bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression profile of MUM1/IRF4, BCL-6, and CD138/syndecan-1 defines novel histogenetic subsets of human immunodeficiency virus–related lymphomas
Authors: Carbone Antonino , Gloghini Annunziata , Larocca Luigi M. , Capello Daniela , Pierconti Francesco , Canzonieri Vincenzo , Tirelli Umberto , Dalla-Favera Riccardo , Gaidano Gianluca 
Published: July 2002

Abstract
This study was aimed at defining the histogenesis of the pathologic spectrum of lymphoma arising in the context of human immunodeficiency virus (HIV) infection. Toward this aim, 87 AIDS-related non-Hodgkin lymphomas (AIDS-NHL) and 16 Hodgkin lymphomas arising in HIV+ patients (HIV-HL) were comparatively analyzed for the expression pattern of several B-cell histogenetic markers, including BCL-6 (expressed by centroblasts and centrocytes), MUM1/IRF4 (expressed by late centrocytes and post–germinal center [GC] B cells), and CD138/syn-1 (expressed by post-GC B cells). Expression of MUM1, BCL-6, and syn-1 segregated 3 major phenotypic patterns among AIDS-NHL and HIV-HL: (1) the BCL-6+/MUM1−/syn-1− pattern, selectively clustering with a large fraction of AIDS-Burkitt lymphoma (17 of 19) and of systemic AIDS–diffuse large cell lymphoma (12 of 16); (2) the BCL-6−/MUM1+/syn-1−pattern, associated with a fraction of AIDS-immunoblastic lymphoma (8 of 24); and (3) the BCL-6−/MUM1+/syn-1+ pattern, associated with systemic and primary central nervous system immunoblastic lymphoma (14 of 24) and with primary effusion lymphoma (10 of 10), plasmablastic lymphoma of the oral cavity (7 of 7), and HIV-HL (15 of 16). Analysis of nonneoplastic lymph nodes showed that the 3 phenotypic patterns detected in AIDS-NHL and HIV-HL correspond to distinct stages of physiologic B-cell development—centroblasts (BCL-6+/MUM1−/syn-1−), late GC/early post-GC B cells (BCL-6−/MUM1+/syn-1−), and post-GC B cells (BCL-6−/MUM1+/syn-1+). Expression of the Epstein-Barr virus-encoded latent membrane protein-1 clustered with the BCL-6−/MUM1+/syn-1+profile throughout the clinicopathologic spectrum of AIDS-NHL and HIV-HL. Overall, these results define novel histogenetic subsets of AIDS-NHL and HIV-HL and may provide novel tools for refining the diagnosis of these disorders.
Plasminogen-mediated matrix invasion and degradation by macrophages is dependent on surface expression of annexin II
Authors: Falcone Domenick J. , Borth Wolfgang , Khan K. M. Faisal , Hajjar Katherine A. 
Published: July 2002

AbstractGenetic evidence demonstrates the importance of plasminogen activation in the migration of macrophages to sites of injury and inflammation, their removal of necrotic debris, and their clearance of fibrin. These studies identified the plasminogen binding protein annexin II on the surface of macrophages and determined its role in their ability to degrade and migrate through extracellular matrices. Calcium-dependent binding of annexin II to RAW264.7 macrophages was shown using flow cytometry and Western blot analysis of EGTA eluates. Ligand blots demonstrated that annexin II comigrates with one of several proteins in lysates and membranes derived from RAW264.7 macrophages that bind plasminogen. Preincubation of RAW264.7 macrophages with monoclonal anti–annexin II IgG inhibited (35%) their binding of 125I-Lys-plasminogen. Likewise, plasmin binding to human monocyte-derived macrophages and THP-1 monocytes was inhibited (50% and 35%, respectively) when cells were preincubated with anti–annexin II IgG. Inhibition of plasminogen binding to annexin II on RAW264.7 macrophages significantly impaired their ability to activate plasminogen and degrade [3H]-glucosamine–labeled extracellular matrices. The migration of THP-1 monocytes through a porous membrane, in response to monocyte chemotactic protein-1, was blocked when the membranes were coated with extracellular matrix. The addition of plasminogen to the monocytes restored their ability to migrate through the matrix-coated membrane. Preincubation of THP-1 monocytes with anti–annexin II IgG inhibited (60%) their plasminogen-dependent chemotaxis through the extracellular matrix. These studies identify annexin II as a plasminogen binding site on macrophages and indicate an important role for annexin II in their invasive and degradative phenotype.
Novel structurally altered P2X1 receptor is preferentially activated by adenosine diphosphate in platelets and megakaryocytic cells
Authors: Greco Nicholas J. , Tonon Giovanni , Chen Weidong , Luo Xunyi , Dalal Rakhi , Jamieson G. A. 
Published: July 2002

