bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison of functions for evaluating the effect of Fe and Al oxides on the particle size distribution of kaolin and quartz
Authors: Arias M. , Lopez E. , Barral M. T. 
Published: December 2006

AbstractAlthough it is generally agreed that Fe and Al can act to bind soil particles, their relative efficiencies as aggregants are still disputed. In this work, the aggregating efficiencies of both aged and non-aged Fe and Al oxides precipitated on kaolin or quartz substrates were characterized by comparing their effects on particle size distributions (PSD). To facilitate comparison of PSD data, these were parameterized by fitting them with five different probability density functions (the normal, lognormal, Jaky, fractal and Rosin-Rammler functions). The best fits were given by the Rosin-Rammler function (R2 = 0.997), whose α parameter was used to compare the aggregating efficiency of Fe and Al oxides: in order of decreasing efficiency, non-aged Al > non-aged Fe ≈ aged Fe > aged Al-precipitates.
Solid-state 27Al and 29Si NMR analysis of hydroxy-Cr and-Al interlayered montmorillonite
Authors: Dubbin W. E. , Goh Tee Boon 
Published: December 2006

AbstractThe ease with which sorbed Cr(III) is released to solution via oxidation or cation exchange depends on its mode of complexation and the broader chemical environment in which it is held. This study was conducted to elucidate the chemical environment of hydrolysed Cr(III) sorbed onto montmorillonite, both alone and coprecipitated with Al. The 27Al MAS NMR revealed that Cr in the coprecipitated hydroxy interlayer created a second environment for AI, slightly more shielded than that of Al in the montmorillonite 2:1 layer. This observation is evidence for the presence of numerous Al-O-Cr linkages, thus revealing a uniform distribution of Al and Cr within the hydroxy polymers. The 29Si MAS NMR revealed a second environment for Si in the tetrahedral sheet of the Cr clays. This environment could be created only through a redistribution of electrons at the siloxane surface caused by inner-sphere complexation of Cr(III). Due to this inner-sphere complexation, sorbed Cr(III) is difficult to displace via simple exchange reactions and, consequently, its bioavailability is decreased.
Antithrombotic properties of aspirin and resistance to aspirin: beyond strictly antiplatelet actions
Authors: Undas Anetta , Brummel-Ziedins Kathleen E. , Mann Kenneth G. 
Published: December 2006

AbstractAspirin is effective in the prevention of cardiovascular events in high-risk patients. The primary established effect of aspirin on hemostasis is to impair platelet aggregation via inhibition of platelet thromboxane A2 synthesis, thus reducing thrombus formation on the surface of the damaged arterial wall. Growing evidence also indicates that aspirin exerts additional antithrombotic effects, which appear to some extent unrelated to platelet thromboxane A2 production. Aspirin can reduce thrombin generation with the subsequent attenuation of thrombin-mediated coagulant reactions such as factor XIII activation. Aspirin also acetylates lysine residues in fibrinogen resulting in increased fibrin clot permeability and enhanced clot lysis as well as directly promoting fibrinolysis with high-dose aspirin. The variable effectiveness of aspirin in terms of clinical outcomes and laboratory findings, which has been termed aspirin resistance, may be related to these additional antithrombotic effects that are altered when associated with common genetic polymorphisms such as the Leu33Pro β3-integrin or Val34Leu factor XIII mutations. However, the clinical relevance of these observations is still unclear. Elucidation of the actual impacts of aspirin other than antiaggregation effects could be important in view of the widespread use of this drug in the prevention of thrombotic manifestations of atherosclerosis.
Inability of memory T cells to induce graft-versus-host disease is a result of an abortive alloresponse
Authors: Chen Benny J. , Deoliveira Divino , Cui Xiuyu , Le Ngocdiep T. , Son Jessica , Whitesides John F. , Chao Nelson J. 
Published: December 2006

