bluuebunny/crossref_metadata_2025_split huggingface dataset:
Poverty Relief, Global Institutions, and the Problem of Compliance
Authors: Fuller Lisa 
Published: September 2005

AbstractThomas Pogge and Andrew Kuper suggest that we should promote an ‘institutional’ solution to global poverty. They advocate the institutional solution because they think that non-governmental organizations (NGOs) can never be the primary agents of justice in the long run. They provide several standard criticisms of NGO aid in support of this claim. However, there is a more serious problem for institutional solutions: how to generate enough goodwill among rich nation-states that they would be willing to commit themselves to supranational institutional reforms. In the current international political climate, the implementation of such institutional reforms introduces several intractable problems, including difficulties of global coordination and enforcement. I defend the solution of NGO aid from the criticisms presented by Pogge and Kuper, and propose how it might be reformed. My main suggestion is that all practising NGOs should be required to be ‘accountable for reasonableness’ in the sense that Norman Daniels and James Sabin have outlined.
Thomas Pogge’s Global Resources Dividend: A Critique and an Alternative
Authors: Hayward Tim 
Published: September 2005

AbstractPogge’s proposal for a Global Resources Dividend (GRD) has been criticized because its likely effects would be less predictable than Pogge supposes and could even be counterproductive to the main aim of relieving poverty. The GRD might also achieve little with respect to its secondary aim of promoting environmental protection. This article traces the problems to Pogge’s inadequate conception of natural resources. It proposes instead to conceive of natural resources in terms of ‘ecological space’. Using this conception, redistributive principles follow with a more definite logic from Pogge’s own supporting moral argument. The proposed alternative approach also promises a more direct contribution to Pogge’s secondary aim of resource conservation and environmental protection. I conclude that if any redistributive resource-based tax should be levied on nations, then there are at least four decisive reasons to favour levying a tax related to a nation’s per capita utilization of ecological space rather than the GRD.
Poverty and the Moral Significance of Contribution
Authors: Øverland Gerhard 
Published: September 2005

AbstractThe main thesis of the article is that one’s responsibility to render assistance is not affected by having contributed to the situation by causing harm. I examine ways in which contribution to need is morally significant. Although contribution is relevant with regard to certain features, such as questions of blame, compensation, and fair distribution of the cost of assistance, I argue that contribution should carry no weight when assessing our duty to assist people in severe need if we can do so at little cost. If this is true we have reason to suspect that it is redundant to know whether or not we have in fact contributed to the need of the global poor when assessing our duty to address global poverty.
Alkylamines cause Vγ9Vδ2 T-cell activation and proliferation by inhibiting the mevalonate pathway
Authors: Thompson Keith , Rojas-Navea Javier , Rogers Michael J. 
Published: September 2005

AbstractThree general classes of small, nonpeptide “antigens” activate Vγ9Vδ2 T cells: pyrophosphomonoesters, such as isopentenyl diphosphate (IPP), nitrogen-containing bisphosphonates (N-BPs), and alkylamines. However, we have shown recently that N-BPs indirectly activate Vγ9Vδ2 T cells as a consequence of inhibition of farnesyl diphosphate synthase (a key enzyme of the mevalonate pathway) and the intracellular accumulation of IPP. We now show that alkylamines activate Vγ9Vδ2 T cells by the same mechanism. Alkylamines were found to be weak inhibitors of farnesyl diphosphate synthase and caused accumulation of unprenylated Rap1A in peripheral blood mononuclear cells and macrophages, indicative of inhibition of the mevalonate pathway. Furthermore, as with N-BPs, the stimulatory effect of the alkylamines on Vγ9Vδ2T cells was abrogated by simultaneous treatment with mevastatin. These findings suggest that only pyrophosphomonoesters such as IPP are true Vγ9Vδ2 T-cell agonists, whereas alkylamines and N-BPs indirectly activate Vγ9Vδ2 T cells through a common mechanism involving the accumulation of IPP.
The inositol phosphatase SHIP-2 down-regulates FcγR-mediated phagocytosis in murine macrophages independently of SHIP-1
Authors: Ai Jing , Maturu Amita , Johnson Wesley , Wang Yijie , Marsh Clay B. , Tridandapani Susheela 
Published: September 2005