AbstractExperimental and clinical data suggest the presence of multiple types of adenosine diphosphate (ADP) receptors, one coupled to ligand-gated cation channels (P2X) and others coupled to G-protein–coupled (P2Y) receptors. This report identifies cDNA for a structurally altered P2X1-like receptor in megakaryocytic cell lines (Dami and CMK 11-5) and platelets that, when transfected into nonresponsive 1321 cells, confers a specific sensitivity to ADP with the pharmacologic rank order of ADP &gt; &gt; ATP &gt; &gt; &gt; α,β-methylene-ATP as measured by Ca++ influx. This receptor (P2X1del) contains a deletion of 17 amino acids (PALLREAENFTLFIKNS) that includes an NFT consensus sequence for N-linked glycosylation. Glycosylated forms of the P2X1deland P2X1wt receptors were indistinguishable electrophoretically by Western blot or by immunoprecipitation using available antihuman and antirat antibodies. These results indicate that the expression of the P2X1del receptor results in an influx of Ca++ induced by ADP. Expression of P2X1delreceptor homomeric subunits is sufficient to express a receptor preferentially activated by ADP and suggests that this altered form, alone or in combination with P2X1wt receptors, is a component of an ADP-activated ion channel.
Type 1 von Willebrand disease mutation Cys1149Arg causes intracellular retention and degradation of heterodimers: a possible general mechanism for dominant mutations of oligomeric proteins
Authors: Bodó Imre , Katsumi Akira , Tuley Elodee A. , Eikenboom Jeroen C. J. , Dong Zhengyu , Sadler J. Evan 
Published: July 2002

AbstractSome families affected by von Willebrand disease type 1 show high penetrance with exceptionally low von Willebrand factor (VWF) levels. Previously, a mutation associated with this dominant phenotype, Cys1149Arg, was found to decrease the secretion of coexpressed normal VWF, and the mutation was proposed to cause intracellular retention of pro-VWF heterodimers. To demonstrate heterodimer formation, a model was developed in which subunits could be distinguished immunologically and by size. Recombinant VWF lacking domain A1 (dA1), A3 (dA3), or both (dA13) was secreted efficiently as a full range of multimers. Cotransfection of Cys1149Arg and dA13 resulted in the secretion of multimeric VWF containing about 250 kd (Cys1149Arg) and about 210 kd (dA13). Cell lysates contained pro-VWF forms of Cys1149Arg and dA13. Immunoprecipitation with an antidomain A1 antibody recovered both subunits in heterodimers, and subunit ratios were consistent with random dimerization. Similar results were obtained for cotransfection of Cys1149Arg and dA1. Normal VWF has a Cys1149-Cys1169 intrachain bond. When cotransfected with normal VWF, Cys1149Arg or the double mutant Cys1149Arg+Cys1169Ser caused a similar decrease in VWF secretion, suggesting that an unpaired Cys1169 does not explain the intracellular retention of Cys1149Arg. VWF Cys1149Arg was not secreted from BHK cells but was degraded intracellularly within about 4 hours, and the proteasome inhibitor lactacystin delayed its clearance more than 16 hours. Thus, dominant von Willebrand disease type 1 may be caused by heterodimerization of mutant and normal subunits in the endoplasmic reticulum followed by proteasomal degradation in the cytoplasm. A similar dominant negative mechanism could cause quantitative deficiencies of other multisubunit proteins.
H ferritin knockout mice: a model of hyperferritinemia in the absence of iron overload
Authors: Ferreira Chrystophe , Santambrogio Paolo , Martin Marie-Elise , Andrieu Valérie , Feldmann Gérard , Hénin Dominique , Beaumont Carole 
Published: July 2002

