bluuebunny/crossref_metadata_2025_split huggingface dataset:
'religious Insults': Christian Critiques of Islam and the Government in Colonial Northern Nigeria
Authors: Barnes Andrew 
Published: May 2004

AbstractThis article discusses two Christian critiques of Islam published during the colonial era, and the response by the colonial government to each. The first goal of the article is to characterize Christian criticisms of Islam during the colonial era. The second is to demonstrate how conflict over Islam could shape relations between British administrators and Christian missionaries. The third goal is to narrate the history of a religious controversy as it developed over two generations. As will be seen, the war of words over government religious policy toward Islam could become quite vicious, even without any active participation by Muslims.
Dignifying Death: the Politics of Burial in Bulawayo
Authors: Ranger Terence 
Published: May 2004

AbstractThere has recently been much more recognition of the African role in the making of the colonial cities of southern Africa. Nevertheless, many kinds of action have still seemed to be impossible for Africans living in tightly controlled municipal townships. Among these is the political and symbolic management of death. While literature on West African towns celebrates 'mausoleum politics' and the struggle over the burial of dead men under the floors of their houses, in colonial Southern African cities it has been assumed that Africans had no choice but to accept the constraining rules of drab municipal cemeteries. Similarly, the initiative and agency, which we know rural Africans in Southern Africa to have exercised in their encounters with mission Christianity, have been much less documented in the towns. In short, it has been assumed that the Southern African town—and particularly the black townships—represented colonial control at its most intense and oppressive, allowing little room for symbolic or practical autonomy whether in social life, politics or religion. This article tests such presuppositions in relation to Southern Rhodesia's second largest town, and major industrial centre, Bulawayo. It argues that from the late 1890s there has always been a black Bulawayo, expressed first in the absence of municipal or state control of the Location and expressed later by the emergence of varying influential men and women there with the capacity to take cultural and symbolic initiatives, perhaps especially in the sphere of death, burial and commemoration. It discusses the successful performance of rites to 'bring back the spirit' a year after death despite missionary and municipal prohibitions; it discusses the role of the innumerable Burial Societies in colonial Bulawayo; it discusses the efforts of educated young men to erect memorials for African kings and chiefs; it discusses the varying focus of three types of African urban Christianity—missionfounded churches, 'Ethiopianist' independent churches and Apostolic prophetic churches—on rituals of death. By so doing it opens up many questions about the social, political, cultural and religious life of an African Location in colonial southern Africa.
Chimerism and clinical outcomes of 110 recipients of unrelated donor bone marrow transplants who underwent conditioning with low-dose, single-exposure total body irradiation and cyclophosphamide
Authors: Girgis Mark , Hallemeier Chris , Blum William , Brown Randy , Lin Hsiu-san , Khoury Hanna , Goodnough L. Tim , Vij Ravi , Devine Steve , Wehde Marita , Postma Stacey , Oza Aarti , DiPersio John , Adkins Douglas 
Published: May 2004

AbstractWe hypothesized that low-dose (550-cGy), single-exposure, high dose rate (30 cGy/min) total body irradiation (TBI) with cyclophosphamide as conditioning for HLA-compatible unrelated donor (URD) bone marrow transplantation (BMT) would result in donor chimerism (DC) with a low risk for serious organ toxicity and treatment-related mortality (TRM). Twenty-six patients with good risk diagnoses (acute leukemia in first complete remission [CR] and chronic-phase chronic myelogenous leukemia [CML]) and 84 with poor risk diagnoses underwent this regimen and URD BMT. Unsorted marrow nucleated cells were assessed for chimerism using VNTR probes. All DC occurred in 78 (86%) of 91 evaluable patients at 1 or more follow-up points. Graft failure occurred in 7 (7.7%) patients. Fatal organ toxicity occurred in only 2% of patients. TRM rates through 2 years of follow-up were 19% and 42% in those with good and poor risk diagnoses, respectively. Overall and disease-free survival rates in the good risk group were 47% and 40%, respectively, and in the poor risk group they were 25% and 21%, respectively, at a median follow-up for living patients of 850 days (range, 354-1588 days). This regimen resulted in 100% DC in most patients undergoing URD BMT with a relatively low risk for fatal organ toxicity and TRM.
Exogenous IL-7 increases recent thymic emigrants in peripheral lymphoid tissue without enhanced thymic function
Authors: Chu Yu-Waye , Memon Sarfraz A. , Sharrow Susan O. , Hakim Frances T. , Eckhaus Michael , Lucas Philip J. , Gress Ronald E. 
Published: May 2004

