bluuebunny/crossref_metadata_2025_split huggingface dataset:
Textures of diffusion-controlled reaction in contact-metamorphosed Mg-rich granulite, Kokchetav area, Kazakhstan
Authors: Ashworth J. R. , Reverdatto V. V. , kolobov V. YU. , Lepetyukha V. V. , Sheplev V. S. , Bryxina N. A. 
Published: July 2002

AbstrsctIn a granulite from the Kokchetav massif, a complex mineral assemblage and intricate textures have resulted from a combination of unusual rock composition and two–stage metamorphic history. The second, contact metamorphism produced mainly cordierite and anthophyllite, reflecting a bulk composition attributed to pre–metamorphic alteration of basic igneous rock. From the first, highpressure metamorphism, garnet relics persist while another mineral has been completely pseudomorphed. The garnet is partly replaced by a symplectite of three minerals: orthopyroxene vermicules in a coarser intergrowth of cordierite and calcic plagioclase. Despite variable proportions of cordierite and plagioclase, the Al:Si ratio of the symplectite is almost constant, because the proportion of orthopyroxene is smaller where the dominant aluminous mineral is cordierite (Al:Si ≈ 0.8) than where the even more aluminous plagioclase (Al:Si ≈ 0.89) is prominent. The bulk Al:Si ratio of this symplectite, approximately 0.69, is very close to that of reactant garnet (0.66), indicating that Al and Si have been retained almost completely during the local reaction, while other elements were more mobile. In the pseudomorphs, aluminous cores (with Al:Si ratios 1.61–1.93) indicate that the mineral which has been completely replaced was probably kyanite. These cores comprise plagioclase, zoisite, corundum and spinel, and are surrounded by layers of plagioclase and cordierite. Fe, Mg, and Ca have diffused to the core, through layers with low bulk concentrations of these elements, probably by grainboundary diffusion in the solid state.
Short-chain fatty acid derivatives stimulate cell proliferation and induce STAT-5 activation
Authors: Boosalis Michael S. , Bandyopadhyay Ram , Bresnick Emery H. , Pace Betty S. , Van DeMark Karyn , Zhang Baohua , Faller Douglas V. , Perrine Susan P. 
Published: July 2002

AbstractCurrent chemotherapeutic and butyrate therapeutics that induce fetal hemoglobin expression generally also suppress erythropoiesis, limiting the production of cells containing fetal hemoglobin (F cells). Recently, selected short-chain fatty acid derivatives (SCFADs) were identified that induce endogenous γ-globin expression in K562 cells and human burst-forming units–erythroid and that increase proliferation of human erythroid progenitors and a multilineage interleukin-3–dependent hematopoietic cell line. In this report, γ-globin inducibility by these SCFADs was further demonstrated in mice transgenic for the locus control region and the entire β-globin gene locus in a yeast artificial chromosome and in 2 globin promoter-reporter assays. Conditioned media experiments strongly suggest that their proliferative activity is a direct effect of the test compounds. Investigation of potential mechanisms of action of these SCFADs demonstrates that these compounds induce prolonged expression of the growth-promoting genes c-myb andc-myc. Both butyrate and specific growth-stimulatory SCFADs induced prolonged signal transducer and activator of transcription (STAT)-5 phosphorylation and activation, and c-cisexpression, persisting for more than 120 minutes, whereas with IL-3 alone phosphorylation disappeared within minutes. In contrast to butyrate treatment, the growth-stimulating SCFADs did not result in bulk histone H4 hyperacetylation or induction of p21Waf/Cip, which mediates the suppression of cellular growth by butyrate. These findings suggest that the absence of bulk histone hyperacetylation and p21 induction, but prolonged induction of cis, myb, myc, and STAT-5 activation, contribute to the cellular proliferation induced by selected SCFADs.
Signal transduction involved in MCP-1–mediated monocytic transendothelial migration
Authors: Cambien Béatrice , Pomeranz Manuel , Millet Marie-Ange , Rossi Bernard , Schmid-Alliana Annie 
Published: July 2002

