ISTOTA SIECI SEMANTYCZNYCH – PUŁAPKI I KORZYŚCI ZASTOSOWANIA W SĄDOWNICTWIE

Semantic Webs increasingly allow the processing of information over the Internet according to their content and purpose. The widespread use of metadata standards has, however, caused interoperability problems between different systems. Enabling users to search for different languages requires translation resources to cross the language barrier can be a serious challenge. The presented tendency to use semantic webs is an opportunity for legislation, facilitating the process of developing and providing legal regula-tions and managing the progress of legislative work and implementation of procedures. The aim of this article is to review semantic web theory in rela-tion to the pitfalls of defining and applying ontology to the machine-based understanding of content stored in the network. The scope of this article is a preliminary analysis of aspects of interdisciplinary cooperation in the metadata creation phase - indexed according to the conceptual analysis (ontology) of a given field. The area of research interest was also the benefits and pitfalls of using open source, XML and the Legal Semantic Web in the common judiciary.Sieci semantyczne (ang. Semantic Web) pozwalają w coraz większym stopniu na przetwarzanie informacji za pośrednictwem Internetu zgodnie z ich zawartością i przeznaczeniem. Rozpowszechnienie standardów metadanych spowodowało jednak problemy z interoperacyjnością między różnymi systemami. Umożliwienie użytkownikom przeszukiwania różnych języków wymaga zasobów tłumaczeniowych, aby przekroczyć barierę językową, może stanowić poważne wyzwanie. Zaprezentowana tendencja do korzystania z sieci semantycznych jest szansą dla prawodawstwa, ułatwiającą procesy opracowania i udostępniania przepisów prawnych oraz zarządzania postępem prac legislacyjnych i realizacji procedur. Celem artykułu jest przegląd teorii sieci semantycznych w odniesieniu do pułapek związanych z definiowaniem i stosowaniem ontologii na potrzeby zrozumienia maszynowego treści przechowywanych w sieci. Zakres artykułu obejmuje wstępną analizę aspektów współpracy grup interdyscyplinarnych na etapie tworzenia metadanych - indeksowane według analiz koncepcyjnych (ontologii) danej dziedziny. Obszarem zainteresowań badawczych były również korzyści i pułapki zastosowania Open- source, XML i Legal Semantic Web w sądownictwie powszechnym

Court Technology jako przykład zastosowania ICT w sądownictwie

Currently, courts in many countries are looking more than ever for ICT applications that would serve to case management and documentation to support their daily activities. The purpose of the article was to present the indicated solutions in the judiciary, which is the Court Technology on the example offered by commercial software company in the US based on the open source model. Significant problems with the possibilities of using such solutions in the judiciary have been only indicated in the article and will provide the basis for further, in-depth research

The etiology of formation and reacting way to a change in the supply chain

Purpose: The aim of this article was to determine the etiological factors of changes occurring in supply chains and to diagnose the reactions to these factors. Design/Methodology/Approach: The study was carried out for separated 19 categories grouping etiological factors. To structure the data in the process of building the categories, a systematic diagram and a code distribution analysis diagram were used. In the next part, when creating the ASPM method, some assumptions of the Scrum and DSDM method were used. Due to the subject matter of the conducted research, it was decided to apply a case study supplemented by a structured interview. The sample consisted of companies conducting business in international supply chains and cooperation with logistics operators, including 4PL. Findings: The results show that the development should be towards a flexible organization. The process of flexible adaptation of an organization that is compound, i.e., the supply chain, to changes of an exo- and endogenous nature requires the operationalization of the entire concept based on the experience in project management, especially due to the non-linearity of emerging interactions within the framework of the change taking place. Practical Implications: Etiology, by focusing on the background of a given phenomenon, fact or process, by isolating etiological factors that cause them, allows us to discover the causes of the existing state of affairs. This applies to virtually every discipline and area of life. Originality/Value: The study identified factors of changes occurring in supply chains and to diagnose the reactions to these factors.peer-reviewe

Mapping of ESE-1 subdomains required to initiate mammary epithelial cell transformation via a cytoplasmic mechanism

