Showing papers by "University of Kiel published in 2007"
TL;DR: G*Power 3 provides improved effect size calculators and graphic options, supports both distribution-based and design-based input modes, and offers all types of power analyses in which users might be interested.
Abstract: G*Power (Erdfelder, Faul, & Buchner, 1996) was designed as a general stand-alone power analysis program for statistical tests commonly used in social and behavioral research. G*Power 3 is a major extension of, and improvement over, the previous versions. It runs on widely used computer platforms (i.e., Windows XP, Windows Vista, and Mac OS X 10.4) and covers many different statistical tests of thet, F, and χ2 test families. In addition, it includes power analyses forz tests and some exact tests. G*Power 3 provides improved effect size calculators and graphic options, supports both distribution-based and design-based input modes, and offers all types of power analyses in which users might be interested. Like its predecessors, G*Power 3 is free.
40,195 citations
TL;DR: A previously unrecognized pathway for the activation of tumor antigen–specific T-cell immunity that involves secretion of the high-mobility-group box 1 (HMGB1) alarmin protein by dying tumor cells and the action of HMGB1 on Toll-like receptor 4 (TLR4) expressed by dendritic cells (DCs) is described.
Abstract: Conventional cancer treatments rely on radiotherapy and chemotherapy. Such treatments supposedly mediate their effects via the direct elimination of tumor cells. Here we show that the success of some protocols for anticancer therapy depends on innate and adaptive antitumor immune responses. We describe in both mice and humans a previously unrecognized pathway for the activation of tumor antigen-specific T-cell immunity that involves secretion of the high-mobility-group box 1 (HMGB1) alarmin protein by dying tumor cells and the action of HMGB1 on Toll-like receptor 4 (TLR4) expressed by dendritic cells (DCs). During chemotherapy or radiotherapy, DCs require signaling through TLR4 and its adaptor MyD88 for efficient processing and cross-presentation of antigen from dying tumor cells. Patients with breast cancer who carry a TLR4 loss-of-function allele relapse more quickly after radiotherapy and chemotherapy than those carrying the normal TLR4 allele. These results delineate a clinically relevant immunoadjuvant pathway triggered by tumor cell death.
2,666 citations
2,271 citations
TL;DR: Adalimumab was well-tolerated, with a safety profile consistent with previous experience with the drug, and was significantly more effective than placebo in maintaining remission in moderate to severe CD through 56 weeks.
2,028 citations
TL;DR: Data suggest that the underlying biological process may be specific to Crohn disease, and that marker rs2241880, a coding SNP (T300A), carries virtually all the disease risk exerted by the ATG16L1 locus.
Abstract: We performed a genome-wide association study of 19,779 nonsynonymous SNPs in 735 individuals with Crohn disease and 368 controls. A total of 7,159 of these SNPs were informative. We followed up on all 72 SNPs with P 0.4), these data suggest that the underlying biological process may be specific to Crohn disease.
1,856 citations
TL;DR: The data uncover a fundamental role of an endogenous antimicrobial peptide in breaking innate tolerance to self-DNA and suggest that this pathway may drive autoimmunity in psoriasis.
Abstract: Plasmacytoid dendritic cells (pDCs) sense viral and microbial DNA through endosomal Toll-like receptors to produce type 1 interferons. pDCs do not normally respond to self-DNA, but this restriction seems to break down in human autoimmune disease by an as yet poorly understood mechanism. Here we identify the antimicrobial peptide LL37 (also known as CAMP) as the key factor that mediates pDC activation in psoriasis, a common autoimmune disease of the skin. LL37 converts inert self-DNA into a potent trigger of interferon production by binding the DNA to form aggregated and condensed structures that are delivered to and retained within early endocytic compartments in pDCs to trigger Toll-like receptor 9. Thus, our data uncover a fundamental role of an endogenous antimicrobial peptide in breaking innate tolerance to self-DNA and suggest that this pathway may drive autoimmunity in psoriasis.