AbstractFcγR-mediated phagocytosis of IgG-coated particles is a complex process involving the activation of multiple signaling enzymes and is regulated by the inositol phosphatases PTEN (phosphatase and tensin homolog deleted on chromosome 10) and SHIP-1 (Src homology [SH2] domain-containing inositol phosphatase). In a recent study we have demonstrated that SHIP-2, an inositol phosphatase with high-level homology to SHIP-1, is involved in FcγR signaling. However, it is not known whether SHIP-2 plays a role in modulating phagocytosis. In this study we have analyzed the role of SHIP-2 in FcγR-mediated phagocytosis using independent cell models that allow for manipulation of SHIP-2 function without influencing the highly homologous SHIP-1. We present evidence that SHIP-2 translocates to the site of phagocytosis and down-regulates FcγR-mediated phagocytosis. Our data indicate that SHIP-2 must contain both the N-terminal SH2 domain and the C-terminal proline-rich domain to mediate its inhibitory effect. The effect of SHIP-2 is independent of SHIP-1, as overexpression of dominant-negative SHIP-2 in SHIP-1-deficient primary macrophages resulted in enhanced phagocytic efficiency. Likewise, specific knockdown of SHIP-2 expression using siRNA resulted in enhanced phagocytosis. Finally, analysis of the molecular mechanism of SHIP-2 down-regulation of phagocytosis revealed that SHIP-2 down-regulates upstream activation of Rac. Thus, we conclude that SHIP-2 is a novel negative regulator of FcγR-mediated phagocytosis independent of SHIP-1. (Blood. 2006;107:813-820)
Suppressor activity and potency among regulatory T cells is discriminated by functionally active CD44
Authors: Firan Mihail , Dhillon Sohita , Estess Pila , Siegelman Mark H. 
Published: September 2005

AbstractCD4CD25+ regulatory T cells are fundamental to the maintenance of peripheral tolerance and have great therapeutic potential. However, efforts in this regard have been hampered by limiting cell numbers in vivo, an anergic phenotype in vitro, and a rudimentary understanding of the molecular basis for the functional state of CD4CD25+ regulatory T cells (Treg cells). Here we show heterogeneity of suppressor activity among activated CD4CD25+ Treg cells and that, within this population, the functionally active, hyaluronan-binding form of CD44 (CD44act) is strikingly correlated with superior suppressor activity. Within 16 hours after in vitro activation, CD44act can discriminate enhanced suppressive function in in vitro proliferation assays and in an in vivo bone marrow engraftment model. The expression of other surface markers and that of Foxp3 are similar irrespective of hyaluronan binding and associated degree of suppressor potency. Furthermore, CD44act is induced on resting CD4CD25+ cells in vivo by allogeneic stimulation, with similar functional consequences. These results reveal a cell-surface marker that delineates functional activity within a population of activated CD4CD25+ regulatory T cells, thereby providing a potential tool for identifying regulatory activity and enriching for maximal suppressor potency.
The leukotriene B4 lipid chemoattractant receptor BLT1 defines antigen-primed T cells in humans
Authors: Islam Sabina A. , Thomas Seddon Y. , Hess Christoph , Medoff Benjamin D. , Means Terry K. , Brander Christian , Lilly Craig M. , Tager Andrew M. , Luster Andrew D. 
Published: September 2005

AbstractWe have recently shown that the leukotriene B4 (LTB4)–BLT1 pathway is important in early effector T-cell recruitment in mouse models of inflammation. Here we characterize the phenotype and function of human peripheral blood BLT1+ T cells in health and illustrate their involvement in asthma and acute infection. In healthy individuals, BLT1+ T cells are a rare peripheral blood T-cell population enriched for the activation markers CD38 and HLA-DR. Compared with BLT1– T cells, a larger proportion of peripheral blood BLT1+ T cells express the effector cytokines IFNγ and IL-4 and inflammatory chemokine receptors, CCR1, CCR2, CCR6, and CXCR1. Consequently, in healthy individuals peripheral blood BLT1+ T cells are a rare antigen-primed T-cell subset with unique phenotypic, migratory, and functional properties. BLT1 expression on T cells is tightly regulated by inflammation and only transiently expressed after naive T-cell activation by dendritic cells. Although rare in the peripheral blood of healthy individuals, BLT1+ T cells are markedly increased in frequency in the peripheral blood in response to acute Epstein-Barr virus (EBV) infection and moderately increased in the airways of asymptomatic allergic asthmatics. Our studies provide novel insights into the LTB4-BLT1 lipid chemoattractant pathway in human T-cell responses, and how it may link innate and adaptive immunity.
Amplification of tumor-specific regulatory T cells following therapeutic cancer vaccines
Authors: Zhou Gang , Drake Charles G. , Levitsky Hyam I. 
Published: September 2005