AbstractFerritin, the iron-storing molecule, is made by the assembly of various proportions of 2 different H and L subunits into a 24-mer protein shell. These heteropolymers have distinct physicochemical properties, owing to the ferroxidase activity of the H subunit, which is necessary for iron uptake by the ferritin molecule, and the ability of the L subunit to facilitate iron core formation inside the protein shell. It has previously been shown that H ferritin is indispensable for normal development, since inactivation of the H ferritin gene by homologous recombination in mice is lethal at an early stage during embryonic development. Here the phenotypic analysis of the mice heterozygous for the H ferritin gene (Fth+/− mice) is reported, and differences in gene regulation between the 2 subunits are shown. The heterozygousFth+/− mice were healthy and fertile and did not present any apparent abnormalities. Although they had iron-overloaded spleens at the adult stage, this is identical to what is observed in normal Fth+/+ mice. However, these heterozygous mice had slightly elevated tissue L ferritin content and 7- to 10-fold more L ferritin in the serum than normal mice, but their serum iron remained unchanged. H ferritin synthesis from the remaining allele was not up-regulated. This probably results from subtle changes in the intracellular labile iron pool, which would stimulate L ferritin but not H ferritin synthesis. These results raise the possibility that reduced H ferritin expression might be responsible for unexplained human cases of hyperferritinemia in the absence of iron overload where the hereditary hyperferritinemia-cataract syndrome has been excluded.
Human natural killer cells with polyclonal lectin and immunoglobulinlike receptors develop from single hematopoietic stem cells with preferential expression of NKG2A and KIR2DL2/L3/S2
Authors: Miller Jeffrey S. , McCullar Valarie 
Published: July 2002

AbstractThe stage of progenitor maturation and factors that determine the fate and clonal acquisition of human natural killer (NK) cell receptors during development are unknown. To study human NK cell receptor ontogeny, umbilical cord blood CD34+/Lin−/CD38− cells were cultured with a murine fetal liver line (AFT024) and defined cytokines. In the absence of lymphocyte-stimulating cytokines or when contact with AFT024 was prohibited, NK cell progeny were killer immunoglobulinlike receptor (KIR) and CD94 lectin receptor negative. In contrast, efficient NK cell differentiation and receptor acquisition was dependent on direct contact of progenitors with AFT024 and the addition of interleukin-15 (IL-15) or IL-2 but not IL-7. To address the question of whether receptor acquisition was determined at the stem cell level, single CD34+/Lin−/CD38−progenitors were studied. More than 400 single cell progeny were analyzed from cultures containing IL-15 or IL-2 and NK cells were always polyclonal, suggesting that receptor fate is determined beyond an uncommitted progenitor and that receptor-negative NK cells acquire class I-recognizing receptors after lineage commitment. KIR2DL2/L3/S2 was expressed more than KIR2DL1/S1 or KIR3DL1, and NKG2A was the dominant CD94 receptor, independent of whether the stem cell source contained the respective major histocompatibility complex class I ligand, suggesting a nonrandom sequence of receptor acquisition. The conclusion is that NK receptor fate is determined after NK cell commitment, does not require stromal presentation of human class I alleles, and is clonally stable after expression but dynamic because new receptors are acquired over time.
Isotype-switched immunoglobulin genes with a high load of somatic hypermutation and lack of ongoing mutational activity are prevalent in mediastinal B-cell lymphoma
Authors: Leithäuser Frank , Bäuerle Martin , Huynh Minh Quang , Möller Peter 
Published: July 2002

AbstractPrimary mediastinal B-cell lymphoma (PMBL) is a subentity of diffuse large B-cell lymphoma with characteristic clinical, histomorphologic, immunophenotypical, and genetic features. Unlike other B-cell lymphomas, PMBL has not yet been the subject of comprehensive molecular studies on the rearranged immunoglobulin (Ig) gene. Such investigations have proved essential to obtaining information about the differentiation stage of the lymphomagenic B cell. In the present study, the clonally rearranged immunoglobulin heavy-chain gene of 13 PMBL cases is analyzed by polymerase chain reaction (PCR) in conjunction with cloning and DNA sequencing. Twelve of 13 rearrangements were potentially functional. All clonally rearranged immunoglobulin genes bore a high load of somatic mutations (average, 13.0%), which appeared to be selected for a functional antibody in the majority of cases. The comparison of cloned PCR products revealed no evidence of ongoing mutation of the immunoglobulin variable gene. By means of reverse-transcriptase PCR, lymphoma-specific immunoglobulin transcripts were detected in 8 of 13 cases, all of which were of the postswitched type, whereas immunoglobulin protein expression was undetectable except for 1 case. A PMBL cell line, MedB-1, generated from an IgG− parental tumor, constitutively expressed IgG protein in a subset of cells, which was moderately suppressed by interleukin-4 and up-regulated in the presence of dexamethasone. PMBL is thus characterized by a heavily mutated, class-switched immunoglobulin gene without evidence of ongoing mutational activity. Moreover, our data indirectly suggest that regulation by extrinsic signals contributes to the immunoglobulin-negative phenotype of PMBL.
Interleukin-3 and interferon β cooperate to induce differentiation of monocytes into dendritic cells with potent helper T-cell stimulatory properties
Authors: Buelens Christel , Bartholomé Emmanuel J. , Amraoui Zoulikha , Boutriaux Michael , Salmon Isabelle , Thielemans Kris , Willems Fabienne , Goldman Michel 
Published: July 2002

