bluuebunny/crossref_metadata_2025_split huggingface dataset:
Every Man is Naturally an Antiquarian: Francis Grose and Polite Antiquities
Authors: Bending Stephen 
Published: December 2003

Stephen Bending is a Lecturer in the English Department at the University of Southampton. He has written numerous articles on landscape and polite culture in the eighteenth century and has co–edited with James Raven and Antonia Forster The English Novel 1770–1799: A Bibliographical Survey of Prose Fiction in the British Isles (Oxford University Press, 2000), and with Stephen Bygrave Henry Mackenzie’s, The Man of Feeling (World’s Classics, 2002), and is editor of the forthcoming anthology, The Writing of Rural England, 1500–1800 (Longman, 2002).Francis Grose produced well over a thousand low–cost antiquarian images of the antiquities of England and Wales. While it may be tempting to dismiss him as a mere popularizer and a charlatan, his works open up to a wide national public the antiquities of their native land. Central to his venture is at once the commodification of the past and an attempt to represent that commodification as nothing of the kind. Grose sets about repackaging the old as the new – a now classic act of consumerism – but also works hard to deny this activity by drawing on the language of scholarship and accuracy. Ultimately, his cheaply produced and mass–marketed images and texts demonstrate an antiquarian past which repeatedly collapses into a commercial present: cheap prints for a mass market create a national past in the very act of contemporary consumer aesthetics.
Voyage: Dominique–Vivant Denon and the Transference of Images of Egypt
Authors: Moore Abigail Harrison 
Published: December 2003

Abigail Harrison Moore is a lecturer in the School of Fine Art, History of Art and Cultural Studies at the University of Leeds. She recently obtained her PhD from the University of Southampton, entitled Imagining Egypt: The Regency Furniture Collections at Harewood House, Leeds and Nineteenth–Century Images of Egypt. Her current research focuses on the theory, history and historiography of material culture and museum studies.Focusing on the images in Dominique–Vivant Denon’s Voyage dans la Basse et la Haute d’Egypte (1802), this article explores the relationship between Denon’s illustrations of Egypt and the creation of a politically charged style of design in France and England at the beginning of the nineteenth century. The process of transcribing a historic site creates something that is at once removed from its original situation and, thus, the meaning of the image is altered depending upon its context of use. Previous regimes had turned to revivalism and its powerful aura of the past to support their hegemonic activities in the present, and Denon is shown to use the past to define the present in post–Revolutionary France. By using the example of Voyage and theorizing it by way of resources provided in the work of Roland Barthes, this essay aims to explain some of the processes that reconfigured the image of Egypt in France and England at the beginning of the nineteenth century.
Specimens of Antient Sculpture: Imperialism and the decline of art
Authors: Ballantyne Andrew 
Published: December 2003

Andrew Ballantyne is Professor of Architecture at the University of Newcastle. He is the author of Architecture, Landscape and Liberty: Richard Payne Knight and the Picturesque (Cambridge University Press, 1997) and Architecture: A Very Short Introduction (Oxford University Press, 2002). He is the editor of What is Architecture? (Routledge, 2002) and Architectures, in the Blackwell/AAH series New Interventions in Art History.When Richard Payne Knight wrote his commentaries on ancient sculpture, his analysis was characteristically wide–ranging. The observations are informative about the sculptures themselves, but scholarship has advanced, and the writings have been superseded. The remarks with which Knight positioned the works in their various cultural and political contexts are of continuing interest, particularly because they show him making connections between the organization of society and the qualities of its art. The great evil of Knight’s own day was, as he saw it, Napoleon’s imperialism; and he projected this current concern back into the analysis of ancient sculpture, so that the unmatched beauty of the works from ancient Greece began its decline from the moment when Alexander the Great started his empire–building campaigns. For Knight, as for Winckelmann, the artistic and architectural productions of the ancient Greeks were ideal because they were the productions of an ideal society. This analysis is complicated by the fact that attributions have changed, and the relative merits of individuals’ works have shifted. The engraved plates that illustrate the commentaries remain impressive, however, and they are themselves artistic productions, the aim of which was to give a clear impression of the sculpture. Knight’s commentary includes critical remarks when their effects were too picturesque, despite his fondness for such effects in their proper place.
Differential effects of sex hormones on autoantibody production and proteinuria in chronic graft-versus-host disease-induced experimental lupus nephritis
Authors: VAN GRIENSVEN M , BERGIJK E C , BAELDE J J , DE HEER E , BRUIJN J A 
Published: December 2003