1,628 citations
TL;DR: In patients with moderate-to-severe Crohn's disease, induction and maintenance therapy with certolizumab pegol was associated with a modest improvement in response rates, as compared with placebo, but with no significant improvement in remission rates.
Abstract: In this article we provide a contemporary overview of available clinical data on certolizumab pegol, a pegylated anti-tumor necrosis factor (TNF) alpha agent that comprises a uniquely small protein, and its emerging role as a therapy for Crohn's disease (CD). The results from a comprehensive clinical trial program suggest that certolizumab pegol offers rapid and sustained remission of moderate to severe CD. Certolizumab pegol is an effective and well-tolerated therapy both in patients who have already received biologics and in patients who are anti-TNF naive. Benefits of therapy include a stable dosing regimen, which allows for rapid induction of a clinical response followed by long-term maintenance of response and remission under one fixed dose. Treatment with certolizumab pegol has been shown to improve function and quality of life in patients with CD, and insights into the potential mechanisms by which certolizumab pegol effects a response in CD suggest that this agent may have the potential to slow or even modify disease progression. Early therapy is particularly effective and could help control CD progression and lessen the burden of disease on patients.
1,023 citations
TL;DR: Patients with moderate-to-severe Crohn's disease who had a response to induction therapy with 400 mg of certolizumab pegol were more likely to have a maintained response and a remission at 26 weeks with continued certolIZumab Pegol treatment than with a switch to placebo.
Abstract: Background Certolizumab pegol is a pegylated humanized Fab′ fragment with a high binding affinity for tumor necrosis factor α that does not induce apoptosis of T cells or monocytes. Methods In our randomized, double-blind, placebo-controlled trial, we evaluated the efficacy of certolizumab pegol maintenance therapy in adults with moderate-to-severe Crohn's disease. As induction therapy, 400 mg of certolizumab pegol was administered subcutaneously at weeks 0, 2, and 4. Patients with a clinical response (defined as reduction of at least 100 from the baseline score on the Crohn's Disease Activity Index [CDAI]) at week 6 were stratified according to their baseline C-reactive protein level and were randomly assigned to receive 400 mg of certolizumab pegol or placebo every 4 weeks through week 24, with follow-up through week 26. Results Among patients with a response to induction therapy at week 6 (428 of 668 [64%]), the response was maintained through week 26 in 62% of patients with a baseline C-reactive prote...
977 citations
TL;DR: In this article, a meta-analysis summarizes teaching effectiveness studies of the past decade and investigates the role of theory and research design in disentangling results, finding that the largest effects for domainspecific components of teaching were most proximal to the executive processes of learning.
Abstract: This meta-analysis summarizes teaching effectiveness studies of the past decade and investigates the role of theory and research design in disentangling results. Compared to past analyses based on the process–product model, a framework based on cognitive models of teaching and learning proved useful in analyzing studies and accounting for variations in effect sizes. Although the effects of teaching on student learning were diverse and complex, they were fairly systematic. The authors found the largest effects for domainspecific components of teaching—teaching most proximal to executive processes of learning. By taking into account research design, the authors further disentangled meta-analytic findings. For example, domain-specific teaching components were mainly studied with quasi-experimental or experimental designs. Finally, correlational survey studies dominated teaching effectiveness studies in the past decade but proved to be more distal from the teaching–learning process.
945 citations
TL;DR: The proposed tumor–node–metastasis (TNM) classifications are based on the recently published ENETS Guidelines for the Diagnosis and Treatment of gastroenteropancreatic NETs and follow the previous proposal for foregut tumors.
Abstract: Criteria for the staging and grading of neuroendocrine tumors (NETs) of midgut and hindgut origin were established at the second Consensus Conference in Frascati (Rome) organized by the European Neuroendocrine Tumor Society (ENETS). The proposed tumor-node-metastasis (TNM) classifications are based on the recently published ENETS Guidelines for the Diagnosis and Treatment of gastroenteropancreatic NETs and follow our previous proposal for foregut tumors. The new TNM classifications for NETs of the ileum, appendix, colon, and rectum, and the grading system were designed, discussed, and consensually approved by all conference participants. These proposals need to be validated and are meant to help clinicians in the stratification, treatment and follow-up of patients.