AbstractThe fate of tumor-specific CD4+ T cells is central to the outcome of the host immune response to cancer. We show that tumor antigen recognition by a subset of CD4+ T cells led to their differentiation into cells capable of suppressing naive and Th1 effector cells. Such tumor-induced regulatory T cells (TMTregs) arose both from precommitted “natural” regulatory T cells and CD4+CD25–GITRlow precursors. Once induced, TMTregs were capable of maintaining suppressor activity long after transfer into antigen-free recipients. Suppression was mediated by GITRhigh cells residing within both CD25+ and CD25– subsets. Vaccination of the tumor-bearing host concomitantly expanded TMTregs and effector cells, but suppression was dominant, blunting the expansion of naive tumor-specific T cells and blocking the execution of effector function in vitro and in vivo. These studies illustrate the possibility that therapeutic vaccination could actually worsen host tolerance to tumor antigens and support treatment paradigms that seek to not only increase the frequency of tumor-specific T cells, but to do so in conjunction with strategies that inactivate or remove regulatory T-cell populations.
Follicular dendritic-like cells derived from human monocytes
Authors: Heinemann Dagmar EH , Peters J Hinrich 
Published: September 2005

Abstract
Background
Follicular dendritic cells (FDCs) play a central role in controlling B-cell response maturation, isotype switching and the maintenance of B-cell memory. These functions are based on prolonged preservation of antigen and its presentation in its native form by FDCs. However, when entrapping entire pathogens, FDCs can turn into dangerous long-term reservoirs that may preserve viruses or prions in highly infectious form.
Despite various efforts, the ontogeny of FDCs has remained elusive. They have been proposed to derive either from bone marrow stromal cells, myeloid cells or local mesenchymal precursors. Still, differentiating FDCs from their precursors in vitro may allow addressing many unsolved issues associated with the (patho-) biology of these important antigen-presenting cells. The aim of our study was to demonstrate that FDC-like cells can be deduced from monocytes, and to develop a protocol in order to quantitatively generate them in vitro.

Results
Employing highly purified human monocytes as a starter population, low concentrations of Il-4 (25 U/ml) and GM-CSF (3 U/ml) in combination with Dexamethasone (Dex) (0.5 μM) in serum-free medium trigger the differentiation into FDC-like cells. After transient de-novo membrane expression of alkaline phosphatase (AP), such cells highly up-regulate surface expression of complement receptor I (CD35). Co-expression of CD68 confirms the monocytic origin of both, APpos and CD35pos cells. The common leukocyte antigen CD45 is strongly down-regulated. Successive stimulation with TNF-α up-regulates adhesion molecules ICAM-1 (CD54) and VCAM (CD106). Importantly, both, APpos as well as APneg FDC-like cells, heterotypically cluster with and emperipolese B cells and exhibit the FDC characteristic ability to entrap functionally preserved antigen for prolonged times. Identical characteristics are found in monocytes which were highly expanded in vitro by higher doses of GM-CSF (25 U/ml) in the absence of Dex and Il-4 before employing the above differentiation cocktail.

Conclusion
In this work we provide evidence that FDC-like cells can be derived from monocytes in vitro. Monocyte-derived FDC-like cells quantitatively produced offer a broad utility covering basic research as well as clinical application.
Association between occupational exposure to mineral oil and rheumatoid arthritis: results from the Swedish EIRA case–control study
Authors: Sverdrup Berit , Källberg Henrik , Bengtsson Camilla , Lundberg Ingvar , Padyukov Leonid , Alfredsson Lars , Klareskog Lars ,   the Epidemiological Investigation of Rheumatoid Arthritis study group
Published: September 2005

