bluuebunny/crossref_metadata_2025_split huggingface dataset:
How much science is there in injury prevention and control?
Authors: Smith C A , Shannon H S 
Published: March 2003

Objectives:To determine what proportion of research papers at an injury prevention conference reported an evaluation.Methods:A random sample of 250 abstracts from the 6th World Conference on Injury Prevention and Control were classified by methodological type. Those that described any evaluation were further subdivided by whether the evaluation was of process or if it used an intermediate or “true” outcome.Results:Of 250 abstracts, 20 (8%; 95% confidence interval 5.0% to 12.1%) showed evaluations with intermediate or true outcomes. Research designs were weak. Among the 20 reports, none was a randomized trial and only two conducted a before and after study with control group. The remaining 17 used before-after or “after only” designs.Conclusion:The conference papers included few evaluations. To ensure that resources are best used, those in the injury prevention field must increase their use of rigorous evaluation.
Diversity of trends in occupational injury mortality in the United States, 1980–96
Authors: Loomis D , Bena J F , Bailer A J 
Published: March 2003

Objectives:Although the United States has generally enjoyed declining rates of fatal occupational injury, the rate of decline has not been uniform. To examine the heterogeneity of trends, changes in fatal occupational injury rates from 1980 to 1996 were estimated by occupation, industry, geographic region, and demographic group.Methods:Deaths due to injury at work during 1980–96 were identified from the US National Traumatic Occupational Fatality database and populations at risk were estimated from the census of population. Mortality rates were computed for unintentional injuries, homicides, and all injuries combined. The annual rate of change was estimated using Poisson regression to model the death rate as a function of time.Results:The estimated average rates for all fatal occupational injuries and for unintentional injuries declined by 3% per year, while the estimated rate of homicide declined <1% per year. The improvement was faster for men (3% per year) than for women (<1% per year) and for younger relative to older workers (7% per yearv2%–3% per year). Trends were also geographically heterogeneous, with the most rapid declines (7%–8% per year) in the South and West. Injury rates for most occupations and industries declined at near the average rate, but some experienced no change or an increase. The rate of homicide also increased in a number of occupations and industries.Conclusions:Broad downward trends in occupational fatality rates may be explained by several factors, including organized safety efforts, product and process changes, and the ongoing shift of employment toward safer sectors. Disparities in fatal injury trends draw attention to potential opportunities to reduce risk: work settings with increasing injury rates are of particular concern.
Principles for Sustainability: From Cooperation and Efficiency to Sufficiency
Authors: Princen Thomas 
Published: March 2003

If analysts of political and ecological economy take seriously critical trends in environmental degradation and accept social responsibility for contributing to the reversal of such trends, they must go beyond the descriptive and predictive to the prescriptive, beyond marginal environmental improvement to sustainability, beyond cooperation and efficiency to sufficiency. Cooperation and efficiency principles are useful when biophysical underpinnings remain intact. Otherwise, sufficiency principles—restraint, precaution, polluter pays, zero, reverse onus—address the defining characteristics of current trends, namely environmental criticality, risk export, and responsibility evasion. They engage overconsumption. They compel decision-makers to ask when too much resource use or too little regeneration risks important values such as ecological integrity and social cohesion, when material gains now preclude material gains in the future, when consumer gratification or investor reward threatens economic security, when benefits internalized depend on costs externalized. Under sufficiency, one necessarily asks what are the risks, not just in the short term and for immediate beneficiaries, but in the longterm and for the under-represented.
Methimazole protects from experimental autoimmune uveitis (EAU) by inhibiting antigen presenting cell function and reducing antigen priming
Authors: Wang Peng , Sun Shu-Hui , Silver Phyllis B , Chan Chi-Chao , Agarwal Rajeev K , Wiggert Barbara , Kohn Leonard D , Jamieson Gordon A , Caspi Rachel R 
Published: March 2003