AbstractInterleukin 7 (IL-7) is critical in maintaining thymic-dependent and thymic-independent pathways of T-cell homeostasis. T-cell receptor (TCR) rearrangement excision circles (TRECs) have been used as markers for recent thymic emigrants (RTEs) in assessing human thymic function. To study the thymic and peripheral effects of IL-7 on RTEs, we measured TREC content and peripheral naive T-cell subsets and turnover in IL-7-treated mice. Short-term administration of IL-7 into thymus-intact mice resulted in increased total TREC numbers, consistent with RTE accumulation. Decreases in TREC frequency were attributable to dilution secondary to increased cell turnover. Significantly, IL-7 administration into thymectomized mice resulted in patterns of decreased TREC frequency and increased total TREC number similar to those in IL-7-treated thymus-intact mice. Distinct patterns of naive cell and RTE distribution among peripheral immune organs and altered expression of CD11a were observed following IL-7 treatment in thymus-intact and thymectomized mice. These results demonstrate (1) that total TREC number and not TREC frequency accurately reflects quantitative changes in RTEs; (2) that short-term IL-7 administration results in preferential accumulations of RTEs among peripheral immune organs, accounting for the increase in TRECs in the total peripheral lymphoid pool; and (3) no evidence for regulation of thymic function by short-term IL-7 administration. (Blood. 2004;104:1110-1119)
Bone marrow angiogenic ability and expression of angiogenic cytokines in myeloma: evidence favoring loss of marrow angiogenesis inhibitory activity with disease progression
Authors: Kumar Shaji , Witzig Thomas E. , Timm Michael , Haug Jessica , Wellik Linda , Kimlinger Teresa K. , Greipp Philip R. , Rajkumar S. Vincent 
Published: May 2004

AbstractWe compared the angiogenic potential of bone marrow plasma and the expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors on plasma cells from patients with monoclonal gammopathy of undetermined significance (MGUS), smoldering multiple myeloma (SMM), and newly diagnosed multiple myeloma (NMM). Cytokine and cytokine-receptor expression was studied by bone marrow immunohistochemistry, quantitative reverse transcription-polymerase chain reaction (RT-PCR) on sorted plasma cells, and quantitative Western blot analysis. Bone marrow angiogenic potential was studied using a human in vitro angiogenesis assay. The expression levels of VEGF, bFGF, and their receptors were similar among MGUS, SMM, and NMM. Sixty-one percent of NMM samples stimulated angiogenesis in the in vitro angiogenesis assay compared with SMM (0%) and MGUS (7%) (P &lt; .001). Importantly, 63% of MGUS samples inhibited angiogenesis compared with SMM (43%) and NMM (4%) (P &lt; .001). The inhibitory activity was heat stable, not overcome by the addition of VEGF, and corresponded to a molecular weight below 10 kd by size-exclusion chromatography. Our results suggest that increasing angiogenesis from MGUS to NMM is, at least in part, explained by increasing tumor burden rather than increased expression of VEGF/bFGF by individual plasma cells. The active inhibition of angiogenesis in MGUS is lost with progression, and the angiogenic switch from MGUS to NMM may involve a loss of inhibitory activity. (Blood. 2004; 104:1159-1165)
Inhibition of intravascular thrombosis in murine endotoxemia by targeted expression of hirudin and tissue factor pathway inhibitor analogs to activated endothelium
Authors: Chen Daxin , Giannopoulos Konstantinos , Shiels Paul G. , Webster Zoe , McVey John H. , Kemball-Cook Geoff , Tuddenham Edward , Moore Marilyn , Lechler Robert , Dorling Anthony 
Published: May 2004