AbstractMonocyte chemoattractant protein-1 (MCP-1) is a major chemoattractant for monocytes and T lymphocytes. The MonoMac6 cell line was used to examine MCP-1 receptor-mediated signal transduction events in relation to MCP-1–mediated monocytic transendothelial migration. MCP-1 stimulates, with distinct time courses, extracellular signal-related kinases (ERK1 and ERK2) and stress-activated protein kinases (SAPK1/JNK1 and SAPK2/p38). SAPK1/JNK1 activation was blocked by piceatannol, indicating that it is regulated by Syk kinase, whereas SAPK2/p38 activation was inhibited by PP2, revealing an upstream regulation by Src-like kinases. In contrast, ERK activation was insensitive to PP2 and piceatannol. Pertussis toxin, a blocker of Go/Gi proteins, abrogated MCP-1–induced ERK activation, but was without any effect on SAPK1/JNK1 and SAPK2/p38 activation. These results underscore the major implication of Go/Gi proteins and nonreceptor tyrosine kinases in the early MCP-1 signaling. Furthermore, MCP-1–mediated chemotaxis and transendothelial migration were significantly diminished by a high concentration of SB202190, a broad SAPK inhibitor, or by SB203580, a specific inhibitor of SAPK2/p38, and abolished by pertussis toxin treatment. Altogether, these data suggest that coordinated action of distinct signal pathways is required to produce a full response to MCP-1 in terms of monocytic locomotion.
Constitutive kinase activation of the TEL-Syk fusion gene in myelodysplastic syndrome with t(9;12)(q22;p12)
Authors: Kuno Yoshie , Abe Akihiro , Emi Nobuhiko , Iida Minako , Yokozawa Toshiya , Towatari Masayuki , Tanimoto Mitsune , Saito Hidehiko 
Published: July 2002

AbstractThe TEL gene on 12p12-13 is a target for a number of translocations associated with various hematological malignancies. The fusion of the TEL gene to the Sykgene in a patient with myelodysplastic syndrome (MDS) with t(9;12)(q22;p12) is reported. Southern blot analysis of patient bone marrow cells with TEL and Syk gene probes detected rearranged fragments. Anchored polymerase chain reaction identified the Syk gene, a nonreceptor tyrosine kinase, on 9q22 fused downstream of TEL exon 5. The TELgene was fused in-frame to Syk and produced a fusion protein that was constitutively phosphorylated in tyrosine with dimerization that was mediated by the helix-loop-helix domain of TEL. A TEL-Syk fusion product transformed the murine hematopoietic cell line BaF3 to interleukin-3 growth factor independence. TEL-Syk is a novel transforming protein and leads to the transformation of hematopoietic cells. These data implicate that the rearranged Syk gene is involved in the pathogenesis of hematopoietic malignancies.
Growth factor–induced angiogenesis in vivo requires specific cleavage of fibrillar type I collagen
Authors: Seandel Marco , Noack-Kunnmann Katharina , Zhu Dan , Aimes Ronald T. , Quigley James P. 
Published: July 2002

Abstract
The contribution of specific type I collagen remodeling in angiogenesis was studied in vivo using a quantitative chick embryo assay that measures new blood vessel growth into well-defined fibrillar collagen implants. In response to a combination of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), a strong angiogenic response was observed, coincident with invasion into the collagen implants of activated fibroblasts, monocytes, heterophils, and endothelial cells. The angiogenic effect was highly dependent on matrix metalloproteinase (MMP) activity, because new vessel growth was inhibited by both a synthetic MMP inhibitor, BB3103, and a natural MMP inhibitor, TIMP-1. Multiple MMPs were detected in the angiogenic tissue including MMP-2, MMP-13, MMP-16, and a recently cloned MMP-9–like gelatinase. Using this assay system, wild-type collagen was compared to a unique collagenase-resistant collagen (r/r), with regard to the ability of the respective collagen implants to support cell invasion and angiogenesis. It was found that collagenase-resistant collagen constitutes a defective substratum for angiogenesis. In implants made with r/r collagen there was a substantial reduction in the number of endothelial cells and newly formed vessels. The presence of the r/r collagen, however, did not reduce the entry into the implants of other cell types, that is, activated fibroblasts and leukocytes. These results indicate that fibrillar collagen cleavage at collagenase-specific sites is a rate-limiting event in growth factor–stimulated angiogenesis in vivo.
Experiences of donors enrolled in a randomized study of allogeneic bone marrow or peripheral blood stem cell transplantation
Authors: Rowley Scott D. , Donaldson Gary , Lilleby Kathy , Bensinger William I. , Appelbaum Frederick R. 
Published: July 2002

