bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interleukin‐15 inhibits sodium nitroprusside–induced apoptosis of synovial fibroblasts and vascular endothelial cells
Authors: Yang Lin , Thornton Sherry , Grom Alexei A. 
Published: November 2002

AbstractObjectiveOne of the pathologic hallmarks of juvenile rheumatoid arthritis (JRA) is a tumor‐like expansion of inflamed synovial tissue, or pannus, which causes much of the joint damage in this disease. The expansion of pannus is supported by extensive formation of new blood vessels. We have previously shown that revascularization of minced JRA synovial tissues engrafted into SCID mice correlated with the intensity of inflammatory activity in the tissues and with interleukin‐15 (IL‐15) expression. Since synovial vascular endothelial cells (VECs) expressed IL‐15 receptors, the present study was undertaken to investigate the hypothesis that IL‐15 might play a role in neovascularization of the pannus.MethodsTo evaluate IL‐15 for possible angiogenic activity, we assessed the ability of recombinant human IL‐15 (rHuIL‐15) to induce VEC growth directly and to stimulate synovial cells to produce endothelial growth factors. Since IL‐15 had been shown to inhibit apoptosis of certain immune cells, we were also interested in whether it might have similar effects on VECs. Apoptosis was induced by addition of sodium nitroprusside (SNP) at 1–2 mM to >80% confluent primary VECs, and numbers of apoptotic cells were determined by annexin V assay.ResultsAddition of rHuIL‐15 at 10–100 ng/ml to primary synovial fibroblast cultures failed to up‐regulate expression of vascular endothelial growth factor and angiopoietin 1 by these cells. Although rHuIL‐15 failed to induce a mitogenic response of VECs, it promoted survival of these cells on Matrigel. Preincubation of VECs with rHuIL‐15 at 50 ng/ml significantly reduced the proportion of VECs undergoing apoptosis.ConclusionIL‐15 promotes survival of VECs on Matrigel and inhibits SNP‐induced apoptosis of endothelial cells. We hypothesize that this mechanism may be relevant to the stabilization of newly formed vascular structures in JRA synovium.
Fast spin echo–T2‐weighted sequences with fat saturation in dactylitis of spondylarthritis
Authors: Olivieri Ignazio , Salvarani Carlo , Cantini Fabrizio , Scarano Enrico , Padula Angela , Niccoli Laura , Ciancio Giovanni , Barozzi Libero 
Published: November 2002

AbstractObjectiveTo establish by means of fast spin echo (FSE)–T2‐weighted sequences with fat saturation if enthesitis of the flexor digitorum superficialis and profundus tendons is the primary lesion in spondylarthritis (SpA) finger dactylitis.MethodsEleven dactylitic fingers and their corresponding normal, contralateral fingers, belonging to 6 patients who met the Amor criteria for SpA, were studied by FSE–T2‐weighted sequences with fat saturation.ResultsAll dactylitic fingers showed moderate or severe fluid collection in the flexor tendon synovial sheaths. Involvement of the joint cavity was simultaneously present in at least one joint in 3 (27.3%) of the 11 fingers. A mild to moderate peritendinous soft tissue edema was observed in 5 (45.5%) of the 11 affected fingers. In no dactylitic finger was bone edema observed near the insertions of the flexor digitorum superficialis or profundus tendons or in other sites of the phalanges. No lesions were observed in the 11 contralateral, clinically normal fingers.ConclusionIn SpA dactylitis there is no evidence of enthesitis of the flexor digitorum tendons and joint capsules.
A shared mission? Changing relationships between government and church health services in Africa
Authors: Green A. , Shaw J. , Dimmock F. , Conn Cath 
Published: November 2002

AbstractThis article reviews the relationships between government and church health providers within sub‐Saharan Africa with a particular focus on East and Southern Africa. This is of particular interest at this time, given the changing configuration of the health sector in many countries as a result of health sector reform policies. The article provides a historical overview of the development and emerging role of the church health services within this changing environment.The factors affecting the relationship between the government and church sector are identified. These include differences in objectives, types of service provided, and the organizational culture and management styles. The paper then explores key issues seen to affect the future pattern of relationships including the changing scene, and identifies different models for relationships and implications for key actors including the Ministry of Health, church health agencies and coordinating bodies. The article concludes that church health services will continue to play a key role in health care in sub‐Saharan Africa; however, there are challenges facing them and both parties need to develop a response to these. Copyright © 2002 John Wiley & Sons, Ltd.
Radiofrequency‐induced temperature increase as a function of cross polarization contact time in 8CB
Authors: Chattah Ana K. , Cucchietti Fernando M. , Hologne Maggy , Raya Jésus , Levstein Patricia R. 
Published: November 2002