Abstract
Methimazole (methyl-mercapto-imidazole, MMI), a compound used clinically in therapy of Graves’ thyroiditis, was found to inhibit development of several autoimmune diseases in animal models. It was suggested on the basis of in vitro data that inhibition is through down-regulation of interferon-γ (IFN-γ)-induced expression of major histocompatibility complex class I and class II molecules. Here, we investigate the effect of MMI on experimental autoimmune uveoretinitis (EAU) and study its mechanism(s). Treatment of EAU with MMI administered in drinking water inhibited induction of the disease and associated antigen (Ag)-specific proliferation and cytokine production by draining lymph node cells (LNCs). The treatment was protective only if administered during the first but not during the second week after immunization, suggesting an effect on the induction phase of EAU. It is interesting that MMI inhibited disease in IFN-γ knockout mice, indicating that the in vivo protective effect is IFN-γ-independent. Flow cytometric analysis of draining LNCs extracted 5 days after immunization showed that MMI partly to completely reversed the increase in Mac-1+/class I+/class II+ cells induced by immunization and reduced the proportion of B7-1 and CD40-positive cells, suggesting a deficit in the Ag-presenting cell (APC) population. APC from untreated mice largely restored antigen-specific proliferation of MMI-treated LNCs. We suggest that MMI inhibits EAU at least in part by preventing the recruitment and/or maturation of APC, resulting in reduced generation of Ag-specific T cells.
Cerivastatin and atorvastatin inhibit IL-3-dependent differentiation and IgE-mediated histamine release in human basophils and downmodulate expression of the basophil-activation antigen CD203c/E-NPP3
Authors: Majlesi Yasamin , Samorapoompichit Puchit , Hauswirth Alexander W , Schernthaner Gerit-Holger , Ghannadan Minoo , Baghestanian Mehrdad , Rezaie-Majd Abdolreza , Valenta Rudolf , Sperr Wolfgang R , Bühring Hans-Jörg , Valent Peter 
Published: March 2003

Abstract
Recent data suggest that the statins, apart from their lipid-lowering activity, exhibit profound anti-inflammatory effects. Basophils are major proinflammatory effector cells in diverse pathologic reactions. We have examined the in vitro effects of five different statins on primary human basophils, their progenitors, and the basophil cell line KU-812. Preincubation of blood basophils with cerivastatin or atorvastatin (0.1–100 μM) for 24 h reduced their capacity to release histamine on immunoglobulin E (IgE)-dependent stimulation in a dose-dependent manner. These statins also inhibited IgE-dependent up-regulation of the basophil-activation antigen CD203c. Moreover, both statins suppressed interleukin-3-induced differentiation of basophils from their progenitors as well as 3H-thymidine uptake in KU-812 cells. All inhibitory effects of cerivastatin and atorvastatin were reversed by mevalonic acid (200 μM). The other statins tested (lovastatin, simvastatin, pravastatin) did not show significant inhibitory effects on basophils. Together, these data identify cerivastatin and atorvastatin as novel inhibitors of growth and activation of human basophils.
Role of MCP-1 and MIP-1α in retinal neovascularization during postischemic inflammation in a mouse model of retinal neovascularization
Authors: Yoshida Shigeo , Yoshida Ayako , Ishibashi Tatsuro , Elner Susan G , Elner Victor M 
Published: March 2003

Abstract
Macrophages are important participants in neovascularization. This study was designed to examine the role of the monocyte/macrophage chemotactic proteins, monocyte chemotactic protein-1 (MCP-1), and macrophage inflammatory protein-1α (MIP-1α) in a mouse model of oxygen-induced ischemic retinopathy and to determine whether the morphology and distribution of macrophages/microglia are concomitantly altered. The MCP-1, MIP-1α mRNA levels increased at 3 h after ischemia. MCP-1, MIP-1α, and vascular endothelial growth factor protein levels were also increased markedly and were maximal on days 1,0.5, and 1, respectively, after ischemia. In situ hybridization showed that MCP-1 and MIP-1α were localized in the hypoxic inner retina. Immunostaining demonstrated that the macrophages/microglia in the retina had morphological changes with enlarged processes, and some were closely associated with neovascular tufts at postnatal day 17. Coadministration of the neutralizing antibodies against MCP-1 and MIP-1α inhibited retinal neovascularization by 30%. Our data suggest that MCP-1 and MIP-1α are involved in the induction of retinal neovascularization and play a role in the inflammation induced by the ischemic retinopathy, possibly by modulating or attracting macrophages/microglia.
Tryptophan availability selectively limits NO-synthase induction in macrophages
Authors: Chiarugi Alberto , Rovida Elisabetta , Dello Sbarba Persio , Moroni Flavio 
Published: March 2003

Abstract
We studied the effects of tryptophan (TRP) availability on the synthesis and release of nitric oxide (NO) and tumor necrosis factor α (TNF-α) in interferon-γ (IFN-γ)-activated murine macrophages of the BAC1.2F5 cell line. IFN-γ (100 U/ml) not only increased the synthesis and release of NO and TNF-α from these cells but also induced indoleamine-2,3-dioxygenase, the rate-limiting enzyme of TRP catabolism. This led to an increased metabolic flow through the kynurenine pathway and significantly decreased TRP levels in macrophage incubation media. Low TRP concentrations in the media, however, modified IFN-γ effects. In TRP-“starved” cultures, in fact, the IFN-γ-mediated NO synthase induction was significantly reduced, and the increased TNF-α synthesis and release were not affected. Our results suggest hat a reduced local TRP availability may modify macrophage function and possibly the outcome of immune responses.
A unique role for IL-23 in promoting cellular immunity
Authors: Lankford Carla S R , Frucht David M 
Published: March 2003