913 citations
TL;DR: A relative quantitative reverse transcriptase-polymerase chain reaction index using only miR-217 and -196a was found to discriminate normal pancreas, chronic pancreatitis and cancerous tissues, establishing a potential utility for miRNAs in diagnostic procedures.
Abstract: Pancreatic ductal adenocarcinoma (PDAC) is known for its very poor overall prognosis. Accurate early diagnosis and new therapeutic modalities are therefore urgently needed. We used 377 feature microRNA (miRNA) arrays to investigate miRNA expression in normal pancreas, chronic pancreatitis, and PDAC tissues as well as PDAC-derived cell lines. A pancreatic miRNome was established comparing the data from normal pancreas with a reference set of 33 human tissues. The expression of miR-216 and -217 and lack of expression of miR-133a were identified as characteristic of pancreas tissue. Unsupervised clustering showed that the three pancreatic tissues types can be classified according to their respective miRNA expression profiles. We identified 26 miRNAs most prominently misregulated in PDAC and a relative quantitative reverse transcriptase-polymerase chain reaction index using only miR-217 and -196a was found to discriminate normal pancreas, chronic pancreatitis and cancerous tissues, establishing a potential utility for miRNAs in diagnostic procedures. Lastly, comparing differentially expressed genes from PDAC with predicted miRNA target genes for the top 26 miRNAs, we identified potential novel links between aberrant miRNA expression and known target genes relevant to PDAC biology. Our data provides novel insights into the miRNA-driven pathophysiological mechanisms involved in PDAC development and offers new candidate targets to be exploited both for diagnostic and therapeutic strategies.
TL;DR: The European Study Group on MRD detection in ALL (ESG-MRD-ALL), consisting of 30 MRD-PCR laboratories worldwide, has developed guidelines for the interpretation of real-time quantitative PCR-based MRD data.
Abstract: Most modern treatment protocols for acute lymphoblastic leukaemia (ALL) include the analysis of minimal residual disease (MRD). To ensure comparable MRD results between different MRD-polymerase chain reaction (PCR) laboratories, standardization and quality control are essential. The European Study Group on MRD detection in ALL (ESG-MRD-ALL), consisting of 30 MRD-PCR laboratories worldwide, has developed guidelines for the interpretation of real-time quantitative PCR-based MRD data. The application of these guidelines ensures identical interpretation of MRD data between different laboratories of the same MRD-based clinical protocol. Furthermore, the ESG-MRD-ALL guidelines will facilitate the comparison of MRD data obtained in different treatment protocols, including those with new drugs.
TL;DR: Time‐lapse cinematography revealed that late endosomes/lysosomes as well as phagosomes lacking LAMP‐1 and LAMP-2 had reduced ability to move toward the microtubule‐organizing center, likely precluding their interaction with each other.
Abstract: Lysosome-associated membrane proteins 1 and 2 (LAMP-1 and LAMP-2) are delivered to phagosomes during the maturation process. We used cells from LAMP-deficient mice to analyze the role of these proteins in phagosome maturation. Macrophages from LAMP-1- or LAMP-2-deficient mice displayed normal fusion of lysosomes with phagosomes. Because ablation of both the lamp-1 and lamp-2 genes yields an embryonic-lethal phenotype, we were unable to study macrophages from double knockouts. Instead, we reconstituted phagocytosis in murine embryonic fibroblasts (MEFs) by transfection of FcγIIA receptors. Phagosomes formed by FcγIIA-transfected MEFs obtained from LAMP-1- or LAMP-2- deficient mice acquired lysosomal markers. Remarkably, although FcγIIA-transfected MEFs from double-deficient mice ingested particles normally, phagosomal maturation was arrested. LAMP-1 and LAMP-2 double-deficient phagosomes acquired Rab5 and accumulated phosphatidylinositol 3-phosphate, but failed to recruit Rab7 and did not fuse with lysosomes. We attribute the deficiency to impaired organellar motility along microtubules. Time-lapse cinematography revealed that late endosomes/lysosomes as well as phagosomes lacking LAMP-1 and LAMP-2 had reduced ability to move toward the microtubule-organizing center, likely precluding their interaction with each other.