SUMMARY
In patients with systemic lupus erythematosus, the female-to-male ratio is as high as 10:1. Sex hormones are thought to play a role in this difference in susceptibility. In a previous study, we demonstrated a high susceptibility of female mice to the development of glomerulonephritis after induction of chronic graft-versus-host disease (GVHD), compared with male mice. In order to unravel further this gender-related difference (C57Bl/10*DBA/2)F1 hybrid mice were either castrated or ovariectomized and treated with 17β-ethinyloestradiol or testosterone-decanoate preceding the induction of chronic GVHD. Testosterone-decanoate reduced significantly the development of albuminuria in females. In contrast, proteinuria of 17β-ethinyloestradiol-treated female mice was in the same range as that of sham-operated mice. Autoantibody levels against glomerular basement membrane, renal tubular epithelium, dsDNA and ssDNA, as determined by ELISA, were higher in 17β-ethinyloestradiol-treated female mice than in all other groups. Immunofluorescence studies showed the presence of immunoglobulin and complement deposits in glomeruli of all animals, without significant differences between the experimental groups. Our findings confirm earlier observations, in that testosterone-decanoate is shown to be an inhibitory compound, whereas 17β-ethinyloestradiol has stimulating properties in autoimmunity. Moreover, our results show for the first time differential hormonal effects on autoantibody levels and proteinuria in experimental lupus nephritis.
21-hydroxylase autoantibodies in adult patients with endocrine autoimmune diseases are highly specific for Addison's disease
Authors: FALORNI A , LAURETI S , NIKOSHKOV A , PICCHIO M L , HALLENGREN B , VANDEWALLE C L , GORUS F K ,   BELGIAN DIABETES REGISTRY, TORTOIOLI C , LUTHMAN H , BRUNETTI P , SANTEUSANIO F 
Published: December 2003

SUMMARY
The diagnostic specificity of recombinant 21-hydroxylase autoantibodies (21OH-Ab) for Addison's disease was tested in adult patients with either Graves' disease (GD), insulin-dependent diabetes mellitus (IDDM), or polyendocrinopathy, as well as in healthy controls. Using a radiobinding assay with in vitro translated recombinant human 21-hydroxylase, we found 21OH-Ab in 24/28 (86%) idiopathic Addison patients, and using an immunofluorescence assay we found adrenal cortex autoantibodies (ACA) in 12/28 (43%) patients (P =0.002). All the 12 ACA-positive sera were also positive for 21OH-Ab and ACA were found in 11/15 (73%) patients with less than 15 years and in 1/13 (8%) patients with 15–38 years of disease duration (P = 0.002). 21OH-Ab were present in 3/92 (3%) patients with GD, in 1/180 (0.6%) with IDDM and in 0/106 healthy subjects. The 21OH-Ab-positive GD and IDDM patients were also positive for ACA. None of 17 patients with polyendocrinopathy, but without Addison's disease, had 21OH-Ab. None of the 180 Belgian IDDM patients had Addison's disease or developed an adrenal insufficiency at follow up. In two out of three Graves patients, the presence of 21OH-Ab was associated with clinical and biochemical signs of adrenal insufficiency. Of the 89 21OH-Ab-negative patients with GD none had Addison's disease at the time of blood sampling, and 79 were followed up for 5.6–7.5 years and none developed clinical signs of adrenal insufficiency. We conclude that the presence of 21OH-Ab in patients with endocrine autoimmune diseases is highly specific for Addison's disease.
Anti-neutrophil monoclonal antibody therapy inhibits the development of adjuvant arthritis
Authors: SANTOS L L , MORAND E F , HUTCHINSON P , BOYCE N W , HOLDSWORTH S R 
Published: December 2003

