bluuebunny/crossref_metadata_2025_split huggingface dataset:
Demystifying Aubrey Beardsley
Authors: Gruetzner Robins Anna 
Published: December 2003

Books reviewed in this article:Stephen Calloway Three Artists (Three Women); Modernism and the Art of Hesse, Krasner and O’KeefeLinda Gertner Zatlin Beardsley Japonisme and the Perversion of the Victorian IdealJane Haville Desmarais The Beardsley Industry. The Critical Reception in England and FrancePeter Raby Aubrey Beardsley and the NinetiesMatthew Sturgis Aubrey Beardsley. A Biography
Government and the Metropolitan Image: ministers, parliament and the concept of a capital city, 1840–1915
Authors: Port M.H. 
Published: December 2003

The two basic obstacles to reconstructing Victorian London as a magnificent capital were its lack of effective local government, and the prevailing system of parliamentary government.Fear of disease forced ministers to act on sanitary issues, but they were reluctant to outface those interests that resisted, on one hand, interference with the peculiar powers of the City of London, and on the other opposed spending any part of national taxation on London. Even necessary improvements in government buildings were attacked as misuse of public money.Improvements in London’s image achieved in the Victorian era were largely the work of a handful of junior ministers influenced by developments in other European capitals, especially Paris. Only at the end of the nineteenth century was a means devised of safeguarding improvement schemes from capricious undermining.
History Painting/Painting History
Authors: Barker Emma 
Published: December 2003

Books reviewed in this article:Christopher Prendergast, Napoleon and History Painting: Antoine‐Jean Gros’s, La Bataille d’EylauBeth S. Wright, Painting and History during the French Restoration: Abandoned by the PastSteven Bann, Paul Delaroche: History PaintedMarc J. Gotlieb, The Plight of Emulation: Ernest Meissonier and French Salon Painting
Repossessions: Postcolonial Perspectives on the Politics of Culture
Authors: Rhodes Colin 
Published: December 2003

Books reviewed in this article:Nicholas Thomas, Possessions: Indigenous Art/Colonial CultureNicholas Thomas and Diane Losche (eds.), Double Vision: Art Histories and Colonial Histories in the PacificNicholas Thomas, Oceanic ArtJulie F. Codell and Dianne Sachko Macleod (eds.), Orientalism Transposed: The Impact of the Colonies on British Culture
Vermeer’s Pregnant Women. On Human Generation and Pictorial Representation
Authors: Leonhard Karin 
Published: December 2003

According to legend, Vermeer's canvas acts like a flawless mirror:The picture is conjured onto it as though it is painted by Nature itself – the canvas reflects undistorted images of the real world. Vermeer seems to be a master in the art of describing; he paints with striking realism.But is there any truth to this legend?We well know that the female body was also seen as a speculum sine macula in the seventeenth century’s eyes. A two–thousand–year–old belief in human generation gave the power of procreation to men alone; the female body was a merely passive matter, a medium in which the embryo could grow.– Vermeer has painted pregnant women.But when we talk about Vermeer, we never ask about this belief, although it was in Delft, only a few streets away from Vermeer's home, that it was challenged and disproved for all time.
Selective depletion of rectal lamina propria rather than lymphoid aggregate CD4 lymphocytes in HIV infection
Authors: CLAYTON F , SNOW G , REKA S , KOTLER D P 
Published: December 2003

SUMMARY
The goal of this study was to examine the changes in lymphocyte populations in rectal mucosa during HIV infection and to study their relationship to mucosal immunity and to systemic depletion of CD4 lymphocytes. Rectal biopsies from 58 HIV-infected subjects and eight controls were studied. Frozen rectal tissue sections were stained with antibodies to CD4, CD3, CD8, and markers for macrophages. HIV-infected subjects were divided into early stage (no opportunistic infections) and AIDS groups. There was profound depletion of rectal lamina propria CD4 lymphocytes (16% and 6% of normal content in early and AIDS groups, respectively). However, lymphoid aggregate CD4 lymphocytes were far less severely depleted (69% and 40% of normal content, respectively). The extent of lymphoid aggregate CD4 lymphocyte depletion generally parallelled the CD4 lymphocyte depletion in the blood. CD8 lymphocyte content in both the lamina propria and lymphoid aggregates usually were increased, particularly in early-stage patients. Macrophage contents were usually normal in the HIV-infected groups. We conclude that rectal lamina propria and lymphoid aggregates are distinct compartments differing markedly in their CD4 lymphocyte content during HIV infection. In light of this and an increased number of apoptotic cells which were noted in rectal lamina propria in HIV-infected subjects, we hypothesize that intestinal lamina propria could be a site of rapid CD4 lymphocyte destruction during HIV infection.
High frequency of Epstein–Barr virus (EBV) lymphoblastoid cell line-reactive lymphocytes in cord blood: evaluation of cytolytic activity and IL-2 production
Authors: MORETTA A , COMOLI P , MONTAGNA D , GASPARONI A , PERCIVALLE E , CARENA I , REVELLO M G , GERNA G , MINGRAT G , LOCATELLI F , RONDINI G , MACCARIO R 
Published: December 2003