AbstractWe have generated transgenic mice expressing the leech anticoagulant hirudin and human tissue factor pathway inhibitor tethered to the cell surface by fusion with fragments of human CD4 and P-selectin. Expression of the transgenes is under the control of the CD31 (platelet endothelial cell adhesion molecule [PECAM]) promoter, limiting expression to endothelial cells, monocytes, and platelets. In addition, the P-selectin sequence directs expression to secretory granules. Functional cell surface expression only occurs when the cells are activated. In a mouse model of systemic lipopolysaccharide (LPS)–induced endotoxemia, we show that expression of either anticoagulant on activated endothelium inhibits the widespread intravascular thrombosis, thrombocytopenia, and consumptive coagulopathy associated with endotoxemia. Importantly, non– LPS-treated transgenic mice had normal baseline bleeding times. We speculate that targeted delivery of anticoagulants to the endothelium may be a strategy worth pursuing in clinical sepsis to improve efficacy of systemic anticoagulation while minimizing potential hemorrhagic side effects.
CD63 tetraspanin slows down cell migration and translocates to the endosomal-lysosomal-MIICs route after extracellular stimuli in human immature dendritic cells
Authors: Mantegazza Adriana R. , Barrio María Marcela , Moutel Sandrine , Bover Laura , Weck Markus , Brossart Peter , Teillaud Jean-Luc , Mordoh José 
Published: May 2004

AbstractWe analyzed herein whether members of the tetraspanin superfamily are involved in human immature dendritic cell (DC) functions such as foreign antigen internalization, phagocytosis, and cell migration. We show that CD63, CD9, CD81, CD82, and CD151 are present in immature DCs. Whereas CD9 and CD81 are mostly expressed at the cell surface, CD63 and CD82 are also located in intracellular organelles. Complexes of monoclonal antibody (Mab) FC-5.01-CD63 or Fab-5.01-CD63 were rapidly translocated “outside-in” and followed the endocytic pathway through early endosomes and lysosomes, reaching major histocompatibility complex (MHC) class II-enriched compartments (MIICs) in less than one hour. Internalization of CD63 was also observed during Saccharomyces cerevisiae phagocytosis. Moreover, an association of CD63 with the β-glycan receptor dectin-1 was observed. Mabs against CD9, CD63, CD81, and CD82 enhanced by 50% the migration induced by the chemokines macrophage inflammatory protein-5 (MIP-5) and MIP-1α. Concomitantly, Mabs against CD63 and CD82 diminished the surface expression of CD29, CD11b, CD18, and α5 integrins. By immunoprecipitation experiments we found that CD63 associated with integrins CD11b and CD18. These results suggest that CD9, CD63, CD81, and CD82 could play a role in modulating the interactions between immature DCs and their environment, slowing their migratory ability. However, only CD63 would intervene in the internalization of complex antigens. (Blood. 2004; 104:1183-1190)
Identification of novel mutations in ADAMTS13 in an adult patient with congenital thrombotic thrombocytopenic purpura
Authors: Uchida Toshihiro , Wada Hideo , Mizutani Minoru , Iwashita Miho , Ishihara Hiroaki , Shibano Toshiro , Suzuki Misako , Matsubara Yumiko , Soejima Kenji , Matsumoto Masanori , Fujimura Yoshihiro , Ikeda Yasuo , Murata Mitsuru ,   for The Research Project on Genetics of Thrombosis
Published: May 2004

Abstract
Congenital thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS) is associated with an inherited von Willebrand factor-cleaving protease (ADAMTS13 [a disintegrin and metalloprotease with thrombospondin type I domains 13]) deficiency. In this study, we identified novel mutations in the ADAMTS13 gene in a patient with TTP. The patient was a 51-year-old Japanese male who exhibited TTP symptoms at frequent intervals. The ADAMTS13 activity during acute episodes was less than 3% that of normal. The enzyme activities of the patient's father and mother were both 46%, and both parents were asymptomatic. Genetic analysis revealed that the patient was a compound heterozygote for 2 mutations. One mutation was a missense mutation in the metalloprotease domain (A250V, exon 7), and the other was a guanine to adenine substitution at the 5′ end of intron 3 (intron 3 G→A). In vitro expression studies revealed that the A250V mutation markedly reduced ADAMTS13 activity and the intron 3 G→A mutation caused abnormal mRNA synthesis. (Blood. 2004;104: 2081-2083)
PECAM-1 is expressed on hematopoietic stem cells throughout ontogeny and identifies a population of erythroid progenitors
Authors: Baumann Christina I. , Bailey Alexis S. , Li Weiming , Ferkowicz Michael J. , Yoder Mervin C. , Fleming William H. 
Published: May 2004