AbstractIn this work we analyse the non‐negligible heating effect that can be produced by the radiofrequency during the contact time in Hartmann–Hahn cross polarization experiments in liquid crystals. We perform the analysis in the nematic phase of 4‐n‐octyl‐4′‐cyanobiphenyl (8CB). The heating effect is quantified through the chemical shifts of the carbon resonances, which move towards their respective positions in the isotropic phase when increasing the contact time. The calibration procedure involves an independent measurement of chemical shift dependence on externally controlled bath temperature. This variation was performed in the range between 300 and 313 K covering the smectic A and nematic mesophases. An overall heating rate of 0.16 K ms−1 is observed during the contact time in a cross polarization experiment performed at ω1/2π ≃ 80 kHz. This rate goes to approximately one‐half for ω1/2π ≃ 60 kHz and becomes unobservable for ω1/2π < 50 kHz under typical experimental conditions. Copyright © 2002 John Wiley & Sons, Ltd.
Engineered design of masonry buildings: fifty years development in Europe
Authors: Hendry A W 
Published: November 2002

AbstractThis paper describes the development of the structural design of multi‐storey, load‐bearing masonry buildings in the United Kingdom and the European Community over the second half of the 20th century. Tall buildings of this type had fallen into disuse in the first half of the century as the empirical rules governing their design led to walls of excessive thickness. The application of engineering principles to load‐bearing masonry was pioneered in Switzerland, and in the United Kingdom a rudimentary code of practice appeared in 1949. This was used for the design of buildings in the following decade, but its limitations led to research work on a number of key problems, and eventually to the publication of a completely new code, based on limit state principles, in 1978. Parallel work by international organizations and later in the European Union led to the publication of a draft code, intended for use in countries of the EU in 1995. Essential problems of overall stability and safety and the design of walls in compression and under combined compressive and lateral loads have been addressed. The paper summarizes the approach to these problems which has been adopted in the UK and EU codes with reference to relevant research work, in particular to projects with which the author has been associated.
New technologies for engineered timber structures
Authors: Natterer Julius K 
Published: November 2002

AbstractNearly every shape of construction can be built in an economical way from timber if the development of the structure is studied carefully. All new construction is a challenge, and the engineer, in collaboration with the architect, must abandon routine to explore the range of techniques for timber construction. Supported by the latest research, the engineer can find the optimal solution, and adapt to the requirements of modern architecture.
Research responsibilities
Authors: THE EDITORS  
Published: November 2002