<p>Abstract</p> <p>Background</p> <p>The ETS family transcription factor ESE-1 is often overexpressed in human breast cancer. ESE-1 initiates transformation of MCF-12A cells via a non-transcriptional, cytoplasmic process that is mediated by a unique 40-amino acid serine and aspartic acid rich (SAR) subdomain, whereas, ESE-1's nuclear transcriptional property is required to maintain the transformed phenotype of MCF7, ZR-75-1 and T47D breast cancer cells.</p> <p>Results</p> <p>To map the minimal functional nuclear localization (NLS) and nuclear export (NES) signals, we fused in-frame putative NLS and NES motifs between GFP and the SAR domain. Using these GFP constructs as reporters of subcellular localization, we mapped a single NLS to six basic amino acids (²⁴²HGKRRR²⁴⁷) in the AT-hook and two CRM1-dependent NES motifs, one to the pointed domain (NES1: ¹⁰²LCNCALEELRL¹¹²) and another to the DNA binding domain (DBD), (NES2: ²⁷⁵LWEFIRDILI²⁸⁴). Moreover, analysis of a putative NLS located in the DBD (³¹⁶GQKKKNSN³²³) by a similar GFP-SAR reporter or by internal deletion of the DBD, revealed this sequence to lack NLS activity. To assess the role of NES2 in regulating ESE-1 subcellular localization and subsequent transformation potency, we site-specifically mutagenized NES2, within full-length GFP-ESE-1 and GFP-NES2-SAR reporter constructs. These studies show that site-specific mutation of NES2 completely abrogates ESE-1 transforming activity. Furthermore, we show that exclusive cytoplasmic targeting of the SAR domain is sufficient to initiate transformation, and we report that an intact SAR domain is required, since block mutagenesis reveals that an intact SAR domain is necessary to maintain its full transforming potency. Finally, using a monoclonal antibody targeting the SAR domain, we demonstrate that the SAR domain contains a region accessible for protein - protein interactions.</p> <p>Conclusions</p> <p>These data highlight that ESE-1 contains NLS and NES signals that play a critical role in regulating its subcellular localization and function, and that an intact SAR domain mediates MEC transformation exclusively in the cytoplasm, via a novel nontranscriptional mechanism, whereby the SAR motif is accessible for ligand and/or protein interactions. These findings are significant, since they provide novel molecular insights into the functions of ETS transcription factors in mammary cell transformation.</p

Preliminary identification of quantitative factors determining the duration of court proceedings in commercial cases

Purpose: The aim of the article was to identify factors that are linear combinations of the variables under scrutiny that affect the duration of court proceedings. Design/Methodology/Approach: This research was conducted on commercial cases, based on the Principal Components Analysis (PCA). The original variables were grouped into factors that are correlated with each other. The Kaiser Criterion (own value >1) was chosen as the main criterion determining the number of factors. The conducted research was subordinated to six phases, largely linked to the data mining scheme (CRISP-DM). Seven variables of a strict numerical nature marked as (vn) were distinguished from the features describing court proceedings. Findings: Based on the analysis, two main quantitative factors characterising the examined cases were identified. The first factor groups the variables:(v4) Number of hearings in the first instance/second instance, (v5) The number of days from the first hearing to the case being settled, (v6) The judgement in the first instance (number of pages), (v7) Volume of files (number of volumes),and the second one:(v1) The court fee paid, (v2) The value of the subject matter of the dispute, (v3) The number of days to the first hearing. Further research will be conducted into the development of relations between the variables in different areas of their variability, particularly with respect to the value of the matter in dispute. Practical Implications: The identified factors can be used at the micro level, in case management by a judge, at the meso level in case management in court, as well as at the macro level the entire justice system. Originality/Value: The study identified factors that affect the efficiency of court proceedings.peer-reviewe

Differentiated Smooth Muscle Cells Generate a Subpopulation of Resident Vascular Progenitor Cells in the Adventitia Regulated by Klf4