AbstractPlatelet endothelial cell adhesion molecule-1 (PECAM-1) (CD31) is an adhesion molecule expressed on endothelial cells and subsets of leukocytes. Analysis of phenotypically defined hematopoietic stem cells (HSCs) from the yolk sac, fetal liver, and adult bone marrow demonstrates CD31 expression on these cells throughout development. CD31+ c-kit+ cells, but not CD31– c-kit+ cells, isolated from day-9.5 yolk sac give rise to multilineage hematopoiesis in vivo. Further evaluation of the CD31+ lineage marker–negative fraction of adult bone marrow reveals functionally distinct cell subsets. Transplantation of CD31+ Lin– c-kit– cells fails to protect lethally irradiated recipients, while CD31+ Lin– c-kit+ Sca-1– cells (CD31+ Sca-1–) provide radioprotection in the absence of long-term donor-derived hematopoiesis. Although donor-derived leukocytes were not detected in CD31+ Sca-1– recipients, donor-derived erythroid cells were transiently produced during the initial phases of bone marrow recovery. These results demonstrate CD31 expression on hematopoietic stem cells throughout ontogeny and identify a population of CD31+ short-term erythroid progenitors cells that confer protection from lethal doses of radiation.
Dimerization: a versatile switch for oncogenesis
Authors: So Chi Wai , Cleary Michael L. 
Published: May 2004

AbstractForced dimerization or oligomerization has emerged as a powerful mechanism for unleashing the oncogenic properties of chimeric transcription factors in acute leukemias. Fusion of transcriptional regulators with a variety of heterologous partner proteins as a consequence of chromosomal rearrangements induces inappropriate self-association, leading to aberrant transcriptional properties and leukemogenesis. Forced dimerization/oligomerization may alter the association of a DNA-binding protein for its transcriptional cofactors, or the dimerization motifs themselves may constitutively recruit transcriptional effector molecules. Oligomerized chimeras may also sequester essential partners or cofactors to exert dominant-negative effects on target gene expression. A key mechanistic feature, and one with major clinical implications, is the nature of the transcriptional cofactors that are recruited by the dimerized oncoprotein. Chimeric RARα and acute myeloid leukemia 1 (AML1) proteins induce constitutive repression after the recruitment of corepressors, whereas inappropriate maintenance of target gene expression by mixed-lineage leukemia (MLL) chimeras may result from the recruitment of coactivators or the basal transcriptional machinery. Molecular therapies directed at enzymatic activities of the aberrantly recruited cofactors, or antagonism of dimerization itself, represent promising avenues of current and future investigation.
Trypanosoma congolenseinfections: antibody-mediated phagocytosis by Kupffer cells
Authors: Shi Meiqing , Wei Guojian , Pan Wanling , Tabel Henry 
Published: May 2004

AbstractImmunohistochemical double-label technique was used to detect trypanosomal antigen in macrophages. Immunoglobulin (Ig)M as well as IgG2a monoclonal antibodies (mAb) specific for the variant surface glycoprotein (VSG) mediated phagocytosis of Trypanosoma congolense variant antigenic type (VAT) TC13 by macrophages [bone marrow-derived macrophage cell line from BALB/c (BALB.BM)] in vitro. Administration of these IgM or IgG2a antibodies to BALB/c mice 30 min after injection of 3 × 108T. congolense mediated phagocytosis of trypanosomes by Kupffer cells of the liver within 1 h. Plasma levels of the monokines interleukin (IL)-1β, IL-10, and IL-12p40 were significantly increased 6–48 h after phagocytosis. In BALB/c mice infected with 103T. congolense, a small degree of phagocytosis of trypanosomes by Kupffer cells, mediated by actively synthesized antibodies, was detected as early as 5 days after infection. Phagocytosis of trypanosomes was dramatically enhanced on day 6. Concomitantly, the Kupffer cells trippled in size. In BALB/c mice infected for 6 days, treatment with IgM or IgG2a mAb specific for T. congolense VSG led to clearance of VAT TC13 parasitemia but did not prevent death at the second parasitemia of a different VAT. We conclude that IgM as well as IgG antibody mediate phagocytosis of trypanosomes by Kupffer cells.
Localization of serglycin in human neutrophil granulocytes and their precursors
Authors: Niemann Carsten Utoft , Cowland Jack Bernard , Klausen Pia , Askaa Jon , Calafat Jero , Borregaard Niels 
Published: May 2004