Abstract
Recent discoveries of interleukin (IL)-23, its receptor, and its signal-transduction pathway add to our understanding of cellular immunity. IL-23 is a heterodimer, comprising IL-12 p40 and the recently cloned IL-23-specific p19 subunit. IL-23 uses many of the same signal-transduction components as IL-12, including IL-12Rβ1, Janus kinase 2, Tyk2, signal transducer and activator of transcription (Stat)1, Stat3, Stat4, and Stat5. This may explain the similar actions of IL-12 and IL-23 in promoting cellular immunity by inducing interferon-γ production and proliferative responses in target cells. Additionally, both cytokines promote the T helper cell type 1 costimulatory function of antigen-presenting cells. IL-23 does differ from IL-12 in the T cell subsets that it targets. Whereas IL-12 acts on naïve CD4+ T cells, IL-23 preferentially acts on memory CD4+ T cells. This review summarizes recent advances regarding IL-23, providing a functional and mechanistic basis for the unique niche that IL-23 occupies in cellular immunity.
Basophils express a type 2 cytokine profile on exposure to proteases from helminths and house dust mites
Authors: Phillips Clair , Coward William R , Pritchard David I , Hewitt Colin R A 
Published: March 2003

Abstract
The proteolytic activities frequently associated with sources of allergens and parasite secretions have been suggested as important immunomodulators. We have investigated whether the protease activity of the house dust mite allergen Der p1 and the secreted proteases of the hookworm Necator americanus are able to directly induce type 2 cytokine production by basophils. Der p1 and the secretions of N. americanus induced interleukin (IL)-4, IL-5, and IL-13 but not interferon-γ mRNA in KU812 basophils. Enzyme-linked immunosorbent assay confirmed that IL-4 and IL-13 were secreted. A nonproteolytic antigen failed to induce cytokine expression, and preincubation of Der p1 or N. americanus secretions with protease inhibitors inhibited cytokine expression. Data were confirmed using basophils purified from human peripheral blood. We speculate that tis innate mechanism may contribute to the development of a cytokine milieu that could promote immunoglobulin E synthesis, eosinophil recruitment, and the development of type 2 T cells.
Cross-talk between tumor cells and neutrophils through the Fas (APO-1, CD95)/FasL system: human glioma cells enhance cell viability and stimulate cytokine production in neutrophils
Authors: Hor Wei-Shio , Huang Wei-Lune , Lin Yee-Shin , Yang Bei-Chang 
Published: March 2003

Abstract
Many tumor cells are resistant to Fas-mediated killing, which has been primarily used as a mechanism to evade immune attack. In this study, we found a new action of Fas on tumors where activation of the Fas signal may force tumor cells to produce survival factors for neutrophils. Human peripheral circulating neutrophils in coculture with glioma cells showed significant delays in spontaneous apoptosis. Interleukin (IL)-6 and IL-8 partially mediated the glioma cell-associated, protective effect on neutrophils. The Fas agonistic antibody CH-11 dose-dependently stimulated the expression of IL-6 and IL-8 in glioma cells. Accordingly, blocking the Fas/FasL interaction reduced IL-6 and IL-8 production in glioma cells and impaired their protective effect on neutrophils. Coculture with glioma cells also affected the expression of cytokines in neutrophils, including IL-8, interferon-γ, and tumor necrosis factor α to various extents. Collectively, our results demonstrate bi-directional cross-talk between tumor and immune cells. Although Fas activation alone cannot induce apoptosis in tumor cells, it may potentially initiate an effective anti-tumor response through a circumvented mechanism.
Activity and subcellular distribution of cathepsins in primary human monocytes
Authors: Greiner Andrea , Lautwein Alfred , Overkleeft Herman S , Weber Ekkehard , Driessen Christoph 
Published: March 2003