SUMMARY
We investigated natural immunity towards autologous EBV lymphoblastoid cell lines (EBV-LCL) in the cord blood. Cord blood lymphocytes (CBL) from 20 healthy neonates were examined together with three EBV+ and one EBV− adult donors. We found that high frequencies of EBV-LCL-reactive cytotoxic lymphocytes, ranging from 1/190 to 1/12 205 were detectable in EBV− and EBV+ donors, as well as in the cord blood of 15 out of 20 neonates. Surface phenotype analysis, depletion experiments with MoAbs specific for T and natural killer (NK) lymphocyte subsets, and T lymphocyte cloning procedures strongly indicate virus-specific cytotoxic T lymphocytes (CTL) as the major population responsible for the lysis of autologous EBV-LCL in EBV+ donors. Conversely, a high frequency of NK cells seems to be involved in the killing activity observed in neonates and in the EBV− donor. Frequencies of EBV-LCL-induced IL-2-producing lymphocytes were high in EBV+ donors (range 1/2247–1/6633) and heterogeneous, but consistent, in cord blood (range 1/5072–1/57 819) and in the EBV− adult (1/17 148). CD8+ lymphocytes were responsible for IL-2 production in EBV+ individuals, while CD4+ T cells were charged with this role in cord blood and in the EBV− donor. These data demonstrate that CBL are able to develop a strong innate immunity, directed against autologous EBV-infected cells, mediated by both NK cells and CD4+ T lymphocytes. This characteristic may be relevant for protection against viral infections in both neonates and patients given cord blood transplantation (CBT).
Phenotypic characterization of T cells in bronchoalveolar lavage fluid (BALF) and peripheral blood of patients with diffuse panbronchiolitis; the importance of cytotoxic T cells
Authors: KAWAKAMI K , KADOTA J , IIDA K , FUJII T , SHIRAI R , MATSUBARA Y , KOHNO S 
Published: December 2003

SUMMARY
We investigated the contribution of T cells in diffuse panbronchiolitis (DPB) by identifying T cell subsets in BALF of 36 patients with DPB, before and after long-term treatment with macrolide antibiotics, and 16 healthy control subjects. The percentages of lymphocytes and CD3+γδ+ cells in BALF of DPB patients and control subjects were similar, but the absolute number of these cells was higher in DPB patients. Treatment resulted in a significant reduction in the absolute number of these cells. A further two-colour analysis of T cell subsets in BALF showed a significantly higher ratio and number of CD8+HLA-DR+ cells in DPB patients. Treatment resulted in a significant reduction of activated T cells. Most BALF CD8+ cells were CD8+CD11b− cytotoxic T cells. The number of these cells in BALF of DPB patients (26.69 ± 5.86 × 103/ml) was higher than the control (2.02 ± 0.38 × 103/ml; P &lt; 0.001), and a significant reduction was observed after treatment (7.69 ± 2.59 × 103/ml; P &lt; 0.01). The number of CD4+ cells was also higher in DPB patients than in controls, and most were CD4+CD29+ memory T cells. However, treatment did not influence the number of these cells. The number of lymphocytes, CD3+γδ+, CD8+CD11b−, CD8+HLA-DR+, and CD4+CD29+ cells was higher in patients with bacterial infection than in those without bacterial infection, and interestingly, macrolide therapy reduced the number of lymphocytes, CD3+γδ+, CD8+CD11b− and CD8+HLA-DR+ cells, irrespective of bacterial infection. In peripheral blood, the percentage of CD8+HLA-DR+ cells was also higher in DPB patients than in healthy subjects, and significantly decreased after treatment. The percentage of CD8+CD11b− cells in peripheral blood was similar in DPB patients and normal subjects, and treatment significantly reduced the percentage of these cells. Finally, the expression of the adhesion molecules CD11a/CD18 (α/β-chains of LFA-1) on lung CD3+ cells and CD49d (α-chain of VLA) on lung CD4+ cells was enhanced compared with that on peripheral blood in DPB patients. Our results suggest that elevation of memory T cells and activation of CD8+ cells, mainly cytotoxic T cells, in the airway lumen of DPB patients may contribute to chronic bronchial inflammation, possibly through up-regulation of adhesion molecules. Our findings also indicate that macrolide antibiotics may have a direct or indirect suppressive effect on cytotoxic T cells, and as such, reduce inflammation and improve clinical condition.
The 80-kD fibronectin fragment increases the production of fibronectin and tumour necrosis factor-alpha (TNF-α) in cultured mesangial cells
Authors: LOPEZ-ARMADA M J , GONZALEZ E , GOMEZ-GUERRERO C , EGIDO J 
Published: December 2003