Leipzig University1, University of Jena2, University of Münster3, Martin Luther University of Halle-Wittenberg4, University of Greifswald5, Heidelberg University6, Augsburg College7, University of Erlangen-Nuremberg8, University of Giessen9, Charité10, University of Göttingen11, Dresden University of Technology12, RWTH Aachen University13, University of Bonn14, University of Kiel15, Hannover Medical School16
TL;DR: The expected number of newly diagnosed cases with severe sepsis in Germany amounts to 76–110 per 100,000 adult inhabitants and future epidemiological studies should use standardized study methodologies with respect to sepsi definitions, hospital size, and daily and monthly variability.
Abstract: To determine the prevalence and mortality of ICU patients with severe sepsis in Germany, with consideration of hospital size. Prospective, observational, cross-sectional 1-day point-prevalence study. 454 ICUs from a representative nationwide sample of 310 hospitals stratified by size. Data were collected via 1-day on-site audits by trained external study physicians. Visits were randomly distributed over 1 year (2003). Inflammatory response of all ICU patients was assessed using the ACCP/SCCM consensus conference criteria. Patients with severe sepsis were followed up after 3 months for hospital mortality and length of ICU stay. Main outcome measures were prevalence and mortality. A total of 3,877 patients were screened. Prevalence was 12.4% (95% CI, 10.9–13.8%) for sepsis and 11.0% (95% CI, 9.7–12.2%) for severe sepsis including septic shock. The ICU and hospital mortality of patients with severe sepsis was 48.4 and 55.2%, respectively, without significant differences between hospital size. Prevalence and mean length of ICU stay of patients with severe sepsis were significantly higher in larger hospitals and universities (≤ 200 beds: 6% and 11.5 days, universities: 19% and 19.2 days, respectively). The expected number of newly diagnosed cases with severe sepsis in Germany amounts to 76–110 per 100,000 adult inhabitants. To allow better comparison between countries, future epidemiological studies should use standardized study methodologies with respect to sepsis definitions, hospital size, and daily and monthly variability.
TL;DR: Consistently favorable results in non-HR patients were achieved with significant treatment reduction in the majority of these patients, and compared without previous trial ALL-BFM 90, consistently favorable results were achieved.
TL;DR: In this paper, a detailed overview of developments in transducer materials technology relating to their current and future applications in micro-scale devices is provided. And a short discussion of structural polymers that are extending the range of micro-fabrication techniques available to designers and production engineers beyond the limitations of silicon fabrication technology is presented.
Abstract: This paper provides a detailed overview of developments in transducer materials technology relating to their current and future applications in micro-scale devices. Recent advances in piezoelectric, magnetostrictive and shape-memory alloy systems are discussed and emerging transducer materials such as magnetic nanoparticles, expandable micro-spheres and conductive polymers are introduced. Materials properties, transducer mechanisms and end applications are described and the potential for integration of the materials with ancillary systems components is viewed as an essential consideration. The review concludes with a short discussion of structural polymers that are extending the range of micro-fabrication techniques available to designers and production engineers beyond the limitations of silicon fabrication technology.
TL;DR: A combination of adaptive control and nano-optics achieves subwavelength dynamic localization of electromagnetic intensity on the nanometre scale and thus overcome the spatial restrictions of conventional optics.