Abstract
Cathepsins (Cat) in antigen presenting cells (APC) control antigen processing as well as major histocompatibility complex class II transport and function. The set of active Cat and the subcellular architecture of the class II antigen presentation compartment are largely unknown in primary human APC, including peripheral blood monocytes. We used novel chemical tools to visualize Cat in an activity-dependent manner. Primary human monocytes cntained active CatS, -B, and -H, while CatL was absent. Expression and activity patterns of Cat in human myelo-monocytoid cell lines were distinct from those found in primary cells. On a subcellular scale, the bulk of active Cat was concentrated in lysosomes in primary monocytes. In late endosomes, only active CatS was found in sizable amounts, colocalizing with C-terminal processing of the class II invariant chain and with cystatin C, the major endogenous Cat inhibitor. Late endosomes of human peripheral blood monocytes contain a well-controlled proteolytic machinery distinct from lysosomes, which is likely to play a key role in class II function.
Differential mRNA expression in circulating γδ T lymphocyte subsets defines unique tissue-specific functions
Authors: Hedges Jodi F , Cockrell Diane , Jackiw Larissa , Meissner Nicole , Jutila Mark A 
Published: March 2003

Abstract
To elucidate the functions of circulating γδ T cells, in the absence of antigen stimulation, the differential gene expression of two circulating γδ T cell subsets was analyzed. The two subsets, with distinct trafficking phenotypes in young calves, were GD3.5+, CD8−, WC1+ or GD3.5−, CD2+, WC1−, and 90–100% CD8+ and were sorted based on GD3.5 and γδ T cell receptor expression. Results from two different human arrays probed with cDNA from these γδ T cell subsets indicated that they have markedly different tissue-specific functions. The genes preferentially expressed by GD3.5+ (CD8−) γδ T cells demonstrated that they were highly activated, proliferative, and inflammatory, whereas those expressed by GD3.5− (primarily CD8+) γδ cells were involved in promoting quiescence, consistent with a role for γδ T cells as sentinel mucosal cells, and several were interferon-regulated genes. Gene expression and phenotypic assays indicated that CD8+ γδ T cells were apoptotic, whereas CD8− γδ T cells were apoptosis-resistant. Differential expression of multiple genes was confirmed in both arrays: That of 14 genes was confirmed by quantitative reverse transcriptase-polymerase chain reaction and that of seven proteins was confirmed by flow cytometry. This novel, genomic analysis of circulating γδ T cell subsets, without confounding effects of the tissue microenvironment, offers new insight into the biology and development of neonatal γδ T cells.
An apoptosis-differentiation program in human polymorphonuclear leukocytes facilitates resolution of inflammation
Authors: Kobayashi Scott D , Voyich Jovanka M , Somerville Greg A , Braughton Kevin R , Malech Harry L , Musser James M , DeLeo Frank R 
Published: March 2003

Abstract
Human polymorphonuclear leukocytes (PMNs) are an essential part of innate immunity and contribute significantly to inflammation. Although much is nderstood about the inflammatory response, the molecular basis for termination of inflammation in humans is largely undefined. We used human oligonucleotide microarrays to identify genes differentially regulated during the onset of apoptosis occurring after PMN phagocytosis. Genes encoding proteins that regulate cell metabolism and vesicle trafficking comprised 198 (98 genes induced, 100 genes repressed) of 867 differentially expressed genes. We discovered that complex cellular pathways involving glutathione and thioredoxin detoxification systems, heme catabolism, ubiquitin-proteasome degradation, purine nucleotide metabolism, and nuclear import were regulated at the level of gene expression during the initial stages of PMN apoptosis. Eleven genes encoding key regulators of glycolysis, the hexose monophosphate shunt, the glycerol-phosphate shuttle, and oxidative phosphorylation were induced. Increased levels of cellular reduced glutathione and γ-glutamyltransferase and glycolytic activity confirmed that several of these metabolic pathways were up-regulated. In contrast, seven genes encoding critical enzymes involved in fatty acid β-oxidation, which can generate toxic lipid peroxides, were down-regulated. Our results indicate that energy metabolism and oxidative stress-response pathways are gene-regulated during PMN apoptosis. We propose that changes in PMN gene expression leading to programmed cell death are part of an apoptosis-differentiation program, a final stage of transcriptionally regulated PMN maturation that is accelerated significantly by phagocytosis. These findings provide new insight into the molecular events that contribute to the resolution of inflammation in humans.
Control of the Magnetic and Optical Properties in Molecular Compounds by Electrochemical, Photochemical and Chemical Methods
Authors: Sato Osamu , Hayami Shinya , Einaga Yasuaki , Gu Zhong-Ze 
Published: March 2003