SUMMARY
The aim of this study was to determine the contribution of neutrophils to adjuvant arthritis (AA) by in vivo depletion of peripheral blood neutrophils. Specific anti-neutrophil MoAb, RP3 (10 mg), or a control antibody was given twice daily on days 8–11 after injection of Mycobacterium tuberculosis in inbred male Sprague-Dawley rats. RP3 treatment inhibited the neutrophil leukocytosis associated with AA (3.3 ± 0.6 × 103/mm3versus 21.2 ± 6.9 × 103/mm3; P &lt; 0.001). On day 12, control animals exhibited severe arthritis as assessed by articular index (AI) (9.2 ± 1.3), increase in paw volume (149.3 ± 10.6%), and synovial fluid (SF) cell count (5.3 ± 0.5 × 105). RP3 treatment significantly reduced AI (1 ± 0.1; P &lt; 0.001), paw volume (103.6 ± 5.8%; P &lt; 0.001) and SF cells (0.6 ± 0.1 × 105; P &lt; 0.001) without affecting cutaneous DTH (treated 0.6 ± 0.1 mm change in thickness, control 0.8 ± 0.2 mm; NS). Additional experiments demonstrated that CD4+ cell depletion but not decomplementation inhibited AA development and synovial neutrophil accumulation. Depletion of circulating neutrophils prevented joint inflammation and synovial leucocyte influx in AA, suggesting a pivotal role for neutrophils in the effector phase of AA. Inhibition of neutrophil accumulation by CD4+ cell depletion and not by decomplementation suggests that neutrophil accumulation in AA is T cell-dependent.
Different Trypanosoma cruzi strains promote neuromyopathic damage mediated by distinct T lymphocyte subsets
Authors: MIRKIN G A , CELENTANO A M , MALCHIODI E L , JONES M , GONZÁLEZ CAPPA S M 
Published: December 2003

SUMMARY
The proliferative response of CD4 and CD8 T lymphocytes obtained from C3H/HeN mice chronically infected with Trypanosoma cruzi strains that differ in virulence, tropism and immunogenicity, was assayed against skeletal muscle, sciatic nerve and spinal cord homogenates. Although both CD4 and CD8 T lymphocytes from mice infected with the RA strain strongly proliferated against the nervous system, no response against skeletal muscle antigens was detected. CD4 and CD8 T lymphocytes from mice infected with the K-98 clone (from CA-I strain) showed low proliferative response against all the antigens assayed. To determine whether the proliferation patterns showed correlation with T cell-mediated neuromuscular damage, passive cell transfer studies were performed. Fifteen days after transfer of CD4 T cells from RA-infected donors (CD4-RA), normal syngeneic recipients displayed exclusively nervous tissue damage, such as perineural, endoneural and/or meningeal inflammatory infiltrates, with predominance of CD4 T cells. Fifteen days after transfer of CD4 T lymphocytes from mice infected with K-98 (CD4-K98), recipients showed inflammatory infiltrates only in skeletal muscle, where CD4 T lymphocytes and macrophages were predominant cells. Recipients of CD8 T cells from RA-infected mice (CD8-RA) showed lesions in both spinal cord and sciatic nerves. Higher percentages of CD8 T cells were observed in comparison with the recipients of CD4-RA or CD4-K98. In contrast, CD8 T cells from K-98-infected donors (CD8-K98) did not induce tissue damage. These results provide evidence that mice infected with T. cruzi populations that differ in their biological characteristics show diverse immune mechanisms that may be involved in the pathogenesis of peripheral nervous system damage.
Effects of interferon-alpha (IFN-α) administration on leucocytes in healthy humans
Authors: CORSSMIT E P M , HEIJLIGENBERG R , HACK C E , ENDERT E , SAUERWEIN H P , ROMIJN J A 
Published: December 2003

SUMMARY
Plasma concentrations of IFN-α are increased in several inflammatory conditions. Several lines of evidence indicate that IFN-α has anti-inflammatory properties. To study the effects of IFN-α on leucocyte subsets and activation and on cytokines, we administered IFN-α (rhIFN-α2b; 5 × 106 U/m2) to eight healthy human subjects in a randomized controlled cross-over study and analysed changes in circulating leucocytes and parameters for neutrophil and monocyte activation. After administration of IFN-α, neutrophil counts increased, monocyte counts decreased transiently, whereas the number of lymphocytes, basophils and eosinophils showed a sustained decrease. IFN-α administration was also associated with neutrophil activation, reflected in an increase in the plasma concentrations of elastase–α1-antitrypsin complexes and lactoferrin. Serum neopterin, a marker for monocyte activation, was significantly increased 10 h after administration of IFN-α. IFN-α significantly increased plasma concentrations of IL-6, IL-8 and IL-10. Although IL-1 and tumour necrosis factor (TNF) remained undetectable, plasma concentrations of soluble TNF receptors p55 and p75 increased after IFN-α administration. We conclude that IFN-α induces multiple alterations in the distribution and functional properties of leucocytes. IFN-α exerts pro- as well as anti-inflammatory effects within the cytokine network.
Identification and characterization of cells infiltrating the graft and aqueous humour in rat corneal allograft rejection
Authors: LARKIN D F P , CALDER V L , LIGHTMAN S L 
Published: December 2003