The debate on the UK Government's recent Research Assessment Exercise (RAE), which
has grown steadily over our past two issues (5/4 and 6/1), reaches a climax in this one.
Perhaps the time has come to ask whether arq is becoming parochial in its focus on a
matter that seems of concern only to the UK. However, we offer no apologies for using
the RAE debate to highlight the research crisis in architecture – a crisis that is by no
means confined to the UK.There are many issues under discussion. There is the simple matter of the
‘accuracy’ of the system in recognising high quality work: our correspondents
(pp. 101–103) seem divided on this. Then there is the question of ‘fairness’ in the size
of the financial reward: the sums available for distribution meant that many who
performed well were awarded less than in the last round. And there is the ever
recurring question of design as ‘research’: Bryan Lawson's contribution (pp. 109–114)
surely provides the last word on this.Three correspondents widen the debate beyond the RAE. Colin Stansfield Smith
(p. 104) writes of a procurement system in which architecture has become
marginalised. John Worthington (p. 104) makes a plea for both the profession and
the schools to look outwards. And, almost incredibly, the letter from the outgoing
RIBA Vice President for Education, Alan Jones (p. 105), seems to suggest that arq's
prodding may have provoked coordinated action within the Institute.The latest news is that the two incoming Vice Presidents for Education and
Practice, Jack Pringle and Richard Saxon, are practitioners who are determined to
bridge the gap between the profession and academia. Each is committed to
promoting, supporting and disseminating research. Both see it not as a problem to
be ignored but as an opportunity to be grasped. We wish them every success.There is much to be done. Real needs must be identified and matched to available
means in academia and practice; valuable unpublished material uncovered;
appropriate methods of dissemination developed; and a realistic implementation
strategy evolved. If the RIBA could, in partnership with practice and academia,
develop such a programme, it would, in the process, acquire the ability to support
the architecture schools in the pursuit of their own (and the profession's) interests.
It would also enable the profession to speak with the kind of authority that the RICS
Foundation has given the surveyors.It is this wider agenda with which arq is concerned. If leading-edge practitioners
and academics have a duty to enhance the profession's knowledge base then
professional institutes have a responsibility as its guardians and sponsors. All must
work together in a world in which architecture is increasingly under threat.
An assay to evaluate the long‐term effects of inflammatory mediators on murine airway smooth muscle: evidence that TNFα up‐regulates 5‐HT2A‐mediated contraction
Authors: Adner Mikael , Rose Andrew C , Zhang Yaping , Swärd Karl , Benson Mikael , Uddman Rolf , Shankley Nigel P , Cardell Lars‐Olaf 
Published: November 2002

Asthma research is arguably limited by an absence of appropriate animal models to study the pharmacology of inflammatory mediators that affect airway hyperresponsiveness and remodelling. Here we assessed an assay based on mouse tracheal segments cultured for 1–32 days, and investigated contractile responses mediated by muscarinic and 5‐hydroxytryptamine (5‐HT) receptors following long‐term exposure to tumour necrosis factor‐alpha (TNFα).
Following culture, in the absence of TNFα, maximum contractile responses to KCl and carbachol were similar, with an increase in response up to day two and a decrease to a stable level after 8 days. Maximal relaxations to isoprenaline were not affected by the culture procedure. The potency of KCl and isoprenaline increased throughout the study. DNA microarray data revealed that global gene expression changes were greater when tissues were introduced to culture than when they were maintained in culture. The morphology of smooth muscle cells was maintained throughout the culture period.
5‐HT induced a weak contraction in both fresh and cultured (up to 8 days) segments. Culture with TNFα produced a time‐ and concentration‐dependent increase in the maximal contraction to 5‐HT, evidently mediated by 5‐HT2A receptors, whereas, the potency for carbachol was reduced.
In conclusion, the phenotype of airway smooth muscle remained largely intact during the culture period, even though minor changes were obtained during the first days of culture. The time‐dependent effect of TNFα indicates the importance of studying the long‐term effect of cytokines on the smooth muscle cells in relation to airway hyperresponsiveness and remodelling.

British Journal of Pharmacology (2002) 137, 971–982. doi:10.1038/sj.bjp.0704928
Protein kinase C (PKC) dependent induction of tissue factor (TF) by mesangial cells in response to inflammatory mediators and release during apoptosis
Authors: Lang Detlef , Terstesse Martin , Dohle Frank , Bangen Philip , Banas Bernhard , Pauels Hans‐Gerd , Heidenreich Stefan 
Published: November 2002

In inflammatory kidney diseases procoagulatory activity (PCA) becomes evident. Glomerular fibrin deposits and capillary microthrombi are histopathological hallmarks in most forms of glomerulonephritis.
Therefore in this study the expression of tissue factor (TF) as the main inducer of thrombogenesis was examined in cultured human mesangial cells (MC) in response to proinflammatory stimuli such as interleukin‐1 (IL‐1β), tumour necrosis factor alpha (TNF‐α) and lipopolysaccharide (LPS). Also main signalling pathways were investigated.
IL‐1β, TNF‐α and LPS induced TF in MC in a time and dose dependent manner on mRNA and protein levels. Highest activity was found after 12 h of stimulation. Induction of TF was completely blockable by BAPTA‐AM, a chelator of intracellular [Ca2+]i as well as calphostin, a protein kinase C (PKC) inhibitor. Activation of the protein kinase A (PKA) pathway had no influence on basal TF expression, but down‐regulated cytokine‐induced TF. The PKA blocker, KT5720, increased TF formation significantly. Since TF exerts its activity primarily on the surface of cells and after release of encrypted receptors we further tested TF activity in MC supernatants. IL‐1β did not significantly increase TF activity in supernatants of intact cells. However, when MC were rendered apoptotic by oxidative metabolites, IL‐1β treated MC released highly stimulated TF activity into the supernatants, suggesting that a paracrine activation of the coagulatory cascade can take place under such conditions.
Inflammatory mediators up‐regulate TF expression in MC by a PKC dependent pathway whereas PKA can serve as a negative feed‐back link. Apoptosis of inflammatory MC may trigger to spread PCA.