Abstract
The experiences of 69 (38 marrow and 31 peripheral blood stem cell [PBSC]) donors participating in a randomized trial comparing allogeneic bone marrow with PBSC transplantation were studied. Marrow was collected by means of standard harvest techniques and general or regional anesthesia. PBSC donors were treated with 5 to 7 days of filgrastim at a dose of 16 μg/kg/d and underwent 1 to 3 days of apheresis to obtain 5 × 106 CD34+ cells per kilogram recipient weight. Donors completed questionnaires describing their health experiences before, during, and then weekly after donation until return to baseline status. Both marrow and PBSC donors reported minimal fluctuation in symptoms measuring emotional status. In contrast, both groups of donors reported deterioration in physical status starting with administration of filgrastim (PBSC donors) or after the marrow collection procedure. The symptom burden reported was similar, with pain a prominent symptom for both groups. Equivalent mean levels of maximal pain, average pain, and pain duration through the day were reported, although toxicity peaks occurred at different time points during the harvest procedures. All PBSC donors but only 79% of marrow donors reported good physical status by 14 days after the harvest procedures. These data demonstrate similar levels of physical discomfort for hematopoietic stem cell donors regardless of the collection procedure used, but a quicker resolution of symptoms for PBSC donors.
Diagnostic and clinical relevance of the number of circulating CD34+ cells in myelofibrosis with myeloid metaplasia
Authors: Barosi Giovanni , Viarengo Gianluca , Pecci Alessandro , Rosti Vittorio , Piaggio Giovanna , Marchetti Monia , Frassoni Francesco 
Published: July 2002

Abstract
The absolute content of CD34+ cells in the peripheral blood of 84 patients with myelofibrosis with myeloid metaplasia (MMM) and 23 patients with other Philadelphia-negative (Ph−) chronic myeloproliferative disorders (CMDs) was investigated. In MMM, the median absolute number of circulating CD34+cells was consistently high (91.6 × 106/L; range, 0-2460 × 106/L). Receiver operating characteristic curve analysis showed that 15 × 106/L as a decision criterion for CD34+cells produced an almost complete discrimination between MMM patients out of therapy and other Ph− CMDs (positive predictive value, 98.4%; negative predictive value, 85.0%). MMM patients with higher numbers of CD34+ cells had a significantly longer disease duration (P = .019) and higher spleen volume index (P = .014), liver volume (P = .000), percentage of circulating immature myeloid cells (P = .020), and percentage of myeloid blasts (P = .000). When CD34+ cells were correlated with the use of Dupriez risk stratification, CD34+ cells increased significantly from low-risk (median, 68.1 × 106/L) to intermediate-risk (median, 112.8 × 106/L) and high-risk patients (median 666.1 × 106/L) (F = 4.95;P = .009). When CD34+ cells were correlated with a severity score on the basis of both myeloproliferative and myelodepletive characteristics of the disease, only the myeloproliferation index was significantly associated with CD34+ cell level (F = 5.7;P = .000). Overall survival and interval to blast transformation from the time of CD34+ cell analysis were significantly shorter in patients with more than 300 × 106/L CD34+ cells (P = .005 and .0005, respectively). In conclusion, the absolute number of CD34+ circulating cells allows MMM to be distinguished from other Ph− CMDs; it is strongly associated with the extent of myeloproliferation and predicts evolution toward blast transformation.
Delayed donor red cell chimerism and pure red cell aplasia following major ABO-incompatible nonmyeloablative hematopoietic stem cell transplantation
Authors: Bolan Charles D. , Leitman Susan F. , Griffith Linda M. , Wesley Robert A. , Procter Jo L. , Stroncek David F. , Barrett A. John , Childs Richard W. 
Published: July 2002

AbstractDelayed donor red cell engraftment and pure red cell aplasia (PRCA) are well-recognized complications of major ABO-incompatible hematopoietic stem cell transplantation (SCT) performed by means of myeloablative conditioning. To evaluate these events following reduced-intensity nonmyeloablative SCT (NST), consecutive series of patients with major ABO incompatibility undergoing either NST (fludarabine/cyclophosphamide conditioning) or myeloablative SCT (cyclophosphamide/high-dose total body irradiation) were compared. Donor red blood cell (RBC) chimerism (initial detection of donor RBCs in peripheral blood) was markedly delayed following NST versus myeloablative SCT (median, 114 versus 40 days;P &lt; .0001) and strongly correlated with decreasing host antidonor isohemagglutinin levels. Antidonor isohemagglutinins declined to clinically insignificant levels more slowly following NST than myeloablative SCT (median, 83 versus 44 days;P = .03). Donor RBC chimerism was delayed more than 100 days in 9 of 14 (64%) and PRCA occurred in 4 of 14 (29%) patients following NST, while neither event occurred in 12 patients following myeloablative SCT. Conversion to full donor myeloid chimerism following NST occurred significantly sooner in cases with, compared with cases without, PRCA (30 versus 98 days; P = .008). Cyclosporine withdrawal appeared to induce graft-mediated immune effects against recipient isohemagglutinin-producing cells, resulting in decreased antidonor isohemagglutinin levels and resolution of PRCA following NST. These data indicate that significantly delayed donor erythropoiesis is (1) common following major ABO-incompatible NST and (2) associated with prolonged persistence of host antidonor isohemagglutinins. The clinical manifestations of these events are affected by the degree and duration of residual host hematopoiesis.
Relationship between transferrin saturation and iron stores in the African American and US Caucasian populations: analysis of data from the third National Health and Nutrition Examination Survey
Authors: McLaren Christine E. , Li Kuo-Tung , Gordeuk Victor R. , Hasselblad Victor , McLaren Gordon D. 
Published: July 2002