Abstract: The size of mechanical tools limits their spatial resolution. In the case of a drill, for instance, its diameter determines the size of the smallest hole that it can make, with 1-mm holes from 10-mm drills an obvious impossibility. But in the world of optics, the 'impossible' can happen. Aeschlimann et al. demonstrate a light-based tool that not only 'drills holes' smaller than its own size (its wavelength), but does so in selectable positions that can be changed at the speed of light. The experiment combines adaptive control with nano-optics, to control interactions between light and matter with sub-wavelength resolution and femtosecond timing. Adaptive shaping of the phase and amplitude of femtosecond laser pulses has been developed into an efficient tool for the directed manipulation of interference phenomena, thus providing coherent control over various quantum-mechanical systems1,2,3,4,5,6,7,8,9,10. Temporal resolution in the femtosecond or even attosecond range has been demonstrated, but spatial resolution is limited by diffraction to approximately half the wavelength of the light field (that is, several hundred nanometres). Theory has indicated11,12 that the spatial limitation to coherent control can be overcome with the illumination of nanostructures: the spatial near-field distribution was shown to depend on the linear chirp of an irradiating laser pulse. An extension of this idea to adaptive control, combining multiparameter pulse shaping with a learning algorithm, demonstrated the generation of user-specified optical near-field distributions in an optimal and flexible fashion13. Shaping of the polarization of the laser pulse14,15 provides a particularly efficient and versatile nano-optical manipulation method16,17. Here we demonstrate the feasibility of this concept experimentally, by tailoring the optical near field in the vicinity of silver nanostructures through adaptive polarization shaping of femtosecond laser pulses14,15 and then probing the lateral field distribution by two-photon photoemission electron microscopy18. In this combination of adaptive control1,2,3,4,5,6,7,8,9,10 and nano-optics19, we achieve subwavelength dynamic localization of electromagnetic intensity on the nanometre scale and thus overcome the spatial restrictions of conventional optics. This experimental realization of theoretical suggestions11,12,13,16,17,20 opens a number of perspectives in coherent control, nano-optics, nonlinear spectroscopy, and other research fields in which optical investigations are carried out with spatial or temporal resolution.
TL;DR: A role for LIMP-2 is supported as the mannose-6-phosphate-independent trafficking receptor for beta-glucocerebrosidase, the enzyme defective in Gaucher disease, which involves a coiled-coil domain within the lumenal domain.
TL;DR: The use of the MDP-containing composite resin Panavia F on air abraded zirconia ceramic can be recommended as promising bonding method.
TL;DR: To enhance comparability of findings among studies, species, and oceanographic regions, a recommendation on standards for the reporting of results in the literature is made.
Abstract: We review the different methods that are used to collect dietary data from marine birds. We consider their limitations and practicalities and emphasize critical data gaps in our knowledge of the feeding ecology of seabirds (na mely diets outside breeding seasons). To enhance comparability of findings among studies, species, and oceanographic regions, we make recommendations on standards for the reporting of results in the literature.
TL;DR: In this paper, a detailed reconstruction of West African monsoon hydrology over the past 155,000 years suggests a close linkage to northern high-latitude climate oscillations, and the onset of enhanced monsoon precipitation lags behind the changes in EEA sea surface temperatures by up to 7000 years during glacial-interglacial transitions.
Abstract: A detailed reconstruction of West African monsoon hydrology over the past 155,000 years suggests a close linkage to northern high-latitude climate oscillations. Ba/Ca ratio and oxygen isotope composition of planktonic foraminifera in a marine sediment core from the Gulf of Guinea, in the eastern equatorial Atlantic (EEA), reveal centennial-scale variations of riverine freshwater input that are synchronous with northern high-latitude stadials and interstadials of the penultimate interglacial and the last deglaciation. EEA Mg/Ca-based sea surface temperatures (SSTs) were decoupled from northern high-latitude millennial-scale fluctuation and primarily responded to changes in atmospheric greenhouse gases and low-latitude solar insolation. The onset of enhanced monsoon precipitation lags behind the changes in EEA SSTs by up to 7000 years during glacial-interglacial transitions. This study demonstrates that the stadial-interstadial and deglacial climate instability of the northern high latitudes exerts dominant control on the West African monsoon dynamics through an atmospheric linkage.
TL;DR: It can be expected that future diagnostic algorithms will include molecular parameters to detect early disease or guide therapies by predicting the individual course of disease.
TL;DR: This study employs a signal sequence trap strategy to isolate cell surface molecules expressed on human AML-LSC and finds that CD96, which is a member of the Ig gene superfamily, is a promising candidate as an LSC-specific antigen.