British Journal of Pharmacology (2002) 137, 1116–1124. doi:10.1038/sj.bjp.0704967
Overexpression of glutathione S‐transferase A1‐1 in ECV 304 cells protects against busulfan mediated G2‐arrest and induces tissue factor expression
Authors: Ritter Christoph A , Sperker Bernhard , Grube Markus , Dressel Dana , Kunert‐Keil Christiane , Kroemer Heyo K 
Published: November 2002

The antineoplastic drug busulfan is frequently used in preconditioning regimens for bone marrow transplantation. Pharmacokinetics vary tremendously between patients due to extensive metabolism in the liver via conjugation to glutathione catalysed by glutathione S‐transferase (GST) A1‐1. Since elevated busulfan plasma levels have been reported to be a risk factor for developing veno‐occlusive disease (VOD), metabolism of busulfan may play a pivotal role in the induction of VOD.
Therefore, we developed a cell model to investigate the influence of busulfan metabolism on its biological effects. GSTA1‐1 cDNA was transfected into the cell line ECV 304 and protein expression was demonstrated by Western blotting. Enzymatic activity could be detected by formation of tetrahydrothiophene. Additionally, effects of busulfan treatment on cell cycle and expression of tissue factor have been investigated.
A busulfan‐induced G2‐arrest was reduced in GSTA1‐1‐transfected cells, which consequently displayed a significantly higher activity of cdc2 kinase (24.1±1.5 AU mg−1 protein) after busulfan treatment compared to controls (14.7±2.3 AU mg−1 protein; P<0.01). Elevated basal expression of tissue factor in GSTA1‐1‐transfected ECV 304 cells could be 4 fold increased by busulfan treatment.
These data demonstrate that ECV 304 cells transfected with GSTA1‐1 provide a valuable tool to assess busulfan metabolism in vitro. Furthermore, overexpression of GSTA1‐1 leads to a partial protection against cell cycle effects of busulfan and affects tissue factor expression.

British Journal of Pharmacology (2002) 137, 1100–1106. doi:10.1038/sj.bjp.0704972
The isolated blood‐perfused rat heart: an inappropriate model for the study of ischaemia‐ and infarction‐related ventricular fibrillation
Authors: Clements‐Jewery Hugh , Hearse David J , Curtis Michael J 
Published: November 2002

Well‐characterized in vivo and in vitro models exist for the study of ischaemia‐ and infarction‐related ventricular fibrillation (VF). In rats in vivo, VF appears to occur in distinct acute ischaemia‐ (early) and infarction‐related (late) phases. Interestingly, isolated buffer‐perfused rat hearts do not develop late VF. This raises the possibility that unidentified components of the blood may be responsible for late VF. We thus sought to characterize an isolated blood‐perfused rat heart in order to investigate the possible influence of blood components on arrhythmias arising from ischaemia and infarction.
Hearts, excised from male Wistar rats, were perfused in the Langendorff mode with blood from support rats (male Wistar, 350–430 g) via an extracorporeal circuit. Perfused hearts underwent left coronary artery occlusion for 240 min or a sham procedure (n=10 group−1).
Only 10% of ischaemic hearts developed late VF (90–240 min). Tissue myeloperoxidase activity (an index of neutrophil accumulation) increased during ischaemia from 0.017±0.004 (six fresh hearts) to 0.056±0.005 units mg protein−1 (P<0.05) at 240 min, but values were similar in sham hearts (0.083±0.013). Likewise, the decline (−1 vs 240 min of ischaemia shown) in circulating total white blood cells from 6.8±0.5 to 1.9±0.2×103 μl−1 and in platelets from 441±32 to 274±16×103 μl−1 (both P<0.05) was similar in time‐matched sham hearts (data not shown).
Surprisingly, only 10% of ischaemic hearts developed early VF (0–90 min), although the incidence of early ventricular tachycardia was 100% in these hearts (P<0.05 vs sham hearts). Blood K+ values were normal (hyperkalaemia suppresses VF).
Although late VF was absent in blood‐perfused hearts, it would be premature to conclude from this that late VF is not mediated by blood components. This is because the similar neutrophil accumulation in ischaemic and sham hearts, the decline in numbers of circulating blood components, and the unexpected paucity of early VF all question the validity of the model.