AbstractIt was observed that interferon β (IFN-β) prevents the down-regulation of the interleukin-3 receptor α chain (IL-3Rα), which spontaneously occurs during culture of human monocytes. The functionality of IL-3R was demonstrated by the fact that IL-3 rescued IFN-β–treated monocytes from apoptosis. Monocytes cultured in the presence of IFN-β and IL-3 acquire a dendritic morphology and express high levels of HLA antigen class I and class II and costimulatory molecules. When stimulated by either lipopolysaccharide or fibroblasts expressing CD40 ligand (CD40L) transfectants, dendritic cells (DCs) generated in IFN-β and IL-3 secreted high levels of IL-6, IL-8, and tumor necrosis factor-α but low levels of IL-12 in comparison with DCs generated in IL-4 and granulocyte-macrophage colony-stimulating factor (GM-CSF). In mixed leukocyte culture, IL-3–IFN-β DCs induced a vigorous proliferative response of allogeneic cord blood T cells and elicited the production of high levels of IFN-γ and IL-5 by naive adult CD4+ T cells. Finally, IL-3–IFN-β DCs were found to produce much higher levels of IFN-α than IL-4–GM-CSF DCs in response to Poly (I:C) but not to influenza virus. It was concluded that monocytes cultured in the presence of IL-3 and IFN-β differentiate into DCs with potent helper T-cell stimulatory capacity despite their low secretion of IL-12.
Tumor Vascularity in the Prognostic Assessment of Primary Cutaneous Melanoma
Authors: Kashani-Sabet Mohammed , Sagebiel Richard W. , Ferreira Carlos M.M. , Nosrati Mehdi , Miller James R. 
Published: July 2002

PURPOSE: The vascular supply of the primary tumor is recognized to play an important role in the progression of a number of solid tumors. However, the role of tumor vascularity in the prognostic assessment of melanoma remains unclear. The purpose of this study was to determine the prognostic impact of patterns of vascularity on the outcome associated with cutaneous melanoma. PATIENTS AND METHODS: Tumor vascularity was documented prospectively using routine histopathologic analysis of 417 primary cutaneous melanomas from the University of California at San Francisco Melanoma Center database. Four patterns of tumor vascularity were recorded: absent, sparse, moderate, and prominent. RESULTS: Increasing tumor vascularity significantly increased the risk of relapse and death associated with melanoma, corresponding to reduced relapse-free and overall survival. By multivariate analysis, tumor vascularity was the most important determinant of overall survival, surpassing tumor thickness. Increasing tumor vascularity was associated with increased incidence of ulceration in the primary tumor. CONCLUSION: Tumor vascularity is an important prognostic factor in melanoma, rivaling tumor thickness. Increasing tumor vascularity is highly correlated with ulceration, possibly helping to explain the biologic basis of this known prognostic factor.
Place of Death and Its Predictors for Local Patients Registered at a Comprehensive Cancer Center
Authors: Bruera Eduardo , Russell Nancy , Sweeney Catherine , Fisch Michael , Palmer J. Lynn 
Published: July 2002

PURPOSE: To help with planning of a palliative care program, we reviewed the place of death of patients who were registered at our comprehensive cancer center and explored factors that predicted death in the hospital versus death at home. PATIENTS AND METHODS: A retrospective study was undertaken of local patients who were registered at the University of Texas M.D. Anderson Cancer Center and died during the 1997/1998 fiscal year. Data from the institutional tumor registry and from the State of Texas Bureau of Vital Statistics file were collected and analyzed. The main outcome measures were place of death, patient characteristics associated with place of death, and time from registration at the institution to death. RESULTS: Of 1,793 local patients, 251 (14%) died at M.D. Anderson Cancer Center; the remaining 86% died elsewhere. A total of 617 (34%) died at home, and 929 (52%) died in an acute hospital setting (including M.D. Anderson). A total of 1,040 (58%) died within 2 years of registration. The risk of hospital death versus home death increased for patients with cancer at a hematologic site (odds ratio [OR], 4.4; 95% confidence interval [CI], 2.8 to 6.8) and black ethnicity (OR, 1.9; 95% CI, 1.4 to 2.6) and decreased for patients who paid with Medicare (OR, 0.71; 95% CI, 0.57 to 0.90). CONCLUSION: Most patients died in an acute care hospital setting and within 2 years of registration. Our data show some predictors of hospital death for cancer patients and suggest that better hospital palliative care services and integrated palliative care systems that bridge community and acute hospitals are needed.
Fabricating and Engineering Woody‐Biomass Aerogels for High‐Performance Triboelectric Nanogenerators for Energy Harvesting and Biomechanical Monitoring
Authors: Li Longwen , Wang Ruolin , Fu Yang , Jin Zhenhui , Chen Jiansong , Du Haishun , Pan Xuejun , Wang Yi‐Cheng 
Published: October 2024