Abstract: Permanent cure of acute myeloid leukemia (AML) by chemotherapy alone remains elusive for most patients because of the inability to effectively eradicate leukemic stem cells (LSCs), the self-renewing component of the leukemia. To develop therapies that effectively target LSC, one potential strategy is to identify cell surface markers that can distinguish LSC from normal hematopoietic stem cells (HSCs). In this study, we employ a signal sequence trap strategy to isolate cell surface molecules expressed on human AML-LSC and find that CD96, which is a member of the Ig gene superfamily, is a promising candidate as an LSC-specific antigen. FACS analysis demonstrates that CD96 is expressed on the majority of CD34+CD38− AML cells in many cases (74.0 ± 25.3% in 19 of 29 cases), whereas only a few (4.9 ± 1.6%) cells in the normal HSC-enriched population (Lin−CD34+CD38−CD90+) expressed CD96 weakly. To examine whether CD96+ AML cells are enriched for LSC activity, we separated AML cells into CD96+ and CD96− fractions and transplanted them into irradiated newborn Rag2−/− γc−/− mice. In four of five samples, only CD96+ cells showed significant levels of engraftment in bone marrow of the recipient mice. These results demonstrate that CD96 is a cell surface marker present on many AML-LSC and may serve as an LSC-specific therapeutic target.
TL;DR: Preclinical animal disease models have provided strong evidence that specific blockade of IL-6-regulated signalling pathways represents a promising approach for the therapy of these diseases.
Abstract: IL-6 plays a pivotal role in immune responses and certain oncologic conditions. The intense investigation of its biological activity and function led to the discovery of two different IL-6-driven signalling pathways. Binding to the membrane-bound IL-6 receptor (mIL-6R, CD126) causes the recruitment of two gp130 co-receptor molecules (CD130) and the activation of intracellular signalling cascades via gp130. Although this classical pathway is mainly limited to hepatocytes, neutrophils, monocytes/macrophages and certain other leukocyte populations, which express IL-6R on their surface, an alternative mechanism has also been described. Proteolytic cleavage of the mIL-6R protein or translation from alternatively spliced mRNA leads to the generation of a soluble form of the IL-6R (sIL-6R), which is likewise able to bind to IL-6. The resulting IL-6/sIL-6R complex is also capable of binding to gp130 and inducing intracellular signalling. Through this so-called 'trans-signalling' mechanism, IL-6 is able to stimulate cells that lack an endogenous mIL-6R. High levels of IL-6 and sIL-6R have been reported in several chronic inflammatory and autoimmune diseases as well as in cancer. Preclinical animal disease models have provided strong evidence that specific blockade of IL-6-regulated signalling pathways represents a promising approach for the therapy of these diseases. An optimised variant of the recently described fusion protein sgp30Fc is now heading towards its clinical evaluation.
TL;DR: Consideration of these patterns of gene distribution underscores the likely significance of gene loss during animal evolution whilst indicating ancient origins for many components of the vertebrate innate immune system.
Abstract: Background
Characterization of the innate immune repertoire of extant cnidarians is of both fundamental and applied interest - it not only provides insights into the basic immunological 'tool kit' of the common ancestor of all animals, but is also likely to be important in understanding the global decline of coral reefs that is presently occurring. Recently, whole genome sequences became available for two cnidarians, Hydra magnipapillata and Nematostella vectensis, and large expressed sequence tag (EST) datasets are available for these and for the coral Acropora millepora.
TL;DR: Once-daily MMX mesalamine was efficacious and well-tolerated for the induction of clinical and endoscopic remission in active ulcerative colitis, potentially improving treatment compliance.
TL;DR: A meta‐analysis of 478 disease‐associated splicing mutations, in 38 different genes, reveals that exon skipping was the preferred phenotype when the immediate vicinity of the affected exon–intron junctions was devoid of alternative splice‐sites, and estimates that some 1.6% of disease‐causing missense substitutions in human genes are likely to affect the mRNA splicing phenotype.