British Journal of Pharmacology (2002) 137, 1089–1099. doi:10.1038/sj.bjp.0704977
Association of ankylosing spondylitis with HLA–B*1403 in a West African population
Authors: López‐Larrea Carlos , Mijiyawa Moustafa , González Segundo , Fernández‐Morera J. Luis , Blanco‐Gelaz Miguel A. , Martínez‐Borra Jesús , López‐Vázquez Antonio 
Published: November 2002

AbstractObjectiveTo investigate the contribution of HLA class I alleles in the susceptibility to primary ankylosing spondylitis (AS) in West African patients living in Togo.MethodsA large epidemiologic analysis of 9,065 West African rheumatology patients living in Togo was performed in order to identify those who had AS. Eight Togolese patients with AS were identified. HLA was typed by polymerase chain reaction using sequence‐specific oligonucleotide probes. DNA typing was also performed on a control population of 85 healthy subjects matched for ethnic background.ResultsA significant association between AS and B*14 was identified. This allele was found in 62.5% of the AS patients (odds ratio 69), but was carried by only 2% of the healthy controls. Analysis for B14 subtypes showed that B*1403 was the predominant allele in AS patients (odds ratio 171), and that this allele was absent in healthy controls. B27 was virtually absent, being observed in only 1 AS patient (B*2705).ConclusionHLA–B*1403 shows the B27 “supertype” motif and may exert an effect on AS susceptibility according to the arthritogenic peptide model. The association of B*1403 with AS has not previously been reported in either population.
Stratification of pedigrees multiplex for systemic lupus erythematosus and for self‐reported rheumatoid arthritis detects a systemic lupus erythematosus susceptibility gene (SLER1) at 5p15.3
Authors: Namjou Bahram , Nath Swapan K. , Kilpatrick Jeff , Kelly Jennifer A. , Reid Jeff , James Judith A. , Harley John B. 
Published: November 2002

AbstractObjectiveArthritis is a common manifestation in systemic lupus erythematosus (SLE), appearing in ∼85% of patients. Often, the polyarthritis at presentation of SLE cannot be distinguished from rheumatoid arthritis (RA) by physical examination or history. Indeed, physicians initially tell many SLE patients that they have RA (one source of “self‐reported RA”), only to have SLE established later. In addition, RA aggregates in families with an SLE proband. We predicted that pedigrees multiplex for both SLE and for self‐reported RA would better isolate particular genetic effects. If this proved to be true, we would then use the increased genetic homogeneity to more easily reveal genetic linkage.MethodsFrom a collection of 160 pedigrees multiplex for SLE, we selected 36 pedigrees that also contained ≥2 members with self‐reported RA (19 pedigrees were African American, 14 were European American, and 3 were of other ethnic origin). Data from a genome scan of 307 microsatellite markers were evaluated for SLE linkage by contemporary genetic epidemiologic techniques.ResultsThe most significant evidence of linkage to SLE was obtained at 5p15.3 in the European American pedigrees by both parametric (logarithm of odds [LOD] score 6.2, P = 9.3 × 10−8) and nonparametric (LOD score 6.9, P = 1.7 × 10−8) methods. The best‐fitting model for this putative SLE gene in this region was a recessive gene with a population frequency of 5% and with 50% penetrance in females and 15% penetrance in males at virtually 100% homogeneity.ConclusionFor a genetically complex disease phenotype, an unusually powerful linkage has been found with SLE at 5p15.3 in European American pedigrees multiplex for SLE and for self‐reported RA. This result predicts the presence of a gene at the top of chromosome 5 in this subset of patients that is important for the pathogenesis of SLE.