RATIONALE: The vascular adventitia is a complex layer of the vessel wall consisting of vasa vasorum microvessels, nerves, fibroblasts, immune cells, and resident progenitor cells. Adventitial progenitors express the stem cell markers, Sca1 and CD34 (adventitial sca1-positive progenitor cells [AdvSca1]), have the potential to differentiate in vitro into multiple lineages, and potentially contribute to intimal lesions in vivo. OBJECTIVE: Although emerging data support the existence of AdvSca1 cells, the goal of this study was to determine their origin, degree of multipotency and heterogeneity, and contribution to vessel remodeling. METHODS AND RESULTS: Using 2 in vivo fate-mapping approaches combined with a smooth muscle cell (SMC) epigenetic lineage mark, we report that a subpopulation of AdvSca1 cells is generated in situ from differentiated SMCs. Our data establish that the vascular adventitia contains phenotypically distinct subpopulations of progenitor cells expressing SMC, myeloid, and hematopoietic progenitor-like properties and that differentiated SMCs are a source to varying degrees of each subpopulation. SMC-derived AdvSca1 cells exhibit a multipotent phenotype capable of differentiating in vivo into mature SMCs, resident macrophages, and endothelial-like cells. After vascular injury, SMC-derived AdvSca1 cells expand in number and are major contributors to adventitial remodeling. Induction of the transcription factor Klf4 in differentiated SMCs is essential for SMC reprogramming in vivo, whereas in vitro approaches demonstrate that Klf4 is essential for the maintenance of the AdvSca1 progenitor phenotype. CONCLUSIONS: We propose that generation of resident vascular progenitor cells from differentiated SMCs is a normal physiological process that contributes to the vascular stem cell pool and plays important roles in arterial homeostasis and disease

Angiotensin type 1 receptor antagonist losartan, reduces MPTP-induced degeneration of dopaminergic neurons in substantia nigra

BACKGROUND: Recent attention has focused on understanding the role of the brain-renin-angiotensin-system (RAS) in stroke and neurodegenerative diseases. Direct evidence of a role for the brain-RAS in Parkinson's disease (PD) comes from studies demonstrating the neuroprotective effect of RAS inhibitors in several neurotoxin based PD models. In this study, we show that an antagonist of the angiotensin II (Ang II) type 1 (AT(1)) receptor, losartan, protects dopaminergic (DA) neurons against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity both in primary ventral mesencephalic (VM) cultures as well as in the substantia nigra pars compacta (SNpc) of C57BL/6 mice (Fig. 1). RESULTS: In the presence of exogenous Ang II, losartan reduced MPP(+ )(5 μM) induced DA neuronal loss by 72% in vitro. Mice challenged with MPTP showed a 62% reduction in the number of DA neurons in the SNpc and a 71% decrease in tyrosine hydroxylase (TH) immunostaining of the striatum, whereas daily treatment with losartan lessened MPTP-induced loss of DA neurons to 25% and reduced the decrease in striatal TH(+ )immunostaining to 34% of control. CONCLUSION: Our study demonstrates that the brain-RAS plays an important neuroprotective role in the MPTP model of PD and points to AT(1 )receptor as a potential novel target for neuroprotection

Plasma lipid biomarker signatures in squamous carcinoma and adenocarcinoma lung cancer patients

There is a clinical need for reliable biomarkers for lung cancer that permit early diagnosis of the disease and provide prediction of histological phenotype. A prospective study design was used with a study population of patients with suspected lung cancer. Blood samples were collected from 17 patients with histologically confirmed squamous cell lung carcinoma, 17 individuals with adenocarcinoma, and 17 control individuals who did not subsequently have a diagnosis of lung cancer or any other cancer. Blood plasma samples were analysed for their lipid profiles using liquid chromatography coupled with high resolution mass spectrometry. Data were analysed using multivariate statistical methods. There was good separation between histological subtypes and control groups and also between individuals with a subsequent diagnosis of adenocarcinoma and squamous cell carcinoma (sensitivity 80 %, specificity 83 %, Q2 = 0.70). Alterations in the levels of different classes of lipids including triglycerides (TGs), phosphatidylinositols (PIs), phosphatidylcholines (PCs), phosphatidylethanolamines (PEs), free fatty acids, lysophospholipids and sphingolipids were observed in squamous carcinoma and adenocarcinoma lung cancer patients when compared with control patients. In conclusion, this study has identified candidate lipid biomarkers of non-small cell lung cancer patients which may be helpful to indicate the tumour subtype and to differentiate them from patients who do not have lung cancer. Measuring these biomarkers has the potential to improve diagnosis in patients with suspected lung cancer and risk stratification in screening

Activation of PPARγ in Myeloid Cells Promotes Lung Cancer Progression and Metastasis