SUMMARY
The presence of fibronectin (FN) fragments has been demonstrated in several inflammatory processes, and they have been implicated in the recruitment of mononuclear cells. However, the interaction of these FN fragments with resident cells has hardly been studied. We have hypothesized that the 80-kD FN fragment, which includes the RGD cell binding domain of FN, could contribute to the pathogenesis of glomerular damage through the interaction with mesangial cells (MC) via α5β1 integrin. Since an increase in the glomerular deposit of matrix components, particularly FN, is frequently observed in progressive glomerulonephritis, we studied whether its synthesis is modulated by the 80-kD FN fragment and the native FN molecule. While the 80-kD FN fragment stimulated FN in a dose-dependent manner, both at the mRNA and protein level, the whole FN molecule exerted a dual effect. High doses produced FN inhibition, while low doses elicited a certain increase. This stimulation was abrogated by the presence of Sam-1, a MoAb against the α-subunit of the α5β1 integrin. Since cytokines play a fundamental role in glomerular injury, we studied the production of TNF-α, one of the most powerful mediators of inflammation. TNF-α synthesis was induced by the 80-kD FN fragment, in a dose-dependent manner, but not by native FN. When MC were incubated with the 29- and 31-kD FN fragments, which lack the RGD cell binding domain, TNF-α secretion was not detected. These results strongly suggest that in cultured MC, the 80-kD FN fragment induces the synthesis of matrix proteins such as FN, and cytokines such as TNF-α, via α5β1 integrin. This mechanism could contribute to the perpetuation of renal injury.
Radiation damage and immune suppression in splenic mononuclear cell populations
Authors: HARRINGTON N P , CHAMBERS K A , ROSS W M , FILION L G 
Published: December 2003

SUMMARY
We have examined alterations in all of the major splenic mononuclear cell (SMNC) populations in C57Bl/6 mice following whole-body irradiation (0–700 cGy) in order to determine which populations may play a role in active immune suppression and/or haematopoietic recovery. A protocol has been established for characterization and differentiation by flow cytometric analysis (FCA) of the major MNC populations in the mouse spleen: T lymphocytes (CD4+ and CD8+ cells), B lymphocytes, natural killer (NK) cells, and monocytes/macrophages. Ionizing radiation caused decreased spleen cellularity and decreased ability of surviving SMNC to respond to mitogen. FCA revealed alterations in the relative composition of the constituent splenic cell populations following irradiation, reflecting differential radiosensitivity, with selective enrichment of NK cells (seven-fold) and CD4+ T lymphocytes (three-fold). Enrichment developed during the 7-day post-irradiation period. In addition, some MNC became activated in a dose- and time-dependent fashion following whole-body irradiation, as indicated by expression of CD71, the transferrin receptor. These cells were CD34+ and Thy1.2+, but were CD4− or CD8− as well as CD45− (B cell). The observed increase in NK cells corresponds with a previously reported increase in natural suppressor (NS) cells following total-lymphoid irradiation (TLI). The balance of recovery-inhibiting NK cells and recovery-enhancing CD4+ T lymphocytes following irradiation may reflect or influence the degree of haematopoietic recovery, and may provide an indication of the extent of damage (biological dosimetry).
Wild isolates of Plasmodium falciparum malaria show decreased sensitivity to in vitro inhibition of parasite growth mediated by autologous host antibodies
Authors: WÅHLIN FLYG B , PERLMANN H , PERLMANN P , ESPOSITO F , BERZINS K 
Published: December 2003