Abstract: Although single base-pair substitutions in splice junctions constitute at least 10% of all mutations causing human inherited disease, the factors that determine their phenotypic consequences at the RNA level remain to be fully elucidated. Employing a neural network for splice-site recognition, we performed a meta-analysis of 478 disease-associated splicing mutations, in 38 different genes, for which detailed laboratory-based mRNA phenotype assessment had been performed. Inspection of the ±50-bp DNA sequence context of the mutations revealed that exon skipping was the preferred phenotype when the immediate vicinity of the affected exon–intron junctions was devoid of alternative splice-sites. By contrast, in the presence of at least one such motif, cryptic splice-site utilization, became more prevalent. This association was, however, confined to donor splice-sites. Outside the obligate dinucleotide, the spatial distribution of pathological mutations was found to differ significantly from that of SNPs. Whereas disease-associated lesions clustered at positions –1 and +3 to +6 for donor sites and –3 for acceptor sites, SNPs were found to be almost evenly distributed over all sequence positions considered. When all putative missense mutations in the vicinity of splice-sites were extracted from the Human Gene Mutation Database for the 38 studied genes, a significantly higher proportion of changes at donor sites (37/152; 24.3%) than at acceptor splice-sites (1/142; 0.7%) was found to reduce the neural network signal emitted by the respective splice-site. Based upon these findings, we estimate that some 1.6% of disease-causing missense substitutions in human genes are likely to affect the mRNA splicing phenotype. Taken together, our results are consistent with correct donor splice-site recognition being a key step in exon recognition. Hum Mutat 28(2), 150–158, 2007. © 2006 Wiley-Liss, Inc.
TL;DR: It is demonstrated that IL6R is shed from apoptotic human neutrophils, which is relevant to the control of acute inflammation, where transition from the initial neutrophil infiltration to a more sustained population of mononuclear cells is essential for the resolution of the inflammatory process.
TL;DR: Several microscopic (agent-based) models of financial markets which have been studied by economists and physicists over the last decade: Kim-Markowitz, Levy-Levy-Solomon, Cont-Bouchaud, Solomon-Weisbuch, Lux-Marchesi, Donangelo- Sneppen and Solomon-Lenz-Huang as mentioned in this paper.
Abstract: This review deals with several microscopic (‘agent-based’) models of financial markets which have been studied by economists and physicists over the last decade: Kim–Markowitz, Levy–Levy–Solomon, Cont–Bouchaud, Solomon–Weisbuch, Lux–Marchesi, Donangelo– Sneppen and Solomon–Levy–Huang. After an overview of simulation approaches in financial economics, we first give a summary of the Donangelo–Sneppen model of monetary exchange and compare it with related models in economics literature. Our selective review then outlines the main ingredients of some influential early models of multi-agent dynamics in financial markets (Kim–Markowitz, Levy–Levy–Solomon). As will be seen, these contributions draw their inspiration from the complex appearance of investors’ interactions in real-life markets. Their main aim is to reproduce (and, thereby, provide possible explanations) for the spectacular bubbles and crashes seen in certain historical episodes, but they lack (like almost all the work before 1998 or so) a perspective in terms of the universal statistical features of financial time series. In fact, awareness of a set of such regularities (power-law tails of the distribution of returns, temporal scaling of volatility) only gradually appeared over the nineties. With the more precise description of the formerly relatively vague characteristics (e.g. moving from the notion of fat tails to the more concrete one of a power law with index around three), it became clear that financial market dynamics give rise to some kind of universal scaling law. Showing similarities with scaling laws for other systems with many interacting sub-units, an exploration of financial markets as multi-agent systems appeared to be a natural consequence. This topic has been pursued by quite a number of contributions appearing in both the physics and economics literature since the late nineties. From the wealth of different flavours of multi-agent models that have appeared up to now, we discuss the Cont–Bouchaud, Solomon–Levy–Huang and Lux–Marchesi models. Open research questions are discussed in our concluding section. 4 Now at Deutsche Bundesbank. The opinions expressed in this review are those of the authors, not those of the banks.