AbstractSeveral groups, including our own, have independently demonstrated that effector memory T cells from non–alloantigen-primed donors do not cause graft-versus-host disease (GVHD). In the current study, we further investigated whether this approach could be extended to all memory T cells, and we studied the underlying mechanisms. Neither total memory T cells nor purified central memory T cells were able to induce GVHD. Memory T cells were at least 3-log less potent than bulk T cells in mediating GVHD. As expected, memory T cells failed to elicit cytotoxicity and proliferated poorly against alloantigens in standard 5-day mixed-lymphocyte cultures. However, the proliferative responses of memory T cells were more comparable with those of bulk and naive T cells when the culture time was shortened. Moreover, the frequencies of IL-2–secreting cells measured by 42-hour enzyme-linked immunosorbent spot (ELISPOT) assay were similar among naive, memory, and bulk T cells. These data indicated that memory T cells are able to respond to alloantigens initially but fail to develop to full potential. The abortive immune response, which was mediated by non–alloantigen-specific memory T cells in response to alloantigens, may explain why memory T cells from unprimed and non–alloantigen-primed donors could not induce GVHD.
Congenital erythropoietic porphyria due to a mutation in GATA1: the first trans-acting mutation causative for a human porphyria
Authors: Phillips John D. , Steensma David P. , Pulsipher Michael A. , Spangrude Gerald J. , Kushner James P. 
Published: December 2006

AbstractCongenital erythropoietic porphyria (CEP), an autosomal recessive disorder, is due to mutations of uroporphyrinogen III synthase (UROS). Deficiency of UROS results in excess uroporphyrin I, which causes photosensitization. We evaluated a 3-year-old boy with CEP. A hypochromic, microcytic anemia was present from birth, and platelet counts averaged 70 × 109/L (70 000/μL). Erythrocyte UROS activity was 21% of controls. Red cell morphology and globin chain labeling studies were compatible with β-thalassemia. Hb electrophoresis revealed 36.3% A, 2.4% A2, 59.5% F, and 1.8% of an unidentified peak. No UROS or α- and β-globin mutations were found in the child or the parents. The molecular basis of the phenotype proved to be a mutation of GATA1, an X-linked transcription factor common to globin genes and heme biosynthetic enzymes in erythrocytes. A mutation at codon 216 in the child and on one allele of his mother changed arginine to tryptophan (R216W). This is the first report of a human porphyria due to a mutation in a trans-acting factor and the first association of CEP with thalassemia and thrombocytopenia. The Hb F level of 59.5% suggests a role for GATA-1 in globin switching. A bone marrow allograft corrected both the porphyria and the thalassemia.
Adenovirus-induced thrombocytopenia: the role of von Willebrand factor and P-selectin in mediating accelerated platelet clearance
Authors: Othman Maha , Labelle Andrea , Mazzetti Ian , Elbatarny Hisham S. , Lillicrap David 
Published: December 2006

AbstractThrombocytopenia has been consistently reported following the administration of adenoviral gene transfer vectors. The mechanism underlying this phenomenon is currently unknown. In this study, we have assessed the influence of von Willebrand Factor (VWF) and P-selectin on the clearance of platelets following adenovirus administration. In mice, thrombocytopenia occurs between 5 and 24 hours after adenovirus delivery. The virus activates platelets and induces platelet-leukocyte aggregate formation. There is an associated increase in platelet and leukocyte-derived microparticles. Adenovirus-induced endothelial cell activation was shown by VCAM-1 expression on virus-treated, cultured endothelial cells and by the release of ultra-large molecular weight multimers of VWF within 1 to 2 hours of virus administration with an accompanying elevation of endothelial microparticles. In contrast, VWF knockout (KO) mice did not show significant thrombocytopenia after adenovirus administration. We have also shown that adenovirus interferes with adhesion of platelets to a fibronectin-coated surface and flow cytometry revealed the presence of the Coxsackie adenovirus receptor on the platelet surface. We conclude that VWF and P-selectin are critically involved in a complex platelet-leukocyte-endothelial interplay, resulting in platelet activation and accelerated platelet clearance following adenovirus administration.
In the absence of IGF-1 signaling, IFN-γ suppresses human malignant T-cell growth
Authors: Conti Laura , Regis Gabriella , Longo Angela , Bernabei Paola , Chiarle Roberto , Giovarelli Mirella , Novelli Francesco 
Published: December 2006