Abstract
In previous analyses of transferrin saturation data in African Americans and Caucasians from the second National Health and Nutrition Examination Survey (NHANES II), subpopulations were found consistent with population genetics for common loci that influence iron metabolism. The goal of this new study was to determine if these transferrin saturation subpopulations have different levels of iron stores. Statistical mixture modeling was applied to transferrin saturation data for African Americans and Caucasians from the third National Health and Nutrition Examination Survey (NHANES III), and then the mean serum ferritin concentrations were determined for the transferrin saturation subpopulations that were identified. After adjustment for diurnal variation, 3 subpopulations of transferrin saturation were identified in each racial group. Satisfying Hardy-Weinberg conditions for major locus effects, in both racial groups the sum of the square roots of the proportion with the lowest mean transferrin saturation and the proportion with the highest mean transferrin saturation was approximately 1. When weighted to reflect the US adult population as a whole, these subpopulations of increasing transferrin saturations had progressively increasing mean age-adjusted serum ferritin concentration values in each ethnic grouping as stratified by sex (trend test, P &lt; .002 for all). These results are consistent with the concept that population transferrin saturation subpopulations reflect different levels of storage iron.
Loss of blood CD11c+ myeloid and CD11c−plasmacytoid dendritic cells in patients with HIV-1 infection correlates with HIV-1 RNA virus load
Authors: Donaghy Heather , Pozniak Anton , Gazzard Brian , Qazi Nad , Gilmour Jill , Gotch Frances , Patterson Steven 
Published: July 2002

AbstractHuman blood contains at least 2 subpopulations of antigen-presenting dendritic cells (DCs) that can be differentiated by their expression of CD11c. Myeloid DCs (myDCs), which are CD11c+, trap invading pathogens in the tissues and then migrate to lymphoid tissues where they stimulate pathogen-specific T-cell responses. Plasmacytoid DCs (pcDCs), which are CD11c−, secrete interferon-α in response to viral infections. This study reports that in HIV-1 infection there is a progressive depletion of both these DC populations and that this correlates with an increasing HIV-1 plasma virus load. The median numbers of myDCs and pcDCs were 6978/mL and 9299/mL, respectively, in healthy male controls and 2298/mL and 1640/mL, respectively, in patients with more than 105 HIV-1 RNA copies/mL. Both DC populations expressed CD4, CCR5, and CXCR4. The findings suggest that loss of DCs in HIV infection may contribute to disease progression.
Sphingosine 1-phosphate antagonizes apoptosis of human leukemia cells by inhibiting release of cytochrome c and Smac/DIABLO from mitochondria
Authors: Cuvillier Olivier , Levade Thierry 
Published: July 2002

AbstractSphingosine 1-phosphate (S-1P) has been implicated as a second messenger preventing apoptosis by counteracting activation of executioner caspases. Here it is reported that S-1P prevents apoptosis and executioner caspase-3 activation by inhibiting the translocation of cytochrome c and Smac/DIABLO from mitochondria to the cytosol induced by anti-Fas, tumor necrosis factor-α (TNF-α), serum deprivation, and cell-permeable ceramides in the human acute leukemia Jurkat, U937, and HL-60 cell lines. Furthermore, the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate, which stimulates sphingosine kinase, the enzyme responsible for S-1P production, also inhibits cytochrome c and Smac/DIABLO release. In contrast, dimethylsphingosine (DMS), a specific inhibitor of sphingosine kinase, sensitizes cells to cytochrome c and Smac/DIABLO release triggered by anti-Fas, TNF-α, serum deprivation, or ceramide. DMS-induced mitochondrial apoptogenic factor leakage can likewise be overcome by S-1P cotreatment. Hence, S-1P, likely generated through a protein kinase C– mediated activation of sphingosine kinase, inhibits the apoptotic cascade upstream of the release of the mitochondrial apoptogenic factors, cytochrome c, and Smac/DIABLO in human acute leukemia cells.
Acidic and neutral sialidase in the erythrocyte membrane of type 2 diabetic patients
Authors: Venerando Bruno , Fiorilli Amelia , Croci Gianluigi , Tringali Cristina , Goi Giancarlo , Mazzanti Laura , Curatola Giovanna , Segalini Giovanni , Massaccesi Luca , Lombardo Adriana , Tettamanti Guido 
Published: July 2002