SUMMARY
Antigenic diversity in field populations of Plasmodium falciparum parasites may delay the acquisition of protective immunity to malaria, the development of which may thus require repeated exposure to infection over a prolonged period of time. In this study we show that P. falciparum parasites may vary in their sensitivity to antibody-mediated invasion/growth inhibition in vitro. Wild isolates of P. falciparum from children living in an endemic area of Burkina Faso were tested for their sensitivity to the growth inhibitory effects of antibodies originating from the same (autologous) and from other donors (heterologous). A significantly lower invasion inhibition activity was obtained when the isolates and antibodies were tested in autologous compared with heterologous combinations. The lower sensitivity to growth inhibition by autologous antibodies may be due to immune pressure in vivo, selecting from a heterogeneous parasite population those with a low expression of the antigens recognized by the host's antibodies. Alternatively, the parasites cultured from each child might represent expanding parasite populations, mainly constituting strains not earlier seen by the immune system of that specific host. The results reinforce the concern about Plasmodium antigenic diversity as a major obstacle towards the development of an effective malaria vaccine.
Mannoproteins of Cryptococcus neoformans induce proliferative response in human peripheral blood mononuclear cells (PBMC) and enhance HIV-1 replication
Authors: ORENDI J M , VERHEUL A F M , DE VOS N M , VISSER M R , SNIPPE H , CHERNIAK R , VAISHNAV V V , RIJKERS G T , VERHOEF J 
Published: December 2003

SUMMARY
To investigate the possible role of Cryptococcus neoformans var. neoformans in HIV disease progression, and to identify the responsible cryptococcal components, an in vitro cell culture model was set up to study the C. neoformans-induced enhancement of HIV replication in HIV-1-infected PBMC. Similar to whole C. neoformans, cell-wall membrane fraction and mannoproteins induced proliferation of PBMC and enhancement of lymphotropic HIV replication in HIV-infected PBMC, while galactoxylomannan did not. MoAbs capable of interfering with MHC class II-mediated antigen presentation prevented the induction of cell proliferation by whole C. neoformans or cryptococcal mannoproteins. MoAb binding to adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) also inhibited C. neoformans-induced cell proliferation. In addition, anti-MHC class II MoAb inhibited the enhancement of HIV replication by C. neoformans. The results suggest that: (i) C. neoformans may accelerate HIV disease progression by stimulation of HIV replication through MHC class II-mediated antigen presentation; and (ii) cryptococcal mannoprotein may be one of the responsible components. The ability to enhance HIV replication in PBMC in vitro is not unique for C. neoformans. However, this is the first report to study in detail a yeast-induced enhancement of HIV replication in PBMC.
Serum amyloid A gene expression in rabbit, mink and mouse
Authors: MARHAUG G , HACKETT B , DOWTON S B 
Published: December 2003

SUMMARY
The expression of serum amyloid A (SAA) protein, a major acute-phase reactant in most species, was examined by in situ hybridization in multiple organs of rabbit, mink and mouse. In livers of unstimulated mice and rabbits a heterogeneous pattern of SAA expression in hepatocytes was observed. In all three species, lipopolysaccharide (LPS) administration resulted in extensive uniform hybridization of SAA probes to hepatocytes and in the rabbit SAA transcripts were detected in cells in the white pulp of the spleen, the adrenal cortex and ovary as well as in the mucosa and lymphatic vessels of the small intestine. Examination of hybridizing SAA signals in the rabbit myocardium showed a speckled distribution in myocytes. The rabbit endocardium was strongly positive, and in the kidney rabbit SAA mRNA was mainly confined to epithelial cells of the proximal and distal convoluted tubules. In the unstimulated mouse, SAA mRNA was detected in the liver and epithelial cells of the small and large intestine. After stimulation of an acute-phase response with LPS a strong response was seen in these organs as well as in the convoluted tubules of the kidney. In extrahepatic organs of the mink, no SAA mRNA was detectable in unstimulated animals, while the convoluted tubules of the kidney and uterine endometrium were strongly positive after systemic LPS injection.
Mercury-induced renal immune complex deposits in young (NZB × NZW)F1 mice: characterization of antibodies/autoantibodies
Authors: ABEDI-VALUGERDI M , HU H , MÖLLER G 
Published: December 2003