AbstractThe aim of the present study was to investigate the association between exposure to mineral oil and the risk of developing rheumatoid arthritis (RA), and in addition to perform a separate analysis on the major subphenotypes for the disease; namely, rheumatoid factor (RF)-positive RA, RF-negative RA, anticitrulline-positive RA and anticitrulline-negative RA, respectively. A population-based case–control study of incident cases of RA was performed among the population aged 18–70 years in a defined area of Sweden during May 1996–December 2003. A case was defined as an individual from the study base who for the first time received a diagnosis of RA according to the American College of Rheumatology criteria of 1987. Controls were randomly selected from the study base with consideration taken for age, gender and residential area. Cases (n = 1,419) and controls (n = 1,674) answered an extensive questionnaire regarding lifestyle factors and occupational exposures, including different types of mineral oils. Sera from cases and controls were investigated for RF and anticitrulline antibodies.Among men, exposure to any mineral oil was associated with a 30% increased relative risk of developing RA (relative risk = 1.3, 95% confidence interval = 1.0–1.7). When cases were subdivided into RF-positive RA and RF-negative RA, an increased risk was only observed for RF-positive RA (relative risk = 1.4, 95% confidence interval 1.0–2.0). When RA cases were subdivided according to the presence of anticitrulline antibodies, an increased risk associated with exposure to any mineral oil was observed only for anticitrulline-positive RA (relative risk = 1.6, 95% confidence interval = 1.1–2.2). Analysis of the interaction between oil exposure and the presence of HLA-DR shared epitope genes regarding the incidence of RA indicated that the increased risk associated with exposure to mineral oil was not related to the presence of shared epitope genotypes.In conclusion, our study shows that exposure to mineral oil is associated with an increased risk to develop RF-positive RA and anticitrulline-positive RA, respectively. The findings are of particular interest since the same mineral oils can induce polyarthritis in rats.
Identification of the Major Oxidative 3α-Hydroxysteroid Dehydrogenase in Human Prostate That Converts 5α-Androstane-3α,17β-diol to 5α-Dihydrotestosterone: A Potential Therapeutic Target for Androgen-Dependent Disease
Authors: Bauman David R. , Steckelbroeck Stephan , Williams Michelle V. , Peehl Donna M. , Penning Trevor M. 
Published: September 2005

AbstractAndrogen-dependent prostate diseases initially require 5α-dihydrotestosterone (DHT) for growth. The DHT product 5α-androstane-3α,17β-diol (3α-diol), is inactive at the androgen receptor (AR), but induces prostate growth, suggesting that an oxidative 3α-hydroxysteroid dehydrogenase (HSD) exists. Candidate enzymes that posses 3α-HSD activity are type 3 3α-HSD (AKR1C2), 11-cis retinol dehydrogenase (RODH 5), L-3-hydroxyacyl coenzyme A dehydrogenase , RODH like 3α-HSD (RL-HSD), novel type of human microsomal 3α-HSD, and retinol dehydrogenase 4 (RODH 4). In mammalian transfection studies all enzymes except AKR1C2 oxidized 3α-diol back to DHT where RODH 5, RODH 4, and RL-HSD were the most efficient. AKR1C2 catalyzed the reduction of DHT to 3α-diol, suggesting that its role is to eliminate DHT. Steady-state kinetic parameters indicated that RODH 4 and RL-HSD were high-affinity, low-capacity enzymes whereas RODH 5 was a low-affinity, high-capacity enzyme. AR-dependent reporter gene assays showed that RL-HSD, RODH 5, and RODH 4 shifted the dose-response curve for 3α-diol a 100-fold, yielding EC50 values of 2.5 × 10−9m, 1.5 × 10−9m, and 1.0 × 10−9m, respectively, when compared with the empty vector (EC50 = 1.9 × 10−7m). Real-time RT-PCR indicated that L-3-hydroxyacyl coenzyme A dehydrogenase and RL-HSD were expressed more than 15-fold higher compared with the other candidate oxidative enzymes in human prostate and that RL-HSD and AR were colocalized in primary prostate stromal cells. The data show that the major oxidative 3α-HSD in normal human prostate is RL-HSD and may be a new therapeutic target for treating prostate diseases.
Increased Plasma Pro-B-Type Natriuretic Peptide in Infants of Women with Type 1 Diabetes
Authors: Halse Karen G , Lindegaard Marie LS , Goetze Jens P , Damm Peter , Mathiesen Elisabeth R , Nielsen Lars B 
Published: September 2005

AbstractBackground: Up to 40% of newborn infants of women with type 1 diabetes have echocardiographic signs of cardiomyopathy. Increased plasma concentrations of B-type natriuretic peptide (BNP) and its precursor (proBNP) are markers of cardiac failure and hypoxia in adults. In this study, we investigated whether plasma concentrations of proBNP and/or BNP are increased in infants of women with type 1 diabetes.Methods: Plasma BNP and proBNP were measured with RIAs. The proBNP assay measures both intact proBNP and NH2-terminal fragments derived from this precursor, whereas the BNP assay measures only BNP-32 and not proBNP.Results: Infants of women with diabetes and hemoglobin A1c (Hb A1c) ≥6.2% before delivery had a higher median plasma proBNP concentration (31 pmol/L; interquartile range, 21–47 pmol/L; n = 16) than infants of healthy women [16 (9–32) pmol/L; n = 21; P = 0.01]. Infants of women with diabetes and Hb A1c &lt;6.2% (n = 15) had intermediate values. The plasma BNP and proBNP concentrations were closely associated (r2 = 0.80; P &lt;0.0001); within the group of infants of women with diabetes and Hb A1c ≥6.2%, both correlated with the degree of fetal stress during labor.Conclusions: Maternal diabetes and suboptimal metabolic control may affect the fetal heart and predominantly stimulate proBNP secretion in conjunction with perinatal stress.
Excitation functions of proton induced reactions on68Zn from threshold up to 71 MeV, with specific reference to the production of67Cu
Authors: Stoll T. , Kastleiner S. , Shubin Yu. N. , Coenen Heinz H. , Qaim Syed M. 
Published: September 2005