AbstractSeveral approaches to target insulin-like growth factor-1 (IGF-1) signaling have resulted in the inhibition of the growth of a broad range of tumor cells. Malignant T cells are insensitive to the antiproliferative effects of the interferon-γ (IFN-γ)/signal transducer and activator of transcription 1 (STAT1) pathway because of the IGF-1–dependent internalization of the IFN-γR2 signaling chain. Here we show that human malignant T cells are also resistant to the growth inhibitory effect of both the IGF-1 receptor–specific inhibitor picropodophyllin (PPP) and retrovirus-mediated gene transfer of a dominant negative IGF-1 receptor. However, blockade of IGF-1 receptor perturbs IFN-γR2 internalization and induces its cell surface accumulation in malignant T cells. This allows the reinstatement of the IFN-γ–induced STAT1 activation, a high expression of proapoptotic molecules, and the suppression of malignant T-cell growth both in vitro and in vivo in a severe combined immunodeficiency (SCID) mouse model. These data indicate that the inhibition of IGF-1 signaling combined with IFN-γ administration could be a promising approach to suppress the growth of neoplastic T cells resistant to each treatment on its own.
Comprehensive analysis of homeobox genes in Hodgkin lymphoma cell lines identifies dysregulated expression of HOXB9 mediated via ERK5 signaling and BMI1
Authors: Nagel Stefan , Burek Christof , Venturini Letizia , Scherr Michaela , Quentmeier Hilmar , Meyer Corinna , Rosenwald Andreas , Drexler Hans G. , MacLeod Roderick A. F. 
Published: December 2006

AbstractMany members of the nearly 200-strong homeobox gene family have been implicated in cancer, mostly following ectopic expression. In this study we analyzed homeobox gene expression in Hodgkin lymphoma (HL) cell lines. Both reverse transcription–polymerase chain reaction (RT-PCR) using degenerate primers and microarray profiling identified consistently up-regulated HOXB9 expression. Analysis of HOXB9 regulation in HL cells revealed E2F3A and BMI1 as activator and repressor, respectively. Furthermore, a constitutively active ERK5 pathway was identified in all HL cell lines analyzed as well as primary HL cells. Our data show that ERK5 probably mediates HOXB9 expression by repressing BMI1. In addition, expression analysis of the neighboring microRNA gene mir-196a1 revealed coregulation with HOXB9. Functional analysis of HOXB9 by knockdown and overexpression assays indicated their influence on both proliferation and apoptosis in HL cells. In summary, we identified up-regulation of HOXB9 in HL mediated by constitutively active ERK5 signaling which may represent novel therapeutic targets in HL.
Development of the hemangioblast defines the onset of hematopoiesis in human ES cell differentiation cultures
Authors: Kennedy Marion , D'Souza Sunita L. , Lynch-Kattman Macarena , Schwantz Staci , Keller Gordon 
Published: December 2006

AbstractThe onset of hematopoiesis in the mouse embryo and in the embryonic stem (ES) cell differentiation model is defined by the emergence of the hemangioblast, a progenitor with both hematopoietic and vascular potential. While there is evidence for the existence of a hemangioblast in the mouse, it is unclear if this progenitor develops during the establishment of the human hematopoietic system. In this report, we have mapped hematopoietic development in human ES cell (hESC) differentiation cultures and demonstrated that a comparable hemangioblast population exists. The human hemangioblasts were identified by their capacity to generate blast colonies that display both hematopoietic and vascular potential. These colony-forming cells express the receptor tyrosine kinase KDR (VEGF receptor 2) and represent a transient population that develops in BMP-4–stimulated embryoid bodies (EBs) between 72 and 96 hours of differentiation, prior to the onset of the primitive erythroid program. Two distinct types of hemangioblasts were identified, those that give rise to primitive erythroid cells, macrophages, and endothelial cells and those that generate only the primitive erythroid population and endothelial cells. These findings demonstrate for the first time the existence of the human hemangioblast and in doing so identify the earliest stage of hematopoietic commitment.
Topology testing of phylogenies using least squares methods
Authors: Czarna Aleksandra , Sanjuán Rafael , González-Candelas Fernando , Wróbel Borys 
Published: December 2006

Abstract

Background
The least squares (LS) method for constructing confidence sets of trees is closely related to LS tree building methods, in which the goodness of fit of the distances measured on the tree (patristic distances) to the observed distances between taxa is the criterion used for selecting the best topology. The generalized LS (GLS) method for topology testing is often frustrated by the computational difficulties in calculating the covariance matrix and its inverse, which in practice requires approximations. The weighted LS (WLS) allows for a more efficient albeit approximate calculation of the test statistic by ignoring the covariances between the distances.