SUMMARY
In a rat model of corneal transplantation, Fischer 344 (RT1lv1) rats received orthotopic corneal isografts or Wistar-Furth (RT1u) donor allografts. Rejection was observed in 25 of 26 allograft recipients, at a median time of 18 days, with all isografts surviving &gt; 100 days. Flow cytometric analysis of aqueous humour identified cellular infiltration of the aqueous at the time of allograft rejection, in contrast to the acellular aqueous found in isografts at corresponding times following transplantation. A higher proportion of CD8+ than CD4+ cells was found at days 1–3 following rejection, whereas there was a higher proportion of CD4+ cells at days 5–8. No changes in peripheral blood T cell subsets were found at the time of rejection. Immunohistochemical analysis of cells infiltrating recipient iris and grafted cornea undertaken at days 1–2, 4 and 7–10 following onset of rejection, demonstrated inflammatory cells in the graft epithelium, stroma and aggregated on the endothelium. Large numbers of macrophages, T cells (CD4+ &gt; CD8+ at all time points), natural killer (NK) cells and neutrophils were detected in graft tissue at days 1–2 and 4, diminishing after that time. Most infiltrating cells expressed MHC class II antigen, and a smaller number expressed IL-2R. Expression of the co-stimulatory marker B7 was identified in a few cells at day 4 in the region of the graft-host wound. The immune response in graft rejection was characterized at day 4 also by expression of intercellular adhesion molecule-1 (ICAM-1) on endothelial cells of iris and corneal vessels, demonstration of interferon-gamma on mononuclear cells in the peripheral (recipient) cornea, and tumour necrosis factor-alpha on aggregated mononuclear cells on the graft, but not recipient, endothelium. Only sparse cellular infiltrates were found in isograft controls, with inflammation located at the graft-host wound. These findings suggest that inflammatory cells reach a corneal allograft by two routes—from vessels in the peripheral recipient cornea, and from vessels in the recipient iris via the aqueous humour. Different aqueous and intragraft T cell subset proportions were seen early in rejection, although a preponderance of CD4+ cells was found in both aqueous and graft at later times.
HIV infection of CD45RA+ and CD45RO+ CD4+ T cells
Authors: HELBERT M R , WALTER J , L'AGE J , BEVERLEY P C L 
Published: December 2003

SUMMARY
HIV preferentially infects the RO+ memory subset of CD4+ lymphocytes, and these cells are lost earlier in HIV infection than their RA+ counterparts. Although both populations express similar amounts of CD4 and bind the HIV envelope glycoprotein (gp120) equally well, calcium signals and CD4 down-regulation subsequent to gp120 binding are not the same in both populations. Data suggest these disparities are mediated by differential tyrosine kinase (TK) regulation. Syncytium formation is enhanced in RO+ cells, partly a consequence of increased leucocyte function antigen-1 (LFA-1) expression and, again, partly due to altered TK regulation. After in vitro HIV infection, reverse transcription is not detected in RA+ cells, is minimal in the RO+ class II− population, but progresses well in RO+ class II+. Infection followed by mitogen stimulation permits reverse transcription in all cells. HIV infection of RO+ cells is enhanced moderately at multiple points in the virus life cycle.
Immunoprecipitation of steroidogenic enzyme autoantigens with autoimmune polyglandular syndrome type I (APS I) sera; further evidence for independent humoral immunity to P450c17 and P450c21
Authors: PETERSON P , UIBO R , PERA¨NEN J , KROHN K 
Published: December 2003