SummaryThe excitation function of the68Zn(p, 2p)67Cu reaction was measured radiochemically up to a proton energy of 71 MeV to obtain accurate data for production of the therapy related β−-emitting radioisotope67Cu (T1/2= 61.9 h). Investigations were also made on the (p, 2n) and (p, 3n) reactions on68Zn. The experimental cross sections of the68Zn(p, 2p)67Cu,68Zn(p, 2n)67Ga and68Zn(p, 3n)66Ga reactions were compared with published data and with theoretical predictions based on the hybrid-precompound model ALICE-IPPE. Thick target yields of67Cu,67Ga (T1/2= 78.3 h) and66Ga (T1/2= 9.4 h) were calculated. Production of67Cu is feasible only at proton energies above 50 MeV. For the target thicknessEp= 70 → 50 MeV, the yield of67Cu amounts to 16.9 MBq/µA·h.
Separation of neptunium and plutonium from acidic medium using 3-phenyl-4-benzoyl-5-isoxazolone
Authors: Mohapatra P. K. , Ruikar P.B. , Manchanda V.K. 
Published: September 2005

Summary
The extraction behaviour of plutonium (IV) and neptunium (IV) was studied from nitric as well as hydrochloric acid employing 3-phenyl-4-benzoyl-5-isoxazolone (PBI) in toluene as the extractant. The forward extraction in hydrochloric acid medium was carried out in presence of several holding oxidants out of which ammonium meta vanadate was found to give the best results. The stripping behaviour of Np and Pu was studied employing a variety of reagents out of which 0.1 M hydroquinione in 1:1 HCl was the most promising. The separation of Np from Pu under simulated conditions was attempted from hydrochloric acid medium giving a decontamination factor value of >104 and ∼60% Pu recovery.
A statistical study of 238U and 234U/238U distributions in coral samples from the Egyptian shoreline of the north-western Red Sea and in fossil mollusk shells from the Atlantic coast of High Atlas in Morocco: Implications for 230Th/234U dating
Authors: Choukri A. , Reyss J.-L. , Hakam O.K. , Plaziat J. C. 
Published: September 2005

Summary
In this work, radiochemical analysis results of 126 unrecrystallized coral samples from the Egyptian shoreline of northwestern Red Sea and 120 fossil mollusk shell samples from the Atlantic coast of Moroccan High Atlas at the North of Agadir City in Morocco are presented and discussed. The coral samples were collected in Egypt from the emerged coral reef terraces over 500 km from The Ras Gharib-Ras Shukeir depression (28°10') in the north to Wadi Lahami (north of Ras Banas, 24°10') in the south. The fossil mollusk shells were collected in Morocco from Agadir-Harbour in the south to Tamri village in the north extending over about 50 km. The statistical distributions of results (238U content, 234U/238U activity ratio and ages) obtained on the dated materials in the two different regions were compared for three fossil sea levels corresponding to three different climatic stages (Holocene, 5e, 7 and/or 9) in the aim to establish methodological criteria for judging validity of the measured ages.
For corals, 238U content varies in narrow interval around the same average value of 3 ppm for the three sea levels, the calculated initial 234U/238U values are in agreement with the actual sea water ratio (1.15) with some values slightly higher than for the older sea levels. The obtained ages are in good agreement with the ages reported previously for the three emerged fossil sea levels on unrecrystallized corals by alpha spectrometry and by mass spectrometry.
For mollusk shells, except for Holocene sea level, 238U and initial 234U/238U activity ratios vary for the older levels in wide intervals, independent of species and calcite contents of samples. The high 238U contents and 234U/238U activity ratio are due eventually to a post-incorporation of secondary uranium from sea water or from continental waters drained away rivers. This incorporation leads to a rejuvenation of mollusk shell ages and is responsible for the wide dispersion of their apparent ages according to the mode and the timing of uranium introduction.