Results
The goal of this paper is to assess the applicability of the LS approach for constructing confidence sets of trees. We show that the approximations inherent to the WLS method did not affect negatively the accuracy and reliability of the test both in the analysis of biological sequences and DNA-DNA hybridization data (for which character-based testing methods cannot be used). On the other hand, we report several problems for the GLS method, at least for the available implementation. For many data sets of biological sequences, the GLS statistic could not be calculated. For some data sets for which it could, the GLS method included all the possible trees in the confidence set despite a strong phylogenetic signal in the data. Finally, contrary to WLS, for simulated sequences GLS showed undercoverage (frequent non-inclusion of the true tree in the confidence set).

Conclusion
The WLS method provides a computationally efficient approximation to the GLS useful especially in exploratory analyses of confidence sets of trees, when assessing the phylogenetic signal in the data, and when other methods are not available.
Gene transfer and expression in human neutrophils. The phox homology domain of p47
phox
translocates to the plasma membrane but not to the membrane of mature phagosomes
Authors: Johnson Jennifer L , Ellis Beverly A , Munafo Daniela B , Brzezinska Agnieszka A , Catz Sergio D 
Published: December 2006

Abstract

Background
Neutrophils are non-dividing cells with poor survival after isolation. Consequently, exogenous gene expression in neutrophils is challenging. We report here the transfection of genes and expression of active proteins in human primary peripheral neutrophils using nucleofection.

Results
Exogenous gene expression in human neutrophils was achieved 2 h post-transfection. We show that neutrophils transfected by nucleofection are functional cells, able to respond to soluble and particulate stimuli. They conserved the ability to undergo physiological processes including phagocytosis. Using this technique, we were able to show that the phox homology (PX) domain of p47
phox
localizes to the plasma membrane in human neutrophils. We also show that RhoB, but not the PX domain of p47
phox
, is translocated to the membrane of mature phagosomes.

Conclusion
We demonstrated that cDNA transfer and expression of exogenous protein in human neutrophils is compatible with cell viability and is no longer a limitation for the study of protein function in human neutrophils.
Erratum to: Identification of specific calcitonin-like receptor residues important for calcitonin gene-related peptide high affinity binding
Authors: Banerjee Sugato , Evanson Janel , Harris Erik , Lowe Stephen L , Speth Robert C , Thomasson Kathryn A , Porter James E 
Published: December 2006

Abstract
This is a correction article.
After publication of this work [1], we became aware of the fact that Robert C. Speth was not included as an author. Dr. Speth put a considerable amount of time and effort into developing and preparing the radiopeptide used to carry out the radioligand binding studies reported in this manuscript and therefore should have originally been included as an author. We apologize to Dr. Speth for any inconvenience that this oversight might have caused and thank him for his invaluable contribution to this project.
Gefitinib (IRESSA) sensitive lung cancer cell lines show phosphorylation of Akt without ligand stimulation
Authors: Noro Rintaro , Gemma Akihiko , Kosaihira Seiji , Kokubo Yutaka , Chen Mingwei , Seike Masahiro , Kataoka Kiyoko , Matsuda Kuniko , Okano Tetsuya , Minegishi Yuji , Yoshimura Akinobu , Kudoh Shoji 
Published: December 2006

AbstractBackgroundPhase III trials evaluating the efficacy of gefitinib (IRESSA) in non-small cell lung cancer (NSCLC) lend support to the need for improved patient selection in terms of gefitinib use. Mutation of the epidermal growth factor receptor (EGFR) gene is reported to be associated with clinical responsiveness to gefitinib. However, gefitinib-sensitive and prolonged stable-disease-defined tumors withoutEGFRgene mutation have also been reported.MethodsTo identify other key factors involved in gefitinib sensitivity, we analyzed the protein expression of molecules within the EGFR family, PI3K-Akt and Ras/MEK/Erk pathways and examined the sensitivity to gefitinib using the MTT cell proliferation assay in 23 lung cancer cell lines.ResultsWe identified one highly sensitive cell line (PC9), eight cell lines displaying intermediate-sensitivity, and 14 resistant cell lines. Only PC9 and PC14 (intermediate-sensitivity) displayed anEGFRgene mutation including amplification. Eight out of the nine cell lines showing sensitivity had Akt phosphorylation without ligand stimulation, while only three out of the 14 resistant lines displayed this characteristic (P= 0.0059). Furthermore, the ratio of phosphor-Akt/total Akt in sensitive cells was higher than that observed in resistant cells (P= 0.0016). Akt phosphorylation was partially inhibited by gefitinib in all sensitive cell lines.ConclusionThese results suggest that Akt phosphorylation without ligand stimulation may play a key signaling role in gefitinib sensitivity, especially intermediate-sensitivity. In addition, expression analyses of the EGFR family,EGFRgene mutation, and FISH (fluorescencein situhybridization) analyses showed that the phosphorylated state of EGFR and Akt might be a useful clinical marker of Akt activation without ligand stimulation, in addition toEGFRgene mutation and amplification, particularly in adenocarcinomas.
Malignant colo-duodenal fistula; case report and review of the literature
Authors: Soulsby Ruth , Leung Edmund , Williams Nigel 
Published: December 2006

