thymocytes from apoptosis. (Blood. 2006;107:2415-2422)
Phenytoin as a novel anti-vitiligo weapon
Authors: Namazi MR 
Published: November 2005

AbstractVitiligo is a psychologically devastating clinical conundrum which affects approximately 1% of the general population. The exact cause of the illness is an enigma, but several hypotheses about its pathogenesis are advanced.The autoimmune hypothesis proposes an autoimmune attack against melanocytes. Although anti-melanocyte autoantibodies have been demonstrated in vitiligo, recent research casts doubt on their pathogenic role and instead supports the involvement of cell-mediated autoimmune response in the pathobiology of this disorder, which is characterized by increase of suppressor T-cells and decrease of the helper/suppressor ratio in association with the presence of type-1 cytokine secreting cytotoxic T cells in the vicinity of disappearing melanocytes.The neural hypothesis proposes that increased release of norepinephrine, a melanocytotoxin, from the autonomic nerve endings in the microenvironment of melanocytes injures these cells. Moreover, norepinephrine induces the catecholamine degrading enzyme monoamine oxidase (MAO), which favors the formation of toxic levels of hydrogen peroxide in the vicinity of melanocytes.Another theory suggests that abnormal permeability of melanosome membrane, which normally prevents the diffusion of toxic melanin precursors into the cytoplasm, may cause melanocyte damage.Phenytoin, the widely-used anticonvulsant, has been employed both topically and systemically in the treatment of some dermatological disorders. The drug has been shown to significantly suppress mitogen-induced activation of lymphocytes and cytotoxic T lymphocyte activity and to polarize the immune response toward the type-2 pathway. It also significantly decreases suppressor T cells and increases the helper/suppressor ratio.At high concentrations, the drug inhibits the release of norepinephrine and the activity of MAO. Moreover, phenytoin is suggested to interact with membrane lipids, which may promote stabilization of the membranes.The hydantoin moiety of phenytoin exerts a direct stimulatory action on melanocytes; facial hyperpigmentation is a recognized side effect of orally administered phenytoin.Altogether, the above evidence suggests that phenytoin could be therapeutically effective against vitiligo. As phenytoin stimulates collagen production and inhibits its breakdown, its concomitant use with topical steroids could prevent steroid-induced skin atrophy while potentiating the anti-vitiligo effect of these agents.
Color Tuning Based on a Six-membered Chelated Iridium(III) Complex with Aza-aromatic Ligand
Authors: Zhu Rui , Lin Jian , Wen Gui-An , Liu Shu-Juan , Wan Jun-Hua , Feng Jia-Chun , Fan Qu-Li , Zhong Gao-Yu , Wei Wei , Huang Wei 
Published: November 2005

Abstract
A six-membered chelated iridium complex containing aza-aromatic ligand is prepared. Emission color tuning from yellow to deep red is observed for electroluminescent devices with different doping concentrations.
Preparation of Gold Nanoplates by an Electrochemical Method
Authors: Zhou Min , Chen Shenhao , Zhao Shiyong , Ma Hongfang 
Published: November 2005

Abstract
Single-crystal triangular and hexangular nanoplates of gold can be obtained by electrochemical reducing AuCl4− in the presence of PVP and a small amount of H2PtCl6. With the concentration of H2PtCl6 increasing from 0 to 1 × 10−3 mol/dm3, the morphology of Au nanoparticles evolved from spheroids to triangular and hexangular nanoplates with well-defined facets.
Cyclization and Ring-expansion Reactions Involving Reductive Formation and Oxidative Ring-opening of Cyclopropanol Derivatives
Authors: Hasegawa Eietsu , Tsuchida Hiroyuki , Tamura Mutsuko 
Published: November 2005

Abstract
FeCl3-promoted regioselective ring-opening reactions of cyclopropyl trimethylsilyl ethers, obtained by SmI2 reduction followed by silylation with Me3SiCl of bromoalkyl ketones and acyl chloride, were performed. Eventually, the sequential reduction and oxidation reactions starting from bromoalkyl ketones to give ring-expanded enones were achieved in one-pot.
Anomalous Magnetic Field Effects Interpreted by the Relaxation Mechanism under Ultrahigh Fields of up to 28 T
Authors: Hamasaki Atom , Nishizawa Kiyoshi , Sakaguchi Yoshio , Okada Toshiyuki , Kido Giyuu , Wakasa Masanobu 
Published: November 2005

Abstract
Magnetic field effects on the triplet sensitization reaction of p-aminophenyl disulfide were studied in a sodium dodecylsulfate micellar solution by a nanosecond laser flash photolysis technique under ultrahigh magnetic fields of up to 28 T. The yield of the escaped p-aminophenyl thiyl radical decreased by 6 ± 2% at 28 T compared with that at 0 T.
Preparation of Mesoporous Titania Particles with Photocatalytic Activity under Visible-light Irradiation
Authors: Shibata Hirobumi , Mukai Tatsuya , Akita Takahito , Ohkubo Takahiro , Sakai Hideki , Abe Masahiko 
Published: November 2005

Abstract
Novel visible light-responsive photocatalytic mesoporous titania particles were prepared using the sol–gel reaction of titanium oxysulfate sulfuric acid hydrate TiOSO4·xH2SO4·xH2O in aqueous solution in the presence of lyotropic cetyltrimethylammonium bromide (CTAB) liquid crystal as template. The absorption threshold of the calcined particles shifted toward the longer wavelength side and they showed a photocatalytic activity in the oxidation of gaseous 2-propanol under visible light (&gt;440 nm) irradiation.