AbstractThe behavior of the 2 sialidase forms present in the erythrocyte membrane was investigated in 117 subjects with type 2 diabetes mellitus versus 95 healthy controls. A significant increase of the acidic form of sialidase, which is anchored to the membrane by a glycosylphosphatidylinositol bridge, was observed in erythrocyte resealed membranes. On the contrary, the neutral form of the enzyme, the only one capable of removing lipid- and protein-bound sialic acid from endogenous and exogenous sialoderivatives, was significantly reduced with a consequent increase of erythrocyte membrane total sialic acid content. Disease duration, therapy, glycemia, parameters of metabolic control, and presence of complications, except nephropathies, had no influence on the tested enzyme activities. Diabetic subjects showed a different erythrocyte age distribution, with an almost double proportion of young red cells and only one quarter of senescent ones compared with controls. In young erythrocytes, diabetic and control subjects had the same distribution of the 2 enzymes, while in senescent cells the acidic enzyme was increased 3.5-fold and the neutral form was reduced by half in the diabetic subjects. The increase of both acidic sialidase and total membrane-bound sialic acid, together with an overpresence of young red cells in diabetics, suggests that in this pathological condition there might be an altered aging process with a diminished expression of the neutral form of the enzyme and an increase of bound sialic acid. It has been suggested that the expression of the neutral enzyme requires some activation mechanism that is impaired in diabetes.
Partial deletion in the JK locus causing a Jknull phenotype
Authors: Lucien Nicole , Chiaroni Jacques , Cartron Jean-Pierre , Bailly Pascal 
Published: July 2002

AbstractA new alteration of the blood group JK*A allele was identified in a Jknull patient from Tunisia with an allo–anti-Jk3 in her serum. Southern blot and exon mapping analyses revealed an internal deletion within the Kidd (JK) locus encompassing exons 4 and 5. Sequence analysis of the Jk transcript showed that exons 4 and 5 were missing but were replaced by a 136–base-pair (bp) intron 3 sequence located 315 bp and 179 bp upstream from exon 4. This sequence is flanked by typical donor–acceptor cryptic splice sites used in the mutant but not in the normal JK gene. Because the translation initiation codon is located in exon 4, the Jk protein is not produced.
Lineage-specific defect in gene expression in human platelet phospholipase C-β2 deficiency
Authors: Mao Guang Fen , Vaidyula Vijender R. , Kunapuli Satya P. , Rao A. Koneti 
Published: July 2002

AbstractPhospholipase C (PLC)–β2 plays a major role in platelet activation. Previous studies have described a unique patient with impaired receptor-mediated platelet aggregation, secretion, calcium mobilization, and phospholipase C (PLC) activation associated with a selective decrease in platelet PLC-β2 isozyme. To identify the mechanisms leading to the defect, platelet RNA from the patient and healthy subjects was subjected to reverse transcription–polymerase chain reaction (RT-PCR) and the products sequenced. The PLC-β2 cDNA sequence in the patient showed no abnormalities. Platelet PLC-β2 and β-actin (internal control) mRNA levels were assessed by RT-PCR; the ratio of PLC-β2 to β-actin mRNA levels was 0.80 to 0.95 in 4 healthy subjects and 0.28 in the patient. PLC-β2 mRNA levels were similarly reduced compared with GPIIb and Gαq mRNA levels. PLC-γ2 and platelet factor 4 mRNA levels were normal. Calcium mobilization was studied in neutrophils upon activation with formyl-Met-Leu-Phe (fMLP), adenosine diphosphate (ADP), platelet-activating factor (PAF), interleukin-8 (IL-8), C5a, and leukotriene B4 (LTB4), and it was normal. Neutrophil elastase secretion upon activation with fMLP, ADP, PAF, IL-8, C5a, and LTB4 was normal, as were neutrophil PLC-β2 mRNA and PLC-β2 on immunoblotting. Thus, responses to activation, PLC-β2 protein, and PLC-β2 mRNA are decreased in patient platelets but not in neutrophils, providing evidence for a hitherto undescribed lineage (platelet)–specific defect in PLC-β2 gene expression. These studies provide a physiologically relevant model to delineate regulation of PLC-β2 gene and its tissue-specific expression.