Abstract

Background
Colo-duodenal fistula is a rare complication of malignant and inflammatory bowel disease. Cases with malignant colo-duodenal fistulae can present with symptoms from the primary, from the fistula or from metastatic disease. The fistula often results in diarrhoea and vomiting with dramatic weight loss. Upper abdominal pain is usually present as is general malaise both from the presence of the disease and from the metabolic sequelae it causes. The diarrhoea relates to colonic bacterial contamination of the upper intestines rather than to a pure mechanical effect. Vomiting may be faeculant or truly faecal and eructation foul smelling but in the case reports this 'classic' symptomatology was often absent despite a fistula being present and patent enough to allow barium through it. Occasionally patients will present with a gastro-intestinal bleed.

Case presentation
We present an unusual case of colorectal carcinoma, where a 65 year old male patient presented with diarrhoea and vomiting secondary to a malignant colo-duodenal fistula near the hepatic flexure. Adenocarcinoma was confirmed on histology from a biopsy obtained during the patient's oesophageogastroduodenoscopy, and the fistula was demonstrated in his barium enema. Staging computed tomography showed a locally advanced carcinoma of the proximal transverse colon, with a fistula to the duodenum and regional lymphadenopathy. The patient was also found to have subcutaneous metastasis. Following discussions at the multidisciplinary meeting, this patient was referred for palliation, and died within 4 months after discharge from hospital.

Conclusion
We present the case, discuss the management and review the literature. Colo-duodenal fistulae from colonic primaries are rare but early diagnosis may allow curative surgery. This case emphasises the importance of accurate staging and repeated clinical examination.
Influenza A virus infection engenders a poor antibody response against the ectodomain of matrix protein 2
Authors: Feng JingQi , Zhang Manxin , Mozdzanowska Krystyna , Zharikova Darya , Hoff Henry , Wunner William , Couch Robert B , Gerhard Walter 
Published: December 2006

AbstractBackgroundMatrix protein 2 (M2) is an integral tetrameric membrane protein of influenza A virus (IAV). Its ectodomain (M2e) shows remarkably little diversity amongst human IAV strains. As M2e-specific antibodies (Abs) have been shown to reduce the severity of infection in animals, M2e is being studied for its capability of providing protection against a broad range of IAV strains. Presently, there is little information about the concentration of M2e-specific Abs in humans. Two previous studies made use of ELISA and Western blot against M2e peptides and recombinant M2 protein as immunosorbents, respectively, and reported Ab titers to be low or undetectable. An important caveat is that these assays may not have detected all Abs capable of binding to native tetrameric M2e. Therefore, we developed an assay likely to detect all M2e tetramer-specific Abs.ResultsWe generated a HeLa cell line that expressed full length tetrameric M2 (HeLa-M2) or empty vector (HeLa-C10) under the control of the tetracycline response element. These cell lines were then used in parallel as immunosorbents in ELISA. The assay was standardized and M2e-specific Ab titers quantified by means of purified murine or chimeric (mouse variable regions, human constant regions) M2e-specific Abs in the analysis of mouse and human sera, respectively. We found that the cell-based ELISA was substantially more effective than immobilized M2e peptide in detecting M2e-specific Abs in sera of mice that had recovered from repetitive IAV infections. Still, titers remained low (< 5 μg/ml) even after two consecutive infections but increased to ~50 μg/ml after the third infection. Competition with free M2e peptide indicated that ~20% of M2e-specific Abs engendered by infection reacted with M2e peptide. In humans presenting with naturally acquired influenza virus infection, 11 of 24 paired sera showed a ≥ 4-fold increase in M2e-specific Ab titer. The Ab response appeared to be of short duration as titers were very low (average 0.2 μg/ml) in all patients at onset of infection and in controls, in spite of evidence for previous exposure to IAV.ConclusionThe results provide convincing evidence that M2e-specific Ab-mediated protection is currently lacking or suboptimal in humans.