SUMMARY
It is well demonstrated that mercury induces a systemic autoimmune disease in susceptible mouse strains. One of the major characteristics of mercury-induced autoimmune disease in mice is the development of renal immune complex deposits. We have previously shown that continual injection of mercury into young autoimmune prone (NZB × NZW)F1 mice induced an increase in antibody/autoantibody production as well as development of early renal immune complex deposits. In the present study, we characterized the isotype, the specificity and the possible pathogenicity of deposited immunoglobulins in the kidneys of mercury-injected (NZB × NZW)F1 hybrids. We found that young (NZB × NZW)F1 mice injected with mercuric chloride (HgCl2) for 6 weeks developed intense antibody formation of all immunoglobulin isotypes (except for IgG2b) as well as high levels of granular deposits of IgM, IgG1, IgG2a and IgG3 antibodies in the renal mesangium. Increased levels of the same antibody isotypes were also found in the kidney eluate of mercury- but not saline-injected mice. The dominant antibody in the kidney eluate of mercury-injected mice was of IgG1 isotype and found to be directed against double-stranded DNA, collagen, cardiolipin, phosphatidylethanolamine, and the hapten trinitrophenol, but not against nucleolar antigens. Further studies demonstrated that mercury-induced renal immune complex deposits in young (NZB × NZW)F1 mice did not lead to a severe kidney injury. Thus, in response to mercury, young (NZB × NZW)F1 mice develop renal immunoglobulin deposits with an isotype and specificity pattern correlating with that seen in the spleen and in the serum.
An assessment of peripheral immunity in patients with sarcoidosis using measurements of serum vitamin D3, cytokines and soluble CD23
Authors: BANSAL A S , BRUCE J , HOGAN P G , ALLEN R K 
Published: December 2003

SUMMARY
The aetiology of the peripheral anergy in sarcoidosis is unclear. To investigate this further we measured the serum levels of several factors important in different aspects of immune regulation to obtain a profile of those factors which promote and inhibit immune activation in sarcoidosis. Thirty-seven patients with sarcoidosis and 20 healthy controls of similar sex and age comprised the study group. Serum IL-10, interferon-gamma (IFN-γ), soluble CD23 (sCD23), IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-1β and tumour necrosis factor-alpha (TNF-α) were measured using in-house ELISAs. Vitamin D3 was measured using a radioreceptor assay. Serum levels of sCD23 and IL-10 were significantly elevated in patients with sarcoidosis relative to controls (median 13.9 versus 9.5 arbitrary units/ml, P &lt; 0.01 for sCD23, and 9.6 versus 5.0 pg/ml, P &lt; 0.04 for IL-10). Regardless of steroid therapy or disease activity, serum levels of IFN-γ, TNF-α, IL-1β, GM-CSF and IL-8 were no different in patients with sarcoidosis and controls. Vitamin D3 levels were significantly higher in patients with sarcoidosis versus normal controls (medians 78.0 versus 56.0, P &lt; 0.001), active sarcoidosis (n = 20) versus inactive disease (n = 17) (medians 81.5 versus 66.0, P &lt; 0.03) and active sarcoidosis versus controls (medians 81.5 versus 56.0, P &lt; 0.0002). The levels were no different between patients with inactive sarcoidosis and controls. We suggest that IL-10 and vitamin D3 may contribute to the peripheral anergy in sarcoidosis. The elevated serum sCD23 suggests an increase in peripheral humoral immunity. Consistent with a quiescent peripheral immune system, factors capable of monocyte/macrophage activation (TNF-α, IFN-γ, GM-CSF and IL-8) were not elevated in the peripheral circulation.
In vitro measurement of cytotoxic T cell activity does not predict clinical progression in paediatric HIV disease—two case studies
Authors: FROEBEL K S , MOK J Y Q , ALDHOUS M C , ARMITAGE M P , ARNOTT M , REYNOLDS L M , PEUTHERER J F , BURNS S M 
Published: December 2003

SUMMARY
Cytotoxic T cells are believed to be an important immune response in HIV infection, both in the initial response to viraemia, and in controlling HIV replication and maintaining clinical stability. We report here the detailed findings in two vertically infected children, from the Edinburgh perinatal cohort. Both were clinically stable for the first 7 years of life. One had vigorous HIV-specific cytotoxic T lymphocyte (CTL) responses, and non-lytic suppression, measured in vitro, while the second had no CTL activity against HIV. Despite her HIV-specific immunity, the first child had a declining CD4 count, and a high and fluctuating viral load, whereas the second child maintained a stable CD4 count, a low viral load and had a virus which could not be cultured in peripheral blood mononuclear cells (PBMC) in vitro. The first child subsequently progressed to AIDS and has now died, while the second remains clinically well. More detailed investigations showed the clinically stable child to be heterozygous for the CCR5 receptor, and to be HLA-B49—both of which markers have been associated with slow HIV disease progression. These findings question the role of CTL in maintaining stable HIV disease, and stress the need for immunological investigations to be considered in the light of the genetic make-up of the patient. They may also reflect a different immunopathogenesis of HIV disease in children compared with adults.