SUMMARY
Three steroidogenic P450 cytochromes, steroid 17α-hydroxylase (P450c17), steroid 21-hydroxylase (P450c21) and side-chain cleavage enzyme (P450scc), have been described as autoantigens in APS I. In this study we report an immunoprecipitation assay for the detection of autoantibodies to these three enzymes using in vitro35S-labelled antigens. Overall, 33 out of 46 (72%) patients with APS I had autoantibodies to at least one of the three proteins and each protein was recognized by patient sera with equal frequency. A higher rate of autoantibody positivity was observed in APS I patients with Addison's disease compared with patients without Addison's disease (85% versus 39%). All 11 patients with ovarian failure had anti-P450c17 or anti-P450scc antibodies. The immunoprecipitation results with P450c17, P450c21 and P450scc correlated well with the results obtained by immunoblotting assays. In addition, the steroidogenic enzymes 11β-hydroxylase (P450c11β), aromatase (P450arom), 3β-hydroxysteroid dehydrogenase (3βHSD) and adrenodoxin were studied by immunoprecipitation assay, but no reaction was found either with 46 APS I or with 26 healthy control sera. To study the suggested immunological cross-reactivity between P450c17 and P450c21 enzymes, nine APS I patient sera were preabsorbed with bacterially expressed P450c17 or P450c21 and subsequently used in immunoprecipitation assay. The absorption experiments clearly indicated that the preincubation inhibited only the reactivity of corresponding antigen, suggesting independent autoantibody response to the two enzymes. Our results suggest that the immune response to some but not to all steroidogenic enzymes is a specific feature of APS I that may be pathogenically significant.
A boy with X-linked hyper-IgM syndrome and natural killer cell deficiency
Authors: ØSTENSTAD B , GILIANI S , MELLBYE O J , NILSEN B R , ABRAHAMSEN T 
Published: December 2003

SUMMARY
We present a boy with hyper-IgM syndrome with a previously not reported mutation in the CD40 ligand gene. He also had a concomitant natural killer (NK) cell deficiency. He had no CD56+ or CD16+ cells and no NK activity as determined in 4 h chromium release cytotoxicity assay. After 5 days in culture with IL-2-containing medium, however, his peripheral blood mononuclear cells lysed both NK-sensitive and NK-resistant targets, showing that he had lymphokine-activated killer cell precursors in the circulation. Due to the associated neutropenia, he was treated with granulocyte colony-stimulating factor (G-CSF) and responded well. In the same period we observed a transient increase in the number of NK cells. Isolated NK cell deficiencies are extremely rare. We suggest that the defect in our patient is part of the hyper-IgM syndrome, probably representing the phenotype of the new mutation described. Thus, it is possible that both the neutropenia and the NK cell deficiency are due to lack of growth-promoting signals normally delivered by the CD40 ligand.
Neutralization of tumour necrosis factor (TNF) but not of IL-1 reduces inflammation in chronic dextran sulphate sodium-induced colitis in mice
Authors: KOJOUHAROFF G , HANS W , OBERMEIER F , MA¨NNEL D N , ANDUS T , SCHO¨LMERICH J , GROSS V , FALK W 
Published: December 2003

SUMMARY
The cytokines TNF and IL-1 have been implicated as mediators of the inflammatory processes in patients with inflammatory bowel disease (IBD). To investigate the role of these cytokines in mucosal inflammation we used anti-cytokine strategies in a mouse model of acute and chronic colitis. Mice which received 5% dextran sulphate sodium (DSS) in their drinking water showed signs of acute colitis on day 4, with severe weight loss and bloody diarrhoea. Chronic colitis was established after four cycles of feeding 5% DSS for 7 days and water for 10 days, with the mice showing diarrhoea but no weight loss. In acute colitis, treatment with anti-IL-1 reagents, anti-TNF MoAb, or dexamethasone (DEX) led to aggravation. By contrast, in chronic colitis, treatment of mice with several IL-1 activity-inhibiting reagents failed to show significant effects, whereas anti-TNF MoAb or DEX significantly reduced the colitis. We conclude that in acute colitis IL-1 and TNF are beneficial, whereas in chronic colitis, TNF but not IL-1 seems to play a major role in perpetuation of chronic inflammation.
Normal human immunoglobulins for intravenous use (IVIg) delay hyperacute xenograft rejection through F(ab′)2-mediated anti-complement activity
Authors: LATREMOUILLE C H , GENEVAZ D , HU M C , SCHUSSLER O , GOUSSEF N , MANDET C , BRUNEVAL P , HAEFFNER-CAVAILLON N , CARPENTIER A , GLOTZ D 
Published: December 2003

SUMMARY
Xenotransplantation between discordant species leads to a hyperacute rejection mediated by natural antibodies, both of the IgG and IgM isotypes, activation of complement and endothelial cell activation. The combination of these mechanisms leads to a transplant survival of minutes to a few hours. Polyclonal human immunoglobulins for intravenous use (IVIg) from normal donors have proved effective in a number of antibody-mediated disorders, as well as in inflammatory disorders. We demonstrate that administration of IVIg in a guinea pig to rat model of cardiac xenografting can effectively delay hyperacute rejection. This effect is mediated by the F(ab′)2 fragments of IVIg, and is correlated to an anti-complementary activity.