AbstractSerglycin is a major proteoglycan of hematopoietic cells. It is thought to play a role in the packaging of granule proteins in human neutrophil granulocytes. The presence of serglycin in myeloid cells has been demonstrated only at the transcriptional level. We generated a polyclonal antibody against recombinant human serglycin. Here, we show the localization of serglycin in humans during neutrophil differentiation. Immunocytochemistry revealed serglycin immunoreactivity in the Golgi area of promyelocytes (PM) and myelocytes (MC), as well as in a few band cells and mature neutrophil granulocytes. Granular staining was detected near the Golgi apparatus in some of the PM, and the major part of the cytoplasm was negative. Immunoelectron microscopy showed serglycin immunoreactivity located to the Golgi apparatus and a few immature granules of PM and MC. The decreasing level of serglycin protein during myeloid differentiation coincided with a decrease of mRNA expression, as evaluated by Northern blotting. Subcellular fractions of neutrophil granulocytes were obtained. Serglycin immunoreactivity was detected in the fraction containing Golgi apparatus, plasma membrane, and secretory vesicles by Western blotting and enzyme-linked immunosorbent assay. Serglycin was not detected in subcellular fractions containing primary, secondary, or tertiary granules. Together, these findings indicate that serglycin is located to the Golgi apparatus and a few immature granules during neutrophil differentiation. This is consistent with a function for serglycin in formation of granules in neutrophil granulocytes. Our findings contrast the view that native serglycin is present in mature granules and plays a role in packaging and regulating the activity of proteolytic enzymes there.
The monocyte Fcγ receptors FcγRI/γ and FcγRIIA differ in their interaction with Syk and with Src-related tyrosine kinases
Authors: Huang Zhen-Yu , Hunter Sharon , Kim Moo-Kyung , Chien Paul , Worth Randall G , Indik Zena K , Schreiber Alan D 
Published: May 2004

AbstractThere are important differences in signaling between the Fc receptor for immunoglobulin G (IgG) FcγRIIA, which uses the Ig tyrosine-activating motif (ITAM) within its own cytoplasmic domain, and FcγRI, which transmits signals by means of an ITAM located within the cytoplasmic domain of its associated γ-chain. For example, in transfected epithelial cells and COS-1 cells, FcγRIIA mediates phagocytosis of IgG-coated red blood cells more efficiently than does FcγRI/γ, and enhancement of phagocytosis by Syk kinase is more pronounced for FcγRI/γ than for FcγRIIA. In addition, structure/function studies indicate that the γ-chain ITAM and the FcγRIIA ITAM have different requirements for mediating the phagocytic signal. To study the differences between FcγRIIA and FcγRI/γ, we examined the interaction of FcγRIIA and the FcγRI/γ chimera FcγRI-γ-γ (extracellular domain–transmembrane domain–cytoplasmic domain) with Syk kinase and with the Src-related tyrosine kinases (SRTKs) Hck and Lyn in transfected COS-1 cells. Our data indicate that FcγRIIA interacts more readily with Syk than does FcγRI-γ-γ and suggest that one consequence may be the greater phagocytic efficiency of FcγRIIA compared with FcγRI/γ. Furthermore, individual SRTKs affect the efficiency of phagocytosis differently for FcγRI-γ-γ and FcγRIIA and also influence the ability of these receptors to interact with Syk kinase. Taken together, the data suggest that differences in signaling by FcγRIIA and FcγRI-γ-γ are related in part to interaction with Syk and Src kinases and that individual SRTKs play different roles in FcγR-mediated phagocytosis.
TGF-β regulation of human macrophage scavenger receptor CD163 is Smad3-dependent
Authors: Pioli Patricia A , Goonan Katie E , Wardwell Kathleen , Guyre Paul M 
Published: May 2004

AbstractTight regulation of the inflammatory response is essential for the maintenance of physiologic homeostasis. A potentially important mediator of this process is CD163, a macrophage-specific member of the scavenger receptor cysteine-rich family. CD163 surface expression is up-regulated by glucocorticoids and the anti-inflammatory cytokine interleukin-10, and CD163 is shed acutely from the cell surface in response to lipopolysaccharide. We now demonstrate that transforming growth factor-β (TGF-β) markedly reduces expression of CD163. Treatment of primary human monocytes with TGF-β inhibited basal as well as dexamethasone-induced CD163 mRNA and protein expression. De novo protein synthesis was not required for this inhibition, suggesting that TGF-β regulates CD163 expression transcriptionally. To delineate this transcriptional regulation, a 2.5-kb fragment of the CD163 promoter was isolated. This promoter was inhibited by TGF-β, and suppression was dependent on Smad3 expression. These results define a novel function for TGF-β and implicate an important role for CD163 in the host response to inflammation.