Activation of peroxisome proliferator-activated receptor-γ (PPARγ) inhibits growth of cancer cells including non-small cell lung cancer (NSCLC). Clinically, use of thiazolidinediones, which are pharmacological activators of PPARγ is associated with a lower risk of developing lung cancer. However, the role of this pathway in lung cancer metastasis has not been examined well. The systemic effect of pioglitazone was examined in two models of lung cancer metastasis in immune-competent mice. In an orthotopic model, murine lung cancer cells implanted into the lungs of syngeneic mice metastasized to the liver and brain. As a second model, cancer cells injected subcutaneously metastasized to the lung. In both models systemic administration of pioglitazone increased the rate of metastasis. Examination of tissues from the orthotopic model demonstrated increased numbers of arginase I-positive macrophages in tumors from pioglitazone-treated animals. In co-culture experiments of cancer cells with bone marrow-derived macrophages, pioglitazone promoted arginase I expression in macrophages and this was dependent on the expression of PPARγ in the macrophages. To assess the contribution of PPARγ in macrophages to cancer progression, experiments were performed in bone marrow-transplanted animals receiving bone marrow from Lys-M-Cre+/PPARγflox/flox mice, in which PPARγ is deleted specifically in myeloid cells (PPARγ-Macneg), or control PPARγflox/flox mice. In both models, mice receiving PPARγ-Macneg bone marrow had a marked decrease in secondary tumors which was not significantly altered by treatment with pioglitazone. This was associated with decreased numbers of arginase I-positive cells in the lung. These data support a model in which activation of PPARγ may have opposing effects on tumor progression, with anti-tumorigenic effects on cancer cells, but pro-tumorigenic effects on cells of the microenvironment, specifically myeloid cells

Benign mammary epithelial cells enhance the transformed phenotype of human breast cancer cells

<p>Abstract</p> <p>Background</p> <p>Recent research has yielded a wealth of data underscoring the key role of the cancer microenvironment, especially immune and stromal cells, in the progression of cancer and the development of metastases. However, the role of adjacent benign epithelial cells, which provide initial cell-cell contacts with cancer cells, in tumor progression has not been thoroughly examined. In this report we addressed the question whether benign MECs alter the transformed phenotype of human breast cancer cells.</p> <p>Methods</p> <p>We used both <it>in vitro </it>and <it>in vivo </it>co-cultivation approaches, whereby we mixed GFP-tagged MCF-10A cells (G2B-10A), as a model of benign mammary epithelial cells (MECs), and RFP-tagged MDA-MB-231-TIAS cells (R2-T1AS), as a model of breast cancer cells.</p> <p>Results</p> <p>The <it>in vitro </it>studies showed that G2B-10A cells increase the colony formation of R2-T1AS cells in both soft agar and clonogenicity assays. Conditioned media derived from G2B-10A cells enhanced colony formation of R2-T1AS cells, whereas prior paraformaldehyde (PFA) fixation of G2B-10A cells abrogated this enhancement effect. Moreover, two other models of benign MECs, MCF-12A and HuMECs, also enhanced R2-T1AS colony growth in soft agar and clonogenicity assays. These data reveal that factors secreted by benign MECs are responsible for the observed enhancement of the R2-T1AS transformed phenotype. To determine whether G2B-10A cells enhance the tumorigenic growth of co-injected R2-T1AS cells <it>in vivo</it>, we used the nude mouse xenograft assay. Co-injecting R2-T1AS cells with G2B-10A cells ± PFA-fixation, revealed that G2B-10A cells promoted a ~3-fold increase in tumor growth, irrespective of PFA pre-treatment. These results indicate that soluble factors secreted by G2B-10A cells play a less important role in promoting R2-T1AS tumorigenesis <it>in vivo</it>, and that additional components are operative in the nude mouse xenograft assay. Finally, using array analysis, we found that both live and PFA-fixed G2B-10A cells induced R2-T1AS cells to secrete specific cytokines (IL-6 and GM-CSF), suggesting that cell-cell contact activates R2-T1AS cells.</p> <p>Conclusions</p> <p>Taken together, these data shift our understanding of adjacent benign epithelial cells in the cancer process, from passive, noncontributory cells to an active and tumor-promoting vicinal cell population that may have significant effects early, when benign cells outnumber malignant cells.</p