Abstract
The electrochemical, photochemical and chemical control of the magnetic properties in molecular compounds is described. The preparation of various thin films of CrCr and FeFe Prussian blue on a conducting electrode allowed us to control the magnetic properties by varying the oxidation state of the component metals. The magnetic properties of CrCr Prussian blue show that the critical temperature and coercive field can be drastically modified by electrochemical treatment. That is, the compound, CrII1.29CrIII0.14[CrIII(CN)6] has ferrimagnetic properties with Tc (critical temperature) = 240 K and Hc (coercive field) = 25 G, while the reduced form, KCrII1.29CrIII0.14[CrII(CN)6], has Tc = 100 K and Hc = 220 G. Similarly, it was found that the critical temperature of FeFe Prussian blue shifts continuously from paramagnetic to magnetic with Tc = 12 K. These changes can be expressed as K4FeII4[FeII(CN)6]3 (paramagnetic) ←→ FeIII4[FeII(CN)6]3 (ferromagnetic, Tc = 4.5 K) + 4 K+ + 4e− and FeIII4[FeII(CN)6]3 (ferromagnetic, Tc = 4.2 K) + 3Cl− − 3e−←→ FeIII4[FeIII(CN)6]3(Cl)3 (Tc = 12 K). Furthermore, we have discovered that the FeCo Prussian blue and Co valence tautomeric compounds exhibit photo-reversible magnetization effects. The photoinduced magnetization in FeCo Prussian blue is expressed as Na0.4CoII-HS0.3CoIII-LS[FeII(CN)6] (paramagnetic) ←→ Na0.4CoII-HS1.3[FeIII(CN)6] (ferrimagnetic, Tc = 26 K and Hc = 6000 G), where HS and LS denote high-spin and low-spin. An example of the photoinduced valence tautomeric behavior is expressed as [CoIII-LS(3,5-dbsq)(3,5-dbcat)(tmeda)] ←→ [CoII-HS(3,5-dbsq)2(tmeda)], where tmeda, 3,5-dbsq and 3,5-dbcat represent N,N,N′,N′-tetramethylethylenediamine, 3,5-di-tert-butyl-1,2-semiquinonate and 3,5-di-tert-butyl-1,2-catecholate, respectively. Additionally, we succeeded in tuning the phase transition temperature by varying the ligand field of the Co ions in the FeCo Prussian blue. Brief comments are also included regarding the first examples of light-induced excited spin state trapping observed in an FeIII complex, i.e. [FeIII-LS(pap)2]ClO4·H2O ←→ [FeIII-HS(pap)2]ClO4·H2O (pap = N-2-pyridylmethylidene-2-hydroxy-phenylaminato) and a photoinduced structural change observed in a CuII complex, [CuII(dieten)2](BF4)2 [dieten = bis(N,N -diethylethylenediamine)].
Syntheses, Structures, and Thermolyses of Three- and Four-Membered Heterocyclic Compounds Containing Highly Coordinate Main Group Elements
Authors: Kawashima Takayuki 
Published: March 2003

Abstract
Most titled compounds were synthesized by taking advantage of the Martin ligand. Their structures were determined by X-ray crystallography. Thermolyses of most of the four-membered ring compounds gave the corresponding Wittig-type products, while those of 1,2-oxasiletanides in the presence of proton source afforded the homo-Brook rearrangement products depending on bulkiness of the substituent at the 3-position. Pentacoordinate thiasiliranides were hydrolyzed to give the corresponding thiol, which seems to be formed via the initial cleavage of the Si–C bond followed by further hydrolysis of the corresponding thia-Brook rearrangement product. On the other hand, the most polarized bond of a pentacoordinate selenaphosphirane was found to be the P–Se bond, which was confirmed by its reaction with CF3SO3Me to give the corresponding 1-(methylseleno)alkylphosphonium triflate and by the solvent-dependent NMR study.
Synthesis and Biological Activities of Lipid A Analogs Possessing β-Glycosidic Linkage at 1-Position
Authors: Fukase Koichi , Ueno Atsushi , Fukase Yoshiyuki , Oikawa Masato , Suda Yasuo , Kusumoto Shoichi 
Published: March 2003

Abstract
New lipid A analogs having acidic groups β-glycosidically linked at the 1-position were synthesized in order to investigate the structural requirement for immunostimulating and endotoxic activity of lipid A. The β-(phosphonoxy)ethyl (PE) and carboxymethyl (CM) analogs of Escherichia coli type having six acyl groups and those of the biosynthetic precursor type having four acyl groups were synthesized via a divergent synthetic route. The E. coli type β-(phosphonoxy)ethyl analog, which was previously reported to be not endotoxic, showed strong immunostimulating activity comparable to the natural-type α-analog. The acidic functional groups are concluded to be essential but their strict spatial arrangement is not required for expression of the biological activity.