AbstractWoody biomass is an abundant renewable resource. In this study, aerogels for versatile triboelectric devices are fabricated from poplar biomass via a dissolution‐and‐regeneration method with concentrated lithium bromide solution as the solvent. To improve the aerogels' structural homogeneity, two treatments—ball‐milling the raw poplar woody biomass before its dissolution, and, separately, ultrasonication following its dissolution—were applied. These treatments altered the porous structures and mechanical properties of the resulting aerogels, leading to a marked increase in their triboelectric performance. Removing the majority of the lignin from the aerogels was also explored, and resulted in triboelectric output ≈5 times greater than that of pristine woody biomass aerogel (i.e., without ball milling, ultrasonication, or lignin reduction). The underlying mechanisms of such increases were found to be both chemical and physical. Next, triboelectric devices were fabricated using the optimal (i.e., low‐lignin) aerogel for energy harvesting and biomechanical monitoring. These devices were able to: 1) respond sensitively to force, likely due to the aerogel's porous structures; 2) capture mechanical energy, charge capacitors, and power small portable electronics; and 3) monitor biomechanical movements including respiration, joint motions, and gait‐pattern changes.
Sergeant‐and‐Soldier Effect in an Organic Room‐Temperature Phosphorescent Host‐Guest System
Authors: Law Anthony W. K. , Cheung Tsz Shing , Zhang Jianyu , Leung Nelson L. C. , Kwok Ryan T. K. , Zhao Zheng , Sung Herman H. Y. , Williams Ian D. , Qiu Zijie , Alam Parvej , Lam Jacky W.Y. , Tang Ben Zhong 
Published: October 2024

AbstractHost‐guest systems have emerged as an efficient strategy for promoting organic room temperature phosphorescence (RTP). Despite the advantages of doping guest molecules into a host matrix, the complexity of these systems and the lack of techniques to visualize host‐guest interactions at the molecular scale pose significant challenges in understanding the underlying mechanisms. Here, a novel host‐guest RTP system is developed by incorporating low concentrations (1–10 mol%) of TPP‐4C‐BI (guest) into crystalline TPP‐4C‐Cz (host). Utilizing structural isomerism, the guest molecules are regularly incorporated into the host crystal lattice, resulting in phosphorescence quantum yields almost ten times higher than the pure compounds. The system enabled resolution of the molecular packing of the single crystal through X‐ray diffraction, providing unprecedented visualization of host‐guest interactions. A “sergeant‐and‐soldier” effect, where the minority dopant molecules (sergeants) significantly influence the packing arrangement of the host molecules (soldiers), enhances RTP is identified. Further analyses revealed that due to the host molecule's inefficient phosphorescence pathway, its long‐lived dark triplets are channeled to the guest via triplet‐triplet energy transfer (TTET), allowing the excited energy to radiatively decay more efficiently. These insights advance the understanding of RTP mechanisms and offer practical implications for designing high‐efficiency phosphorescent materials.
Optoelectric‐Driven Wetting Transition on Artificially Micropatterned Surfaces With Long‐Range Virtual Electrodes
Authors: Zamboni Riccardo , Ray Debdatta , Denz Cornelia , Imbrock Jörg 
Published: October 2024

AbstractThe manipulation of droplets and wetting properties is crucial in many applications that involve surface‐liquid interactions, especially on artificial superhydrophobic substrates. This study presents an active optoelectronic method to achieve transport and transition between two wetting states on patterned surfaces, namely Cassie–Baxter (CB) and Wenzel (W). The approach employs a photovoltaic iron‐doped lithium niobate crystal placed on the bottom of a micropatterned substrate without any adhesive or sticky bonding. Taking advantage of the bulk photovoltaic effect, charge separation can be induced by light inside the crystal, thus leading to virtual electrodes. The long‐range interaction between these virtual electrodes and the droplets on the top of the substrate allows for transitions between wetting states and droplet transport. Superhydrophobic wetting transitions between Cassie–Baxter and Wenzel are observed on different substrates using this technique. The forces acting on the droplet that cause the transition are determined numerically. The evolution of droplet deformation and contact angle during the generation of the virtual electrode depends on the shape and intensity of the light beam used for photoinduction, as well as on the compositional properties of the crystal.