Arbitration proceedings in the Czech Republic

The theme of this thesis is the arbitration proceedings in the Czech Republic, which is one of the alternative disputes resolutions. The goal of this thesis is to provide a complete summary of legal regulation of the arbitration proceedings. The thesis is divided into eight chapters. The first three chapters deal with general issues of the arbitration proceedings. The first chapter which is further subdivided into six subchapters is focused on the basic definition of the arbitration proceedings, its theoretical concepts, its advantages and disadvantages, as well as its different types. The second chapter provides a summary mainly of national legal regulation. Chapter three explains the objective conditions under which a certain range of disputes can be heard and decided in the arbitration proceedings, including some specific examples. Chapter four is concerned with the arbitration agreement which is the major institute and the basis condition of the arbitration proceedings. This chapter is subdivided into three subchapters dealing with for example the different types of arbitration agreements, their mandatory requirements and also their invalidity and termination. In a separate subchapter author discusses the arbitration agreement for resolving disputes arising from consumer contracts. Chapter..

Comparison of changes in rheumatologic conditions between the patients with high and low anti-<i>Porphyromonas gingivalis</i> peptidylarginine deiminase (PPAD) immunoglobulin G (IgG) titers.

<p>Comparison of changes in rheumatologic conditions between the patients with high and low anti-<i>Porphyromonas gingivalis</i> peptidylarginine deiminase (PPAD) immunoglobulin G (IgG) titers.</p

Baseline characteristics of the study patients with rheumatoid arthritis (RA).

<p>Baseline characteristics of the study patients with rheumatoid arthritis (RA).</p

Relevance of the serum anti-PPAD IgG levels to changes in the DAS28-CRP and serum anti-CCP IgG levels after 3 and 6 months of bDMARD therapy (A and B).

<p>Relevance of the serum anti-PPAD IgG levels to changes in the DAS28-CRP and serum anti-CCP IgG levels after 3 and 6 months of bDMARD therapy (A and B).</p

Comparison of genotype and allele frequencies of 8 polymorphisms between the patients with high and low anti-<i>Porphyromonas gingivalis</i> peptidylarginine deiminase (PPAD) immunoglobulin G (IgG) titers.

<p>Comparison of genotype and allele frequencies of 8 polymorphisms between the patients with high and low anti-<i>Porphyromonas gingivalis</i> peptidylarginine deiminase (PPAD) immunoglobulin G (IgG) titers.</p

Comparison of characteristics after 6 months of biological disease-modifying antirheumatic drug (bDMARD) therapy between the patients with high and low anti-<i>Porphyromonas gingivalis</i> peptidylarginine deiminase (PPAD) immunoglobulin G (IgG) titers.

<p>Comparison of characteristics after 6 months of biological disease-modifying antirheumatic drug (bDMARD) therapy between the patients with high and low anti-<i>Porphyromonas gingivalis</i> peptidylarginine deiminase (PPAD) immunoglobulin G (IgG) titers.</p

Cumulative proportion of the incidence of hospitalization owing to fractures.

<p>ACEI: angiotensin converting enzyme inhibitor, ARB: angiotensin II receptor blocker.</p

Multivariate-adjusted hazard ratios of hospitalization owing to fractures associated with angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker use considering patients with different levels of parathyroid hormone, sex, or systolic blood pressure.

<p>The hazard ratio was obtained from the Cox regression model adjusted for the distribution of age; sex; duration of dialysis; causes of end-stage kidney disease; body mass index; Kt/V; comorbidity of cardiovascular disease or diabetes mellitus; smoking; history of parathyroidectomy; prescriptions of anti-coagulants, vitamin D receptor activators, and phosphate binders; and serum levels of albumin, calcium, phosphorus, parathyroid hormone, alkaline phosphatase, and blood hemoglobin, in addition to systolic and diastolic blood pressure and the use of antihypertensive drugs (β-blockers, calcium channel blockers, diuretics, and others). P values for interactions were obtained from the likelihood ratio test. CI: confidence interval, HR: hazard ratio, iPTH: intact parathyroid hormone, ACEI: angiotensin-converting enzyme inhibitor, ARB: angiotensin II receptor blocker.</p

Baseline characteristics of the participants.

<p>For continuous variables, median and interquartile ranges (IQR) are shown.</p><p>ACEI: angiotensin converting enzyme inhibitor, ARB: angiotensin II receptor blocker</p><p>Baseline characteristics of the participants.</p

DDX3X Induces Primary EGFR-TKI Resistance Based on Intratumor Heterogeneity in Lung Cancer Cells Harboring EGFR-Activating Mutations

<div><p>The specific mechanisms how lung cancer cells harboring epidermal growth factor receptor (EGFR) activating mutations can survive treatment with EGFR-tyrosine kinase inhibitors (TKIs) until they eventually acquire treatment-resistance genetic mutations are unclear. The phenotypic diversity of cancer cells caused by genetic or epigenetic alterations (intratumor heterogeneity) confers treatment failure and may foster tumor evolution through Darwinian selection. Recently, we found DDX3X as the protein that was preferentially expressed in murine melanoma with cancer stem cell (CSC)-like phenotypes by proteome analysis. In this study, we transfected PC9, human lung cancer cells harboring EGFR exon19 deletion, with cDNA encoding DDX3X and found that DDX3X, an ATP-dependent RNA helicase, induced CSC-like phenotypes and the epithelial-mesenchymal transition (EMT) accompanied with loss of sensitivity to EGFR-TKI. DDX3X expression was associated with upregulation of Sox2 and increase of cancer cells exhibiting CSC-like phenotypes, such as anchorage-independent proliferation, strong expression of CD44, and aldehyde dehydrogenase (ALDH). The EMT with switching from E-cadherin to N-cadherin was also facilitated by DDX3X. Either ligand-independent or ligand-induced EGFR phosphorylation was inhibited in lung cancer cells that strongly expressed DDX3X. Lack of EGFR signal addiction resulted in resistance to EGFR-TKI. Moreover, we found a small nonadherent subpopulation that strongly expressed DDX3X accompanied by the same stem cell-like properties and the EMT in parental PC9 cells. The unique subpopulation lacked EGFR signaling and was highly resistant to EGFR-TKI. In conclusion, our data indicate that DDX3X may play a critical role for inducing phenotypic diversity, and that treatment targeting DDX3X may overcome primary resistance to EGFR-TKI resulting from intratumor heterogeneity.</p></div